A condition of abnormally high level of PHOSPHATES in the blood, usually significantly above the normal range of 0.84-1.58 mmol per liter of serum.
Disorders in the processing of phosphorus in the body: its absorption, transport, storage, and utilization.
Inorganic salts of phosphoric acid.
A non-metal element that has the atomic symbol P, atomic number 15, and atomic weight 31. It is an essential element that takes part in a broad variety of biochemical reactions.
A condition of an abnormally low level of PHOSPHATES in the blood.
A hereditary syndrome clinically similar to HYPOPARATHYROIDISM. It is characterized by HYPOCALCEMIA; HYPERPHOSPHATEMIA; and associated skeletal development impairment and caused by failure of response to PARATHYROID HORMONE rather than deficiencies. A severe form with resistance to multiple hormones is referred to as Type 1a and is associated with maternal mutant allele of the ALPHA CHAIN OF STIMULATORY G PROTEIN.
Abnormally elevated PARATHYROID HORMONE secretion as a response to HYPOCALCEMIA. It is caused by chronic KIDNEY FAILURE or other abnormalities in the controls of bone and mineral metabolism, leading to various BONE DISEASES, such as RENAL OSTEODYSTROPHY.
Inorganic compounds that contain calcium as an integral part of the molecule.
Pathologic deposition of calcium salts in tissues.
Reduction of the blood calcium below normal. Manifestations include hyperactive deep tendon reflexes, Chvostek's sign, muscle and abdominal cramps, and carpopedal spasm. (Dorland, 27th ed)
Decalcification of bone or abnormal bone development due to chronic KIDNEY DISEASES, in which 1,25-DIHYDROXYVITAMIN D3 synthesis by the kidneys is impaired, leading to reduced negative feedback on PARATHYROID HORMONE. The resulting SECONDARY HYPERPARATHYROIDISM eventually leads to bone disorders.
A polypeptide hormone (84 amino acid residues) secreted by the PARATHYROID GLANDS which performs the essential role of maintaining intracellular CALCIUM levels in the body. Parathyroid hormone increases intracellular calcium by promoting the release of CALCIUM from BONE, increases the intestinal absorption of calcium, increases the renal tubular reabsorption of calcium, and increases the renal excretion of phosphates.
A family of small polypeptide growth factors that share several common features including a strong affinity for HEPARIN, and a central barrel-shaped core region of 140 amino acids that is highly homologous between family members. Although originally studied as proteins that stimulate the growth of fibroblasts this distinction is no longer a requirement for membership in the fibroblast growth factor family.
Carbonic acid calcium salt (CaCO3). An odorless, tasteless powder or crystal that occurs in nature. It is used therapeutically as a phosphate buffer in hemodialysis patients and as a calcium supplement.
The end-stage of CHRONIC RENAL INSUFFICIENCY. It is characterized by the severe irreversible kidney damage (as measured by the level of PROTEINURIA) and the reduction in GLOMERULAR FILTRATION RATE to less than 15 ml per min (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002). These patients generally require HEMODIALYSIS or KIDNEY TRANSPLANTATION.
Therapy for the insufficient cleansing of the BLOOD by the kidneys based on dialysis and including hemodialysis, PERITONEAL DIALYSIS, and HEMODIAFILTRATION.
Agents that produce a soft formed stool, and relax and loosen the bowels, typically used over a protracted period, to relieve CONSTIPATION.
Phosphorus used in foods or obtained from food. This element is a major intracellular component which plays an important role in many biochemical pathways relating to normal physiological functions. High concentrations of dietary phosphorus can cause nephrocalcinosis which is associated with impaired kidney function. Low concentrations of dietary phosphorus cause an increase in calcitriol in the blood and osteoporosis.
Lanthanum. The prototypical element in the rare earth family of metals. It has the atomic symbol La, atomic number 57, and atomic weight 138.91. Lanthanide ion is used in experimental biology as a calcium antagonist; lanthanum oxide improves the optical properties of glass.
Polyamines are organic compounds with more than one amino group, involved in various biological processes such as cell growth, differentiation, and apoptosis, and found to be increased in certain diseases including cancer.
Glucuronidase is an enzyme (specifically, a glycosidase) that catalyzes the hydrolysis of glucuronic acid from various substrates, playing crucial roles in metabolic processes like detoxification and biotransformation within organisms.
A sodium-dependent phosphate transporter present primarily at apical sites of EPITHELIAL CELLS in the SMALL INTESTINE.
Pathological processes of the KIDNEY or its component tissues.
Enzymes that catalyze the transfer of N-acetylgalactosamine from a nucleoside diphosphate N-acetylgalactosamine to an acceptor molecule which is frequently another carbohydrate. EC 2.4.1.-.
Conditions in which the KIDNEYS perform below the normal level for more than three months. Chronic kidney insufficiency is classified by five stages according to the decline in GLOMERULAR FILTRATION RATE and the degree of kidney damage (as measured by the level of PROTEINURIA). The most severe form is the end-stage renal disease (CHRONIC KIDNEY FAILURE). (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002)
A condition of abnormally elevated output of PARATHYROID HORMONE (or PTH) triggering responses that increase blood CALCIUM. It is characterized by HYPERCALCEMIA and BONE RESORPTION, eventually leading to bone diseases. PRIMARY HYPERPARATHYROIDISM is caused by parathyroid HYPERPLASIA or PARATHYROID NEOPLASMS. SECONDARY HYPERPARATHYROIDISM is increased PTH secretion in response to HYPOCALCEMIA, usually caused by chronic KIDNEY DISEASES.
A family of symporters that facilitate sodium-dependent membrane transport of phosphate.
A condition caused by a deficiency of PARATHYROID HORMONE (or PTH). It is characterized by HYPOCALCEMIA and hyperphosphatemia. Hypocalcemia leads to TETANY. The acquired form is due to removal or injuries to the PARATHYROID GLANDS. The congenital form is due to mutations of genes, such as TBX1; (see DIGEORGE SYNDROME); CASR encoding CALCIUM-SENSING RECEPTOR; or PTH encoding parathyroid hormone.
Diseases of BONES.
Condition of induced systemic hypersensitivity in which tissues respond to appropriate challenging agents with a sudden local calcification.
A membrane-bound metalloendopeptidase that may play a role in the degradation or activation of a variety of PEPTIDE HORMONES and INTERCELLULAR SIGNALING PEPTIDES AND PROTEINS. Genetic mutations that result in loss of function of this protein are a cause of HYPOPHOSPHATEMIC RICKETS, X-LINKED DOMINANT.
A vitamin that includes both CHOLECALCIFEROLS and ERGOCALCIFEROLS, which have the common effect of preventing or curing RICKETS in animals. It can also be viewed as a hormone since it can be formed in SKIN by action of ULTRAVIOLET RAYS upon the precursors, 7-dehydrocholesterol and ERGOSTEROL, and acts on VITAMIN D RECEPTORS to regulate CALCIUM in opposition to PARATHYROID HORMONE.
A syndrome resulting from cytotoxic therapy, occurring generally in aggressive, rapidly proliferating lymphoproliferative disorders. It is characterized by combinations of hyperuricemia, lactic acidosis, hyperkalemia, hyperphosphatemia and hypocalcemia.
Chemicals that bind to and remove ions from solutions. Many chelating agents function through the formation of COORDINATION COMPLEXES with METALS.
Two pairs of small oval-shaped glands located in the front and the base of the NECK and adjacent to the two lobes of THYROID GLAND. They secrete PARATHYROID HORMONE that regulates the balance of CALCIUM; PHOSPHORUS; and MAGNESIUM in the body.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
Pathological processes involving any of the BLOOD VESSELS in the cardiac or peripheral circulation. They include diseases of ARTERIES; VEINS; and rest of the vasculature system in the body.
The physiologically active form of vitamin D. It is formed primarily in the kidney by enzymatic hydroxylation of 25-hydroxycholecalciferol (CALCIFEDIOL). Its production is stimulated by low blood calcium levels and parathyroid hormone. Calcitriol increases intestinal absorption of calcium and phosphorus, and in concert with parathyroid hormone increases bone resorption.
A family of highly conserved and widely expressed sodium-phosphate cotransporter proteins. They are electrogenic sodium-dependent transporters of phosphate that were originally identified as retroviral receptors in HUMANS and have been described in yeast and many other organisms.
Derivatives of ERGOSTEROL formed by ULTRAVIOLET RAYS breaking of the C9-C10 bond. They differ from CHOLECALCIFEROL in having a double bond between C22 and C23 and a methyl group at C24.
A clinical syndrome associated with the retention of renal waste products or uremic toxins in the blood. It is usually the result of RENAL INSUFFICIENCY. Most uremic toxins are end products of protein or nitrogen CATABOLISM, such as UREA or CREATININE. Severe uremia can lead to multiple organ dysfunctions with a constellation of symptoms.
Derivatives of ACETIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain the carboxymethane structure.
A family of heterotrimeric GTP-binding protein alpha subunits that activate ADENYLYL CYCLASES.
Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care. (Dictionary of Health Services Management, 2d ed)
Abnormally high level of calcium in the blood.
A class of G-protein-coupled receptors that react to varying extracellular CALCIUM levels. Calcium-sensing receptors in the PARATHYROID GLANDS play an important role in the maintenance of calcium HOMEOSTASIS by regulating the release of PARATHYROID HORMONE. They differ from INTRACELLULAR CALCIUM-SENSING PROTEINS which sense intracellular calcium levels.
A specialized CONNECTIVE TISSUE that is the main constituent of the SKELETON. The principle cellular component of bone is comprised of OSTEOBLASTS; OSTEOCYTES; and OSTEOCLASTS, while FIBRILLAR COLLAGENS and hydroxyapatite crystals form the BONE MATRIX.
Two-ring crystalline hydrocarbons isolated from coal tar. They are used as intermediates in chemical synthesis, as insect repellents, fungicides, lubricants, preservatives, and, formerly, as topical antiseptics.
The processes whereby the internal environment of an organism tends to remain balanced and stable.
An enzyme that catalyzes the conversion of an orthophosphoric monoester and water to an alcohol and orthophosphate. EC 3.1.3.1.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.
Creatinine is a waste product that's generated from muscle metabolism, typically filtered through the kidneys and released in urine, with increased levels in blood indicating impaired kidney function.
Elements of limited time intervals, contributing to particular results or situations.
Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.

Left ventricular hypertrophy: is hyperphosphatemia among dialysis patients a risk factor? (1/179)

Cardiovascular disease occurs in ESRD patients at rates that are far higher than is seen in the general population, and cardiovascular deaths account for the majority of deaths among dialysis patients. Abnormal mineral metabolism is a novel cardiovascular risk factor among dialysis patients. Recently published results demonstrated that even with good control of BP and anemia, conventional hemodialysis is associated with significant left ventricular hypertrophy (LVH); however, daily hemodialysis was associated with a significant reduction in LV mass index (LVMI). Furthermore, it was shown that control of serum phosphorus correlates with the reduction in LVMI. These data suggest a novel mechanism for the deleterious effect of elevated serum phosphorus on cardiovascular outcomes among hemodialysis patients: LVH. Other investigators have noted an association of hyperphosphatemia and LVH; however, this study was the first to demonstrate that improvement in serum phosphorus is associated with reduction in LVM. In addition, it is shown that daily hemodialysis is an effective modality in improving serum phosphorus through significantly improved phosphorus removal. Elevated serum phosphorus leads to vascular calcification, which can lead to LVH by decreasing vascular compliance. However, our study showed an improvement in LVMI during a 12-mo period. Because vascular calcification is unlikely to remit over this time period, it is proposed that serum phosphorus has a reversible, cardiotoxic effect that leads to LVH that can be reversed successfully with good control of serum phosphorus.  (+info)

How fibroblast growth factor 23 works. (2/179)

There is a discontinuum of hereditary and acquired disorders of phosphate homeostasis that are caused by either high or low circulating levels of the novel phosphaturic hormone fibroblastic growth factor 23 (FGF23). Disorders that are caused by high circulating levels of FGF23 are characterized by hypophosphatemia, decreased production of 1,25-dihydroxyvitamin D, and rickets/osteomalacia. On the other end of the spectrum are disorders that are caused by low circulating levels of FGF23, which are characterized by hyperphosphatemia, elevated production of 1,25-dihydroxyvitamin D, soft tissue calcifications, and hyperostosis. Knowledge of the genetic basis of these hereditary disorders of phosphate homeostasis and studies of their mouse homologues have uncovered a bone-kidney axis and new systems biology that govern bone mineralization, vitamin D metabolism, parathyroid gland function, and renal phosphate handling. Further understanding of this primary phosphate homeostatic pathway has the potential to have a significant impact on the diagnosis and treatment of disorders of bone and mineral metabolism.  (+info)

High plasma phosphate as a risk factor for decline in renal function and mortality in pre-dialysis patients. (3/179)

BACKGROUND: Hyperphosphataemia is associated with increased mortality in patients with chronic kidney disease (CKD) stage IV or on dialysis. Furthermore, in animal studies, elevated plasma phosphate has been shown to be associated with an accelerated decline in renal function. The aim of this study was to determine the association of plasma phosphate with renal function loss and mortality in CKD stage IV-V pre-dialysis patients with GFR <20 ml/min/1.73 m(2). METHODS: Incident pre-dialysis patients were included between 1999 and 2001 in the multi-centre PREPARE study, and followed until 2003 or death. Rate of decline in renal function for each patient was calculated by linear regression using the Modification of Diet in Renal Disease (MDRD) formula to estimate GFR (eGFR). RESULTS: A total of 448 patients were included [mean (SD) age 60 (15) years, eGFR 13 (5.4) ml/min/1.73 m(2), decline in renal function 0.38 (0.95) ml/min/month]. Phosphate concentration at baseline was 4.71 (1.16) mg/dl, calcium 9.25 (0.77) mg/dl and calcium-phosphate product 43.5 (10.9) mg(2)/dl(2). For each mg/dl higher phosphate concentration, the mean (95% CI) decline in renal function increased with 0.154 (0.071-0.237) ml/min/month. After adjustment, this association remained [beta 0.178 (0.082-0.275)]. Seven percent of the patients died. Crude mortality risk was 1.25 (0.85-1.84) per mg/dl increase in phosphate, which increased to 1.62 (1.02-2.59) after adjustment. CONCLUSIONS: High plasma phosphate is an independent risk factor for a more rapid decline in renal function and a higher mortality during the pre-dialysis phase. Plasma phosphate within the normal range is likely of vital importance in pre-dialysis patients.  (+info)

Economic evaluation of sevelamer in patients with end-stage renal disease. (4/179)

BACKGROUND: There is uncertainty about the most cost-effective way to treat hyperphosphataemia in patients with end-stage renal disease. Methods. We performed an economic analysis which compared the use of sevelamer with calcium carbonate in a simulated cohort of North American dialysis patients, using the perspective of the health care purchaser and a lifetime horizon. Outcomes considered were quality-adjusted life years (QALYs) gained and health care costs. To account for uncertainty, we considered four separate modelling strategies, obtaining data on the relative effectiveness of sevelamer from the recent Dialysis Clinical Outcomes Revisited study. RESULTS: In the base analysis, the use of sevelamer was associated with a cost per QALY gained of CAN$157,00, compared with calcium carbonate. Assuming no survival or hospitalization advantage for sevelamer, use of sevelamer resulted in an incremental cost of CAN$17,00 per patient. In alternate models which assumed sevelamer to be more effective than calcium-based phosphate binders, the use of sevelamer was associated with a cost per QALY gained ranging from CAN$127,00-$278,00. Assuming that sevelamer resulted in a differential reduction in mortality in patients > or = 65 years of age, use of sevelamer in this subgroup was associated with a cost per QALY of CAN$105,500. Results were similar in groups defined by age > or = 55 or by > or = 45 years. Since dialysis is expensive, interventions for dialysis patients that improve survival without reducing the need for dialysis will be associated with a cost-utility ratio at least as great as that of dialysis itself. As such, we repeated the primary analysis excluding the costs of dialysis and transplantation and found that the cost per QALY gained for sevelamer was $77,600. CONCLUSIONS: The cost per QALY gained for treating all dialysis patients with sevelamer exceeds what would usually be considered good value for the money. While the high cost per QALY was in part due to the inclusion of the costs of dialysis and transplant in the analysis, the cost per QALY gained remained relatively unattractive even when these costs were excluded. Although a lower cost per QALY gained is realized when only patients older than 65 years are treated, this strategy remains economically unattractive, particularly given the uncertainty of clinical benefit in this group.  (+info)

Systematic review of the clinical efficacy and safety of sevelamer in dialysis patients. (5/179)

BACKGROUND: The relative effectiveness and safety of sevelamer for treatment of hyperphosphataemia in dialysis patients is uncertain, as compared with calcium-based phosphate binders. METHODS: We conducted a comprehensive search to identify all randomized cross-over or parallel group studies comparing sevelamer to any other therapy or placebo in adult dialysis patients. Study quality was assessed using the Chalmers Index. Data was extracted and checked using a standardized form and combined using a random effects model. RESULTS: We identified 14 primary publications of randomized trials (3193 participants) that were eligible for efficacy analysis. In analyses pooling, the 10 studies reporting on serum phosphate and calcium (2501 participants), serum phosphate was significantly lower with calcium-based phosphate binders by 0.12 mmol/l [95% confidence interval (CI) 0.05-0.19], compared with sevelamer. On-treatment calcium-phosphate product was not significantly lower in patients receiving calcium-based phosphate binders (0.12 mmol(2)/l(2), -0.05 to 0.29), compared with sevelamer. Overall mean difference in serum calcium was significantly lower with sevelamer therapy by 0.10 mmol/l (-0.12 to -0.07) and pooled on-treatment decrease in serum bicarbonate was significantly greater with sevelamer therapy by 2.8 mmol/l (2.2 to -3.5). In the five trials which reported all-cause mortality (2429 participants), the overall risk difference for all cause mortality in these five trials was similar between therapies (-2%, 95% CI -6-2). In the three trials which reported serious adverse events (2185 participants), there was a trend towards a lower risk in patients receiving calcium-based phosphate binders (13% lower, 95% CI -2-29). CONCLUSIONS: Compared with calcium-based phosphate binders, use of sevelamer in dialysis patients is associated with similar to slightly higher phosphate levels, similar calcium phosphate product, and slightly lower serum calcium levels. There was no evidence that sevelamer reduced all-cause mortality, cardiovascular mortality, the frequency of symptomatic bone disease or health-related quality of life.  (+info)

Intraperitoneal calcitriol in infants on peritoneal dialysis. (6/179)

BACKGROUND: Calcitriol has long been used as the main therapy in renal osteodystrophy, but the efficacy of the oral route is not always as high as expected. OBJECTIVE: To asses the safety and efficacy of intraperitoneal calcitriol in infants undergoing peritoneal dialysis (PD). PATIENTS AND METHODS: PD patients on oral calcitriol therapy, with serum parathyroid hormone (PTH) >1000 pg/mL during the previous 3 months of treatment, were switched to intraperitoneal calcitriol therapy, 1 microg twice per week. Dose was increased to 1 microg three times per week if PTH remained >1000 pg/mL, and was later readjusted. Target PTH was 200-300 pg/mL according DOQI guidelines. STATISTICS: All results are expressed as mean +/- SE. The Wilcoxon signed rank test was used to evaluate differences in measurements for each pair of values. The confidence interval for differences between population medians was 96.9%. A p value less than 0.05 was considered significant. RESULTS: Six male children, mean age 17 +/- 3.86 months, completed a 12-month follow-up. Mean pretreatment PTH was 1654 +/- 209 pg/mL. Mean PTH at months 0, 3, 6, 9, and 12 was 1448 +/- 439*, 1277 +/- 723, 910 +/- 704, 582 +/- 282*, and 465 +/- 224* pg/mL, respectively (*p < 0.05). Twelve hypercalcemic and 10 hyperphosphatemic episodes were successfully treated. CONCLUSION: Infants on PD who fail to respond to oral calcitriol therapy can be safely treated with intraperitoneal administration of active vitamin D.  (+info)

Sevelamer hydrochloride in peritoneal dialysis patients: results of a multicenter cross-sectional study. (7/179)

BACKGROUND: Sevelamer hydrochloride is a phosphate binder widely employed in hemodialysis patients. Until now, information about its efficacy and safety in peritoneal dialysis patients has been scarce. PATIENTS AND METHODS: In September 2005 a cross-sectional study of demographic, biochemical, and therapeutic data of patients from 10 peritoneal dialysis units in Catalonia and the Balearic Islands, Spain, was conducted. RESULTS: We analyzed data from 228 patients. At the time of the study, 128 patients (56%) were receiving sevelamer. Patients receiving sevelamer were younger (p < 0.01), showed a longer period of time on dialysis (p < 0.01), and had a lower Charlson Comorbidity Index (p < 0.01). Serum calcium and intact parathyroid hormone levels were not different between the two groups, while phosphate levels <5.5 mg/dL were observed more frequently in patients not receiving sevelamer (79% vs 61%, p < 0.01). Serum total cholesterol (167 +/- 41 vs 189 +/- 42 mg/dL, p < 0.01) and low density lipoprotein (LDL) cholesterol (90 +/- 34 vs 109 +/- 34 mg/dL, p < 0.01), but not high density lipoprotein cholesterol or triglycerides, were lower in sevelamer-treated patients. Moreover, sevelamer-treated patients displayed a higher serum albumin (38 +/- 5 vs 36 +/- 4 g/L, p < 0.01) and a lower C-reactive protein (4.9 +/- 12.8 vs 8.8 +/- 15.7 mg/L, p < 0.01). Blood bicarbonate levels <22 mmol/L were observed more frequently in patients receiving sevelamer (22% vs 5%, p < 0.01). Logistic regression analysis adjusting by confounding variables confirmed that sevelamer therapy was associated with serum total cholesterol <200 mg/dL [relative risk (RR): 2.77, 95% confidence interval (CI): 1.44 - 5.26, p = 0.002] and blood bicarbonate <22 mmol/L (RR: 8.5, 95% CI: 2.6 - 27.0, p < 0.001), but not with serum phosphate >5.5 mg/dL, calcium-phosphate product >55 mg(2)/dL(2), serum albumin <35 g/L, or C-reactive protein >5 mg/L. CONCLUSIONS: This uncontrolled cross-sectional study in peritoneal dialysis patients showed that sevelamer hydrochloride treatment allows an adequate serum phosphate level in about 60% of patients and significantly reduces total and LDL-cholesterol levels. Since this treatment is associated with metabolic acidosis in 22% of patients, we recommend close monitoring of bicarbonate levels in this group of patients until the clinical significance of this result is clarified.  (+info)

Parathyroidectomy as a therapeutic tool for targeting the recommended NKF-K/DOQI ranges for serum calcium, phosphate and parathyroid hormone in dialysis patients. (8/179)

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Hyperphosphatemia is a medical condition characterized by an excessively high level of phosphate (a form of the chemical element phosphorus) in the blood. Phosphate is an important component of various biological molecules, such as DNA, RNA, and ATP, and it plays a crucial role in many cellular processes, including energy metabolism and signal transduction.

In healthy individuals, the concentration of phosphate in the blood is tightly regulated within a narrow range to maintain normal physiological functions. However, when the phosphate level rises above this range (typically defined as a serum phosphate level greater than 4.5 mg/dL or 1.46 mmol/L), it can lead to hyperphosphatemia.

Hyperphosphatemia can result from various underlying medical conditions, including:

* Kidney dysfunction: The kidneys are responsible for filtering excess phosphate out of the blood and excreting it in the urine. When the kidneys fail to function properly, they may be unable to remove enough phosphate, leading to its accumulation in the blood.
* Hypoparathyroidism: The parathyroid glands produce a hormone called parathyroid hormone (PTH), which helps regulate calcium and phosphate levels in the body. In hypoparathyroidism, the production of PTH is insufficient, leading to an increase in phosphate levels.
* Hyperparathyroidism: In contrast, excessive production of PTH can also lead to hyperphosphatemia by increasing the release of phosphate from bones and decreasing its reabsorption in the kidneys.
* Excessive intake of phosphate-rich foods or supplements: Consuming large amounts of phosphate-rich foods, such as dairy products, nuts, and legumes, or taking phosphate supplements can raise blood phosphate levels.
* Tumor lysis syndrome: This is a complication that can occur after the treatment of certain types of cancer, particularly hematological malignancies. The rapid destruction of cancer cells releases large amounts of intracellular contents, including phosphate, into the bloodstream, leading to hyperphosphatemia.
* Rhabdomyolysis: This is a condition in which muscle tissue breaks down, releasing its contents, including phosphate, into the bloodstream. It can be caused by various factors, such as trauma, infection, or drug toxicity.

Hyperphosphatemia can have several adverse effects on the body, including calcification of soft tissues, kidney damage, and metabolic disturbances. Therefore, it is essential to diagnose and manage hyperphosphatemia promptly to prevent complications. Treatment options may include dietary modifications, medications that bind phosphate in the gastrointestinal tract, and dialysis in severe cases.

Phosphorus metabolism disorders refer to a group of conditions that affect the body's ability to properly regulate the levels and utilization of phosphorus. Phosphorus is an essential mineral that plays a critical role in many biological processes, including energy production, bone formation, and nerve function.

Disorders of phosphorus metabolism can result from genetic defects, kidney dysfunction, vitamin D deficiency, or other medical conditions. These disorders can lead to abnormal levels of phosphorus in the blood, which can cause a range of symptoms, including muscle weakness, bone pain, seizures, and respiratory failure.

Examples of phosphorus metabolism disorders include:

1. Hypophosphatemia: This is a condition characterized by low levels of phosphorus in the blood. It can be caused by various factors, such as malnutrition, vitamin D deficiency, and kidney dysfunction.
2. Hyperphosphatemia: This is a condition characterized by high levels of phosphorus in the blood. It can be caused by kidney failure, tumor lysis syndrome, and certain medications.
3. Hereditary hypophosphatemic rickets: This is a genetic disorder that affects the body's ability to regulate vitamin D and phosphorus metabolism. It can lead to weakened bones and skeletal deformities.
4. Oncogenic osteomalacia: This is a rare condition that occurs when tumors produce substances that interfere with phosphorus metabolism, leading to bone pain and weakness.

Treatment for phosphorus metabolism disorders depends on the underlying cause of the disorder and may include dietary changes, supplements, medications, or surgery.

Phosphates, in a medical context, refer to the salts or esters of phosphoric acid. Phosphates play crucial roles in various biological processes within the human body. They are essential components of bones and teeth, where they combine with calcium to form hydroxyapatite crystals. Phosphates also participate in energy transfer reactions as phosphate groups attached to adenosine diphosphate (ADP) and adenosine triphosphate (ATP). Additionally, they contribute to buffer systems that help maintain normal pH levels in the body.

Abnormal levels of phosphates in the blood can indicate certain medical conditions. High phosphate levels (hyperphosphatemia) may be associated with kidney dysfunction, hyperparathyroidism, or excessive intake of phosphate-containing products. Low phosphate levels (hypophosphatemia) might result from malnutrition, vitamin D deficiency, or certain diseases affecting the small intestine or kidneys. Both hypophosphatemia and hyperphosphatemia can have significant impacts on various organ systems and may require medical intervention.

Phosphorus is an essential mineral that is required by every cell in the body for normal functioning. It is a key component of several important biomolecules, including adenosine triphosphate (ATP), which is the primary source of energy for cells, and deoxyribonucleic acid (DNA) and ribonucleic acid (RNA), which are the genetic materials in cells.

Phosphorus is also a major constituent of bones and teeth, where it combines with calcium to provide strength and structure. In addition, phosphorus plays a critical role in various metabolic processes, including energy production, nerve impulse transmission, and pH regulation.

The medical definition of phosphorus refers to the chemical element with the atomic number 15 and the symbol P. It is a highly reactive non-metal that exists in several forms, including white phosphorus, red phosphorus, and black phosphorus. In the body, phosphorus is primarily found in the form of organic compounds, such as phospholipids, phosphoproteins, and nucleic acids.

Abnormal levels of phosphorus in the body can lead to various health problems. For example, high levels of phosphorus (hyperphosphatemia) can occur in patients with kidney disease or those who consume large amounts of phosphorus-rich foods, and can contribute to the development of calcification of soft tissues and cardiovascular disease. On the other hand, low levels of phosphorus (hypophosphatemia) can occur in patients with malnutrition, vitamin D deficiency, or alcoholism, and can lead to muscle weakness, bone pain, and an increased risk of infection.

Hypophosphatemia is a medical condition characterized by abnormally low levels of phosphate (phosphorus) in the blood, specifically below 2.5 mg/dL. Phosphate is an essential electrolyte that plays a crucial role in various bodily functions such as energy production, bone formation, and maintaining acid-base balance.

Hypophosphatemia can result from several factors, including malnutrition, vitamin D deficiency, alcoholism, hormonal imbalances, and certain medications. Symptoms of hypophosphatemia may include muscle weakness, fatigue, bone pain, confusion, and respiratory failure in severe cases. Treatment typically involves correcting the underlying cause and administering phosphate supplements to restore normal levels.

Pseudohypoparathyroidism (PHP) is a rare genetic disorder characterized by the body's resistance to the action of parathyroid hormone (PTH), leading to hypocalcemia (low serum calcium levels) and hyperphosphatemia (high serum phosphate levels). Despite normal or elevated PTH levels, target organs such as the kidneys and bones do not respond appropriately to its actions.

There are several types of PHP, with the most common being type Ia, which is caused by mutations in the GNAS gene. This gene provides instructions for making a protein called the alpha-subunit of the stimulatory G protein (Gs-alpha), which plays a crucial role in transmitting signals within cells. In PHP type Ia, there is a reduced amount or functionally impaired Gs-alpha protein, leading to resistance to PTH and other hormones that use this signaling pathway, such as thyroid-stimulating hormone (TSH) and gonadotropins.

PHP type Ia patients often exhibit physical features known as Albright's hereditary osteodystrophy (AHO), including short stature, round face, obesity, brachydactyly (shortened fingers and toes), and ectopic ossifications (formation of bone in abnormal places). However, it is important to note that not all individuals with AHO have PHP, and not all PHP patients display AHO features.

PHP type Ib is another common form of the disorder, characterized by PTH resistance without the physical manifestations of AHO. This type is caused by mutations in the STX16 gene or other genes involved in the intracellular trafficking of Gs-alpha protein.

Pseudohypoparathyroidism should be differentiated from hypoparathyroidism, a condition where there is an insufficient production or secretion of PTH by the parathyroid glands, leading to similar biochemical abnormalities but without resistance to PTH action.

Secondary hyperparathyroidism is a condition characterized by an overproduction of parathyroid hormone (PTH) from the parathyroid glands due to hypocalcemia (low levels of calcium in the blood). This condition is usually a result of chronic kidney disease, where the kidneys fail to convert vitamin D into its active form, leading to decreased absorption of calcium in the intestines. The body responds by increasing PTH production to maintain normal calcium levels, but over time, this results in high PTH levels and associated complications such as bone disease, kidney stones, and cardiovascular calcification.

Calcium compounds are chemical substances that contain calcium ions (Ca2+) bonded to various anions. Calcium is an essential mineral for human health, and calcium compounds have numerous biological and industrial applications. Here are some examples of calcium compounds with their medical definitions:

1. Calcium carbonate (CaCO3): A common mineral found in rocks and sediments, calcium carbonate is also a major component of shells, pearls, and bones. It is used as a dietary supplement to prevent or treat calcium deficiency and as an antacid to neutralize stomach acid.
2. Calcium citrate (C6H8CaO7): A calcium salt of citric acid, calcium citrate is often used as a dietary supplement to prevent or treat calcium deficiency. It is more soluble in water and gastric juice than calcium carbonate, making it easier to absorb, especially for people with low stomach acid.
3. Calcium gluconate (C12H22CaO14): A calcium salt of gluconic acid, calcium gluconate is used as a medication to treat or prevent hypocalcemia (low blood calcium levels) and hyperkalemia (high blood potassium levels). It can be given intravenously, orally, or topically.
4. Calcium chloride (CaCl2): A white, deliquescent salt, calcium chloride is used as a de-icing agent, a food additive, and a desiccant. In medical settings, it can be used to treat hypocalcemia or hyperkalemia, or as an antidote for magnesium overdose.
5. Calcium lactate (C6H10CaO6): A calcium salt of lactic acid, calcium lactate is used as a dietary supplement to prevent or treat calcium deficiency. It is less commonly used than calcium carbonate or calcium citrate but may be better tolerated by some people.
6. Calcium phosphate (Ca3(PO4)2): A mineral found in rocks and bones, calcium phosphate is used as a dietary supplement to prevent or treat calcium deficiency. It can also be used as a food additive or a pharmaceutical excipient.
7. Calcium sulfate (CaSO4): A white, insoluble powder, calcium sulfate is used as a desiccant, a plaster, and a fertilizer. In medical settings, it can be used to treat hypocalcemia or as an antidote for magnesium overdose.
8. Calcium hydroxide (Ca(OH)2): A white, alkaline powder, calcium hydroxide is used as a disinfectant, a flocculant, and a building material. In medical settings, it can be used to treat hyperkalemia or as an antidote for aluminum overdose.
9. Calcium acetate (Ca(C2H3O2)2): A white, crystalline powder, calcium acetate is used as a food additive and a medication. It can be used to treat hyperphosphatemia (high blood phosphate levels) in patients with kidney disease.
10. Calcium carbonate (CaCO3): A white, chalky powder, calcium carbonate is used as a dietary supplement, a food additive, and a pharmaceutical excipient. It can also be used as a building material and a mineral supplement.

Calcinosis is a medical condition characterized by the abnormal deposit of calcium salts in various tissues of the body, commonly under the skin or in the muscles and tendons. These calcium deposits can form hard lumps or nodules that can cause pain, inflammation, and restricted mobility. Calcinosis can occur as a complication of other medical conditions, such as autoimmune disorders, kidney disease, and hypercalcemia (high levels of calcium in the blood). In some cases, the cause of calcinosis may be unknown. Treatment for calcinosis depends on the underlying cause and may include medications to manage calcium levels, physical therapy, and surgical removal of large deposits.

Hypocalcemia is a medical condition characterized by an abnormally low level of calcium in the blood. Calcium is a vital mineral that plays a crucial role in various bodily functions, including muscle contraction, nerve impulse transmission, and bone formation. Normal calcium levels in the blood usually range from 8.5 to 10.2 milligrams per deciliter (mg/dL). Hypocalcemia is typically defined as a serum calcium level below 8.5 mg/dL or, when adjusted for albumin (a protein that binds to calcium), below 8.4 mg/dL (ionized calcium).

Hypocalcemia can result from several factors, such as vitamin D deficiency, hypoparathyroidism (underactive parathyroid glands), kidney dysfunction, certain medications, and severe magnesium deficiency. Symptoms of hypocalcemia may include numbness or tingling in the fingers, toes, or lips; muscle cramps or spasms; seizures; and, in severe cases, cognitive impairment or cardiac arrhythmias. Treatment typically involves correcting the underlying cause and administering calcium and vitamin D supplements to restore normal calcium levels in the blood.

Renal osteodystrophy is a bone disease that occurs in individuals with chronic kidney disease (CKD). It is characterized by abnormalities in the bones' structure and mineral composition due to disturbances in the metabolism of calcium, phosphorus, and vitamin D. These metabolic disturbances result from the kidneys' decreased ability to maintain balance in the levels of these minerals and hormones.

Renal osteodystrophy can manifest as several bone disorders, including:

1. Osteitis fibrosa cystica: Increased bone turnover due to excessive parathyroid hormone (PTH) production, leading to high levels of alkaline phosphatase and increased resorption of bones.
2. Adynamic bone disease: Decreased bone turnover due to reduced PTH levels, resulting in low bone formation rates and increased fracture risk.
3. Mixed uremic osteodystrophy: A combination of high and low bone turnover, with varying degrees of mineralization defects.
4. Osteomalacia: Defective mineralization of bones due to vitamin D deficiency or resistance, leading to soft and weak bones.

Symptoms of renal osteodystrophy may include bone pain, muscle weakness, fractures, deformities, and growth retardation in children. Diagnosis typically involves laboratory tests, imaging studies, and sometimes bone biopsies. Treatment focuses on correcting the metabolic imbalances through dietary modifications, medications (such as phosphate binders, vitamin D analogs, and calcimimetics), and addressing any secondary hyperparathyroidism if present.

Parathyroid hormone (PTH) is a polypeptide hormone that plays a crucial role in the regulation of calcium and phosphate levels in the body. It is produced and secreted by the parathyroid glands, which are four small endocrine glands located on the back surface of the thyroid gland.

The primary function of PTH is to maintain normal calcium levels in the blood by increasing calcium absorption from the gut, mobilizing calcium from bones, and decreasing calcium excretion by the kidneys. PTH also increases phosphate excretion by the kidneys, which helps to lower serum phosphate levels.

In addition to its role in calcium and phosphate homeostasis, PTH has been shown to have anabolic effects on bone tissue, stimulating bone formation and preventing bone loss. However, chronic elevations in PTH levels can lead to excessive bone resorption and osteoporosis.

Overall, Parathyroid Hormone is a critical hormone that helps maintain mineral homeostasis and supports healthy bone metabolism.

Fibroblast Growth Factors (FGFs) are a family of growth factors that play crucial roles in various biological processes, including cell survival, proliferation, migration, and differentiation. They bind to specific tyrosine kinase receptors (FGFRs) on the cell surface, leading to intracellular signaling cascades that regulate gene expression and downstream cellular responses. FGFs are involved in embryonic development, tissue repair, and angiogenesis (the formation of new blood vessels). There are at least 22 distinct FGFs identified in humans, each with unique functions and patterns of expression. Some FGFs, like FGF1 and FGF2, have mitogenic effects on fibroblasts and other cell types, while others, such as FGF7 and FGF10, are essential for epithelial-mesenchymal interactions during organ development. Dysregulation of FGF signaling has been implicated in various pathological conditions, including cancer, fibrosis, and developmental disorders.

Calcium carbonate is a chemical compound with the formula CaCO3. It is a common substance found in rocks and in the shells of many marine animals. As a mineral, it is known as calcite or aragonite.

In the medical field, calcium carbonate is often used as a dietary supplement to prevent or treat calcium deficiency. It is also commonly used as an antacid to neutralize stomach acid and relieve symptoms of heartburn, acid reflux, and indigestion.

Calcium carbonate works by reacting with hydrochloric acid in the stomach to form water, carbon dioxide, and calcium chloride. This reaction helps to raise the pH level in the stomach and neutralize excess acid.

It is important to note that excessive use of calcium carbonate can lead to hypercalcemia, a condition characterized by high levels of calcium in the blood, which can cause symptoms such as nausea, vomiting, constipation, confusion, and muscle weakness. Therefore, it is recommended to consult with a healthcare provider before starting any new supplement regimen.

Chronic kidney failure, also known as chronic kidney disease (CKD) stage 5 or end-stage renal disease (ESRD), is a permanent loss of kidney function that occurs gradually over a period of months to years. It is defined as a glomerular filtration rate (GFR) of less than 15 ml/min, which means the kidneys are filtering waste and excess fluids at less than 15% of their normal capacity.

CKD can be caused by various underlying conditions such as diabetes, hypertension, glomerulonephritis, polycystic kidney disease, and recurrent kidney infections. Over time, the damage to the kidneys can lead to a buildup of waste products and fluids in the body, which can cause a range of symptoms including fatigue, weakness, shortness of breath, nausea, vomiting, and confusion.

Treatment for chronic kidney failure typically involves managing the underlying condition, making lifestyle changes such as following a healthy diet, and receiving supportive care such as dialysis or a kidney transplant to replace lost kidney function.

Renal dialysis is a medical procedure that is used to artificially remove waste products, toxins, and excess fluids from the blood when the kidneys are no longer able to perform these functions effectively. This process is also known as hemodialysis.

During renal dialysis, the patient's blood is circulated through a special machine called a dialyzer or an artificial kidney, which contains a semi-permeable membrane that filters out waste products and excess fluids from the blood. The cleaned blood is then returned to the patient's body.

Renal dialysis is typically recommended for patients with advanced kidney disease or kidney failure, such as those with end-stage renal disease (ESRD). It is a life-sustaining treatment that helps to maintain the balance of fluids and electrolytes in the body, prevent the buildup of waste products and toxins, and control blood pressure.

There are two main types of renal dialysis: hemodialysis and peritoneal dialysis. Hemodialysis is the most common type and involves using a dialyzer to filter the blood outside the body. Peritoneal dialysis, on the other hand, involves placing a catheter in the abdomen and using the lining of the abdomen (peritoneum) as a natural filter to remove waste products and excess fluids from the body.

Overall, renal dialysis is an essential treatment option for patients with kidney failure, helping them to maintain their quality of life and prolong their survival.

Laxatives are substances or medications that are used to promote bowel movements or loosen the stools, thereby helping in the treatment of constipation. They work by increasing the amount of water in the stool or stimulating the muscles in the intestines to contract and push the stool through. Laxatives can be categorized into several types based on their mechanism of action, including bulk-forming laxatives, lubricant laxatives, osmotic laxatives, saline laxatives, stimulant laxatives, and stool softeners. It is important to use laxatives only as directed by a healthcare professional, as overuse or misuse can lead to serious health complications.

Dietary Phosphorus is a mineral that is an essential nutrient for human health. It is required for the growth, maintenance, and repair of body tissues, including bones and teeth. Phosphorus is also necessary for the production of energy, the formation of DNA and RNA, and the regulation of various physiological processes.

In the diet, phosphorus is primarily found in protein-containing foods such as meat, poultry, fish, dairy products, legumes, and nuts. It can also be found in processed foods that contain additives such as phosphoric acid, which is used to enhance flavor or as a preservative.

The recommended daily intake of phosphorus for adults is 700 milligrams (mg) per day. However, it's important to note that excessive intake of phosphorus, particularly from supplements and fortified foods, can lead to health problems such as kidney damage and calcification of soft tissues. Therefore, it's recommended to obtain phosphorus primarily from whole foods rather than supplements.

Lanthanum is not a medical term itself, but it is a chemical element with the symbol "La" and atomic number 57. It is a soft, ductile, silvery-white metal that belongs to the lanthanide series in the periodic table.

However, in medical contexts, lanthanum may be mentioned as a component of certain medications or medical devices. For example, lanthanum carbonate (trade name Fosrenol) is a medication used to treat hyperphosphatemia (elevated levels of phosphate in the blood) in patients with chronic kidney disease. Lanthanum carbonate works by binding to phosphate in the gastrointestinal tract, preventing its absorption into the bloodstream.

It is important to note that lanthanum compounds are not biologically active and do not have any specific medical effects on their own. Any medical uses of lanthanum are related to its physical or chemical properties, rather than its biological activity.

Polyamines are organic compounds with more than one amino group (-NH2) and at least one carbon atom bonded to two or more amino groups. They are found in various tissues and fluids of living organisms and play important roles in many biological processes, such as cell growth, differentiation, and apoptosis (programmed cell death). Polyamines are also involved in the regulation of ion channels and transporters, DNA replication and gene expression. The most common polyamines found in mammalian cells are putrescine, spermidine, and spermine. They are derived from the decarboxylation of amino acids such as ornithine and methionine. Abnormal levels of polyamines have been associated with various pathological conditions, including cancer and neurodegenerative diseases.

Glucuronidase is an enzyme that catalyzes the hydrolysis of glucuronic acid from various substrates, including molecules that have been conjugated with glucuronic acid as part of the detoxification process in the body. This enzyme plays a role in the breakdown and elimination of certain drugs, toxins, and endogenous compounds, such as bilirubin. It is found in various tissues and organisms, including humans, bacteria, and insects. In clinical contexts, glucuronidase activity may be measured to assess liver function or to identify the presence of certain bacterial infections.

Sodium-phosphate cotransporter proteins, type IIb (NaPi-IIb), are membrane transport proteins found in the kidney's brush border membrane of proximal tubule cells. They play a crucial role in reabsorbing inorganic phosphate from the primary urine back into the bloodstream. These cotransporters facilitate the active transport of phosphate ions (PO4^3-) coupled with sodium ions (Na+) through the cell membrane, using the energy derived from the electrochemical gradient of sodium ions.

Type IIb sodium-phosphate cotransporters are specifically expressed in the kidney and contribute to maintaining phosphate homeostasis in the body. Disorders in NaPi-IIb function can lead to abnormal phosphate levels, which may be associated with various medical conditions such as hypophosphatemia or hyperphosphatemia.

Kidney disease, also known as nephropathy or renal disease, refers to any functional or structural damage to the kidneys that impairs their ability to filter blood, regulate electrolytes, produce hormones, and maintain fluid balance. This damage can result from a wide range of causes, including diabetes, hypertension, glomerulonephritis, polycystic kidney disease, lupus, infections, drugs, toxins, and congenital or inherited disorders.

Depending on the severity and progression of the kidney damage, kidney diseases can be classified into two main categories: acute kidney injury (AKI) and chronic kidney disease (CKD). AKI is a sudden and often reversible loss of kidney function that occurs over hours to days, while CKD is a progressive and irreversible decline in kidney function that develops over months or years.

Symptoms of kidney diseases may include edema, proteinuria, hematuria, hypertension, electrolyte imbalances, metabolic acidosis, anemia, and decreased urine output. Treatment options depend on the underlying cause and severity of the disease and may include medications, dietary modifications, dialysis, or kidney transplantation.

N-Acetylgalactosaminyltransferases (GalNAc-Ts) are a family of enzymes that play a crucial role in the process of protein glycosylation. Protein glycosylation is the attachment of carbohydrate groups, also known as glycans, to proteins. This modification significantly influences various biological processes such as protein folding, stability, trafficking, and recognition.

GalNAc-Ts specifically catalyze the transfer of N-acetylgalactosamine (GalNAc) from a donor molecule, UDP-GalNAc, to serine or threonine residues on acceptor proteins. This initial step of adding GalNAc to proteins is called mucin-type O-glycosylation and sets the stage for further glycan additions by other enzymes.

There are at least 20 different isoforms of GalNAc-Ts identified in humans, each with distinct substrate specificities, tissue distributions, and subcellular localizations. Aberrant expression or dysfunction of these enzymes has been implicated in various diseases, including cancer, where altered glycosylation patterns contribute to tumor progression and metastasis.

Chronic Renal Insufficiency (CRI) is a medical condition characterized by a gradual and progressive loss of kidney function over a period of months or years. It is also known as Chronic Kidney Disease (CKD). The main function of the kidneys is to filter waste products and excess fluids from the blood, which are then excreted in the urine. When the kidneys become insufficient, these waste products and fluids accumulate in the body, leading to various complications.

CRI is defined as a glomerular filtration rate (GFR) of less than 60 ml/min/1.73m2 for three months or more, regardless of cause. GFR is a measure of kidney function that estimates how well the kidneys are filtering waste products from the blood. The condition is classified into five stages based on the severity of the disease and the GFR value.

Stage 1: GFR greater than or equal to 90 ml/min/1.73m2
Stage 2: GFR between 60-89 ml/min/1.73m2
Stage 3: GFR between 30-59 ml/min/1.73m2
Stage 4: GFR between 15-29 ml/min/1.73m2
Stage 5: GFR less than 15 ml/min/1.73m2 or dialysis

CRI can be caused by various underlying conditions such as diabetes, hypertension, glomerulonephritis, polycystic kidney disease, and other genetic or acquired disorders. Symptoms of CRI may include fatigue, weakness, loss of appetite, swelling in the legs and ankles, shortness of breath, and changes in urination patterns. Treatment for CRI focuses on slowing down the progression of the disease, managing symptoms, and preventing complications. This may involve lifestyle modifications, medication, dialysis, or kidney transplantation.

Hyperparathyroidism is a condition in which the parathyroid glands produce excessive amounts of parathyroid hormone (PTH). There are four small parathyroid glands located in the neck, near or within the thyroid gland. They release PTH into the bloodstream to help regulate the levels of calcium and phosphorus in the body.

In hyperparathyroidism, overproduction of PTH can lead to an imbalance in these minerals, causing high blood calcium levels (hypercalcemia) and low phosphate levels (hypophosphatemia). This can result in various symptoms such as fatigue, weakness, bone pain, kidney stones, and cognitive issues.

There are two types of hyperparathyroidism: primary and secondary. Primary hyperparathyroidism occurs when there is a problem with one or more of the parathyroid glands, causing them to become overactive and produce too much PTH. Secondary hyperparathyroidism develops as a response to low calcium levels in the body due to conditions like vitamin D deficiency, chronic kidney disease, or malabsorption syndromes.

Treatment for hyperparathyroidism depends on the underlying cause and severity of symptoms. In primary hyperparathyroidism, surgery to remove the overactive parathyroid gland(s) is often recommended. For secondary hyperparathyroidism, treating the underlying condition and managing calcium levels with medications or dietary changes may be sufficient.

Sodium-phosphate cotransporter proteins are membrane transport proteins that facilitate the active transport of sodium and inorganic phosphate ions across biological membranes. These proteins play a crucial role in maintaining phosphate homeostasis within the body by regulating the absorption and excretion of phosphate in the kidneys and intestines. They exist in two major types, type I (NaPi-I) and type II (NaPi-II), each having multiple subtypes with distinct tissue distributions and regulatory mechanisms.

Type I sodium-phosphate cotransporters are primarily expressed in the kidney's proximal tubules and play a significant role in reabsorbing phosphate from the primary urine back into the bloodstream. Type II sodium-phosphate cotransporters, on the other hand, are found in both the kidneys and intestines. In the kidneys, they contribute to phosphate reabsorption, while in the intestines, they facilitate phosphate absorption from food.

These proteins function by coupling the passive downhill movement of sodium ions (driven by the electrochemical gradient) with the active uphill transport of phosphate ions against their concentration gradient. This coupled transport process enables cells to maintain intracellular phosphate concentrations within a narrow range, despite fluctuations in dietary intake and renal function.

Dysregulation of sodium-phosphate cotransporter proteins has been implicated in various pathological conditions, such as chronic kidney disease (CKD), tumoral calcinosis, and certain genetic disorders affecting phosphate homeostasis.

Hypoparathyroidism is a medical condition characterized by decreased levels or insufficient function of parathyroid hormone (PTH), which is produced and released by the parathyroid glands. These glands are located in the neck, near the thyroid gland, and play a crucial role in regulating calcium and phosphorus levels in the body.

In hypoparathyroidism, low PTH levels result in decreased absorption of calcium from the gut, increased excretion of calcium through the kidneys, and impaired regulation of bone metabolism. This leads to low serum calcium levels (hypocalcemia) and high serum phosphorus levels (hyperphosphatemia).

Symptoms of hypoparathyroidism can include muscle cramps, spasms, or tetany (involuntary muscle contractions), numbness or tingling sensations in the fingers, toes, and around the mouth, fatigue, weakness, anxiety, cognitive impairment, and in severe cases, seizures. Hypoparathyroidism can be caused by various factors, including surgical removal or damage to the parathyroid glands, autoimmune disorders, radiation therapy, genetic defects, or low magnesium levels. Treatment typically involves calcium and vitamin D supplementation to maintain normal serum calcium levels and alleviate symptoms. In some cases, recombinant PTH (Natpara) may be prescribed as well.

Bone diseases is a broad term that refers to various medical conditions that affect the bones. These conditions can be categorized into several groups, including:

1. Developmental and congenital bone diseases: These are conditions that affect bone growth and development before or at birth. Examples include osteogenesis imperfecta (brittle bone disease), achondroplasia (dwarfism), and cleidocranial dysostosis.
2. Metabolic bone diseases: These are conditions that affect the body's ability to maintain healthy bones. They are often caused by hormonal imbalances, vitamin deficiencies, or problems with mineral metabolism. Examples include osteoporosis, osteomalacia, and Paget's disease of bone.
3. Inflammatory bone diseases: These are conditions that cause inflammation in the bones. They can be caused by infections, autoimmune disorders, or other medical conditions. Examples include osteomyelitis, rheumatoid arthritis, and ankylosing spondylitis.
4. Degenerative bone diseases: These are conditions that cause the bones to break down over time. They can be caused by aging, injury, or disease. Examples include osteoarthritis, avascular necrosis, and diffuse idiopathic skeletal hyperostosis (DISH).
5. Tumors and cancers of the bone: These are conditions that involve abnormal growths in the bones. They can be benign or malignant. Examples include osteosarcoma, chondrosarcoma, and Ewing sarcoma.
6. Fractures and injuries: While not strictly a "disease," fractures and injuries are common conditions that affect the bones. They can result from trauma, overuse, or weakened bones. Examples include stress fractures, compound fractures, and dislocations.

Overall, bone diseases can cause a wide range of symptoms, including pain, stiffness, deformity, and decreased mobility. Treatment for these conditions varies depending on the specific diagnosis but may include medication, surgery, physical therapy, or lifestyle changes.

Calciphylaxis is a rare but serious medical condition characterized by the formation of calcium deposits in small blood vessels and surrounding tissues, particularly in the skin and fatty tissue beneath the skin. This can lead to tissue death (necrosis) and ulceration, often resulting in severe pain, infection, and other complications.

Calciphylaxis is most commonly seen in patients with chronic kidney disease or end-stage renal failure, although it has also been reported in patients with normal kidney function. Other risk factors include obesity, female gender, diabetes, and use of warfarin or corticosteroids.

The exact cause of calciphylaxis is not fully understood, but it is believed to involve a combination of factors such as abnormal mineral metabolism, inflammation, and vascular injury. Treatment typically involves addressing any underlying medical conditions, wound care, and sometimes surgical debridement or skin grafting. In some cases, medications such as sodium thiosulfate or bisphosphonates may be used to help dissolve the calcium deposits and improve symptoms.

PHEX (Phosphate Regulating Endopeptidase Homolog, X-Linked) is a gene that encodes for an enzyme called phosphate regulating neutral endopeptidase. This enzyme is primarily expressed in osteoblasts, which are cells responsible for bone formation.

The main function of the PHEX protein is to regulate the levels of a hormone called fibroblast growth factor 23 (FGF23) by breaking it down. FGF23 plays an essential role in maintaining phosphate homeostasis by regulating its reabsorption in the kidneys and its absorption from the gut.

Inactivating mutations in the PHEX gene can lead to X-linked hypophosphatemia (XLH), a genetic disorder characterized by low levels of phosphate in the blood, impaired bone mineralization, and rickets. In XLH, the production of FGF23 is increased due to the lack of regulation by PHEX, leading to excessive excretion of phosphate in the urine and decreased absorption from the gut. This results in hypophosphatemia, impaired bone mineralization, and other skeletal abnormalities.

Vitamin D is a fat-soluble secosteroid that is crucial for the regulation of calcium and phosphate levels in the body, which are essential for maintaining healthy bones and teeth. It can be synthesized by the human body when skin is exposed to ultraviolet-B (UVB) rays from sunlight, or it can be obtained through dietary sources such as fatty fish, fortified dairy products, and supplements. There are two major forms of vitamin D: vitamin D2 (ergocalciferol), which is found in some plants and fungi, and vitamin D3 (cholecalciferol), which is produced in the skin or obtained from animal-derived foods. Both forms need to undergo two hydroxylations in the body to become biologically active as calcitriol (1,25-dihydroxyvitamin D3), the hormonally active form of vitamin D. This activated form exerts its effects by binding to the vitamin D receptor (VDR) found in various tissues, including the small intestine, bone, kidney, and immune cells, thereby influencing numerous physiological processes such as calcium homeostasis, bone metabolism, cell growth, and immune function.

Tumor Lysis Syndrome (TLS) is a metabolic complication that can occur following the rapid destruction of malignant cells, most commonly seen in hematologic malignancies such as acute leukemias and high-grade non-Hodgkin lymphomas. The rapid breakdown of these cancer cells releases a large amount of intracellular contents, including potassium, phosphorus, and nucleic acids, into the bloodstream.

This sudden influx of substances can lead to three major metabolic abnormalities: hyperkalemia (elevated potassium levels), hyperphosphatemia (elevated phosphate levels), and hypocalcemia (low calcium levels). Hyperuricemia (elevated uric acid levels) may also occur due to the breakdown of nucleic acids. These metabolic disturbances can cause various clinical manifestations, such as cardiac arrhythmias, seizures, renal failure, and even death if not promptly recognized and treated.

TLS is classified into two types: laboratory TLS (LTLS) and clinical TLS (CTLS). LTLS is defined by the presence of abnormal laboratory values without any related clinical symptoms, while CTLS is characterized by laboratory abnormalities accompanied by clinical signs or symptoms. Preventive measures, such as aggressive hydration, urinary alkalinization, and prophylactic medications to lower uric acid levels, are often employed in high-risk patients to prevent the development of TLS.

Chelating agents are substances that can bind and form stable complexes with certain metal ions, preventing them from participating in chemical reactions. In medicine, chelating agents are used to remove toxic or excessive amounts of metal ions from the body. For example, ethylenediaminetetraacetic acid (EDTA) is a commonly used chelating agent that can bind with heavy metals such as lead and mercury, helping to eliminate them from the body and reduce their toxic effects. Other chelating agents include dimercaprol (BAL), penicillamine, and deferoxamine. These agents are used to treat metal poisoning, including lead poisoning, iron overload, and copper toxicity.

The parathyroid glands are four small endocrine glands located in the neck, usually near or behind the thyroid gland. They secrete parathyroid hormone (PTH), which plays a critical role in regulating calcium and phosphate levels in the blood and bones. PTH helps maintain the balance of these minerals by increasing the absorption of calcium from food in the intestines, promoting reabsorption of calcium in the kidneys, and stimulating the release of calcium from bones when needed. Additionally, PTH decreases the excretion of calcium through urine and reduces phosphate reabsorption in the kidneys, leading to increased phosphate excretion. Disorders of the parathyroid glands can result in conditions such as hyperparathyroidism (overactive glands) or hypoparathyroidism (underactive glands), which can have significant impacts on calcium and phosphate homeostasis and overall health.

Calcium is an essential mineral that is vital for various physiological processes in the human body. The medical definition of calcium is as follows:

Calcium (Ca2+) is a crucial cation and the most abundant mineral in the human body, with approximately 99% of it found in bones and teeth. It plays a vital role in maintaining structural integrity, nerve impulse transmission, muscle contraction, hormonal secretion, blood coagulation, and enzyme activation.

Calcium homeostasis is tightly regulated through the interplay of several hormones, including parathyroid hormone (PTH), calcitonin, and vitamin D. Dietary calcium intake, absorption, and excretion are also critical factors in maintaining optimal calcium levels in the body.

Hypocalcemia refers to low serum calcium levels, while hypercalcemia indicates high serum calcium levels. Both conditions can have detrimental effects on various organ systems and require medical intervention to correct.

Vascular diseases are medical conditions that affect the circulatory system, specifically the blood vessels (arteries, veins, and capillaries). These diseases can include conditions such as:

1. Atherosclerosis: The buildup of fats, cholesterol, and other substances in and on the walls of the arteries, which can restrict blood flow.
2. Peripheral Artery Disease (PAD): A condition caused by atherosclerosis where there is narrowing or blockage of the peripheral arteries, most commonly in the legs. This can lead to pain, numbness, and cramping.
3. Coronary Artery Disease (CAD): Atherosclerosis of the coronary arteries that supply blood to the heart muscle. This can lead to chest pain, shortness of breath, or a heart attack.
4. Carotid Artery Disease: Atherosclerosis of the carotid arteries in the neck that supply blood to the brain. This can increase the risk of stroke.
5. Cerebrovascular Disease: Conditions that affect blood flow to the brain, including stroke and transient ischemic attack (TIA or "mini-stroke").
6. Aneurysm: A weakened area in the wall of a blood vessel that causes it to bulge outward and potentially rupture.
7. Deep Vein Thrombosis (DVT): A blood clot that forms in the deep veins, usually in the legs, which can cause pain, swelling, and increased risk of pulmonary embolism if the clot travels to the lungs.
8. Varicose Veins: Swollen, twisted, and often painful veins that have filled with an abnormal collection of blood, usually appearing in the legs.
9. Vasculitis: Inflammation of the blood vessels, which can cause damage and narrowing, leading to reduced blood flow.
10. Raynaud's Phenomenon: A condition where the small arteries that supply blood to the skin become narrowed, causing decreased blood flow, typically in response to cold temperatures or stress.

These are just a few examples of vascular conditions that fall under the umbrella term "cerebrovascular disease." Early diagnosis and treatment can significantly improve outcomes for many of these conditions.

Calcitriol is the active form of vitamin D, also known as 1,25-dihydroxyvitamin D. It is a steroid hormone that plays a crucial role in regulating calcium and phosphate levels in the body to maintain healthy bones. Calcitriol is produced in the kidneys from its precursor, calcidiol (25-hydroxyvitamin D), which is derived from dietary sources or synthesized in the skin upon exposure to sunlight.

Calcitriol promotes calcium absorption in the intestines, helps regulate calcium and phosphate levels in the kidneys, and stimulates bone cells (osteoblasts) to form new bone tissue while inhibiting the activity of osteoclasts, which resorb bone. This hormone is essential for normal bone mineralization and growth, as well as for preventing hypocalcemia (low calcium levels).

In addition to its role in bone health, calcitriol has various other physiological functions, including modulating immune responses, cell proliferation, differentiation, and apoptosis. Calcitriol deficiency or resistance can lead to conditions such as rickets in children and osteomalacia or osteoporosis in adults.

Sodium-phosphate cotransporter proteins, type III (NPTIII), are a subfamily of sodium-dependent phosphate transporters that play a crucial role in the regulation of phosphate homeostasis within the body. They are located primarily in the proximal tubule cells of the kidney and facilitate the active transport of inorganic phosphate (Pi) from the lumen into the cell, coupled with the movement of sodium ions (Na+) in the same direction.

The type III sodium-phosphate cotransporters consist of two isoforms, NaPi-IIa and NaPi-IIc, which are encoded by the SLC34A1 and SLC34A3 genes, respectively. These proteins have a molecular weight of approximately 80-90 kDa and contain 13 transmembrane domains, with both the N- and C-termini located intracellularly.

NaPi-IIa is responsible for the majority of sodium-dependent phosphate reabsorption in the kidney, while NaPi-IIc plays a modulatory role under conditions of high dietary phosphate intake or during development. Dysregulation of these cotransporters has been implicated in various pathological conditions, such as chronic kidney disease (CKD), tumoral calcinosis, and certain forms of hypophosphatemic rickets.

In summary, sodium-phosphate cotransporter proteins, type III, are essential for maintaining phosphate balance by mediating the active reabsorption of inorganic phosphate from the kidney tubular lumen into the bloodstream.

Ergocalciferols are a form of vitamin D, specifically vitamin D2, that is found in some plants. They are not produced by the human body and must be obtained through diet or supplementation. Ergocalciferols can be converted into an active form of vitamin D in the body, which is important for maintaining healthy bones and calcium levels. However, vitamin D3 (cholecalciferol), which is produced by the body in response to sunlight exposure, is generally considered to be more effective at raising and maintaining vitamin D levels in the body than ergocalciferols.

Uremia is not a disease itself, but rather it's a condition that results from the buildup of waste products in the blood due to kidney failure. The term "uremia" comes from the word "urea," which is one of the waste products that accumulate when the kidneys are not functioning properly.

In uremia, the kidneys are unable to effectively filter waste and excess fluids from the blood, leading to a variety of symptoms such as nausea, vomiting, fatigue, itching, mental confusion, and ultimately, if left untreated, can lead to coma and death. It is a serious condition that requires immediate medical attention, often involving dialysis or a kidney transplant to manage the underlying kidney dysfunction.

Acetates, in a medical context, most commonly refer to compounds that contain the acetate group, which is an functional group consisting of a carbon atom bonded to two hydrogen atoms and an oxygen atom (-COO-). An example of an acetate is sodium acetate (CH3COONa), which is a salt formed from acetic acid (CH3COOH) and is often used as a buffering agent in medical solutions.

Acetates can also refer to a group of medications that contain acetate as an active ingredient, such as magnesium acetate, which is used as a laxative, or calcium acetate, which is used to treat high levels of phosphate in the blood.

In addition, acetates can also refer to a process called acetylation, which is the addition of an acetyl group (-COCH3) to a molecule. This process can be important in the metabolism and regulation of various substances within the body.

GTP-binding protein alpha subunits, Gs, are a type of heterotrimeric G proteins that play a crucial role in the transmission of signals within cells. These proteins are composed of three subunits: alpha, beta, and gamma. The alpha subunit of Gs proteins (Gs-alpha) is responsible for activating adenylyl cyclase, an enzyme that converts ATP to cyclic AMP (cAMP), a secondary messenger involved in various cellular processes.

When a G protein-coupled receptor (GPCR) is activated by an extracellular signal, it interacts with and activates the Gs protein. This activation causes the exchange of guanosine diphosphate (GDP) bound to the alpha subunit with guanosine triphosphate (GTP). The GTP-bound Gs-alpha then dissociates from the beta-gamma subunits and interacts with adenylyl cyclase, activating it and leading to an increase in cAMP levels. This signaling cascade ultimately results in various cellular responses, such as changes in gene expression, metabolism, or cell growth and differentiation.

It is important to note that mutations in the GNAS gene, which encodes the Gs-alpha subunit, can lead to several endocrine and non-endocrine disorders, such as McCune-Albright syndrome, fibrous dysplasia, and various hormone-related diseases.

A chronic disease is a long-term medical condition that often progresses slowly over a period of years and requires ongoing management and care. These diseases are typically not fully curable, but symptoms can be managed to improve quality of life. Common chronic diseases include heart disease, stroke, cancer, diabetes, arthritis, and COPD (chronic obstructive pulmonary disease). They are often associated with advanced age, although they can also affect children and younger adults. Chronic diseases can have significant impacts on individuals' physical, emotional, and social well-being, as well as on healthcare systems and society at large.

Hypercalcemia is a medical condition characterized by an excess of calcium ( Ca2+ ) in the blood. While the normal range for serum calcium levels is typically between 8.5 to 10.2 mg/dL (milligrams per deciliter) or 2.14 to 2.55 mmol/L (millimoles per liter), hypercalcemia is generally defined as a serum calcium level greater than 10.5 mg/dL or 2.6 mmol/L.

Hypercalcemia can result from various underlying medical disorders, including primary hyperparathyroidism, malignancy (cancer), certain medications, granulomatous diseases, and excessive vitamin D intake or production. Symptoms of hypercalcemia may include fatigue, weakness, confusion, memory loss, depression, constipation, nausea, vomiting, increased thirst, frequent urination, bone pain, and kidney stones. Severe or prolonged hypercalcemia can lead to serious complications such as kidney failure, cardiac arrhythmias, and calcification of soft tissues. Treatment depends on the underlying cause and severity of the condition.

Calcium-sensing receptors (CaSR) are a type of G protein-coupled receptor that play a crucial role in the regulation of extracellular calcium homeostasis. They are widely expressed in various tissues, including the parathyroid gland, kidney, and bone.

The primary function of CaSR is to detect changes in extracellular calcium concentrations and transmit signals to regulate the release of parathyroid hormone (PTH) from the parathyroid gland. When the concentration of extracellular calcium increases, CaSR is activated, which leads to a decrease in PTH secretion, thereby preventing further elevation of calcium levels. Conversely, when calcium levels decrease, CaSR is inhibited, leading to an increase in PTH release and restoration of normal calcium levels.

In addition to regulating calcium homeostasis, CaSR also plays a role in other physiological processes, including cell proliferation, differentiation, and apoptosis. Dysregulation of CaSR has been implicated in various diseases, such as hyperparathyroidism, hypoparathyroidism, and cancer. Therefore, understanding the function and regulation of CaSR is essential for developing new therapeutic strategies to treat these conditions.

"Bone" is the hard, dense connective tissue that makes up the skeleton of vertebrate animals. It provides support and protection for the body's internal organs, and serves as a attachment site for muscles, tendons, and ligaments. Bone is composed of cells called osteoblasts and osteoclasts, which are responsible for bone formation and resorption, respectively, and an extracellular matrix made up of collagen fibers and mineral crystals.

Bones can be classified into two main types: compact bone and spongy bone. Compact bone is dense and hard, and makes up the outer layer of all bones and the shafts of long bones. Spongy bone is less dense and contains large spaces, and makes up the ends of long bones and the interior of flat and irregular bones.

The human body has 206 bones in total. They can be further classified into five categories based on their shape: long bones, short bones, flat bones, irregular bones, and sesamoid bones.

Naphthalene is not typically referred to as a medical term, but it is a chemical compound with the formula C10H8. It is a white crystalline solid that is aromatic and volatile, and it is known for its distinctive mothball smell. In a medical context, naphthalene is primarily relevant as a potential toxin or irritant.

Naphthalene can be found in some chemical products, such as mothballs and toilet deodorant blocks. Exposure to high levels of naphthalene can cause symptoms such as nausea, vomiting, diarrhea, and headaches. Long-term exposure has been linked to anemia and damage to the liver and nervous system.

In addition, naphthalene is a known environmental pollutant that can be found in air, water, and soil. It is produced by the combustion of fossil fuels and is also released from some industrial processes. Naphthalene has been shown to have toxic effects on aquatic life and may pose a risk to human health if exposure levels are high enough.

Homeostasis is a fundamental concept in the field of medicine and physiology, referring to the body's ability to maintain a stable internal environment, despite changes in external conditions. It is the process by which biological systems regulate their internal environment to remain in a state of dynamic equilibrium. This is achieved through various feedback mechanisms that involve sensors, control centers, and effectors, working together to detect, interpret, and respond to disturbances in the system.

For example, the body maintains homeostasis through mechanisms such as temperature regulation (through sweating or shivering), fluid balance (through kidney function and thirst), and blood glucose levels (through insulin and glucagon secretion). When homeostasis is disrupted, it can lead to disease or dysfunction in the body.

In summary, homeostasis is the maintenance of a stable internal environment within biological systems, through various regulatory mechanisms that respond to changes in external conditions.

Alkaline phosphatase (ALP) is an enzyme found in various body tissues, including the liver, bile ducts, digestive system, bones, and kidneys. It plays a role in breaking down proteins and minerals, such as phosphate, in the body.

The medical definition of alkaline phosphatase refers to its function as a hydrolase enzyme that removes phosphate groups from molecules at an alkaline pH level. In clinical settings, ALP is often measured through blood tests as a biomarker for various health conditions.

Elevated levels of ALP in the blood may indicate liver or bone diseases, such as hepatitis, cirrhosis, bone fractures, or cancer. Therefore, physicians may order an alkaline phosphatase test to help diagnose and monitor these conditions. However, it is essential to interpret ALP results in conjunction with other diagnostic tests and clinical findings for accurate diagnosis and treatment.

A kidney, in medical terms, is one of two bean-shaped organs located in the lower back region of the body. They are essential for maintaining homeostasis within the body by performing several crucial functions such as:

1. Regulation of water and electrolyte balance: Kidneys help regulate the amount of water and various electrolytes like sodium, potassium, and calcium in the bloodstream to maintain a stable internal environment.

2. Excretion of waste products: They filter waste products from the blood, including urea (a byproduct of protein metabolism), creatinine (a breakdown product of muscle tissue), and other harmful substances that result from normal cellular functions or external sources like medications and toxins.

3. Endocrine function: Kidneys produce several hormones with important roles in the body, such as erythropoietin (stimulates red blood cell production), renin (regulates blood pressure), and calcitriol (activated form of vitamin D that helps regulate calcium homeostasis).

4. pH balance regulation: Kidneys maintain the proper acid-base balance in the body by excreting either hydrogen ions or bicarbonate ions, depending on whether the blood is too acidic or too alkaline.

5. Blood pressure control: The kidneys play a significant role in regulating blood pressure through the renin-angiotensin-aldosterone system (RAAS), which constricts blood vessels and promotes sodium and water retention to increase blood volume and, consequently, blood pressure.

Anatomically, each kidney is approximately 10-12 cm long, 5-7 cm wide, and 3 cm thick, with a weight of about 120-170 grams. They are surrounded by a protective layer of fat and connected to the urinary system through the renal pelvis, ureters, bladder, and urethra.

A biological marker, often referred to as a biomarker, is a measurable indicator that reflects the presence or severity of a disease state, or a response to a therapeutic intervention. Biomarkers can be found in various materials such as blood, tissues, or bodily fluids, and they can take many forms, including molecular, histologic, radiographic, or physiological measurements.

In the context of medical research and clinical practice, biomarkers are used for a variety of purposes, such as:

1. Diagnosis: Biomarkers can help diagnose a disease by indicating the presence or absence of a particular condition. For example, prostate-specific antigen (PSA) is a biomarker used to detect prostate cancer.
2. Monitoring: Biomarkers can be used to monitor the progression or regression of a disease over time. For instance, hemoglobin A1c (HbA1c) levels are monitored in diabetes patients to assess long-term blood glucose control.
3. Predicting: Biomarkers can help predict the likelihood of developing a particular disease or the risk of a negative outcome. For example, the presence of certain genetic mutations can indicate an increased risk for breast cancer.
4. Response to treatment: Biomarkers can be used to evaluate the effectiveness of a specific treatment by measuring changes in the biomarker levels before and after the intervention. This is particularly useful in personalized medicine, where treatments are tailored to individual patients based on their unique biomarker profiles.

It's important to note that for a biomarker to be considered clinically valid and useful, it must undergo rigorous validation through well-designed studies, including demonstrating sensitivity, specificity, reproducibility, and clinical relevance.

Creatinine is a waste product that's produced by your muscles and removed from your body by your kidneys. Creatinine is a breakdown product of creatine, a compound found in meat and fish, as well as in the muscles of vertebrates, including humans.

In healthy individuals, the kidneys filter out most of the creatinine and eliminate it through urine. However, when the kidneys are not functioning properly, creatinine levels in the blood can rise. Therefore, measuring the amount of creatinine in the blood or urine is a common way to test how well the kidneys are working. High creatinine levels in the blood may indicate kidney damage or kidney disease.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

Cardiovascular diseases (CVDs) are a class of diseases that affect the heart and blood vessels. They are the leading cause of death globally, according to the World Health Organization (WHO). The term "cardiovascular disease" refers to a group of conditions that include:

1. Coronary artery disease (CAD): This is the most common type of heart disease and occurs when the arteries that supply blood to the heart become narrowed or blocked due to the buildup of cholesterol, fat, and other substances in the walls of the arteries. This can lead to chest pain, shortness of breath, or a heart attack.
2. Heart failure: This occurs when the heart is unable to pump blood efficiently to meet the body's needs. It can be caused by various conditions, including coronary artery disease, high blood pressure, and cardiomyopathy.
3. Stroke: A stroke occurs when the blood supply to a part of the brain is interrupted or reduced, often due to a clot or a ruptured blood vessel. This can cause brain damage or death.
4. Peripheral artery disease (PAD): This occurs when the arteries that supply blood to the limbs become narrowed or blocked, leading to pain, numbness, or weakness in the legs or arms.
5. Rheumatic heart disease: This is a complication of untreated strep throat and can cause damage to the heart valves, leading to heart failure or other complications.
6. Congenital heart defects: These are structural problems with the heart that are present at birth. They can range from mild to severe and may require medical intervention.
7. Cardiomyopathy: This is a disease of the heart muscle that makes it harder for the heart to pump blood efficiently. It can be caused by various factors, including genetics, infections, and certain medications.
8. Heart arrhythmias: These are abnormal heart rhythms that can cause the heart to beat too fast, too slow, or irregularly. They can lead to symptoms such as palpitations, dizziness, or fainting.
9. Valvular heart disease: This occurs when one or more of the heart valves become damaged or diseased, leading to problems with blood flow through the heart.
10. Aortic aneurysm and dissection: These are conditions that affect the aorta, the largest artery in the body. An aneurysm is a bulge in the aorta, while a dissection is a tear in the inner layer of the aorta. Both can be life-threatening if not treated promptly.

It's important to note that many of these conditions can be managed or treated with medical interventions such as medications, surgery, or lifestyle changes. If you have any concerns about your heart health, it's important to speak with a healthcare provider.

Hyperphosphatemia is an electrolyte disorder in which there is an elevated level of phosphate in the blood. Most people have no ... The diagnosis of hyperphosphatemia is made through measuring the concentration of phosphate in the blood. A phosphate ... "Hyperphosphatemia". Merck Manuals Professional Edition. Retrieved 27 October 2018. Ronco, Claudio; Bellomo, Rinaldo; Kellum, ... Abnormalities in phosphate metabolism such as hyperphosphatemia are included in the definition of the new chronic kidney ...
Hyperphosphatemia, that is, an abnormally high serum phosphate level, can result from increased phosphate (PO4) intake, ... The major strategies for treating hyperphosphatemia are as follows:. * Diagnose and treat the cause: Eg, hyperphosphatemia due ... Hyperphosphatemia in renal disease. Hyperphosphatemia is a risk factor for mortality in multiple populations, including kidney ... encoded search term (Hyperphosphatemia) and Hyperphosphatemia What to Read Next on Medscape ...
Figure 16 Russia Hyperphosphatemia Drugs Market 2019-2027 ($ Million). Figure 17 Rest of Europe Hyperphosphatemia Drugs Market ... Figure 10 Europe Hyperphosphatemia Drugs Market 2019-2027 ($ Million). Figure 11 United Kingdom Hyperphosphatemia Drugs Market ... Figure 12 France Hyperphosphatemia Drugs Market 2019-2027 ($ Million). Figure 13 Germany Hyperphosphatemia Drugs Market 2019- ... Figure 14 Spain Hyperphosphatemia Drugs Market 2019-2027 ($ Million). Figure 15 Italy Hyperphosphatemia Drugs Market 2019-2027 ...
Sidley Represented Alebund in Option and License Agreement with Chugai for EOS789 Under Development for Hyperphosphatemia. July ... an oral inhibitor of phosphate transporters under development for the treatment of hyperphosphatemia. Alebund plans to conduct ...
A Phase III Study of PA21 With Calcium Carbonate in Hemodialysis Patients With Hyperphosphatemia. ... A Phase III Study of PA21 With Calcium Carbonate in Hemodialysis Patients With Hyperphosphatemia * Share on Facebook ... Close more info about A Phase III Study of PA21 With Calcium Carbonate in Hemodialysis Patients With Hyperphosphatemia ... Close more info about A Phase III Study of PA21 With Calcium Carbonate in Hemodialysis Patients With Hyperphosphatemia ...
The global hyperphosphatemia drugs market is driven by advancements in medical research and drug development and the increasing ... Hyperphosphatemia drugs are medications used to treat a medical condition called hyperphosphatemia, characterized by abnormally ... Global Hyperphosphatemia Drugs Market Trends:. The increasing prevalence of chronic kidney disease (CKD) and end-stage renal ... Global Hyperphosphatemia Drugs Market to Reach US$ 6.1 Billion by 2028, Stimulated by Increasing Prevalence of Chronic Kidney ...
... Ardelik (ARDX) on Xphozahs orphan designation for hyperphosphatemia. November 17, 2023. by Jinny Loop ... ARDX announced that the FDA granted orphan designation to Xphozah (tenapanor) for the treatment of hyperphosphatemia in ...
Hyperphosphatemia, that is, an abnormally high serum phosphate level, can result from increased phosphate (PO4) intake, ... encoded search term (Hyperphosphatemia) and Hyperphosphatemia What to Read Next on Medscape ... resulting in resolution of the hyperphosphatemia. In contrast, under conditions of renal failure, sustained hyperphosphatemia ... Hyperphosphatemia in Dialysis Patients: Beyond Nonadherence to Diet and Binders. Am J Kidney Dis. 2016 Feb. 67 (2):182-6. [QxMD ...
The global prevalence of Chronic Kidney Diseases (CKD) is expected to drive the hyperphosphatemia drugs market revenue growth. ... Hyperphosphatemia Treatment Market is expected to register a steady revenue CAGR during the forecast period. ... Hyperphosphatemia is extremely common in people with Chronic Kidney Disease, and it occurs even more frequently in people with ... Hyperphosphatemia is a condition caused by a high phosphate or phosphorous level in the blood. This condition affects nearly 90 ...
Hyperphosphatemia - Etiology, pathophysiology, symptoms, signs, diagnosis & prognosis from the MSD Manuals - Medical ... Pathophysiology of Hyperphosphatemia Hyperphosphatemia plays a critical role in the development of secondary ... Symptoms and Signs of Hyperphosphatemia Most patients with hyperphosphatemia are asymptomatic, although symptoms of ... Hyperphosphatemia can be spurious in cases of hyperproteinemia (eg, in multiple myeloma Multiple Myeloma Multiple myeloma is a ...
Hyperphosphatemia and Soft Tissue Mineralization Inform patients that BALVERSA may cause hyperphosphatemia and soft tissue ... 5.2 Hyperphosphatemia and Soft Tissue Mineralization. BALVERSA can cause hyperphosphatemia leading to soft tissue ... Hyperphosphatemia: Increases in phosphate levels are a pharmacodynamic effect of BALVERSA. Monitor for hyperphosphatemia and ... High phosphate levels in the blood (hyperphosphatemia). Hyperphosphatemia is common with BALVERSA but can also be serious. High ...
Effects of hyperphosphatemia on diaphragmatic strength and endurance. / Bark, H.; Nizri, M.; Tarasuik, A. et al. In: Journal of ... Effects of hyperphosphatemia on diaphragmatic strength and endurance. In: Journal of Applied Physiology. 1992 ; Vol. 73, No. 1 ... title = "Effects of hyperphosphatemia on diaphragmatic strength and endurance",. abstract = "Effects of an infusion of Na2HPO4 ... Bark H, Nizri M, Tarasuik A, Heimer D. Effects of hyperphosphatemia on diaphragmatic strength and endurance. Journal of Applied ...
title = "Sucroferric oxyhydroxide for hyperphosphatemia: a review of real-world evidence",. abstract = "Hyperphosphatemia is a ... Sucroferric oxyhydroxide for hyperphosphatemia: a review of real-world evidence. Daniel W. Coyne, Stuart M. Sprague, Marc ... Sucroferric oxyhydroxide for hyperphosphatemia : a review of real-world evidence. In: Journal of nephrology. 2022 ; Vol. 35, No ... Sucroferric oxyhydroxide for hyperphosphatemia: a review of real-world evidence. / Coyne, Daniel W.; Sprague, Stuart M.; ...
Management of hyperphosphatemia By Marcello Tonelli Published in Mineral and bone disorders ...
Dermatologic manifestations of renal disease are not uncommon findings in patients with end-stage renal disease (ESRD). Cutaneous examination of patients with ESRD has shown that 50-100% of patients have at least 1 dermatologic condition.
Hyperphosphatemia. Potassium. Hypokalemia. Hyperkalemia. Sodium. Hyponatremia. Hypernatremia. How are electrolyte imbalances ...
Hyperphosphatemia: Hyperphosphatemia is a medical condition involving too much phosphate in the blood.This can lead to bone ...
Hyperphosphatemia. *Infected urinary phosphate stones. *Severe kidney impairment. *Use with caution in patients in whom sodium ...
Hyperphosphatemia: This condition develops when there is too much phosphate in the bloodstream. It can lead to kidney failure. ...
Hyperphosphatemia * 2001/s/viewarticle/964521. Journal Article Impact of Persistent Subclinical Hypothyroidism on Clinical ...
Hyperphosphatemia Market. DelveInsights "Hyperphosphatemia - Market Insights, Epidemiology, and Market Forecast-2030" report. ...
Hyperphosphatemia may result from any of the following:. * Decreased renal phosphate excretion (eg, reduced GFR, renal failure ... See Hyperphosphatemia.) Another long-term effect of such elevations is soft-tissue calcification. ... Serum phosphate concentrations above the reference interval for the appropriate age and gender reflect a hyperphosphatemia ...
Calcium acetate is used to treat hyperphosphatemia (too much phosphate in the blood) in patients with end stage kidney disease ...
hyperphosphatemia. The last two are not invariable findings in vitamin D toxicity, though they are common. ...
by Neisslabs , Oct 20, 2015 , Disease Center, NEWS. An interesting fact is that the 208 bones present in your body are your hardest mass of living tissues. Their main function is providing support to your body and protecting your internal organs from injury. Did you know throughout your lifespan, your bones are ...
Tenapanor for Hyperphosphatemia Approved in Japan * Alvotech Announces Approval in Japan of AVT04 (ustekinumab), a Biosimilar ...
Innovation in the Managmement of Hyperphosphatemia. Three Ways We Are Revolutionizing Renal Care. ...
... hyperphosphatemia; hypomagnesemia. *acid-base disorders: metabolic acidosis; metabolic alkalosis; respiratory acidosis; ...
After an FDA review in July 2021 of tenapanor to treat hyperphosphatemia, the medication was pivoted again and launched in ... While its aim with hyperphosphatemia patients was to stop phosphorus absorption, in people with IBS-C, it inhibits dietary ... Ardelyx, the manufacturer of tenapanor, switched gears to target hyperphosphatemia, a condition that causes extra phosphorus in ... Elevated water secretion likely played a role in why hyperphosphatemia patients without constipation experienced diarrhea while ...
  • The aging population can be considered as the most crucial reason for the rising prevalence of hyperphosphatemia disorders that is driving the growth of the Spain market. (researchandmarkets.com)
  • Elderly individuals are more susceptible to kidney-related conditions, leading to a higher prevalence of hyperphosphatemia in this demographic. (imarcgroup.com)
  • When examined collectively, the population attributable risk percentage for disorders of mineral metabolism was 17.5%, owing largely to the high prevalence of hyperphosphatemia. (nih.gov)
  • Hyperphosphatemia-that is, abnormally high serum phosphate levels-can result from increased phosphate intake, decreased phosphate excretion, or a disorder that shifts intracellular phosphate to extracellular space. (medscape.com)
  • In cases of chronic kidney diseases and elderly people, the loss of phosphorus homeostasis due to phosphorus excretion failure causes hyperphosphatemia. (researchandmarkets.com)
  • In renal insufficiency , phosphorus excretion declines and hyperphosphatemia develops. (bvsalud.org)
  • A woman has hypocalcemia, hyperphosphatemia, and decreased urinary phosphate excretion. (proprofs.com)
  • Abnormalities in phosphate metabolism such as hyperphosphatemia are included in the definition of the new chronic kidney disease-mineral and bone disorder (CKD-MBD). (wikipedia.org)
  • Hyperphosphatemia is extremely common in people with Chronic Kidney Disease , and it occurs even more frequently in people with end-stage kidney disease. (reportsanddata.com)
  • Hyperphosphatemia is a common complication in dialysis-dependent patients with chronic kidney disease. (amsterdamumc.org)
  • [ 2 ] Although chronic kidney disease (CKD) often leads to hyperphosphatemia, abnormalities in phosphorus levels have been observed in populations with and without kidney disease. (medscape.com)
  • The diagnosis of hyperphosphatemia is made through measuring the concentration of phosphate in the blood. (wikipedia.org)
  • Furthermore, the increasing awareness and diagnosis of hyperphosphatemia in patients with CKD and ESRD have also contributed to market expansion. (imarcgroup.com)
  • Disorders of mineral metabolism (hyperphosphatemia, hypercalcemia, and secondary hyperparathyroidism) are potentially modifiable. (nih.gov)
  • Rarely, if the cause of hyperphosphatemia is not clear, 24-hour measurement of urinary phosphate can be performed. (medscape.com)
  • Hyperphosphatemia drugs are medications used to treat a medical condition called hyperphosphatemia, characterized by abnormally high levels of phosphate in the blood. (imarcgroup.com)
  • The pathophysiology of hyperphosphatemia associated with end-stage renal disease and treatment with phosphate binders are discussed. (bvsalud.org)
  • Hyperphosphatemia in Dialysis Patients: Beyond Nonadherence to Diet and Binders. (medscape.com)
  • Hyperphosphatemia and hs-CRP Initiate the Coronary Artery Calcification in Peritoneal Dialysis Patients. (medscape.com)
  • The use of various phosphate-binders in dialysis patients has prompted several studies in the U.S., driving revenue growth of the North America hyperphosphatemia treatment market. (reportsanddata.com)
  • Calcium acetate is used to treat hyperphosphatemia (too much phosphate in the blood) in patients with end stage kidney disease who are on dialysis. (drugs.com)
  • The treatment of hyperphosphatemia in patients with chronic renal failure includes dialysis , dietary phosphorus restrictions, phosphate -binding medications, and vitamin D analogs. (bvsalud.org)
  • [ 5 ] In dialysis and kidney transplant patients, hyperphosphatemia is associated with anemia independent of other mineral bone disease components. (medscape.com)
  • Hyperphosphatemia can also be caused by Diabetic Ketoacidosis , uncontrolled diabetes, high Vitamin D levels, and low parathyroid hormone levels. (reportsanddata.com)
  • Although most patients with hyperphosphatemia are asymptomatic, they occasionally report hypocalcemic symptoms, such as muscle cramps, tetany, and perioral numbness or tingling. (medscape.com)
  • More commonly, patients report symptoms related to the underlying cause of the hyperphosphatemia. (medscape.com)
  • While its aim with hyperphosphatemia patients was to stop phosphorus absorption, in people with IBS-C, it inhibits dietary sodium uptake. (healthline.com)
  • Elevated water secretion likely played a role in why hyperphosphatemia patients without constipation experienced diarrhea while taking this medication. (healthline.com)
  • Les patients étaient inclus en accord avec les critères de consensus internationaux. (bvsalud.org)
  • Elle a mis en exergue l'intérêt de la réorganisation de la prise en charge de ces patients en période de crise sanitaire, l'éducation thérapeutique des patients et le recours à la télémédecine pour assurer la continuité des soins. (bvsalud.org)
  • Spurious hyperphosphatemia due to sample contamination with heparinized saline from an indwelling catheter. (medscape.com)
  • Ardelik, Inc. ARDX announced that the FDA granted orphan designation to Xphozah (tenapanor) for the treatment of hyperphosphatemia in children. (booblogs.com)
  • Ardelyx, the manufacturer of tenapanor, switched gears to target hyperphosphatemia, a condition that causes extra phosphorus in the blood, instead of IBS-C. (healthline.com)
  • After an FDA review in July 2021 of tenapanor to treat hyperphosphatemia, the medication was pivoted again and launched in April 2022 as the first and only NHE3 inhibitor for the treatment of IBS-C. (healthline.com)
  • [ 13-15 ] In murine models that lack FGF-23 or klotho, the resultant hyperphosphatemia is associated with cell toxicity, premature aging and vascular calcifications. (medscape.com)
  • If left untreated, hyperphosphatemia can result in secondary hyperparathyroidism , renal osteodystrophy , and metastatic calcification of blood vessels and soft tissue . (bvsalud.org)
  • Hyperphosphatemia is an electrolyte disorder in which there is an elevated level of phosphate in the blood. (wikipedia.org)
  • In the CKD clients, conditions within the bones remodeling can lead to extreme launch of phosphorus and calcium supplements on the blood, and this exacerbates hyperphosphatemia and vascular calcification and you can accelerates the fresh decline off kidney function. (kaamcha.com)
  • The increasing aging population in Spain is considered as the major driving factor to strengthen the demand of the hyperphosphatemia drugs market in the country. (researchandmarkets.com)
  • And this is growing the demand for the hyperphosphatemia drugs market in the country. (researchandmarkets.com)
  • Moreover, the growing aging population is contributing to the expansion of the hyperphosphatemia drugs market. (imarcgroup.com)
  • The global prevalence of Chronic Kidney Diseases (CKD) is expected to drive the hyperphosphatemia drugs market revenue growth. (reportsanddata.com)
  • Strategic mergers and acquisitions by key market players are also expected to create a profitable environment for revenue growth of the hyperphosphatemia drugs market. (reportsanddata.com)
  • Hyperphosphatemia can also occur with excessive oral phosphate administration and occasionally with overzealous use of enemas containing phosphate. (msdmanuals.com)
  • Sidley represented Alebund Pharmaceuticals (Alebund) in its option and license agreement with Chugai Pharmaceutical Co., Ltd. (Chugai) in relation to EOS789, an oral inhibitor of phosphate transporters under development for the treatment of hyperphosphatemia. (sidley.com)
  • The hyperphosphatemia treatment market is expected to register a steady revenue CAGR during the forecast period. (reportsanddata.com)
  • Increasing number of drug launches in developing economies is expected to drive hyperphosphatemia treatment market growth. (reportsanddata.com)
  • In the hyperphosphatemia treatment market, there appears to be an unmet need for developing calcium acetate/magnesium combination products. (reportsanddata.com)
  • North America has emerged as a potentially profitable region in the global hyperphosphatemia treatment market, with healthcare providers increasingly focusing on implementing the Kidney Disease Improving Global Outcomes (KDIGO) guidelines. (reportsanddata.com)
  • However, even severe hyperphosphatemia is for the most part clinically asymptomatic. (medscape.com)
  • citation needed] Drugs: hyperphosphatemia can also be caused by taking oral sodium phosphate solutions prescribed for bowel preparation for colonoscopy in children. (wikipedia.org)
  • This article reviews the key results from these observational studies of sucroferric oxyhydroxide and evaluates its role in the management of hyperphosphatemia in clinical practice. (amsterdamumc.org)
  • Monitor for hyperphosphatemia and manage with dose modifications when required. (nih.gov)
  • Hyperphosphatemia occasionally results from a transcellular shift of phosphate into the extracellular space that is so large that the renal excretory capacity is overwhelmed. (msdmanuals.com)
  • Hyperphosphatemia: Increases in phosphate levels are a pharmacodynamic effect of BALVERSA. (nih.gov)
  • Hyperphosphatemia is a condition caused by a high phosphate or phosphorous level in the blood. (reportsanddata.com)
  • Hyperphosphatemia is a medical condition involving too much phosphate in the blood. (medicalnewstoday.com)