Uremia
Azotemia
Renal Dialysis
Kidney Failure, Chronic
Urea
Blood Urea Nitrogen
Parathyroid Hormone
Anuria
Kidneys, Artificial
Parathyroid Glands
Hemorrhagic Disorders
Peritoneal Dialysis
Glycosylation End Products, Advanced
Mechanism of parathyroid tumourigenesis in uraemia. (1/1382)
Clonal analysis has shown that in renal hyperparathyroidism (2-HPT), parathyroid glands initially grow diffusely and polyclonally after which the foci of nodular hyperplasia are transformed to monoclonal neoplasia. There is a great deal of information about genetic abnormalities contributing to the tumourigenesis of parathyroid neoplasia in primary hyperparathyroidism. It is speculated that allelic loss of the MEN1 suppressor gene and overexpression of cyclin D1 induced by rearrangement of the parathyroid hormone gene may be the major genetic abnormality in sporadic parathyroid adenoma but not in 2-HPT. The pathogenesis of 2-HPT, abnormality of the Ca2+-sensing receptor (CaR) gene and the vitamin D receptor gene may possibly contribute to parathyroid tumourigenesis in 2-HPT. However, this is not yet clear and heterogeneous and multiple genetic abnormalities may be responsible for the progression of secondary parathyroid hyperplasia. (+info)Implication of carbonyl stress in long-term uraemic complications. (2/1382)
Advanced glycation end products (AGEs) are formed during non-enzymatic glycation and oxidation (glycoxidation) reactions. AGEs, such as pentosidine and carboxymethyllysine are increased in plasma proteins and skin collagen of uraemic patients several times more than in normal subjects and non-uraemic diabetic patients. However, AGEs do not differ between diabetics and non-diabetics in uraemic patients. The AGE accumulation in uraemia, therefore, cannot be attributed to hyperglycaemia, nor simply to a decreased removal by glomerular filtration of AGE-modified proteins. Recent evidence has suggested that, in uraemia, the increased carbonyl compounds, derived from both carbohydrates and lipids, modify proteins not only by glycoxidation but also by lipoxidation reactions, leading to the increased production of AGEs and advanced lipoxidation end products (ALEs). Thus, uraemia might be a state of increased carbonyl compounds with potentially damaging proteins ('carbonyl stress'). Carbonyl stress in uraemia appears relevant to long-term complications, such as dialysis-related amyloidosis. The increased AGEs and ALEs in uraemic plasma and tissue proteins may indicate alterations in the non-enzymatic chemistry involving both carbohydrates and lipids in uraemia. (+info)Maintenance of normal agonist-induced endothelium-dependent relaxation in uraemic and hypertensive resistance vessels. (3/1382)
BACKGROUND: The nitric oxide system has been implicated in several diseases with vascular complications including diabetes mellitus and hypertension. Despite the high prevalence of hypertension and cardiovascular complications in renal failure few studies have examined vascular and endothelial function in uraemia. We therefore chose to study possible abnormalities of the nitric oxide vasodilator system in an animal model of chronic renal failure. METHODS: Adult spontaneous hypertensive rats and Wistar Kyoto rats were subjected to a 5/6 nephrectomy with control animals having sham operations. After 4 weeks blood pressure was recorded and the animals were sacrificed. Branches of the mesenteric arteries were isolated and mounted on a Mulvany myograph. All experiments were performed in the presence of indomethacin (10(-5) M). The vessels were first preconstricted with noradrenaline, exposed to increasing concentrations of acetylcholine (10(-8) to 10(-4) M) and subsequently to sodium nitroprusside (10(-5) M). RESULTS: There was no difference in the relaxation of the four groups of vessels to any of the concentrations of acetylcholine used nor was there any significant difference in the EC50s (control Wistar Kyoto 6.1+/-1.4 x 10(-8) M; uraemic Wistar Kyoto 5.4+/-0.8 x 10(-8) M; control spontaneous hypertensive rats 4.5+/-0.6 x 10(-8) M; uraemic spontaneous hypertensive rats 6+/-0.7 x 10(-8) M). Vasodilatation in response to sodium nitroprusside was unchanged in uraemic vessels. In addition the vascular responses to both acetylcholine and sodium nitroprusside were unaltered in spontaneous hypertensive rats. CONCLUSIONS: We conclude that normal agonist-induced endothelium-dependent relaxation is maintained in experimental uraemia and hypertension. (+info)The impact of an amino acid-based peritoneal dialysis fluid on plasma total homocysteine levels, lipid profile and body fat mass. (4/1382)
BACKGROUND: The caloric load from glucose-based peritoneal dialysis (PD) fluids contributes to hypertriglyceridaemia, adiposity and, as result of anorexia, protein malnutrition in PD patients. It has been suggested that replacement of a glucose-based by an amino acids-based PD fluid (AA-PDF) for one exchange per day might improve the nutritional status and lipid profile. Due to the uptake of methionine from the dialysate, however, exposure to AA-PDF might aggravate hyperhomocysteinaemia, a frequently occurring risk factor for atherosclerosis in uraemic patients. METHODS: We studied the impact of a once daily exchange with 1.1% AA-PDF instead of glucose-based PD fluid for 2 months on plasma methionine and total homocysteine (tHcy) levels, lipid profile, butyrylcholinesterase (BChE) and body fat mass of seven stable PD patients. Results are expressed as mean+/-SEM. RESULTS: Methionine levels did not increase significantly during therapy, but tHcy levels increased substantially from 60+/-12 to 84+/-19 micromol/l after 1 month (P=0.039), and to 85+/-22 micromol/l after 2 months of AA-PDF treatment. Serum triglyceride concentration decreased from 3.0+/-0.4 mmol/l at entry to 2.6+/-0.5 mmol/l (at 1 month, P=0.041 vs baseline). Serum BChE also decreased from 6.9+/-0.4 U/ml at entry to 6.3+/-0.4 U/ml after 2 months (P=0.014). Total cholesterol concentration and cholesterol fractions did not change. The reduced exposure to glucose-based PD fluid for 2 months resulted in a 0.5 kg reduction in fat mass which was due mainly to a reduction in fat mass of the trunk region (0.3 kg, P=0.031). CONCLUSIONS: It is concluded that methionine-containing AA-PDF induces an increase in the plasma tHcy level. This might, potentially, offset the beneficial effects of an improved serum lipid profile and reduced fat mass on the risk of cardiovascular disease in PD patients. Lowering the methionine content of the fluid, therefore, may be required to overcome this adverse effect. (+info)Decreased calcium-sensing receptor expression in hyperplastic parathyroid glands of uremic rats: role of dietary phosphate. (5/1382)
BACKGROUND: The abnormal control of parathyroid hormone secretion in chronic renal failure is attributed, in part, to down-regulation of the calcium-sensing receptor (CaR) in hyperplastic parathyroid tissue. The cause of this down-regulation is unknown. Here we examined the roles of uremia and parathyroid hyperplasia on parathyroid gland (PTG) CaR expression in the rat model of renal failure. METHODS: Rats made uremic by 5/6 nephrectomy were maintained for one month on diets containing 0.2% P (low phosphate), 0.5% P (normal phosphate) or 1.2% P (high phosphate); intact rats (controls) were maintained on the normal-phosphate diet. RESULTS: CaR mRNA was reduced only in uremic rats fed the high-phosphate diet (55% less than in controls, P < 0.05). Immunohistochemical staining revealed decreased CaR protein expression in uremic high-phosphate rat PTG compared with controls (41% decrease as determined by computer-assisted quantitation, P < 0.01). PTG size was increased in uremic rats fed the high-phosphate diet compared with controls (2.77 +/- 0.95 vs. 0.77 +/- 0.16 microgram/g body wt, P < 0.0001). There was no increase in PTG size in uremic rats fed the low-phosphate and normal-phosphate diets (0.92 +/- 0.31 and 1.01 +/- 0.31 micrograms/g) compared with controls (0.77 +/- 0.16 microgram/g body wt). Immunohistochemical staining for proliferating cell nuclear antigen in hyperplastic PTG from uremic rats showed that CaR was decreased primarily in areas of active cell proliferation. CONCLUSION: These results suggest that CaR down-regulation cannot be attributed to uremia per se, but rather, is associated with parathyroid cell proliferation. Furthermore, dietary phosphate restriction prevents both the parathyroid hyperplasia and decreased CaR expression in renal failure. (+info)Evidence of splanchnic-brain signaling in inhibition of ingestive behavior by middle molecules. (6/1382)
Anorexia, nausea, and vomiting are common symptoms of uremic intoxication. Fractions in the middle molecule weight range, isolated from normal urine and uremic plasma ultrafiltrate, inhibit ingestive behavior in the rat. To investigate their site of action and specificity, male rats were injected intraperitoneally, intravenously, or intracerebroventricularly with concentrated fractions of uremic plasma ultrafiltrate or normal urine (molecular weight range: 1.0 to 5.0 kD) and tested for ingestive and sexual behavior. An intraperitoneal injection of 0.5 ml of urine fraction (10:1) or 2.0 ml of uremic plasma ultrafiltrate fraction (25:1) inhibited carbohydrate intake by 76.3 and 45.9%, respectively, but an intravenous injection had no effect. However, intravenous injection of higher doses inhibited carbohydrate ingestion. An intracerebroventricular injection of 5 or 10 microl of urine (20:1) middle molecule fraction inhibited carbohydrate intake by 13.4 and 41.6%, respectively. An injection of 5 or 10 microl of uremic plasma ultrafiltrate (125:1) middle molecule fraction inhibited carbohydrate intake by 22.6 and 49.5%, respectively. Injections of the corresponding fraction from normal plasma ultrafiltrate had no effect. Injection of urine or uremic plasma ultrafiltrate middle molecule fractions did not affect the display of sexual behavior. These results suggest that middle molecule fractions from uremic plasma ultrafiltrate or normal urine act in the splanchnic region and/or brain to inhibit food intake and that the effect is specific for ingestive behavior. (+info)Association of morbidity with markers of nutrition and inflammation in chronic hemodialysis patients: a prospective study. (7/1382)
BACKGROUND: Numerous studies suggest a strong association between nutrition and clinical outcome in chronic hemodialysis (CHD) patients. Nevertheless, the pathophysiological link between malnutrition and morbidity remains to be clarified. In addition, recent evidence suggests that nutritional indices may reflect an inflammatory response, as well as protein-calorie malnutrition. In this study, we prospectively assessed the relative importance of markers of nutritional status and inflammatory response as determinants of hospitalization in CHD patients. METHODS: The study consisted of serial measurements of concentrations of serum albumin, creatinine, transferrin, prealbumin, C-reactive protein (CRP), and reactance values by bio-electrical impedance analysis (BIA) as an indirect measure of lean body mass every 3 months over a period of 15 months in 73 CHD patients. Outcome was determined by hospitalizations over the subsequent three months following each collection of data. RESULTS: Patients who required hospitalization in the three months following each of the measurement sets had significantly different values for all parameters than patients who were not hospitalized. Thus, serum albumin (3.93 +/- 0.39 vs. 3.74 +/- 0.39 g/dl), serum creatinine (11.0 +/- 3.7 vs. 9.1 +/- 3.5 mg/dl), serum transferrin (181 +/- 35 vs. 170 +/- 34 mg/dl), serum prealbumin (33.6 +/- 9.2 vs. 30.0 +/- 10.1 mg/dl), and reactance (50.4 +/- 15.6 vs. 43.0 +/- 13.0 ohms) were higher for patients not hospitalized, whereas CRP (0.78 +/- 0.89 vs. 2.25 +/- 2.72 mg/dl) was lower in patients who were not hospitalized. All differences were statistically significant (P < 0.05 for all parameters). When multivariate analysis was performed, serum CRP and reactance values were the only statistically significant predictors of hospitalization (P < 0.05 for both). When a serum CRP concentration of 0.12 mg/dl was considered as a reference range (relative risk 1.0), the relative risk for hospitalization was 7% higher (relative risk = 1.07) for a CRP concentration of 0.92 mg/dl and was 30% (relative risk = 1.30) higher for a CRP concentration of 3.4 mg/dl. When a reactance value of 70 ohms was considered as a reference range with a relative risk of 1.0, the relative risk of hospitalization increased to 1.09 for a reactance value of 43 ohms and further increased to 1.14 for a reactance value of 31 ohms. CONCLUSIONS: The results of this study strongly indicate that both nutritional status and inflammatory response are independent predictors of hospitalization in CHD patients. CRP and reactance values by BIA are reliable indicators of hospitalization. Visceral proteins such as serum albumin, prealbumin, and transferrin are influenced by inflammation when predicting hospitalization. When short-term clinical outcomes such as hospitalizations are considered, markers of both inflammation and nutrition should be evaluated. (+info)Increased erythrocyte 3-DG and AGEs in diabetic hemodialysis patients: role of the polyol pathway. (8/1382)
BACKGROUND: 3-Deoxyglucosone (3-DG) accumulating in uremic serum plays an important role in the formation of advanced glycation end products (AGEs). To determine if 3-DG is involved in the formation of intracellular AGEs, we measured the erythrocyte levels of 3-DG and AGEs such as imidazolone and N epsilon-carboxymethyllysine (CML) in hemodialysis (HD) patients with diabetes. Further, to determine if the polyol pathway is involved in the formation of erythrocyte 3-DG and AGEs, an aldose reductase inhibitor (ARI) was administered to these patients. METHODS: The erythrocyte levels of sorbitol, 3-DG, imidazolone, and CML were measured in ten diabetic HD patients before and after treatment with ARI (epalrestat) for eight weeks, and were compared with those in eleven healthy subjects. 3-DG was incubated in vitro with hemoglobin for two weeks to determine if imidazolone and CML are formed by reacting 3-DG with hemoglobin. RESULTS: The erythrocyte levels of sorbitol, 3-DG, imidazolone, and CML were significantly elevated in diabetic HD patients as compared with healthy subjects. The erythrocyte levels of 3-DG significantly decreased after HD, but sorbitol, imidazolone or CML did not. The administration of ARI significantly decreased the erythrocyte levels of sorbitol, 3-DG and imidazolone, and tended to decrease the CML level. Imidazolone was rapidly produced in vitro by incubating 3-DG with hemoglobin, and CML was also produced, but less markedly as compared with imidazolone. CONCLUSION: The erythrocyte levels of 3-DG and AGEs are elevated in diabetic HD patients. The administration of ARI reduces the erythrocyte levels of 3-DG and AGEs, especially imidazolone, as well as sorbitol. Thus, 3-DG and AGEs, especially imidazolone, in the erythrocytes are produced mainly via the polyol pathway. ARI may prevent diabetic and uremic complications associated with AGEs. (+info)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.
Azotemia is a medical term that refers to an elevated level of urea and other nitrogenous waste products in the blood. This condition is typically caused by impaired kidney function, which can lead to the accumulation of these substances in the body.
Normally, the kidneys filter waste products from the blood and excrete them in the urine. However, when the kidneys are not functioning properly, they may be unable to remove these waste products efficiently, leading to their buildup in the bloodstream. This can cause a range of symptoms, including nausea, vomiting, fatigue, and confusion.
Azotemia is often classified based on the level of urea in the blood, with mild azotemia defined as a blood urea nitrogen (BUN) level between 20 and 39 mg/dL, moderate azotemia defined as a BUN level between 40 and 89 mg/dL, and severe azotemia defined as a BUN level of 90 mg/dL or higher.
Treatment for azotemia typically involves addressing the underlying cause of the condition, which may involve medications to control high blood pressure or diabetes, dietary changes, or dialysis in severe cases.
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.
Nephrectomy is a surgical procedure in which all or part of a kidney is removed. It may be performed due to various reasons such as severe kidney damage, kidney cancer, or living donor transplantation. The type of nephrectomy depends on the reason for the surgery - a simple nephrectomy involves removing only the affected portion of the kidney, while a radical nephrectomy includes removal of the whole kidney along with its surrounding tissues like the adrenal gland and lymph nodes.
Urea is not a medical condition but it is a medically relevant substance. Here's the definition:
Urea is a colorless, odorless solid that is the primary nitrogen-containing compound in the urine of mammals. It is a normal metabolic end product that is excreted by the kidneys and is also used as a fertilizer and in various industrial applications. Chemically, urea is a carbamide, consisting of two amino groups (NH2) joined by a carbon atom and having a hydrogen atom and a hydroxyl group (OH) attached to the carbon atom. Urea is produced in the liver as an end product of protein metabolism and is then eliminated from the body by the kidneys through urination. Abnormal levels of urea in the blood, known as uremia, can indicate impaired kidney function or other medical conditions.
Blood Urea Nitrogen (BUN) is a laboratory value that measures the amount of urea nitrogen in the blood. Urea nitrogen is a waste product that is formed when proteins are broken down in the liver. The kidneys filter urea nitrogen from the blood and excrete it as urine.
A high BUN level may indicate impaired kidney function, as the kidneys are not effectively removing urea nitrogen from the blood. However, BUN levels can also be affected by other factors such as dehydration, heart failure, or gastrointestinal bleeding. Therefore, BUN should be interpreted in conjunction with other laboratory values and clinical findings.
The normal range for BUN is typically between 7-20 mg/dL (milligrams per deciliter) or 2.5-7.1 mmol/L (millimoles per liter), but the reference range may vary depending on the laboratory.
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.
Anuria is a medical condition characterized by the absence or near-absence of urine output, typically defined as less than 100 milliliters in 24 hours. This occurs when the kidneys are unable to produce urine due to a complete or nearly complete failure of both kidneys' function. Anuria can be caused by various underlying medical conditions such as severe dehydration, kidney damage, obstruction in the urinary tract, or certain medications that affect kidney function. It is considered a serious medical emergency and requires immediate evaluation and treatment to prevent further complications, including potential permanent kidney damage or even death.
Artificial kidney, also known as a renal replacement therapy or dialysis, is a device that performs the essential functions of the human kidney when the natural kidneys are unable to do so. The main function of an artificial kidney is to filter and remove waste, excess water, and toxic substances from the blood, helping to maintain the body's chemical balance and regulate blood pressure.
There are two primary types of artificial kidney treatments: hemodialysis and peritoneal dialysis. Hemodialysis involves circulating the patient's blood through an external filter (dialyzer) that contains a semi-permeable membrane, which separates waste products and excess fluids from the blood. The cleaned blood is then returned to the body. This process typically takes place in a clinical setting, such as a hospital or dialysis center, for about 3-5 hours, several times a week.
Peritoneal dialysis, on the other hand, uses the patient's own peritoneum (a membrane lining the abdominal cavity) as a natural filter. A special solution called dialysate is introduced into the peritoneal cavity via a catheter, and waste products and excess fluids pass from the blood vessels in the peritoneum into the dialysate. After a dwell time of several hours, the used dialysate is drained out and replaced with fresh solution. This process can be performed manually (continuous ambulatory peritoneal dialysis) or using a machine (automated peritoneal dialysis), typically at home and during sleep.
Artificial kidneys are life-saving treatments for patients with end-stage renal disease, helping them maintain their quality of life and extend their lifespan until a kidney transplant becomes available.
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.
Hemorrhagic disorders are medical conditions characterized by abnormal bleeding due to impaired blood clotting. This can result from deficiencies in coagulation factors, platelet dysfunction, or the use of medications that interfere with normal clotting processes. Examples include hemophilia, von Willebrand disease, and disseminated intravascular coagulation (DIC). Treatment often involves replacing the missing clotting factor or administering medications to help control bleeding.
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.
Advanced Glycosylation End Products (AGEs) are formed through the non-enzymatic glycation and oxidative modification of proteins, lipids, and nucleic acids. This process occurs when a sugar molecule, such as glucose, binds to a protein or lipid without the regulation of an enzyme, leading to the formation of a Schiff base. This then rearranges to form a more stable ketoamine, known as an Amadori product. Over time, these Amadori products can undergo further reactions, including oxidation, fragmentation, and cross-linking, resulting in the formation of AGEs.
AGEs can alter the structure and function of proteins and lipids, leading to damage in tissues and organs. They have been implicated in the development and progression of several age-related diseases, including diabetes, atherosclerosis, kidney disease, and Alzheimer's disease. AGEs can also contribute to inflammation and oxidative stress, which can further exacerbate tissue damage.
In summary, Advanced Glycosylation End Products (AGEs) are the result of non-enzymatic glycation and oxidation of proteins, lipids, and nucleic acids, leading to structural and functional changes in tissues and organs, and contributing to the development and progression of several age-related diseases.
Bleeding time is a medical test that measures the time it takes for a small blood vessel to stop bleeding after being cut. It's used to evaluate platelet function and the effectiveness of blood clotting. The most common method used to measure bleeding time is the Ivy method, which involves making a standardized incision on the forearm and measuring the time it takes for the bleeding to stop. A normal bleeding time ranges from 2 to 9 minutes, but this can vary depending on the specific method used. Prolonged bleeding time may indicate an impairment in platelet function or clotting factor deficiency.
Uremia
Nephritis
Protein toxicity
Kidney failure
B cell growth and differentiation factors
Robert Earl Hughes
Norepinephrine
Jean Harlow
John Janvier Black
Ann Stone Minot
Diffuse proliferative nephritis
Fred Cavens
Jack Pierce (make-up artist)
Joseph Scott (attorney)
Alpha-2-HS-glycoprotein
Feline lower urinary tract disease
David Handelsman
Robert Edward Lee Mountcastle
William J. Connors
Granulomatosis with polyangiitis
Pindolol
William Anthony McGuire
John A. Widtsoe
Studs Bancker
Fibrothorax
Azotemia
Leo McLaughlin
Ben Hur Lampman
Brothers (Yu novel)
Sri Aurobindo
Uremia - Wikipedia
Monocytes in Uremia
Pathophysiology
Uremia Workup: Approach Considerations, Glomerular Filtration Rate, Ultrasonography
Plasma protein carbamylation and decreased acidic drug protein binding in uremia
Dermatologic Manifestations of Renal Disease: Overview, Dermatologic Manifestations of Diseases Associated With ESRD,...
Uremia %
The pathology of butterfly densities in uraemia | Thorax
The pathology of butterfly densities in uraemia | Thorax
Aggressive Approach in a Case of Cancer Cervix with Uremia - Indian Journal of Palliative Care
The pro-inflammatory effect of uraemia overrules the anti-atherogenic potential of immunization with oxidized LDL in apoE-/-...
An Analysis of Iranian Electronic Cities Case Study: Uremia City (Challenges and Opportunities) | Alizadeh Asl | Environmental...
Uraemia Treatment Market Forecast, Trend Analysis & Competition Tracking - Global Review 2018 to 2028
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Uremia: Background, Pathophysiology, Etiology
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Uremia: Symptoms, Causes & Risks, Do's and Don'ts, Treatment
uraemia- Meaning in Marathi - HinKhoj English Marathi Dictionary
Edema - Glossary Definition
Hemolytic-uremic syndrome: MedlinePlus Medical Encyclopedia
Uremia experimental en la rata: el modelo de nefrectomÃa 5/6 | Documents - Universidad de León
Table - One-Year Retrospective Review of Psychiatric Consultations in Lassa Fever, Southern Nigeria - Volume 26, Number 12...
Arsenic Toxicity: Clinical Assessment | Environmental Medicine | ATSDR
Kidney fibroblast growth factor 23 does not contribute to elevation of its circulating levels in uremia | Gubra
Reduce Uric Acid 579 and Creatinine 866 In Uremia Stage Fundamentally With Chinese Medicine - Kidney Disease Treatment
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Dialysis15
- Without intervention via dialysis or kidney transplant, uremia due to renal failure will progress and cause stupor, coma, and death. (wikipedia.org)
- The ultimate treatment for uremia is renal replacement therapy, which can be accomplished by hemodialysis, peritoneal dialysis, or kidney transplantation. (medscape.com)
- Initiation of dialysis is indicated, regardless of the GFR level, when signs or symptoms of uremia are present and are not treatable by other medical means. (medscape.com)
- Educate patients and their families about dialysis to avoid the shock of emergent dialysis and the decreased quality of life that can occur with uremia. (medscape.com)
- Patients on dialysis frequently have "residual syndrome" (Depner) with partially treated uremia manifested by illness from extracellular fluid volume fluctuations, exposure to bioincompatible materials , inorganic ion abnormalities, acidosis, hyperphosphatemia with complications of systemic diseases and advanced age responsible for the loss of renal function. (standardofcare.com)
- People suffering from uraemia need dialysis to filter the blood. (factmr.com)
- Haemodialysis and peritoneal dialysis are uraemia treatments that involve the removal of waste matter from the blood with the help of a machine. (factmr.com)
- Moreover, increasing demand for advanced dialysis machines and increased R&D activities for uraemia treatment are boosting the uraemia treatment market. (factmr.com)
- In addition, the availability of favourable reimbursement policies and the rising demand for home dialysis are boosting the uraemia treatment market. (factmr.com)
- On the basis of treatment type in uraemia treatment market, peritoneal dialysis segment dominates the uraemia treatment market owing to the advantages of peritoneal dialysis over haemodialysis, which include easy-to-use machines, negligible usage of needles and reduction in clinical visits. (factmr.com)
- Increase in the number of dialysis centres across the globe is expected to fuel the uraemia treatment market during the forecast period. (factmr.com)
- The uraemia treatment market in Europe is the second largest worldwide due to an increase in the number of dialysis centres and improved healthcare infrastructure. (factmr.com)
- Uremia is always fatal if left untreated, and it was always so before dialysis and transplantation were accessible. (medicoverhospitals.in)
- Although the toxin (or toxins) of uremia has yet to be identified, the rapid improvement that follows dialysis points strongly to a toxic component. (britannica.com)
- I conduct translational research focused on uremia and dialysis. (stanford.edu)
Urea8
- Uremia is the term for high levels of urea in the blood. (wikipedia.org)
- Both uremia and uremic syndrome have been used interchangeably to denote a very high plasma urea concentration that is the result of renal failure. (wikipedia.org)
- Uremia is a clinical syndrome marked by elevated concentrations of urea in the blood and associated with fluid, electrolyte, and hormone imbalances and metabolic abnormalities, which develop in parallel with deterioration of kidney function. (medscape.com)
- Spontaneous subdural hematomas occur in patients with uremia, particularly if the blood urea nitrogen (BUN) level is greater than 150-200 mg/dL. (medscape.com)
- If cyanate is produced in vivo from urea in patients with uremia, plasma protein carbamylation may play a role in the decreased plasma protein binding of some acidic drugs. (nih.gov)
- Uremia is a condition in which the kidneys are not able to function properly , which leads to a buildup of toxins in your bloodstream, specifically urea. (stdwatch.com)
- Educational Opportunity: September 12, 2014 Thrombocytopathy due to Uremia: Is urea just an innocent bystander? (kidneyhealth.ca)
- The term uremia , though it is sometimes used as if it were interchangeable with chronic renal failure , really means an increase in the concentration of urea in the blood. (britannica.com)
Discoloration or hyperpigmentation1
- sallow discoloration or hyperpigmentation as uremia worsens Patients may become hyperpigmented as uremia worsens (melanosis). (medscape.com)
Effect of uraemia3
- The results suggest that the pro-inflammatory and pro-atherogenic effect of uraemia overrules the anti-atherogenic potential of oxLDL immunization in apoE-/- mice. (lu.se)
- These differences were so prominent that we would have drawn quite different conclusions about the effect of uraemia on urinary phenotype depending on which batch of animals we had used. (biomedcentral.com)
- We actually found that the effect of shipment batch had a larger effect in both areas than uraemia and that conclusions drawn about the effect of uraemia on gut-derived metabolites would have been radically different depending on the batch of animals used. (biomedcentral.com)
Urine3
- [ 1 ] The term uremia, which literally means urine in the blood, was first used by Piorry to describe the clinical condition associated with kidney failure. (medscape.com)
- However, urine doesn't literally come into contact with your blood during uremia. (stdwatch.com)
- Uremia, which means "urine in the blood," refers to the effects of waste product accumulation, affecting the entire body. (medicoverhospitals.in)
Uremic1
- Keep reading this article to learn everything you need to know about uremia or uremic poisoning. (stdwatch.com)
Azotemia2
- Uremia describes the pathological and symptomatic manifestations of severe azotemia. (wikipedia.org)
- Azotemia is a similar condition, but it's less severe than uremia. (stdwatch.com)
Onset2
- There is no specific time for the onset of uremia for people with progressive loss of kidney function. (wikipedia.org)
- No specific point in time delineates the onset of uremia. (standardofcare.com)
Complications1
- If uremia is not treated, it may result in serious complications. (medicoverhospitals.in)
Symptoms4
- Because uremia is mostly a consequence of kidney failure, its signs and symptoms often occur concomitantly with other signs and symptoms of kidney failure. (wikipedia.org)
- Residual syndrome is a non-life-threatening disease which is displayed as toxic effects causing many of the same signs and symptoms that uremia displays. (wikipedia.org)
- Uraemia patients show signs of metabolic acidosis in which the body produces excess of acid, nausea, vomiting and loss of appetite, which are some of the symptoms seen in uraemia patients. (factmr.com)
- Uremia symptoms are similar to those of chronic kidney disease. (medicoverhospitals.in)
Renal failure2
- Therefore, this review aims to provide an overview about the impairment and activation of monocytes by uremia and the resulting clinical consequences for renal failure patients. (nih.gov)
- Uremia usually develops only after the creatinine clearance falls to less than 10 mL/min, although some patients may be symptomatic at higher clearance levels, especially if renal failure develops acutely. (medscape.com)
Chronic5
- A detailed and accurate history and physical examination will help determine if uremia is acute or chronic. (wikipedia.org)
- Uremia more commonly develops with chronic kidney disease (CKD), especially the later stages of CKD, but it also may occur with acute kidney injury (AKI) if loss of kidney function is rapid. (medscape.com)
- Uremia is usually caused by chronic kidney disease , but it can also occur as a result of an injury or poisoning. (stdwatch.com)
- Uremia is most common in people with chronic kidney disease. (medicoverhospitals.in)
- 4. Identify acute and chronic treatment options and the role of the blood bank in the management of thrombocytopathy due to uremia. (kidneyhealth.ca)
Develops3
- Uraemia is a clinical syndrome associated with electrolyte, fluid, hormone imbalance and metabolic abnormalities, which develops due to the deterioration of the renal function. (factmr.com)
- Uremia can be a sign of end-stage kidney disease, and according to StatPearls , it usually develops over time as a result of worsening renal function. (stdwatch.com)
- Uremia is a severe disorder that develops when waste products related to impaired kidney function accumulate in the blood. (medicoverhospitals.in)
Severe4
- Spontaneous bleeding can occur with severe uremia and may include gastrointestinal (GI) bleeding, spontaneous subdural hematomas, increased bleeding from any underlying disorder, or bleeding associated with trauma. (medscape.com)
- Uraemia is caused due to long-running health problems, such as high blood pressure and diabetes, because of infections that damage the kidney as well as severe injury. (factmr.com)
- Uremia is a severe disorder that can be fatal. (medicoverhospitals.in)
- Uremia ought to represent a purely chemical statement, but it is sometimes used to denote a clinical picture, that of severe renal insufficiency. (britannica.com)
Kidneys1
- But in some cases, your kidneys lose the ability to filter blood efficiently, and a condition known as uremia can happen as a result. (stdwatch.com)
Blood5
- People suffering from uraemia have proteins, creatine and other substances in the blood, which can affect all the systems of the body. (factmr.com)
- Uraemia is usually diagnosed by blood tests that check the level of creatinine. (factmr.com)
- Major factors driving the market of uraemia treatment are increasing incidence of diabetes, high blood pressure, increasing prevalence of end-stage renal disease and increasing number of kidney transplants. (factmr.com)
- North America is expected to be the leading uraemia treatment market worldwide owing to the increasing incidence of diabetes and high blood pressure. (factmr.com)
- With uremia, a kidney can't filter out waste because it no longer works well, so the waste stays in the blood. (webmd.com)
Dysfunction2
- Uremia-related immune dysfunction can reduce responsiveness to infection. (medscape.com)
- 2. Identify the pathogenesis of platelet dysfunction in uremia. (kidneyhealth.ca)
Metabolic2
- Classical signs of uremia are: progressive weakness and easy fatigue, loss of appetite due to nausea and vomiting, muscle atrophy, tremors, abnormal mental function, frequent shallow respiration, and metabolic acidosis. (wikipedia.org)
- Based on an assumption of metabolic similarity between experimental animals, we sought to investigate this 'gut-kidney axis' in a rodent model of uraemia, by demonstrating the effect of experimental uraemia on the urinary metabolome and gut microbiota of rats, purchased from the same supplier in two separate shipment batches for logistical reasons. (biomedcentral.com)
Patients2
- In patients with uremia, the diagnosis of kidney failure is based primarily on an abnormal glomerular filtration rate (GFR) or abnormal creatinine clearance. (medscape.com)
- Scatchard plots for sulfadiazine binding in plasma from patients with uremia and in normal plasma carbamylated in vitro with potassium cyanate showed changes in the 2 groups when compared with those in normal individuals. (nih.gov)
Acute kidney1
- However, acute kidney injury is another possible cause of uremia which progresses quickly. (stdwatch.com)
Electrolyte1
- Uremia is often associated with other problems, such as electrolyte and hormone imbalances. (stdwatch.com)
Kidney disease3
- However, high cost of uraemia treatment, stringent regulations and lack of awareness about kidney disease are among factors hampering the growth of the uraemia treatment market. (factmr.com)
- Because of these similarities, people with kidney disease who experience kidney failure may be unaware they have uremia. (medicoverhospitals.in)
- Kidney disease is a potentially fatal condition, so anyone who suspects they have kidney disease or uremia should consult a doctor immediately. (medicoverhospitals.in)
Occur1
- Moderate and isolated increases occur when glomerular filtration is inhibited in the early stages of uremia. (cdc.gov)
Diabetic1
- The global market for uraemia treatment is expected to register significant growth over the forecast period due to increasing diabetic population. (factmr.com)
Transplantation1
- Consequently, dermatologic manifestations of renal disease may be divided into 3 general categories including: (1) dermatologic manifestations of diseases associated with the development of ESRD, (2) dermatologic manifestations of uremia, and (3) dermatologic disorders associated with renal transplantation. (medscape.com)
Increases1
- Uraemia increases oxidative stress, plasma titres of antibodies recognizing oxidized low-density lipoprotein (oxLDL) and development of atherosclerosis. (lu.se)
Urinary2
- Here, we set out to demonstrate the effect of experimental uraemia on the rat urinary metabolome and gut microbiome but found instead that the effect of vendor shipment batch was larger in both areas than that of uraemia. (biomedcentral.com)
- Whilst we also demonstrated differences in both the urinary metabolome and gut microbiota associated with uraemia, these effects were smaller in size than those associated with shipment batch. (biomedcentral.com)
Glomerular1
- People with kidney function below 50% (i.e. a glomerular filtration rate [GFR] between 50 and 60 mL/min) and over 30 years of age may have uremia to a degree. (wikipedia.org)
Secondary1
- Terminal butterfly densities associated with hypertensive heart failure in uraemia represent variable haemorrhagic and fibrinous pulmonary oedema with secondary cellular changes and organization (uraemic pneumonia). (bmj.com)
Means1
- Marathi meaning of uraemia, What uraemia means in Marathi, uraemia meaning in Marathi, marathi mein uraemia ka matlab, pronunciation, example sentences of uraemia in Marathi language. (hinkhojdictionary.com)
Conditions1
- In addition, uremia and conditions associated with renal replacement therapy are fraught with numerous and, often, relatively unique cutaneous disorders. (medscape.com)
Treatment6
- Increasing healthcare expenditure, rising geriatric population and increased disposable income drive the uraemia treatment market. (factmr.com)
- Several service providers are present in the uraemia treatment market in developed as well as developing countries. (factmr.com)
- Geographically, the global uraemia treatment market is segmented into North America, Latin America, Europe, Asia-Pacific excluding Japan (APEJ), Japan and the Middle East & Africa (MEA). (factmr.com)
- The Asia Pacific excluding Japan and Latin America regions in uraemia treatment market are expected to witness fast growth as compared to other regions due to large patient population, increased number of end users and increased awareness about kidney-related diseases. (factmr.com)
- However, Latin America and Middle East & Africa region in uraemia treatment market is expected to account for slow growth during the forecast period. (factmr.com)
- The global uraemia treatment market is highly fragmented owing to the presence of a large number of service providers. (factmr.com)
Mice2
- We have investigated whether immunization with oxLDL might also prevent uraemia-induced atherosclerosis in apolipoprotein E knockout (apoE-/-) mice. (lu.se)
- ApoE-/- mice were immunized with either native LDL (n = 25), Cu2+-oxidized LDL (n = 25), PBS (n = 25), the apolipoprotein B-derived peptide P45 (apoB-peptide P45) conjugated to bovine serum albumin (BSA) (n = 25) or BSA (n = 25) prior to induction of uraemia by 5/6 nephrectomy (NX). (lu.se)