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 fibrous degeneration, cyst formation, and the presence of fibrous nodules in bone, usually due to HYPERPARATHYROIDISM.
Disorder caused by an interruption of the mineralization of organic bone matrix leading to bone softening, bone pain, and weakness. It is the adult form of rickets resulting from disruption of VITAMIN D; PHOSPHORUS; or CALCIUM homeostasis.
FIBROUS DYSPLASIA OF BONE affecting several bones. When melanotic pigmentation (CAFE-AU-LAIT SPOTS) and multiple endocrine hyperfunction are additionally associated it is referred to as Albright syndrome.
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 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.
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.
Diseases of BONES.
Hydroxy analogs of vitamin D 3; (CHOLECALCIFEROL); including CALCIFEDIOL; CALCITRIOL; and 24,25-DIHYDROXYVITAMIN D 3.
The largest of three bones that make up each half of the pelvic girdle.
The continuous turnover of BONE MATRIX and mineral that involves first an increase in BONE RESORPTION (osteoclastic activity) and later, reactive BONE FORMATION (osteoblastic activity). The process of bone remodeling takes place in the adult skeleton at discrete foci. The process ensures the mechanical integrity of the skeleton throughout life and plays an important role in calcium HOMEOSTASIS. An imbalance in the regulation of bone remodeling's two contrasting events, bone resorption and bone formation, results in many of the metabolic bone diseases, such as OSTEOPOROSIS.
A form of PSEUDOHYPOPARATHYROIDISM characterized by the same features except for the abnormal response to hormones such as PARATHYROID HORMONE. It is associated with paternally inherited mutant alleles of the ALPHA CHAIN OF STIMULATORY G PROTEIN.
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.
A metallic element that has the atomic number 13, atomic symbol Al, and atomic weight 26.98.
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.
Therapy for the insufficient cleansing of the BLOOD by the kidneys based on dialysis and including hemodialysis, PERITONEAL DIALYSIS, and HEMODIAFILTRATION.
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.
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.
Americium. A completely man-made radioactive actinide with atomic symbol Am, atomic number 95, and atomic weight 243. Its valence can range from +3 to +6. Because of its nonmagnetic ground state, it is an excellent superconductor. It is also used in bone mineral analysis and as a radiation source for radiotherapy.
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.
Cholecalciferols substituted with two hydroxy groups in any position.
Metabolic bone diseases are a group of disorders that affect the bones' structure and strength, caused by disturbances in the normal metabolic processes involved in bone formation, resorption, or mineralization, including conditions like osteoporosis, osteomalacia, Paget's disease, and renal osteodystrophy.
Process by which organic tissue becomes hardened by the physiologic deposit of calcium salts.
An enzyme that catalyzes the conversion of an orthophosphoric monoester and water to an alcohol and orthophosphate. EC 3.1.3.1.
A family of heterotrimeric GTP-binding protein alpha subunits that activate ADENYLYL CYCLASES.
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.
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.
A condition of an abnormally low level of PHOSPHATES in the blood.
Inorganic salts of phosphoric acid.
Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.
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.
The amount of mineral per square centimeter of BONE. This is the definition used in clinical practice. Actual bone density would be expressed in grams per milliliter. It is most frequently measured by X-RAY ABSORPTIOMETRY or TOMOGRAPHY, X RAY COMPUTED. Bone density is an important predictor for OSTEOPOROSIS.
Vitamin K-dependent calcium-binding protein synthesized by OSTEOBLASTS and found primarily in BONES. Serum osteocalcin measurements provide a noninvasive specific marker of bone metabolism. The protein contains three residues of the amino acid gamma-carboxyglutamic acid (Gla), which, in the presence of CALCIUM, promotes binding to HYDROXYAPATITE and subsequent accumulation in BONE MATRIX.
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.
The development of bony substance in normally soft structures.
Bone loss due to osteoclastic activity.
The region of the HAND between the WRIST and the FINGERS.
Dialysis fluid being introduced into and removed from the peritoneal cavity as either a continuous or an intermittent procedure.
Developmental bone diseases are a category of skeletal disorders that arise from disturbances in the normal growth and development of bones, including abnormalities in size, shape, structure, or composition, which can lead to various musculoskeletal impairments and deformities.
Pathologic deposition of calcium salts in tissues.
An acquired blood vessel disorder caused by severe deficiency of vitamin C (ASCORBIC ACID) in the diet leading to defective collagen formation in small blood vessels. Scurvy is characterized by bleeding in any tissue, weakness, ANEMIA, spongy gums, and a brawny induration of the muscles of the calves and legs.
Pathological processes of the KIDNEY or its component tissues.
Congenital structural deformities, malformations, or other abnormalities of the maxilla and face or facial bones.
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.

Elevated carboxy terminal cross linked telopeptide of type I collagen in alcoholic cirrhosis: relation to liver and kidney function and bone metabolism. (1/209)

BACKGROUND: The carboxy terminal cross linked telopeptide of type I collagen (ICTP) has been put forward as a marker of bone resorption. Patients with alcoholic liver disease may have osteodystrophy. AIMS: To assess circulating and regional concentrations of ICTP in relation to liver dysfunction, bone metabolism, and fibrosis. METHODS: In 15 patients with alcoholic cirrhosis and 20 controls, hepatic venous, renal venous, and femoral arterial concentrations of ICTP, and bone mass and metabolism were measured. RESULTS: Circulating ICTP was higher in patients with cirrhosis than in controls. No overall significant hepatic disposal or production was found in the patient or control groups but slightly increased production was found in a subset of patients with advanced disease. Significant renal extraction was observed in the controls, whereas only a borderline significant extraction was observed in the patients. Measurements of bone mass and metabolism indicated only a mild degree of osteodystrophy in the patients with cirrhosis. ICTP correlated significantly in the cirrhotic patients with hepatic and renal dysfunction and fibrosis, but not with measurements of bone mass or metabolism. CONCLUSIONS: ICTP is highly elevated in patients with cirrhosis, with no detectable hepatic net production or disposal. No relation between ICTP and markers of bone metabolism was identified, but there was a relation to indicators of liver dysfunction and fibrosis. As the cirrhotic patients conceivably only had mild osteopenia, the elevated ICTP in cirrhosis may therefore primarily reflect liver failure and hepatic fibrosis.  (+info)

Is low plasma 25-(OH)vitamin D a major risk factor for hyperparathyroidism and Looser's zones independent of calcitriol? (2/209)

BACKGROUND: Recent reports suggest that calcitriol might not be the sole active metabolite of vitamin D and that plasma concentrations of 25-(OH)vitamin D (25OHD) are often abnormally low in hemodialysis patients. We have therefore evaluated plasma 25OHD as a risk factor for parathyroid hormone (PTH) hypersecretion and radiological bone disease. We carried out a cross-sectional study during the month of September in an Algerian dialysis center of 113 patients who were not taking supplements of alphacalcidol or calcitriol. METHODS: Plasma 25OHD, calcitriol, PTH, calcium, phosphate, bicarbonate, and aluminum were measured, and x-rays of the hands and pelvis were obtained for evaluation of subperiosteal resorption and Looser's zones. RESULTS: The median plasma 25OHD was 47.5 nmol/liter (range 2.5 to 170.0). Univariate analysis showed that plasma PTH was correlated positively with months on maintenance dialysis and negatively with plasma 25OHD, calcitriol, calcium, bicarbonate and aluminum, but not with that of phosphate. plasma 25OHD was positively correlated with calcium and calcitriol. Using multiple regression analysis, only plasma 25OHD (negative) and the duration on maintenance dialysis (positive) were independently linked to plasma PTH. The prevalence of isolated subperiosteal resorption (ISR) was 34%, and that of the combination of resorption with Looser's zones (CRLZ) was 9%; thus, only 57% of the patients had a normal x-ray appearance. These groups were comparable with regards to age, gender, and duration on dialysis. When the biochemical measurements of the patients with CRLZ were compared with those from patients without radiological lesions, plasma 25OHD was the only parameter to show a statistically significant difference, being significantly lower in the CRLZ group (26 +/- 18 vs. 57 nmol/liter, ANOVA, P < 0.004). Plasma 25OHD was also significantly lower in the ISR group (44, P < 0.05) than in the normal x-ray group, and plasma Ca (P < 0.003) and bicarbonate (P < 0.02) were lower. Logistical analysis showed that the presence of resorption was independently linked only with plasma PTH. Looser's zones and subperiosteal resorption were not seen in patients with plasma 25OHD of more than 40 (Looser's zones) and more than 100 nmol/liter (subperiosteal resorption). The optimal range for intact PTH in hemodialysis patients with mild aluminum overload is 10 to 25 pmol/liter. We found that plasma PTH was inappropriately high only when plasma 25OHD was less than 100 nmol/liter. With a plasma 25OHD of between 100 and 170 nmol/liter, hypercalcemia was present with a plasma PTH of less than 10 pmol/liter in only one case. CONCLUSIONS: This cross sectional study shows that low plasma 25OHD is a major risk factor for hyperparathyroidism and Looser's zones. In dialysis patients, we suggest that the plasma levels of 25OHD are maintained around the upper limit of the reference range of sunny countries.  (+info)

Bone scintigraphy in renal osteodystrophy. (3/209)

Bone scintigraphy with Tc-99m HEDP was performed in 30 patients on maintenance hemodialysis, and the results of quantitative analysis were compared with those of a normal group. To permit this comparison, elevated background activity due to the absence of renal radiotracer excretion was reduced by hemodialysis to levels found in the normals. Histologic proof of renal osteodystrophy had been obtained in all patients. The incidence of radiographic abnormalities was 46%, whereas abnormal scans were found in 25 patients (83%); skeletal lesions were also more pronounced and detected earlier. However, even when the scans appeared normal, the quantitative analysis showed increased skeletal activity in all patients. The total skeletal activity proved to be a good index of the severity of renal osteodystrophy and appeared dependent on both osteomalacia and hyperparathyroidism. These findings show that bone scintigraphy is a sensitive method to detect skeletal involvement in renal osteodystrophy.  (+info)

Renal osteodystrophy in pre-dialysis patients: ethnic difference? (4/209)

The purpose of the present study is to investigate whether an ethnic difference exists in the incidence of renal osteodystrophy between Asian and Western countries in end-stage renal disease (ESRD) patients. We evaluated bone histology in 58 pre-dialysis patients (28 male, 30 female; mean age: 47.7 years). All patients had bone biopsies with quantitative histomorphometry and serological parameters such as intact PTH, osteocalcin, total alkaline phosphatase, and basal and deferoxamine-stimulated serum aluminum levels. We observed that 91.4% of all evaluated patients showed renal osteodystrophy before the start of dialytic therapy. Mild osteitis fibrosa were observed in 21 patients (36.2%), severe osteitis fibrosa in 5 patients (8.6%), mixed lesions in 7 patients (12.1%), osteomalacia in 6 patients (10.3%), aplastic bone disease in 14 patients (24.1%), and normal bone in 5 patients (8.6%). Among the bone histomorphometric parameters, fibrosis area rate (%) showed the best correlation with intact PTH, and osteocalcin and osteoid area rate (%) with total alkaline phosphatase. Aluminum-related bone disease was not observed. Among patients with aplastic bone disease, only 14.3% showed aluminum deposition of any significance (5% < stainable bone surface aluminum < 25%). In the diabetic patients, aplastic bone disease was most common, but no case was related to aluminum intoxication. In conclusion, the distribution of renal osteodystrophy in our study was different from that of Western countries in pre-dialysis patients. Our patients tended to have more mild-form osteitis fibrosa and normal findings, and less severe-form osteitis fibrosa and aplastic bone disease. Aluminum-related bone disease was not observed.  (+info)

Bone mineral density and biochemical markers of bone turnover in patients with predialysis chronic renal failure. (5/209)

BACKGROUND: Metabolic bone disease might commence early in the course of renal failure. This study therefore examined the frequency and severity of the skeletal changes in predialysis chronic renal failure by measurements of bone mineral density (BMD), biochemical markers of bone turnover (osteocalcin, bone-specific alkaline phosphatase, carboxy terminal propeptide of type I collagen, and carboxy-terminal telopeptide of type I collagen), parathyroid hormone (PTH), ionized calcium (Ca++), phosphate (P), and vitamin D metabolites. METHODS: The study was performed in 113 patients (male/female: 82/31) with chronic renal diseases [mean glomerular filtration rate (GFR) of 37 ml/min] and in 89 matched, normal control subjects. RESULTS: The patients had significantly (P<0.05) reduced BMD in the spine (-6.3%), the femur (-12.1%), the forearm (-5.7%), and the total body (-4.2%) as compared with the control subjects. Dividing the patients into quartiles according to GFR revealed that BMD decreased with the gradual decline in renal function at all the measured skeletal sites, but was most pronounced in the femur: 0.63+/-0.03, 0.74+/-0.02, 0.77+/-0.02, and 0.82+/-0.03 g/cm2 in each quartile from lowest to highest GFR compared with 0.82+/-0.02 g/cm2 in the control group (P<0.0001). All of the measured bone markers showed increasing plasma levels with the more advanced stages of renal failure. Serum PTH and serum P levels increased, whereas serum Ca++ and 1,25-dihydroxyvitamin D decreased. BMD Z-scores of the femur and of the forearm correlated to the biochemical markers and to PTH (P<0.05 to P<0.0001). The biochemical markers all showed strong correlations to PTH, also when corrected for the effect of the decline in GFR (r = 0.40 to 0.92, P<0.01 to P< 0.0001). CONCLUSION: Skeletal changes are initiated at an early stage of chronic renal failure, as estimated from reduced BMD and elevated levels of PTH and from the biochemical markers of both bone formation and bone resorption.  (+info)

22-Oxacalcitriol ameliorates high-turnover bone and marked osteitis fibrosa in rats with slowly progressive nephritis. (6/209)

22-Oxacalcitriol ameliorates high-turnover bone and marked osteitis fibrosa in rats with slowly progressive nephritis. BACKGROUND: 22-Oxacalcitriol (OCT) is a unique vitamin D analogue with less calcemic activity than calcitriol, and it effectively suppresses parathyroid hormone (PTH) secretion in uremic rats. This study was performed to examine the long-term effect of intravenously administered OCT on high-turnover bone disease in model rats of slowly progressive renal failure. METHODS: Slowly progressive renal failure rats were made by a single injection of glycopeptide isolated from rat renal cortical tissues. At 250 days, glycopeptide-induced nephritis (GN) rats were divided into three groups with the same levels of serum creatinine and PTH, and they received either OCT (0.03 or 0.15 microg/kg body wt) or vehicle given intravenously three times per week for 15 weeks. RESULTS: Renal function of GN rats deteriorated very slowly but progressively, as assessed by the increase of serum creatinine concentration. At sacrifice, serum PTH levels, bone formation markers, bone resorption markers, and fibrosis volume were significantly elevated in vehicle-treated GN rats compared with those of sham-operated rats, suggesting the development of high-turnover bone disease with osteitis fibrosa. In contrast, in the GN-OCT 0.15 microg/kg group, these high PTH levels and high-turnover bone and fibrosis were significantly decreased. Such amelioration of bone abnormalities by OCT was not accompanied by either hypercalcemia or further deterioration of renal function. CONCLUSIONS: These data indicate that OCT may be a useful and safe agent not only for the suppression of PTH, but also for the amelioration of osteitis fibrosa and high-turnover bone without causing hypercalcemia in chronic dialysis patients.  (+info)

Insulin-like growth factor system components in hyperparathyroidism and renal osteodystrophy. (7/209)

BACKGROUND: The insulin-like growth factor (IGF) system plays a key role in regulation of bone formation. In patients with renal osteodystrophy, an elevation of some IGF binding proteins (IGFBPs) has been described, but there is no study measuring serum levels of both IGF-I and IGF-II as well as IGFBP-1 to -6 in different forms of renal osteodystrophy and hyperparathyroidism. METHODS: In a cross-sectional study, we investigated 319 patients with mild (N = 29), moderate (N = 48), preuremic (N = 37), and end-stage renal failure (ESRF; N = 205). The ESRF group was treated by hemodialysis (HD; N = 148), peritoneal dialysis (PD; N = 27), or renal transplantation (RTX; N = 30). As controls without renal failure, we recruited age-matched healthy subjects (N = 87) and patients with primary hyperparathyroidism (pHPT; N = 25). Serum levels of total and free IGF-I, IGF-II, IGFBP-1 to -6, and biochemical bone markers including intact parathyroid hormone (PTH), bone alkaline phosphatase (B-ALP), and osteocalcin (OSC) were measured by specific immunometric assays. IGF system components and bone markers were correlated with clinical and bone histologic findings. Mean values +/- SEM are given. RESULTS: With declining renal function a significant increase was measured for IGFBP-1 (range 7- to 14-fold), IGFBP-2 (3- to 8-fold), IGFBP-3 (1.5- to 3-fold), IGFBP-4 (3- to 19-fold), and IGFBP-6 (8- to 25-fold), whereas IGFBP-5 levels tended to decrease (1.3- to 1. 6-fold). In contrast, serum levels of IGF-I, free IGF-I, and IGF-II remained constant in most patients. Compared with renal failure patients, pHPT patients showed a similar decline in IGFBP-5 levels and less elevated levels of IGFBP-1 (3.5-fold), IGFBP-2 (2-fold), IGFBP-3 (1.2-fold), and IGFBP-6 (4-fold) but no elevation of IGFBP-4 levels. In all subjects, free and total IGF-I levels showed significant negative correlations with IGFBP-1, IGFBP-2, and IGFBP-4 (that is, inhibitory IGF system components) and significant positive correlations with IGFBP-3 and IGFBP-5 (that is, stimulatory IGF system components). A positive correlation was observed between IGF-II and IGFBP-6. ESRF patients with mixed uremic bone disease and histologic evidence for osteopenia revealed significantly (P < 0.05) higher levels of IGFBP-2 and IGFBP-4 but lower IGFBP-5 levels. Histologic parameters of bone formation showed significant positive correlations with serum levels of IGF-I, IGF-II, and IGFBP-5. In contrast, IGFBP-2 and IGFBP-4 correlated positively with indices of bone loss. Moreover, dialysis patients with low bone turnover (N = 24) showed significantly (P < 0.05) lower levels of IGFBP-5, PTH, B-ALP, and OSC than patients with high bone turnover. CONCLUSION: Patients with primary and secondary hyperparathyroidism showed lower levels of the putative stimulatory IGFBP-5 but higher levels of IGFBP-1, -2, -3, and -6, whereas total IGF-I and IGF-II levels were not or only moderately increased. The marked increase in serum levels of IGFBP-4 appeared to be characteristic for chronic renal failure. IGFBP-5 correlated with biochemical markers and histologic indices of bone formation in renal osteodystrophy patients and was not influenced by renal function. Therefore, IGFBP-5 may gain significance as a serological marker for osteopenia and low bone turnover in long-term dialysis patients.  (+info)

Increased bone strontium levels in hemodialysis patients with osteomalacia. (8/209)

BACKGROUND: In this study, we report on the association between increased bone strontium levels and the presence of osteomalacia in end-stage renal failure patients treated by hemodialysis. METHODS: We performed a histologic examination and determined the strontium content and strontium/calcium ratios in bone biopsies of 100 hemodialysis patients recruited from various centers all over the world. Aside from the bone strontium concentration, the bone aluminum content was assessed. The bone zinc concentration, a nonrelevant element for bone toxicity, was also measured. RESULTS: Bone strontium levels and bone strontium/calcium ratios were increased in subjects with osteomalacia when compared with those with the other types of renal osteodystrophy. Bone strontium and bone calcium levels correlated with each other. The slope of the linear regression curve correlating these parameters was much steeper in the osteomalacic group (Y = 2.22X - 120) as compared with the other types of renal osteodystrophy (Y = 0.52X - 5.7). Within the group of patients with osteomalacia, bone strontium levels also significantly correlated with the bone aluminum content (r = 0.72, P = 0.018). No such correlation was found for the other types of renal osteodystrophy. The bone zinc concentration of subjects with normal renal function did not differ significantly from the values noted for the various types of renal osteodystrophy taken as separate groups, nor could increased bone zinc concentrations be associated with a particular bone lesion. CONCLUSIONS: Our data demonstrate an association between osteomalacia and increased bone strontium concentrations in dialysis patients. Further studies are warranted to establish whether strontium plays either a primary, secondary, or contributive role in the development of the latter type of renal osteodystrophy.  (+info)

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.

Osteitis fibrosa cystica is a medical condition that refers to the abnormal bone remodeling process characterized by increased bone resorption and formation, leading to bone thickening and weakening. It is also known as "von Recklinghausen's disease of bone" or "monostotic fibrous dysplasia."

This condition is typically caused by excessive production of parathyroid hormone (PTH) due to a benign or malignant tumor of the parathyroid gland, known as hyperparathyroidism. The overproduction of PTH leads to an imbalance in calcium and phosphorus metabolism, resulting in increased bone resorption and fibrous tissue deposition within the bone marrow.

The clinical features of osteitis fibrosa cystica include bone pain, fractures, bone deformities, and elevated levels of calcium and alkaline phosphatase in the blood. Radiographic findings may show characteristic "rugger jersey" or "salt and pepper" patterns of alternating areas of increased and decreased bone density.

Treatment typically involves surgical removal of the abnormal parathyroid gland tissue, followed by medical management to prevent further bone loss and promote healing.

Osteomalacia is a medical condition characterized by the softening of bones due to defective bone mineralization, resulting from inadequate vitamin D, phosphate, or calcium. It mainly affects adults and is different from rickets, which occurs in children. The primary symptom is bone pain, but muscle weakness can also occur. Prolonged osteomalacia may lead to skeletal deformities and an increased risk of fractures. Treatment typically involves supplementation with vitamin D, calcium, and sometimes phosphate.

Fibrous Dysplasia, Polyostotic is a rare genetic disorder that affects the bone tissue. It is characterized by the replacement of normal bone tissue with fibrous (scar-like) tissue, leading to weak and fragile bones that are prone to fractures and deformities. The term "polyostotic" refers to the involvement of multiple bones in the body.

In this condition, there is an abnormal development of the bone during fetal growth or early childhood due to a mutation in the GNAS gene. This results in the formation of fibrous tissue instead of normal bone tissue, leading to the characteristic features of Fibrous Dysplasia, Polyostotic.

The symptoms of this condition can vary widely depending on the severity and location of the affected bones. Common symptoms include:

* Bone pain and tenderness
* Bone deformities (such as bowing of the legs)
* Increased risk of fractures
* Skin pigmentation changes (cafe-au-lait spots)
* Hearing loss or other hearing problems (if the skull is affected)

Fibrous Dysplasia, Polyostotic can also be associated with endocrine disorders such as precocious puberty and hyperthyroidism. Treatment typically involves a combination of medications to manage pain and prevent fractures, as well as surgical intervention to correct bone deformities or stabilize fractures.

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.

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.

"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.

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.

Hydroxycholecalciferols are metabolites of vitamin D that are formed in the liver and kidneys. They are important for maintaining calcium homeostasis in the body by promoting the absorption of calcium from the gut and reabsorption of calcium from the kidneys.

The two main forms of hydroxycholecalciferols are 25-hydroxyvitamin D (25(OH)D) and 1,25-dihydroxyvitamin D (1,25(OH)2D). 25-hydroxyvitamin D is the major circulating form of vitamin D in the body and is used as a clinical measure of vitamin D status. It is converted to 1,25-dihydroxyvitamin D in the kidneys by the enzyme 1α-hydroxylase, which is activated in response to low serum calcium or high phosphate levels.

1,25-dihydroxyvitamin D is the biologically active form of vitamin D and plays a critical role in regulating calcium homeostasis by increasing intestinal calcium absorption and promoting bone health. Deficiency in hydroxycholecalciferols can lead to rickets in children and osteomalacia or osteoporosis in adults, characterized by weakened bones and increased risk of fractures.

The ilium is the largest and broadest of the three parts that make up the hip bone or coxal bone. It is the uppermost portion of the pelvis and forms the side of the waist. The ilium has a curved, fan-like shape and articulates with the sacrum at the back to form the sacroiliac joint. The large, concave surface on the top of the ilium is called the iliac crest, which can be felt as a prominent ridge extending from the front of the hip to the lower back. This region is significant in orthopedics and physical examinations for its use in assessing various medical conditions and performing certain maneuvers during the physical examination.

Bone remodeling is the normal and continuous process by which bone tissue is removed from the skeleton (a process called resorption) and new bone tissue is formed (a process called formation). This ongoing cycle allows bones to repair microdamage, adjust their size and shape in response to mechanical stress, and maintain mineral homeostasis. The cells responsible for bone resorption are osteoclasts, while the cells responsible for bone formation are osteoblasts. These two cell types work together to maintain the structural integrity and health of bones throughout an individual's life.

During bone remodeling, the process can be divided into several stages:

1. Activation: The initiation of bone remodeling is triggered by various factors such as microdamage, hormonal changes, or mechanical stress. This leads to the recruitment and activation of osteoclast precursor cells.
2. Resorption: Osteoclasts attach to the bone surface and create a sealed compartment called a resorption lacuna. They then secrete acid and enzymes that dissolve and digest the mineralized matrix, creating pits or cavities on the bone surface. This process helps remove old or damaged bone tissue and releases calcium and phosphate ions into the bloodstream.
3. Reversal: After resorption is complete, the osteoclasts undergo apoptosis (programmed cell death), and mononuclear cells called reversal cells appear on the resorbed surface. These cells prepare the bone surface for the next stage by cleaning up debris and releasing signals that attract osteoblast precursors.
4. Formation: Osteoblasts, derived from mesenchymal stem cells, migrate to the resorbed surface and begin producing a new organic matrix called osteoid. As the osteoid mineralizes, it forms a hard, calcified structure that gradually replaces the resorbed bone tissue. The osteoblasts may become embedded within this newly formed bone as they differentiate into osteocytes, which are mature bone cells responsible for maintaining bone homeostasis and responding to mechanical stress.
5. Mineralization: Over time, the newly formed bone continues to mineralize, becoming stronger and more dense. This process helps maintain the structural integrity of the skeleton and ensures adequate calcium storage.

Throughout this continuous cycle of bone remodeling, hormones, growth factors, and mechanical stress play crucial roles in regulating the balance between resorption and formation. Disruptions to this delicate equilibrium can lead to various bone diseases, such as osteoporosis, where excessive resorption results in weakened bones and increased fracture risk.

Pseudopseudohypoparathyroidism (PPHP) is a rare genetic disorder that is characterized by resistance to the action of parathyroid hormone (PTH), but without the associated biochemical abnormalities seen in pseudohypoparathyroidism (PHP). PPHP is caused by mutations in the gene responsible for the production of the alpha subunit of the Gs protein, which is involved in the transmission of signals from the PTH receptor to the interior of the cell.

Individuals with PPHP typically have normal or elevated levels of serum calcium and phosphorus, and normal PTH levels, despite the resistance to PTH. The disorder is often characterized by a constellation of physical features known as Albright's hereditary osteodystrophy (AHO), which may include short stature, round face, brachydactyly (shortened fingers and toes), and ectopic calcifications. However, unlike PHP, individuals with PPHP do not have cognitive impairment or other endocrine abnormalities.

PPHP is inherited in an autosomal dominant manner, meaning that a child has a 50% chance of inheriting the disorder if one parent is affected. The disorder was named "pseudopseudohypoparathyroidism" because it was initially misdiagnosed as pseudohypoparathyroidism, which is a similar but distinct disorder with different biochemical and clinical features.

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.

The chemical element aluminum (or aluminium in British English) is a silvery-white, soft, non-magnetic, ductile metal. The atomic number of aluminum is 13 and its symbol on the periodic table is Al. It is the most abundant metallic element in the Earth's crust and is found in a variety of minerals such as bauxite.

Aluminum is resistant to corrosion due to the formation of a thin layer of aluminum oxide on its surface that protects it from further oxidation. It is lightweight, has good thermal and electrical conductivity, and can be easily formed and machined. These properties make aluminum a widely used metal in various industries such as construction, packaging, transportation, and electronics.

In the medical field, aluminum is used in some medications and medical devices. For example, aluminum hydroxide is commonly used as an antacid to neutralize stomach acid and treat heartburn, while aluminum salts are used as adjuvants in vaccines to enhance the immune response. However, excessive exposure to aluminum can be harmful and has been linked to neurological disorders such as Alzheimer's disease, although the exact relationship between aluminum and these conditions is not fully understood.

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.

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.

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.

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.

Americium (Am-241) is a radioactive metallic element with the symbol "Am" and atomic number 95. It is a member of the actinide series and does not occur naturally, but can be produced in nuclear reactors. Americium-241 is most commonly used as a source of ionizing radiation in smoke detectors.

It is important to note that handling and storing americium requires proper training and equipment due to its radioactive nature. Improper handling or disposal can result in serious health risks, including radiation exposure and contamination.

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.

Dihydroxycholecalciferols are a form of calcifediol, which is a type of secosteroid hormone that is produced in the body as a result of the exposure to sunlight and the dietary intake of vitamin D. The term "dihydroxycholecalciferols" specifically refers to the compounds 1,25-dihydroxycholecalciferol (calcitriol) and 24,25-dihydroxycholecalciferol. These compounds are produced in the body through a series of chemical reactions involving enzymes that convert vitamin D into its active forms.

Calcitriol is the biologically active form of vitamin D and plays an important role in regulating the levels of calcium and phosphorus in the blood, as well as promoting the absorption of these minerals from the gut. It also has other functions, such as modulating cell growth and immune function.

24,25-dihydroxycholecalciferol is a less active form of vitamin D that is produced in larger quantities than calcitriol. Its exact role in the body is not well understood, but it is thought to have some effects on calcium metabolism and may play a role in regulating the levels of other hormones in the body.

Dihydroxycholecalciferols are typically measured in the blood as part of an evaluation for vitamin D deficiency or to monitor treatment with vitamin D supplements. Low levels of these compounds can indicate a deficiency, while high levels may indicate excessive intake or impaired metabolism.

Metabolic bone diseases are a group of conditions that affect the bones and are caused by disorders in the body's metabolism. These disorders can result in changes to the bone structure, density, and strength, leading to an increased risk of fractures and other complications. Some common examples of metabolic bone diseases include:

1. Osteoporosis: a condition characterized by weak and brittle bones that are more likely to break, often as a result of age-related bone loss or hormonal changes.
2. Paget's disease of bone: a chronic disorder that causes abnormal bone growth and deformities, leading to fragile and enlarged bones.
3. Osteomalacia: a condition caused by a lack of vitamin D or problems with the body's ability to absorb it, resulting in weak and soft bones.
4. Hyperparathyroidism: a hormonal disorder that causes too much parathyroid hormone to be produced, leading to bone loss and other complications.
5. Hypoparathyroidism: a hormonal disorder that results in low levels of parathyroid hormone, causing weak and brittle bones.
6. Renal osteodystrophy: a group of bone disorders that occur as a result of chronic kidney disease, including osteomalacia, osteoporosis, and high turnover bone disease.

Treatment for metabolic bone diseases may include medications to improve bone density and strength, dietary changes, exercise, and lifestyle modifications. In some cases, surgery may be necessary to correct bone deformities or fractures.

Physiologic calcification is the normal deposit of calcium salts in body tissues and organs. It is a natural process that occurs as part of the growth and development of the human body, as well as during the repair and remodeling of tissues.

Calcium is an essential mineral that plays a critical role in many bodily functions, including bone formation, muscle contraction, nerve impulse transmission, and blood clotting. In order to maintain proper levels of calcium in the body, excess calcium that is not needed for these functions may be deposited in various tissues as a normal part of the aging process.

Physiologic calcification typically occurs in areas such as the walls of blood vessels, the lungs, and the heart valves. While these calcifications are generally harmless, they can sometimes lead to complications, particularly if they occur in large amounts or in sensitive areas. For example, calcification of the coronary arteries can increase the risk of heart disease, while calcification of the lung tissue can cause respiratory symptoms.

It is important to note that pathologic calcification, on the other hand, refers to the abnormal deposit of calcium salts in tissues and organs, which can be caused by various medical conditions such as chronic kidney disease, hyperparathyroidism, and certain infections. Pathologic calcification is not a normal process and can lead to serious health complications if left untreated.

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.

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.

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.

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.

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.

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.

A biopsy is a medical procedure in which a small sample of tissue is taken from the body to be examined under a microscope for the presence of disease. This can help doctors diagnose and monitor various medical conditions, such as cancer, infections, or autoimmune disorders. The type of biopsy performed will depend on the location and nature of the suspected condition. Some common types of biopsies include:

1. Incisional biopsy: In this procedure, a surgeon removes a piece of tissue from an abnormal area using a scalpel or other surgical instrument. This type of biopsy is often used when the lesion is too large to be removed entirely during the initial biopsy.

2. Excisional biopsy: An excisional biopsy involves removing the entire abnormal area, along with a margin of healthy tissue surrounding it. This technique is typically employed for smaller lesions or when cancer is suspected.

3. Needle biopsy: A needle biopsy uses a thin, hollow needle to extract cells or fluid from the body. There are two main types of needle biopsies: fine-needle aspiration (FNA) and core needle biopsy. FNA extracts loose cells, while a core needle biopsy removes a small piece of tissue.

4. Punch biopsy: In a punch biopsy, a round, sharp tool is used to remove a small cylindrical sample of skin tissue. This type of biopsy is often used for evaluating rashes or other skin abnormalities.

5. Shave biopsy: During a shave biopsy, a thin slice of tissue is removed from the surface of the skin using a sharp razor-like instrument. This technique is typically used for superficial lesions or growths on the skin.

After the biopsy sample has been collected, it is sent to a laboratory where a pathologist will examine the tissue under a microscope and provide a diagnosis based on their findings. The results of the biopsy can help guide further treatment decisions and determine the best course of action for managing the patient's condition.

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.

Bone density refers to the amount of bone mineral content (usually measured in grams) in a given volume of bone (usually measured in cubic centimeters). It is often used as an indicator of bone strength and fracture risk. Bone density is typically measured using dual-energy X-ray absorptiometry (DXA) scans, which provide a T-score that compares the patient's bone density to that of a young adult reference population. A T-score of -1 or above is considered normal, while a T-score between -1 and -2.5 indicates osteopenia (low bone mass), and a T-score below -2.5 indicates osteoporosis (porous bones). Regular exercise, adequate calcium and vitamin D intake, and medication (if necessary) can help maintain or improve bone density and prevent fractures.

Osteocalcin is a protein that is produced by osteoblasts, which are the cells responsible for bone formation. It is one of the most abundant non-collagenous proteins found in bones and plays a crucial role in the regulation of bone metabolism. Osteocalcin contains a high affinity for calcium ions, making it essential for the mineralization of the bone matrix.

Once synthesized, osteocalcin is secreted into the extracellular matrix, where it binds to hydroxyapatite crystals, helping to regulate their growth and contributing to the overall strength and integrity of the bones. Osteocalcin also has been found to play a role in other physiological processes outside of bone metabolism, such as modulating insulin sensitivity, energy metabolism, and male fertility.

In summary, osteocalcin is a protein produced by osteoblasts that plays a critical role in bone formation, mineralization, and turnover, and has been implicated in various other physiological processes.

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.

Heterotopic ossification (HO) is a medical condition where bone tissue forms outside the skeleton, in locations where it does not typically exist. This process can occur in various soft tissues, such as muscles, tendons, ligaments, or even inside joint capsules. The abnormal bone growth can lead to pain, stiffness, limited range of motion, and, in some cases, loss of function in the affected area.

There are several types of heterotopic ossification, including:

1. Myositis ossificans - This form is often associated with trauma or injury, such as muscle damage from a fracture, surgery, or direct blow. It typically affects young, active individuals and usually resolves on its own within months to a few years.
2. Neurogenic heterotopic ossification (NHO) - Also known as "traumatic heterotopic ossification," this form is often linked to spinal cord injuries, brain injuries, or central nervous system damage. NHO can cause significant impairment and may require surgical intervention in some cases.
3. Fibrodysplasia ossificans progressiva (FOP) - This rare, genetic disorder causes progressive heterotopic ossification throughout the body, starting in early childhood. The condition significantly impacts mobility and quality of life, with no known cure.

The exact mechanisms behind heterotopic ossification are not fully understood, but it is believed that a combination of factors, including inflammation, tissue injury, and genetic predisposition, contribute to its development. Treatment options may include nonsteroidal anti-inflammatory drugs (NSAIDs), radiation therapy, physical therapy, or surgical removal of the abnormal bone growth, depending on the severity and location of the HO.

Bone resorption is the process by which bone tissue is broken down and absorbed into the body. It is a normal part of bone remodeling, in which old or damaged bone tissue is removed and new tissue is formed. However, excessive bone resorption can lead to conditions such as osteoporosis, in which bones become weak and fragile due to a loss of density. This process is carried out by cells called osteoclasts, which break down the bone tissue and release minerals such as calcium into the bloodstream.

The metacarpus is the medical term for the part of the hand located between the carpus (wrist) and the digits (fingers). It consists of five bones, known as the metacarpal bones, which are numbered 1 to 5 from the thumb side to the little finger side. Each metacarpal bone has a base, a shaft, and a head. The bases of the metacarpal bones articulate with the carpal bones to form the wrist joint, while the heads of the metacarpal bones form the knuckles at the back of the hand.

The metacarpus plays an essential role in hand function as it provides stability and support for the movement of the fingers and thumb. Injuries or conditions affecting the metacarpus can significantly impact hand function, causing pain, stiffness, weakness, or deformity.

Peritoneal dialysis is a type of renal replacement therapy used to treat patients with severe kidney dysfunction or end-stage renal disease. It is a process that utilizes the peritoneum, a membranous sac lining the abdominal cavity, as a natural semipermeable membrane for filtering waste products, excess fluids, and electrolytes from the bloodstream.

In peritoneal dialysis, a sterile dialysate solution is infused into the peritoneal cavity via a permanently implanted catheter. The dialysate contains various substances such as glucose or other osmotic agents, electrolytes, and buffer solutions that facilitate the diffusion of waste products and fluids from the blood vessels surrounding the peritoneum into the dialysate.

There are two primary types of peritoneal dialysis: continuous ambulatory peritoneal dialysis (CAPD) and automated peritoneal dialysis (APD). CAPD is performed manually, several times a day, while APD is carried out using a cycler machine overnight.

Peritoneal dialysis offers certain advantages over hemodialysis, such as better preservation of residual renal function, fewer dietary restrictions, and greater flexibility in scheduling treatments. However, it also has potential complications, including peritonitis (inflammation of the peritoneum), catheter-related infections, fluid imbalances, and membrane failure over time.

Developmental bone diseases are a group of medical conditions that affect the growth and development of bones. These diseases are present at birth or develop during childhood and adolescence, when bones are growing rapidly. They can result from genetic mutations, hormonal imbalances, or environmental factors such as poor nutrition.

Some examples of developmental bone diseases include:

1. Osteogenesis imperfecta (OI): Also known as brittle bone disease, OI is a genetic disorder that affects the body's production of collagen, a protein necessary for healthy bones. People with OI have fragile bones that break easily and may also experience other symptoms such as blue sclerae (whites of the eyes), hearing loss, and joint laxity.
2. Achondroplasia: This is the most common form of dwarfism, caused by a genetic mutation that affects bone growth. People with achondroplasia have short limbs and a large head relative to their body size.
3. Rickets: A condition caused by vitamin D deficiency or an inability to absorb or use vitamin D properly. This leads to weak, soft bones that can bow or bend easily, particularly in children.
4. Fibrous dysplasia: A rare bone disorder where normal bone is replaced with fibrous tissue, leading to weakened bones and deformities.
5. Scoliosis: An abnormal curvature of the spine that can develop during childhood or adolescence. While not strictly a developmental bone disease, scoliosis can be caused by various underlying conditions such as cerebral palsy, muscular dystrophy, or spina bifida.

Treatment for developmental bone diseases varies depending on the specific condition and its severity. Treatment may include medication, physical therapy, bracing, or surgery to correct deformities and improve function. Regular follow-up with a healthcare provider is essential to monitor growth, manage symptoms, and prevent complications.

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.

Scurvy is a medical condition caused by a deficiency of vitamin C (ascorbic acid) in the diet, which leads to the breakdown of collagen. This results in various symptoms such as anemia, gum disease, and skin hemorrhages. In severe cases, it can lead to death. It was prevalent among sailors during long voyages before the 18th century when fresh fruits and vegetables were not available, and the condition was eventually linked to the lack of vitamin C in their diet. Nowadays, scurvy is rare in developed countries but can still occur in individuals with extreme diets deficient in vitamin C.

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.

Maxillofacial abnormalities, also known as craniofacial anomalies, refer to a broad range of structural and functional disorders that affect the development of the skull, face, jaws, and related soft tissues. These abnormalities can result from genetic factors, environmental influences, or a combination of both. They can vary in severity, from minor cosmetic issues to significant impairments of vital functions such as breathing, speaking, and eating.

Examples of maxillofacial abnormalities include cleft lip and palate, craniosynostosis (premature fusion of the skull bones), hemifacial microsomia (underdevelopment of one side of the face), and various other congenital anomalies. These conditions may require multidisciplinary treatment involving surgeons, orthodontists, speech therapists, and other healthcare professionals to address both functional and aesthetic concerns.

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.

... renal osteodystrophy); and 3) vascular or other soft-tissue calcification. Renal osteodystrophy may exhibit no symptoms; if it ... Renal osteodystrophy is usually diagnosed after treatment for end-stage kidney disease begins; however the CKD-MBD starts early ... Renal osteodystrophy/adynamic bone disease is currently defined as an alteration of bone morphology in patients with chronic ... Treatment for renal osteodystrophy includes the following:[citation needed] calcium and/or native vitamin D supplementation ...
Renal complications OFC is a common presentation of renal osteodystrophy, which is a term used to refer to the skeletal ... The concept of renal osteodystrophy is currently included into the broader term chronic kidney disease-mineral and bone ... Delmez, James (January 2005). "Renal Osteodystrophy" (PDF). National Institute of Health. U.S. Department of Health and Human ... or renal osteodystrophy. Osteoclastic bone resorption releases minerals, including calcium, from the bone into the bloodstream ...
One form is renal osteodystrophy. List of radiographic findings associated with cutaneous conditions "Renal osteodystrophy ( ... Osteodystrophy is any dystrophic growth of the bone. It is defective bone development that is usually attributable to renal ...
Chronic kidney disease can lead to renal osteodystrophy. Hematologic disorders linked to osteoporosis are multiple myeloma and ... or osteomalacia in renal osteodystrophy. However, radiography is relatively insensitive to detection of early disease and ...
25-dihydroxycholecalciferol in renal osteodystrophy". Canadian Medical Association Journal. 112 (2): 190, 193-5. PMC 1956416. ... 25-dihydroxyvitamin D3 and 1α-hydroxyvitamin D3 to treat renal osteodystrophy, hypoparathyroidism, vitamin D dependent rickets ...
Lack of calcium can lead to renal osteodystrophy (bone weakening). On the other hand, too much calcium can cause calcification ...
Diagnosis of osteosarcoma, ameloblastoma, renal osteodystrophy affecting jaws and hypophosphatemia. Diagnosis, and pre- and ...
It differs from renal osteodystrophy, where the latter shows hyperphosphatemia. The causes of adult osteomalacia are varied, ... except in cases of renal osteodystrophy Elevated serum alkaline phosphatase (due to an increase in compensatory osteoblast ... In addition to low systemic levels of circulating mineral ions (for example, caused by vitamin D deficiency or renal phosphate ... phosphate deficiency caused by increased renal losses. Symptoms: Diffuse joint and bone pain (especially of spine, pelvis, and ...
Signs and symptoms include ectopic calcification, secondary hyperparathyroidism, and renal osteodystrophy. Abnormalities in ...
"Treatment of a murine model of high-turnover renal osteodystrophy by exogenous BMP-7". Kidney International. 61 (4): 1322-31. ... This type of fibrosis often leads to renal failure, and is predictive of end stage renal disease. BMP7 has been discovered to ... "Bone morphogenetic protein-7 improves renal fibrosis and accelerates the return of renal function". Journal of the American ... Renal Physiology. 285 (6): F1060-7. doi:10.1152/ajprenal.00191.2002. PMID 12915382. Kalluri R, Weinberg RA (June 2009). "The ...
Short dialysis (at home) five times a week is thought to reduce renal osteodystrophy. SDHHD and nocturnal dialysis avoid large ... From CMS's point of view any form of dialysis is still more expensive than renal transplantation if looked at over a three-year ... Mehrotra R, Marsh D, Vonesh E, Peters V, Nissenson A (2005). "Patient education and access of ESRD patients to renal ... A good kidney transplant (one that lasts five years) remains the cheapest long term renal replacement therapy. In many ...
... and renal osteodystrophy among others. Temporary hemiepiphysiodesis is increasingly been viewed as more simple and efficient ... "Correction of lower limb deformities in children with renal osteodystrophy by guided growth technique". Journal of Children's ...
The bone disease in secondary hyperparathyroidism caused by kidney failure is termed renal osteodystrophy. Tertiary ... and renal osteodystrophy. Radiation exposure increases the risk of primary hyperparathyroidism. A number of genetic conditions ... Blaine J, Chonchol M, Levi M (July 2015). "Renal control of calcium, phosphate, and magnesium homeostasis". Clinical Journal of ... Hyperparathyroidism can cause hyperchloremia and increase renal bicarbonate loss, which may result in a normal anion gap ...
... s may be rarely associated with ectopic parathyroid adenomas or end stage renal osteodystrophy. Histologically, it ... Brown tumor in end-stage renal disease". The New England Journal of Medicine. 341 (22): 1652. doi:10.1056/nejm199911253412204. ...
2006). "Renal osteodystrophy: alpha-Heremans Schmid glycoprotein/fetuin-A, matrix GLA protein serum levels, and bone ...
... such as renal osteodystrophy, produce widening, while ochronosis results in calcific deposits in the symphysis. Inflammatory ...
... "renal osteodystrophy", which now should be restricted to describing the bone pathology associated with CKD. Thus, renal ... The traditional definition of renal osteodystrophy did not accurately encompass this more diverse clinical spectrum, based on ... The absence of a generally accepted definition and diagnosis of renal osteodystrophy prompted Kidney Disease: Improving Global ... 2006). "Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving ...
... also rarely occurs in Paget's disease of bone, hyperparathyroidism, renal osteodystrophy, osteogenesis ...
... fluoride ion in renal osteodystrophy: correlation with bone histomorphometry". Journal of Clinical Endocrinology & Metabolism. ... 18F]NaF renal clearance is affected by diet and pH level, due to its re-absorption in the nephron, which is mediated by ... Renal Physiology. 235 (3): F254-F264. doi:10.1152/ajprenal.1978.235.3.f254. ISSN 1931-857X. PMID 696835. Staffurth, J. S.; ... Ekstrand, J.; Spak, C. J.; Ehrnebo, M. (2009-03-13). "Renal Clearance of Fluoride in a Steady State Condition in Man: Influence ...
... and renal osteodystrophy. Sometimes no single cause accounts for SCFE, and several factors play a role in the development of a ...
Acid buffering leads to loss of bone density, resulting in an increased risk of bone fractures, renal osteodystrophy, and bone ... measurement of serum ketones indicative of ketoacidosis and renal function tests and urinanalysis to detect renal dysfunction. ... and failure of renal excretion of products of metabolism such as sulphates and phosphates. Adjunctive tests are useful in ... and additional renal generation. The buffer reactions are: H + + HCO 3 − ↽ − − ⇀ H 2 CO 3 ↽ − − ⇀ CO 2 + H 2 O {\displaystyle ...
... hyperparathyroidism and renal osteodystrophy.[citation needed] The common form is that in which one or other maxilla is ...
Chow Chows can be affected by renal dysplasia that progresses to kidney failure and secondary fibrous renal osteodystrophy, ... Familial renal disease is an uncommon cause of kidney failure in dogs and cats. Most causes are breed-related (familial) and ... It progresses to renal failure. Findings include protein in the urine. It is inherited. Persians can be affected by polycystic ... Secondary fibrous osteodystrophy can be seen. Welsh Corgis can be affected by kidney telangiectasias between the ages of five ...
For example, children with renal osteodystrophy or renal bone disease, certain hematological disorders and diseases causing ... renal osteodystrophy and immune-compromised status. In adults vulnerable groups include an artificial joint, prior arthritis, ...
... such as renal osteodystrophy and hypertension. A physician who has undertaken additional training and become certified in ... and the Renal Association represents renal physicians and works closely with the National Service Framework for kidney disease ... renal physiology) and kidney disease (renal pathophysiology), the preservation of kidney health, and the treatment of kidney ... other experts have advocated preserving the use of renal and nephro as appropriate including in "nephrology" and "renal ...
... renal osteodystrophy MeSH C05.116.198.816 - rickets MeSH C05.116.231.030 - adamantinoma MeSH C05.116.231.343 - femoral ...
Osteomyelitis Osteopenia Osteopetrosis Osteoporosis Porotic hyperostosis Primary hyperparathyroidism Renal osteodystrophy ...
... renal osteodystrophy MeSH C19.642.482.500 - digeorge syndrome MeSH C19.700.159.750 - diabetes insipidus, neurogenic MeSH ...
... renal osteodystrophy, chronic kidney disease Treatment of osteoporosis Prevention of corticosteroid-induced osteoporosis ... Increasing renal tubular reabsorption of calcium, thus reducing the loss of calcium in the urine. Stimulating release of ... This will produce greater effects than other vitamin D precursors in patients with kidney disease who have loss of the renal 1- ...
... hypocalcemia and renal osteodystrophy and, with calcium, in primary or corticosteroid-induced osteoporosis. Calcifediol may ... placenta and parathyroid gland and extra-renal synthesis of calcitriol from calcifediol has been shown to have biological ...
... renal osteodystrophy); and 3) vascular or other soft-tissue calcification. Renal osteodystrophy may exhibit no symptoms; if it ... Renal osteodystrophy is usually diagnosed after treatment for end-stage kidney disease begins; however the CKD-MBD starts early ... Renal osteodystrophy/adynamic bone disease is currently defined as an alteration of bone morphology in patients with chronic ... Treatment for renal osteodystrophy includes the following:[citation needed] calcium and/or native vitamin D supplementation ...
Cite this: Vitamin D metabolism in the pathogenesis of renal osteodystrophy and secondary hyperparathyroidism - Medscape - Jul ... Vitamin D metabolism in the pathogenesis of renal osteodystrophy and secondary hyperparathyroidism ...
Osteomalacia may be part of the spectrum of osseous abnormalities that can be observed in patients with chronic renal ... encoded search term (Osteomalacia and Renal Osteodystrophy Imaging) and Osteomalacia and Renal Osteodystrophy Imaging What to ... this condition is referred to as renal osteodystrophy. Renal osteodystrophy combines features of secondary hyperparathyroidism ... Renal osteodystrophy is a global term applied to all pathologic features of bone in patients with renal failure. The primary ...
Bone Disease in Nephropathic Cystinosis: Beyond Renal Osteodystrophy Irma Machuca-Gayet 1 , Thomas Quinaux 1 2 , Aurélia ... Bone Disease in Nephropathic Cystinosis: Beyond Renal Osteodystrophy Irma Machuca-Gayet et al. Int J Mol Sci. 2020. . ... Keywords: Bone; CKD-MBD; Nephropathic cystinosis; Orphan disease; Osteoblast; Osteoclast; Renal osteodystrophy (ROD); mTor ... and classification of renal osteodystrophy: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO) Kidney ...
End-stage renal failure is a chronic, progressive, debilitating disease that causes disability and high mortality, and the ... Renal osteodystrophy, Anesthesia, Outcome, Kidney retransplantation.. Introduction. Chronic Kidney Disease (CKD) is a worldwide ... Multimodal anesthesia for kidney retransplantation in patients with advanced renal osteodystrophy.. Lucia Caroline Schons1, ... Computed Tomography: Infra-renal Vein Hypoplasia. Two previous renal implants in right and left iliac arteries [10]. Anesthesia ...
Dive into the research topics of Renal osteodystrophy. Together they form a unique fingerprint. ...
Renal Osteodystrophy. Chronic Kidney Disease-Mineral and Bone Disorder. RNA Recognition Motif (RRM) Proteins. RNA Recognition ...
Diffuse calcification of a transplanted kindney: a manifestation of renal osteodystrophy  Jaber, Hesham; Hiari, Asem; Jmean, ...
261 Results for Renal Osteodystrophy near Ashburn, VA 20147 Sort: Recommended. Recommended Distance Rating: High to Low ... Montgomery Renal Associates: 15225 Shady Grove Rd Ste 104 Rockville, MD 20850 ...
The NIDDK Kidney Clinical Research and Epidemiology program advances clinical studies and epidemiologic research on renal ... Kevin Chan, M.D. Epidemiology; Renal Osteodystrophy; Clinical Trials; Dialysis and CKD Clinical Studies ... Randomized clinical trials are also conducted to test new therapies to prevent the progression of renal disease and its ... Advances clinical studies and epidemiologic research on renal disease. The Kidney Clinical Research and Epidemiology program ...
... while the long-term regulation of renal phosphate handling requires the IP3/PKC signaling pathway. Dr. Jueppner developed one ...
1 reviews for Renal Osteodystrophy. 9 medications. Add your review. Reviews for Ergocalciferol. Search keyword Search ...
Diffuse calcification of a transplanted kindney: a manifestation of renal osteodystrophy  Jaber, Hesham; Hiari, Asem; Jmean, ...
Renal Osteodystrophy ... I have a rare condition (FMD) that causes renal and carotid ...
Bone metabolism disorder except osteoporosis (e.g., Pagets disease, renal osteodystrophy, osteomalacia) ...
Renal osteodystrophy (2): its treatment in renal insufficiency before dialysis].. Hottelart C; Bako G; Oprisiu R; Georgita A; ... Renal osteodystrophy Guidelines].. Messa P;. G Ital Nefrol; 2003; 20 Suppl 24():S83-95. PubMed ID: 14666505. [TBL] ... 9. [Renal osteodystrophy (3); its treatment in dialysis patients].. Ghitu S; Oprisiu R; Benamar L; Said S; Tataru Albu A; ... 8. Renal osteodystrophy in dialysis patients: diagnosis and treatment.. Fournier A; Oprisiu R; Hottelart C; Yverneau PH; ...
Adult renal osteodystrophy and TLSO. Mitchell Visser. Prosthetic socks (hole-in-toe) with minimal distal thickness ...
Repression of osteocyte Wnt/β-catenin signaling is an early event in the progression of renal osteodystrophy. J. Bone Miner. ...
... affect bone turnover rate and may result in renal osteodystrophy. ... Renal and Urinary Disorders. Renal Failure Chronic. 2. (3.3%). ... Renal Impairment Following administration of paricalcitol capsules, the pharmacokinetic profile of paricalcitol for CKD Stage 5 ...
Renal Function and Chronic Kidney Disease in Aging (R01) PA-09-165. NIA ... and renal osteodystrophy; hematologic problems (anemia and thrombosis) and impaired immune function; and the development of ... According to United States Renal Data System (USRDS) data, the number of older patients with end-stage renal disease (ESRD) has ... CKD is a decline in renal function defined by decreased glomerular filtration rate (GFR) and/or other evidence of renal damage ...
Abid F, Lalani I, Zakaria A, Facchini SA, Hunter JV "Cranial nerve palsies in renal osteodystrophy.." Pediatr. Neurol.. 2007 ...
"Pharmacologic management of renal osteodystrophy" Invited presentation. Local chapter of the American Nephrology Nurses ... "Estimating renal function for drug dosing: CG versus MDRD" American Society of Health-System Pharmacists Midyear Meeting. ... "Drug-induced renal dysfunction" Utah Society of Health-System Pharmacists Meeting. Salt Lake City, Utah. Presentation, ... "Management of hypertension in end stage renal disease" Invited presentation. Local Chapter of the American Nephrology Nurses ...
Haynatzki GR, Dunlay RW, Stegman MR, Recker RR: The use of bone ultrasound in managing renal osteodystrophy. American Society ... Rhabdomyolysis and acute renal failure after changing statin-fibrate combinations. Oldemeyer B, Lund R, Koch M, Meares A, ...
Scientific and technologic improvements during the second half of the 20th century provided renal replacement therapy as a life ... and renal failure (RF) have been recognized as significant medical problems for most of the last 2 centuries and, until ... and future interventions to prevent renal osteodystrophy should be discussed. Subtle signs of renal osteodystrophy begin to be ... Predictors of renal recovery in Australian and New Zealand end-stage renal failure patients treated with peritoneal dialysis. ...
The Prevalence of Renal Osteodystrophy in Chronic Renal Failure Patients in Urban Niger Delta of Nigeria By U. R. Onyemekeihia ...
Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global ... Hou Y, Li X, Sun L, Qu Z, Jiang L, Du Y. Phosphorus and mortality risk in end-stage renal disease: A meta-analysis. Clin Chim ... Special nutritional needs of chronic kidney disease and end-stage renal disease patients: rationale for the use of plant-based ... Relationship of dietary phosphate intake with risk of end-stage renal disease and mortality in chronic kidney disease stages 3- ...
mineral and bone disorder, CKD-MBD, renal osteodystrophy, calcitriol, calcium, phosphorus, parathyroid hormone, PTH, ...
Hyperparathyroidism has the potential to provoke renal osteodystrophy, hypertension, cardiomyocyte hypertrophy, insulin ... A. Karamé, M. Labeeuw, P. Trolliet et al., "The impact of type 2 diabetes on mortality in end-stage renal disease patients ... A. Trombetti, C. Stoermann, J. H. Robert et al., "Survival after parathyroidectomy in patients with end-stage renal disease and ... Data for end-stage renal disease (ESRD) patients who underwent maintenance hemodialysis at Ditmanson Medical Foundation Chia-yi ...

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