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)

In this paper we studied the effects of a low-protein, low-phosphorus supplemented diet in 8 type I diabetics with 'overt' diabetic nephropathy and mild or severe renal insufficiency. We examined the following parameters: the rate of decline of creatinine clearance, the urinary protein loss, the total serum protein, the daily insulin requirement, the serum fasting glucose, the pattern of serum lipids (serum total cholesterol, HDL cholesterol and serum triglycerides), the mean blood pressure and body weight. The rate of decline of creatinine clearance decreased monthly from 1.48 +/- 0.20 ml/min during a previous 15.6-month period of unrestricted protein diet (UPD), to 0.13 +/- 0.3 ml/min during the 11.4 months on the supplemented diet (SD). The mean blood pressure did not differ during UPD (130.9 +/- 7.0 mmHg) and during SD (128.1 +/- 1.6 mmHg). Urinary protein loss significantly decreased on SD, and total serum protein increased. The daily insulin requirement and the serum fasting glucose levels significantly decreased on SD. Serum cholesterol was lower during SD than during UPD, while serum HDL cholesterol and serum triglycerides were not significantly modified. In some patients the body weight decreased on SD as a consequence of the disappearance of edema. In conclusion, on the basis of these preliminary observations, the SD slows the progression of renal failure and seems to exert several beneficial and no unwanted side-effects in renal failure of type I diabetics.
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PMID:Effects of a low-phosphorus, low-protein diet supplemented with essential amino acids and keto analogues on 'overt' diabetic nephropathy. 343 63

Previous clinical studies indicate that the metabolic clearance of oral (+/-)-propranolol is reduced in end-stage renal failure patients. Animal models are needed to explore the mechanism(s) underlying the observed metabolic inhibition in man. The disposition kinetics of S(-)-propranolol were characterized after intravenous and peroral administration in rats with acute renal failure induced by bilateral ureteral ligation (BUL). No alteration in either the systemic clearance or the apparent volumes of distribution of S(-)-propranolol was observed in renal failure animals after a single intravenous dose of 1.5 mg/kg. In contrast, acute uremia did elicit a change in the bioavailability of orally administered S(-)-propranolol. At 36 h after ureteral ligation, the area under the serum concentration-time curve after a 6 mg/kg oral dose of S(-)-propranolol was significantly elevated in renal failure animals, which corresponded to an approximate two fold increase in its systemic availability (from 7.7 to 20.5%). Such an effect could not be demonstrated at times earlier than 36 h after ureteral ligation. Additional experiments were performed to evaluate whether concomitant changes in gastrointestinal absorption or serum protein binding of S(-)-propranolol could have contributed to the apparent increase in oral availability. The results lead to the hypothesis of an inhibited first-pass hepatic metabolism of S(-)-propranolol in acute renal failure and suggest a significant time delay in the onset of inhibition.
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PMID:Altered S(--)-propranolol disposition in bilateral ureter-ligated rats. 362 24

A long-term clinical and therapeutic study was performed in 47 patients with mesangial IgA glomerulonephritis. The male to female ration was 2.9:1. An episode of gross haematuria or the incidental discovery of asymptomatic microscopic haematuria with associated mild proteinuria heralded the apparent onset of renal disease. At the onset of observation 18 patients (38.2%) had high blood pressure. Other 17 patients developed hypertension during observation. Anaemia was uncommon. No essential abnormalities in serum protein and lipid patterns were found. Twenty-nine patients (61.6%) had higher levels of serum immunoglobulins--most frequently of IgA (42.5%). Twenty-two patients had low serum C3 levels (46.8%). The percentage of patients with renal failure increased from 21.2 to 36.1 during observation. Male sex, hypertension, proteinuria higher than 2 g/24 h, elevated ESR, high serum IgA levels, longer duration of the disease and older age of patients suggest an unfavourable outcome. Long-term treatment with a combination of azathioprine/acenocumarol, or indomethacin, or levamisole has no effect on the clinical manifestation and evolution.
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PMID:Clinical and therapeutic studies in mesangial immunoglobulin A glomerulonephritis. 366 42

To examine the development of pulmonary edema during experimental renal dysfunction, left atrial pressure was altered in 14 mongrel dogs divided into two groups. Group 1 was composed of seven control animals, and Group 2 was composed of seven animals with surgically induced renal failure (1 week of bilateral ureteral ligation). Data were obtained at two levels of matched transmural pulmonary vascular pressure (defined as mean left atrial pressure less serum protein osmotic pressure). In the animals with renal dysfunction, extravascular lung water (EVLW) (thermal-green dye technique) was higher at moderately (-1 to -2 mm Hg) and severely elevated (11 to 12 mm Hg) vascular driving pressures (11.5 +/- 1.2 cc/kg vs 10.6 +/- 0.8 cc/kg and 14.8 +/- 1.3 cc/kg vs 13.0 +/- 1.9 cc/kg, respectively, both P less than 0.05 vs control). Because protein osmotic pressure was lower in the renal failure group (15.0 +/- 1.8 mm Hg vs 18.4 +/- 1.4 mm Hg, P less than 0.05), greater accumulations of extravascular lung water occurred at lower levels of left atrial pressure (14.2 +/- 1.4 mm Hg vs 17.1 +/- 1.2 mm Hg, P less than 0.05; 26.8 +/- 2.6 mm Hg vs 29.5 +/- 2.3 mm Hg, P less than 0.01). In addition, when the ratio of EVLW/PBV (pulmonary blood volume) was examined in both groups at each stage of the experiment, the ratio was greater in the Group 2 animals at each elevated pressure, suggesting increased permeability with renal dysfunction. In conclusion, pulmonary edema formation occurs at lower left atrial pressures in the setting of sustained renal dysfunction, this phenomenon can be partially explained by lower protein osmotic pressure though altered pulmonary microvascular permeability may contribute to edema formation.
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PMID:Effect of prolonged renal dysfunction on intravascular and extravascular pulmonary fluid volumes during left atrial hypertension. 330 34

The kinetics of oral ketoconazole in serum and peritoneal fluid were studied in six patients with renal failure receiving peritoneal dialysis. A dose of 400 mg ketoconazole resulted in a maximum blood concentration of 2.3 +/- 1.7 microgram/ml (mean +/- SD), which occurred 3.3 +/- 1.6 hours after dosing. The serum t1/2 was 2.4 +/- 0.8 hours. Peritoneal clearance values were less than 1 ml/min, and peritoneal penetration reached 3.4% of the serum concentration by 5 hours. Protein binding studies were also performed. Compared with healthy controls, patients receiving peritoneal dialysis have significantly less ketoconazole serum protein binding. Fifty to eighty percent of the drug is protein bound in the peritoneal fluid, and the unbound concentration is in the same range as that in the serum of healthy individuals with "therapeutic" total ketoconazole levels of 1 to 2 micrograms/ml.
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PMID:Ketoconazole kinetics in chronic peritoneal dialysis. 397 56

We previously identified endogenous digoxin-like immunoactivity in serum from pregnant women, newborn infants, and patients in renal failure. This activity is due to an endogenous factor(s) that cross-reacts with antibodies raised against digoxin. Using serum from the above sources as well as serum and urine from normal individuals, we further characterized these immunoreactive factors. The factors are water soluble, heat stable, and neutral in molecular charge. That isolated from serum has an apparent mol wt of 200 daltons, as estimated by membrane partitioning. The factor from urine has twice this apparent mol wt, an apparent higher affinity for the digoxin antisera, and is less resistant to acid hydrolysis. It may represent a conjugated metabolite of the factor from serum. The immunoactive factor in serum is noncovalently bound to serum protein, and we describe methods for estimating total, weakly protein-bound (i.e. heat-dissociable), tightly protein-bound (i.e. not heat-dissociable), and unbound (free) activity. Levels measured directly in serum by RIA represent the unbound and weakly protein-bound serum components. In normal subjects, over 90% of the total endogenous immunoactivity in serum is tightly but reversibly bound to protein and not detectable by direct measurement with conventional RIAs. Concentrations determined by direct measurement in serum from patients with renal failure [128 +/- 38 pg digoxin equivalents/ml (mean +/- SE)], pregnant women (141 +/- 12), and neonates (230 +/- 7) consistently exceeded those in normal subjects (61 +/- 3). Chromatography and ultrafiltration studies suggest that these differences are due to increased amounts of weakly protein-bound factor in these subjects rather than to a greater amount of total immunoactive factor. Altered protein binding of this endogenous factor seems to play a predominant role in the detection of digoxin-like immunoactivity in human serum. Our data also suggest that carrier proteins may play a prominent role in the transport of this endogenous immunoactive factor in blood.
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PMID:Protein binding of endogenous digoxin-immunoactive factors in human serum and its variation with clinical condition. 399 64

The serum protein binding of tiaprofenic acid (Surgam) has been investigated in vitro by equilibrium dialysis in a physiological buffer of pH 7.40 with a 14C-labelled tiaprofenic acid isotope. The stability of labelled and unlabelled tiaprofenic acid was good during dialysis and an irregular distribution of 6% impurities in the 14C-labelled tiaprofenic acid isotope preparation was corrected for. No differences were found between elderly (74 +/- 4 yrs) and young (32 +/- 6 yrs) individuals, both groups showing a serum protein binding of tiaprofenic acid of 99.0 +/- 0.15%. However, patients with impaired renal function (creatinine clearance 24 +/- 8 ml/min) showed a significantly lower binding of 98.5 +/- 0.35%. Albumin was identified as the main tiaprofenic acid binding protein in human serum with a high affinity binding site characterized by an in vitro dissociation constant, KD, of 3.8 x 10(-6) mol/l and a number of available binding sites, n, of 0.34. Tiaprofenic acid was found not to be displaced from serum protein binding sites by other highly bound drugs. It is concluded that tiaprofenic acid protein binding is characterized by small interindividual variations, but that the decreased binding of tiaprofenic acid in patients with renal failure should be paid some attention to.
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PMID:Binding of tiaprofenic acid to human sera and isolated serum proteins. 402 26

The aims of this study were to investigate the time course of carbamylation of serum proteins in animals with experimental renal failure (RF) or with high blood urea levels without RF and finally, to document the effect of these states on the binding of sulfacetamide. RF (mean serum creatinine of 24.5 mg/dL and BUN 190 mg/dL) was originated by administrating i.v. uranyl nitrate. Uremia (mean BUN of 94 mg/dL and serum creatinine of 1.3 mg/dL) was induced by giving multiple doses of urea by gavage. RF was associated with a marked increase in the carbamylation of serum proteins and in the free fraction of sulfacetamide (Sff), but the degree of carbamylation did not correlate with Sff. Uremia without RF increased the carbamylation of serum proteins and in this case, the degree of carbamylation correlated with Sff. It is concluded that in vivo, carbamylation of serum proteins modifies, in a limited manner, drug binding to serum protein.
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PMID:Carbamylation of proteins and sulfacetamide free fraction in serum in experimentally-induced high blood urea states. 408 13

The effects and pharmacokinetics of thiopental were studied in eight patients undergoing renal transplantation. The results were compared with findings in a group of patients with normal renal function. No differences were observed in induction doses or between arterial or venous sleep concentrations. The average V3 in the renal failure group was 1441 or 2.5 times the value of the control group (P less than 0.01). The apparent differences indicating longer elimination half-lives and higher serum clearances in the renal patients were not significant. The average binding of thiopental to serum protein shortly after the induction was 83.9% (78.2-88.1) in the renal patients and 89.0% (85.2-91.6) in the control patients (P less than 0.05). The difference in V3 could be explained by the differences in protein binding and when the serum clearance was calculated by using the unbound fraction, this "intrinsic clearance" was significantly lower in the renal failure group (P less than 0.05). Haemodynamic parameters were determined during the initial 5 min. No significant difference was observed between the thiopental-induced changes in stroke volume. Cardiac output was unchanged in both patient groups.
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PMID:Pharmacokinetics and pharmacodynamics of thiopental in patients undergoing renal transplantation. 636 79

Ten normal subjects and ten patients with chronic renal failure requiring hemodialysis were given intravenous infusions of moxalactam ranging from 500 mg to 2 g. Serum and urine concentrations were measured for up to 12 h. Renal failure subjects were given doses both during and between hemodialysis treatments. Protein binding of moxalactam in both normal and uremic serum was determined by ultracentrifugation. The serum half-life in normal subjects was 2.1 and 2.3 h for the 1- and 2-g doses, respectively. The half-life of moxalactam in patients with renal failure was 13.9 h on the 500-mg dose and 13.3 h on the 1.0-g dose. During hemodialysis the serum half-life fell to 4.4 and 5.7 h, respectively. Moxalactam protein binding ranged from 52% in normal serum to 36% in renal failure patient serum. Unbound moxalactam appeared to distribute with the entire body water based on the serum pharmacokinetics and antibiotic serum protein binding determined in this study.
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PMID:Pharmacokinetics, protein binding, and predicted extravascular distribution of moxalactam in normal and renal failure subjects. 645 35


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