Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many acyl glucuronides are labile, reactive and form covalent adducts with proteins. In the present experiment, the stability of salicyl acyl glucuronide (SAG), its reactivity with serum albumin in vitro and the influence of renal failure in rats on the disposition of SAG and covalent binding of salicylate (SA) to rat plasma proteins were investigated. In vitro studies showed that SAG was hydrolyzed to SA or undergoes isomerization to positional isomers. The half-life of SAG was 1.3 hr in 0.15 M phosphate buffer at pH 7.4 and 37 degrees C, but the stability of its isomers was much greater with an apparent half-life of 19 hr. Incubation of SAG in solutions of human serum albumin revealed the formation of covalent adducts with the protein, with maximal binding of 2.8% of total SA equivalents added to the solution. For in vivo studies, one group of rats was administered 5 mg/kg of uranyl nitrate i.p. to induce renal failure. After administration of 100 mg/kg of SA i.v., the AUC 0-26 hr of SAG in rats with renal failure was 9 times higher than that observed in control rats. The apparent clearance of SA decreased from 64 +/- 21 ml/hr in control rats 28 +/- 8.7 ml/hr in rats with renal failure. The level of SA covalent adducts with plasma proteins reached about 0.5 ng/mg of protein in control rats, whereas in rats with renal failure the binding was increased significantly and achieved an average peak concentration of 18 ng/mg of protein when measured 26 hr after dosing. The data indicate that reactive SAG can accumulate in renal failure which then increases covalent addition of SA to proteins. Such binding may have a role in enhancing the potential for toxicity of acidic drugs such as SA in renal disease.
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PMID:Influence of renal failure in rats on the disposition of salicyl acyl glucuronide and covalent binding of salicylate to plasma proteins. 876 61

Low serum albumin levels are common in patients with cirrhosis and liver failure. Decreased synthesis is the main but not the only mechanism leading to decreased serum levels. The consequences of low albumin concentrations are a decreased plasma colloid osmotic pressure and a decreased binding of liposoluble xenobiotics and endogenous substances. Besides the fluid accumulation in pleura and peritoneum, the complications directly related to low serum albumin levels have been only poorly assessed. An increase in serum albumin levels (by a few g.L-1) for a few days can be achieved by the infusion of large amounts of human albumin (approximately 120 g over 3 days). The efficacy of this treatment has been only tested in association with large paracentesis: albumin infusion, which induces volume expansion, reduced the incidence of hyponatremia and functional renal failure. No significant effect on ascites production rate or survival has been observed. Similar results were achieved through polygelin or dextran-70 infusions. No well-conducted controlled study on the value of albumin infusion in other circumstances apart from cirrhotic patients is available. In conclusion, albumin infusion should be reserved to the treatment of hyponatraemia or functional renal failure complicating cirrhosis with severe liver failure and marked hypoalbuminaemia, when the infusion of colloids failed to correct these anomalies.
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PMID:[Indications and role of albumin, plasma volume expansion excluded, in the preoperative or postoperative management of portal hypertension]. 888 92

We have adapted the cardiac troponin T (TnT) immunoassay system (ELISA troponin T, Boehringer Mannheim, Germany), which is based upon streptavidin-biotin immunoassay technology, to a sensitive microplate system. A coating of microplates with biotinylated bovine serum albumin (biotin-LC-BSA) remained stable for months. A secondary streptavidin coating was prepared as the first step of the assay. By using o-phenylenediamine (o-PD) as a substrate for the peroxidase-anti-TnT conjugate, the system allowed rapid kinetic measurement of TnT levels. The upper limit of a reference population (97.5th percentile) was found to be 0.04 mu g l-1. Intra-assay imprecision at 0.08 mu g l-1 was 8%, and 3-4% between 0.28 and 4 mu g l-1. Between-assay imprecision was 6.2% at 0.28 mu g l-1. Studies of TnT and CK-MB mass concentration in acute myocardial infarction patients, treated with streptokinase, demonstrated a clinical sensitivity of the TnT microplate system similar to that of the CK-MB mass concentration test, during the first 8 h after initiation of thrombolytic therapy, at discriminator levels of 0.1 mu g l-1 (TnT) and 8 mu g l-1 (CK-MB mass concentration). The early CK-MB/TnT ratio was lower in patients with signs of successful reperfusion (early peak CK-MB) than in the remaining patients (p<0.001). Serum samples from two patients with renal failure and one patient with rhabdomyolysis demonstrated strong non-linear behaviour with dilution, indicating the presence of an interfering factor. Kinetic measurement compared favourably with end-point analysis with respect to sensitivity and total analysis time. The system described greatly reduces the costs of TnT measurements compared to the ES systems. The total assay time is 70-90 min.
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PMID:Cardiac troponin T immunoassay on biotin--streptavidin-coated microplates: preliminary performance in acute myocardial infarction. 890 40

In attempting to identify variables that might account for the frequent absence of edema in HIV-infected patients with end-stage renal disease, we evaluated 24 consecutive patients at our institution who had HIV infection and developed end-stage renal disease. Clinical and laboratory data prior to the initiation of hemodialysis were recorded and compared between patients with and without edema. Only 11 of the 24 study patients had edema while the remainder did not. The prevalence of diarrhea was significantly less in patients with edema (one of 11 patients compared to eight of 13 with no edema, p < 0.02, odds ratio 0.063). Prior weight loss was significantly less in the patients with edema (9.1 +/- 1.3 kg vs 15.5 +/- 2.2 kg, p < 0.05). Use of antiretroviral therapy was significantly greater in patients with edema (p < 0.05, odds ratio 10.1). None of the patients were receiving diuretics. Blood pressure was significantly higher (p < 0.001) in patients with edema, and serum albumin was low in both groups but did not differ (edema, 24 +/- 2 g/L; no edema, 21 +/- 3 g/L). Four patients had albumin levels as low as 2, 8, 9, and 10 g/L, yet they had no edema. CD4 counts were lower in patients without edema (62 +/- 16 x 10(6) cells/L vs 283 +/- 38 x 10(6) cells/L, p < 0.001). Absence of diarrhea was predictive of the presence of edema with a sensitivity of 91% and specificity of 62% while mean arterial blood pressure > 95 mm Hg was predictive of the presence of edema with a sensitivity of 82% and specificity of 77%. CD4 of > 100 x 10(6) cells/L was predictive of the presence of edema with a sensitivity of 91% and specificity of 77%. These data support the hypothesis that hemodynamic factors may play a role in the frequent absence of edema in patients with HIV infection and renal failure, and variables including diarrhea, low blood pressure, weight loss, and more advanced stage of HIV infection may account for this observation. Hence, the absence of edema should not dissuade the clinician from considering the possibility of advanced renal failure in HIV-infected patients.
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PMID:Absence of edema in HIV-infected patients with end-stage renal disease. 894 76

Many inner-city residents with progressive renal disease do not receive specialist care from a nephrologist, and often arrive in the emergency room manifesting life-threatening uremic symptoms requiring emergency rescue dialysis. We examined the relationship between the quality of medical care received during progression to end-stage renal disease, and the clinical condition and morbidity at initiation of renal replacement therapy. During a 5-year period (January 1990 to December 1994), we prospectively studied 139 consecutive inner-city residents with a confirmed diagnosis of chronic renal failure who were starting uremia therapy. At onset of study, subjects were sorted into one of three groups depending on the extent of medical care received during the 3 years immediately preceding initiation of hemodialysis: nephrologist, nonnephrologist (physician), or no medical care. Information obtained from each subject included length of hospital stay during the admission for initiation of dialysis therapy and the type of hemodialysis vascular access used for first dialysis treatment (permanent v temporary). Predialysis blood urea nitrogen concentration, serum creatinine concentration, serum albumin concentration, and serum bicarbonate concentration were measured once immediately before the first dialysis. The 139 study subjects (62 men and 77 women) comprised 116 blacks (83%), 15 Hispanics (11%), and eight whites (6%), and had a mean age of 56 +/- 15 years (+/-SD). Only 59 (43%) subjects received prior specialist nephrologist care, and their mean length of hospital stay (12 +/- 23 days) was shorter than that of subjects who received nonnephrologist care (n = 63 [45%]; 25 +/- 21 days) or those who received no prior medical care (n = 17 [12%]; 29 +/- 23 days) (P = 0.002). Temporary hemodialysis vascular access was used for the first dialysis in all 17 (100%) of the subjects with no prior medical care, in 56 (89%) of the 63 subjects who received prior care from a nonnephrologist, and in 21 (36%) of the 59 subjects who received prior care from a nephrologist (P = 0.0001). Subjects who received prior care from a nephrologist had a lower mean serum creatinine concentration at initiation of dialysis (11 +/- 4.4 mg/dL) than did either the subjects who received nonnephrologist care (13 +/- 5.4 mg/dL) or no medical care (16 +/- 5.7 mg/dL) (P = 0.003). In addition, subjects who received prior care from a nephrologist had less severe metabolic acidosis than the subjects in the other two groups (P = 0.04). We infer that initiation of uremia therapy is delayed in inner-city residents with progressive renal failure who do not receive specialist nephrologic care, and that as a consequence these patients suffer excess short-term morbidity.
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PMID:Excess morbidity in patients starting uremia therapy without prior care by a nephrologist. 895 35

We studied the outcome of 436 patients with primary biliary cirrhosis (PBC) or primary sclerosing cholangitis (PSC) who underwent orthotopic liver transplant (OLT) at three major liver transplant centers. Univariate predictors of outcome included age, Karnofsky score, Child's class, Mayo risk score, United Network for Organ Sharing (UNOS) status, nutritional status, serum albumin, serum bilirubin, international normalized ratio, and the presence of ascites, encephalopathy, renal failure (serum creatinine > 2 mg/dL), and edema refractory to diuretics. Using these predictors, we developed a four variable mathematical prognostic model to help the liver transplant physician predict the following: 1) the amount of intraoperative blood loss; 2) the number of days in the intensive care unit (ICU); and 3) severe complications after surgery. The model uses age, renal failure, Child's class, and United Network for Organ Sharing status. This study is the first to model the outcome of liver transplant in patients with a specific etiology of chronic liver disease (PBC or PSC). The model may be used to help select patients for OLT and to plan the timing of their transplantation.
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PMID:A prognostic model for the outcome of liver transplantation in patients with cholestatic liver disease. 904 17

We recently demonstrated that pentosidine, an advanced glycation end product, accumulates markedly as albumin-linked form (Palb) and in free-form (Pfree) in the plasma of patients with end-stage renal failure. The present study was undertaken to examine the clearance of Palb and Pfree by different modalities of renal replacement therapy, that is, hemodialysis (HD), continuous ambulatory peritoneal dialysis (CAPD), and renal transplantation. HD cleared Pfree (9.4 +/- 4.3 nmol/kg/HD) but not Palb, by diffusion but not by membrane adsorption, whereas CAPD cleared both Palb (4.03 +/- 2.01 nmol/kg/day) and Pfree (2.43 +/- 1.24 nmol/kg/day). Plasma total pentosidine levels were significantly (P < 0.05) lower in CAPD (0.97 +/- 0.41 nmol/ml) than in HD (1.19 +/- 0.41 nmol/ml), as the result of a lower serum albumin level in the former patients. Indeed, Palb expressed per mg albumin was virtually identical in HD and CAPD. By contrast, Pfree was significantly lower in CAPD than in HD. Palb levels were significantly correlated with plasma Pfree levels in both HD and CAPD patients, but not in the CAPD dialysate. Pentosidine transport across the peritoneum occurs mainly by diffusion, both as Palb and Pfree. Interestingly, peritoneal Palb clearance (0.17 +/- 0.07 ml/min) significantly (P < 0.00001) exceeded albumin clearance (0.11 +/- 0.05 ml/min). Palb levels being significantly higher (P < 0.0005) in the peritoneal fluid (36.28 +/- 18.55 pmol/mg) than in the serum (27.12 +/- 11.71 pmol/mg), thus raises the possibility of a facilitated diffusion of Palb or an active transport mechanism for protein-linked pentosidine into the peritoneal cavity. After renal transplantation, plasma Pfree fell rapidly, remained barely detectable after one month, and returned to normal at six months. By contrast, Palb fell more slowly and remained significantly above normal at six months, but returned eventually to normal levels. These findings demonstrate that: (1) both HD and CAPD remove Pfree; (2) the peritoneal clearance of Palb, might contribute to the lower level of plasma pentosidine in CAPD than in HD patients; and (3) renal transplantation is the best therapeutic modality to normalize both Palb and Pfree levels.
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PMID:Clearance of pentosidine, an advanced glycation end product, by different modalities of renal replacement therapy. 906 25

We conducted a cross-sectional survey to determine the relative course of patients with end-stage renal disease (ESRD) and human immunodeficiency virus (HIV) infection sustained on maintenance hemodialysis. All 34 patients with ESRD and HIV infection receiving hemodialysis in one hospital-based and three community-based outpatient hemodialysis facilities in Brooklyn, NY, were studied. We documented their known duration of HIV infection, duration of ESRD, and hemodialysis prescription, and noted the presence of clinical acquired immunodeficiency syndrome (AIDS). Total CD4 count, serum albumin concentration, and percent reduction of urea (predialysis blood urea nitrogen minus postdialysis blood urea nitrogen, divided by predialysis blood urea nitrogen x 100) were measured. The 34 study subjects (26 men and eight women) included 31 blacks (91%) and three Hispanics (9%) with a mean age of 42 +/- 7.5 years, 29 (85%) of whom had AIDS. Twenty subjects (59%) had a history of intravenous drug abuse. Only six subjects (18%) were receiving an antiretroviral drug (zidovudine = five, dideoxyinosine = one). In 23 subjects (68%), AIDS was diagnosed prior to ESRD and was presumed to be the cause of renal failure (HIV-associated nephropathy). The mean known duration of HIV infection was 50.5 +/- 34 months (median, 48 months); the mean duration of ESRD was 57 +/- 50 months, the mean total CD4 count was 140 +/- 150 cells/microL (median, 70 cells/microL), the mean hematocrit was 28% +/- 5%, and the mean serum albumin concentration was 3.5 +/- 0.37 g/dL. All subjects were receiving erythropoietin for anemia correction. The mean length of the prescribed thrice-weekly hemodialysis sessions was 3.5 +/- 0.4 hours. Our results suggest that the survival of many ESRD patients with HIV infection receiving hemodialysis has improved compared with the uniformly dismal survival rate reported in the 1980s. Decisions on whether to initiate renal replacement therapy in patients with AIDS and advanced renal failure should be individualized because the combination of ESRD and HIV infection does not necessarily signal near-term death.
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PMID:Uremia therapy in patients with end-stage renal disease and human immunodeficiency virus infection: has the outcome changed in the 1990s? 910 43

A progressive decline in glomerular function occurs in diabetic nephropathy. The predictive effects of progression promoters were examined in 182 non-insulin-dependent diabetic patients from a baseline serum creatinine concentration of 133 mumol/l. During a total of 605 person-years follow-up, 107 patients developed end-stage renal failure requiring dialysis. The rate of decline of renal function was highly variable. Urinary protein excretion was the strongest predictor correlated to the rate of decline, followed by diastolic and systolic blood pressure, total cholesterol and platelet count, while the protective effects were seen in serum albumin and haematocrit. Adjustment for urinary protein excretion revealed that diastolic blood pressure, familial predisposition to hypertension, serum albumin, and smoking were independent significant predictors. Angiotensin converting enzyme inhibitors (ACE-I) significantly retarded the development of end-stage renal failure compared to antihypertensives other than ACE-I (mostly nifedipine), and the effect was evident particularly in patients with proteinuria below the median (2.5 g/24 h) (presumably those who responded to ACE-I). A complex effect of proteinuria in association with blood pressure elevation, familial predisposition to hypertension, hypoalbuminaemia, and smoking may play an important role in the progression of nephropathy.
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PMID:Predictors of the progression of diabetic nephropathy and the beneficial effect of angiotensin-converting enzyme inhibitors in NIDDM patients. 911 17

Renal function was assessed in prestroke and poststroke Kyoto-Wistar stroke-prone spontaneously hypertensive rats (SHRsp) fed high-K+ (2.11%) and low-K+ (0.75%) diets containing 4% NaCl and in stroke-resistant SHR (srSHR) fed a low-K+ diet. Elevations in dietary K+ retarded the onset of stroke development in SHRsp, but did not alter the life-span of SHRsp between the onset of stroke and death. At ages < 12 weeks, renal function, measured by serum urea and creatinine levels and urinary protein loss, was comparable in high and low K+ fed prestroke SHRsp, and age-matched srSHR. At ages > 12 weeks, hemorrhagic stroke rapidly developed in SHRsp. When compared with srSHR, prestroke SHRsp exhibited higher serum creatinine and urea levels, a greater excretion of protein into the urine, and lower serum albumin levels. The severity of the above indices of renal failure was amplified in similar-aged poststroke SHRsp. Poststroke SHRsp also had elevated levels of hemoglobin in the urine. Increases in dietary K+ did not significantly decrease the severity of uremia and proteinuria in age-matched prestroke or poststroke SHRsp. It was concluded that a decrease in glomerular filtration, uremia, and proteinuria preceded stroke development in SHRsp. The onset of proteinuria and uremia in SHRsp could potentiate stroke development. The latter indices of renal function were not altered by modifications in dietary K+ that retard stroke development in SHRsp.
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PMID:Renal function in stroke-prone rats fed a high-K+ diet. 931 46


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