Kidney Failure, Chronic
Blood Urea Nitrogen
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)
Treatment for uremia typically involves dialysis or kidney transplantation to remove excess urea from the blood and restore normal kidney function. In some cases, medications may be prescribed to help manage symptoms such as high blood pressure, anemia, or electrolyte imbalances.
The term "uremia" is derived from the Greek words "oura," meaning "urea," and "emia," meaning "in the blood." It was first used in the medical literature in the late 19th century to describe a condition caused by excess urea in the blood. Today, it remains an important diagnostic term in nephrology and is often used interchangeably with the term "uremic syndrome."
A condition in which the kidneys gradually lose their function over time, leading to the accumulation of waste products in the body. Also known as chronic kidney disease (CKD).
Chronic kidney failure affects approximately 20 million people worldwide and is a major public health concern. In the United States, it is estimated that 1 in 5 adults has CKD, with African Americans being disproportionately affected.
The causes of chronic kidney failure are numerous and include:
1. Diabetes: High blood sugar levels can damage the kidneys over time.
2. Hypertension: Uncontrolled high blood pressure can cause damage to the blood vessels in the kidneys.
3. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste and excess fluids from the blood.
4. Interstitial nephritis: Inflammation of the tissue between the kidney tubules.
5. Pyelonephritis: Infection of the kidneys, usually caused by bacteria or viruses.
6. Polycystic kidney disease: A genetic disorder that causes cysts to grow on the kidneys.
7. Obesity: Excess weight can increase blood pressure and strain on the kidneys.
8. Family history: A family history of kidney disease increases the risk of developing chronic kidney failure.
Early stages of chronic kidney failure may not cause any symptoms, but as the disease progresses, symptoms can include:
1. Fatigue: Feeling tired or weak.
2. Swelling: In the legs, ankles, and feet.
3. Nausea and vomiting: Due to the buildup of waste products in the body.
4. Poor appetite: Loss of interest in food.
5. Difficulty concentrating: Cognitive impairment due to the buildup of waste products in the brain.
6. Shortness of breath: Due to fluid buildup in the lungs.
7. Pain: In the back, flank, or abdomen.
8. Urination changes: Decreased urine production, dark-colored urine, or blood in the urine.
9. Heart problems: Chronic kidney failure can increase the risk of heart disease and heart attack.
Chronic kidney failure is typically diagnosed based on a combination of physical examination findings, medical history, laboratory tests, and imaging studies. Laboratory tests may include:
1. Blood urea nitrogen (BUN) and creatinine: Waste products in the blood that increase with decreased kidney function.
2. Electrolyte levels: Imbalances in electrolytes such as sodium, potassium, and phosphorus can indicate kidney dysfunction.
3. Kidney function tests: Measurement of glomerular filtration rate (GFR) to determine the level of kidney function.
4. Urinalysis: Examination of urine for protein, blood, or white blood cells.
Imaging studies may include:
1. Ultrasound: To assess the size and shape of the kidneys, detect any blockages, and identify any other abnormalities.
2. Computed tomography (CT) scan: To provide detailed images of the kidneys and detect any obstructions or abscesses.
3. Magnetic resonance imaging (MRI): To evaluate the kidneys and detect any damage or scarring.
Treatment for chronic kidney failure depends on the underlying cause and the severity of the disease. The goals of treatment are to slow progression of the disease, manage symptoms, and improve quality of life. Treatment may include:
1. Medications: To control high blood pressure, lower cholesterol levels, reduce proteinuria, and manage anemia.
2. Diet: A healthy diet that limits protein intake, controls salt and water intake, and emphasizes low-fat dairy products, fruits, and vegetables.
3. Fluid management: Monitoring and control of fluid intake to prevent fluid buildup in the body.
4. Dialysis: A machine that filters waste products from the blood when the kidneys are no longer able to do so.
5. Transplantation: A kidney transplant may be considered for some patients with advanced chronic kidney failure.
Chronic kidney failure can lead to several complications, including:
1. Heart disease: High blood pressure and anemia can increase the risk of heart disease.
2. Anemia: A decrease in red blood cells can cause fatigue, weakness, and shortness of breath.
3. Bone disease: A disorder that can lead to bone pain, weakness, and an increased risk of fractures.
4. Electrolyte imbalance: Imbalances of electrolytes such as potassium, phosphorus, and sodium can cause muscle weakness, heart arrhythmias, and other complications.
5. Infections: A decrease in immune function can increase the risk of infections.
6. Nutritional deficiencies: Poor appetite, nausea, and vomiting can lead to malnutrition and nutrient deficiencies.
7. Cardiovascular disease: High blood pressure, anemia, and other complications can increase the risk of cardiovascular disease.
8. Pain: Chronic kidney failure can cause pain, particularly in the back, flank, and abdomen.
9. Sleep disorders: Insomnia, sleep apnea, and restless leg syndrome are common complications.
10. Depression and anxiety: The emotional burden of chronic kidney failure can lead to depression and anxiety.
Anuria is often associated with other conditions such as chronic kidney disease, sepsis, or bladder outlet obstruction. The symptoms of anuria may include decreased urine output, swelling in the legs and abdomen, nausea, vomiting, and electrolyte imbalances.
Treatment of anuria depends on the underlying cause, and may involve medications to relieve symptoms, drainage of obstructions, or other interventions such as hemodialysis or peritoneal dialysis. In severe cases, anuria can lead to uremia, a buildup of waste products in the blood that can be life-threatening. Therefore, prompt medical attention is essential for effective management and prevention of complications.
There are several types of hemorrhagic disorders, including:
1. Hemophilia: A genetic disorder that affects the blood's ability to clot and stop bleeding. People with hemophilia may experience spontaneous bleeding or bleeding after injury or surgery.
2. von Willebrand disease: A mild bleeding disorder caused by a deficiency of a protein called von Willebrand factor, which is important for blood clotting.
3. Platelet disorders: Disorders that affect the platelets, such as thrombocytopenia (low platelet count) or thrombocytosis (high platelet count).
4. Bleeding and clotting disorders caused by medications or drugs.
5. Hemorrhagic stroke: A type of stroke that is caused by bleeding in the brain.
6. Gastrointestinal bleeding: Bleeding in the digestive tract, which can be caused by a variety of factors such as ulcers, inflammation, or tumors.
7. Pulmonary hemorrhage: Bleeding in the lungs, which can be caused by a variety of factors such as pneumonia, injury, or tumors.
8. Retinal hemorrhage: Bleeding in the blood vessels of the retina, which can be caused by high blood pressure, diabetes, or other eye disorders.
Symptoms of hemorrhagic disorders can vary depending on the specific condition and the location of the bleeding. Common symptoms include bruising, petechiae (small red spots on the skin), nosebleeds, gum bleeding, and heavy menstrual periods. Treatment for hemorrhagic disorders depends on the underlying cause and may include medications, blood transfusions, or surgery.
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- Consider any type of surgery carefully in patients with uremia because of the increased risk for uremic bleeding, cardiovascular events, acute kidney injury, respiratory depression, and decreased metabolism of certain drugs. (medscape.com)
- Good reproducibility could be obtained by applying immobilized pH gradient 2DE to separate and identify the proteome in sera, which contributes to the further study on uremia toxins pertaining to protein. (ejgm.org)
- Initiation of dialysis is indicated when signs or symptoms of uremia (eg, nausea, vomiting, volume overload, hyperkalemia, severe acidosis) are present and are not treatable by other medical means. (medscape.com)
- Identifying prognostic factors of severe metabolic acidosis and uraemia in African children with severe falciparum malaria: a secondary analysis of a randomized trial. (ox.ac.uk)
- METHODS: A retrospective analysis of the 'Artesunate versus quinine in the treatment of severe falciparum malaria in African children' (AQUAMAT) trial was conducted to identify clinical features of severe metabolic acidosis and uraemia in 5425 children from nine African countries. (ox.ac.uk)
- Separate models were fitted for uraemia and severe metabolic acidosis. (ox.ac.uk)
- Separate univariable and multivariable logistic regression were performed to identify prognostic factors for severe metabolic acidosis and uraemia. (ox.ac.uk)
- RESULTS: There were 2296 children identified with severe metabolic acidosis and 1110 with uraemia. (ox.ac.uk)
- CI 1.09-2.27), jaundice (OR: 3.46 CI 2.21-5.43), severe anaemia (OR: 1.77, CI 1.36-2.29) and hypoglycaemia (OR: 2.77, CI 2.22-3.46) CONCLUSION: Clinical and laboratory parameters representing contributors and consequences of severe metabolic acidosis and uraemia were independently associated with these outcomes. (ox.ac.uk)
- ARF may be recognized by an abrupt onset of azotemia or oliguria, rapidly progressive azotemia, or sudden onset of clinical signs of uremia in a previously healthy patient. (vin.com)
- Bleeding secondary to uremia may occur Consequently, dangerous activities may need to be restricted and potential bleeding sites may need to be assessed in the event of a fall (eg, for a subdural hematoma). (medscape.com)
- Severe uremia can lead to multiple organ dysfunctions with a constellation of symptoms. (nih.gov)
- The test is frequently requested in conjunction with the serum creatinine test for the differential diagnosis of prerenal, renal, and postrenal uremia. (cdc.gov)
- Patients with uremia must have dialysis initiated as soon as symptoms appear, regardless of the glomerular filtration rate (GFR). (medscape.com)
- Activity for patients with uremia is self-restricted based on their level of fatigue. (medscape.com)
- Aim: To establish and optimize two-dimensional electrophoresis (2DE) and relevant techniques for the study of serum proteome of the patients with uremia, and compare serum protein 2DE pattern between the uremia patients and the normal. (ejgm.org)
- Immobilized pH gradient two-dimensional polyacrylamide gel electrophoresis,silver staining, ImageMaster 2D 5.0 analysis software, matrix assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF-TOF-MS) and IPI human database searching, were used to separate and indentify the proteome of the sera from the patients with uremia. (ejgm.org)
- Les IFN et les IL-10 étaient signi cativement élevés chez ceux qui présentaient une néphropathie diabétique (ND) et une maladie rénale en phase terminale (MRPT) par rapport aux témoins et aux patients diabétiques sans ND. (who.int)
- In addition, uremia and conditions associated with renal replacement therapy are fraught with numerous and, often, relatively unique cutaneous disorders. (medscape.com)