Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of captopril on proteinuria was evaluated in twenty patients with various glomerular diseases excreting heavy proteinuria (> 3.0 g/day). Captopril in a daily dose of 37.5 mg was administered orally three times a day to all patients and they were followed for eight weeks. Twenty-four hour urinary excretion of protein, creatinine, sodium, selective protein index (SPI), and blood chemistry including serum electrolytes were measured every two weeks. Twenty-four hour urinary protein excretion per gram creatinine started to fall within two weeks of captopril administration and became nearly stable after four weeks of therapy (p < 0.05). Mean 24-hour urinary protein excretion decreased significantly from a pretreatment value of 9.0 +/- 6.0 gm/gm of cr. to 4.4 +/- 3.5 gm/gm of cr. after eight weeks of captopril treatment. The serum albumin level increased progressively at six and eight weeks after the captopril treatment period and was significantly higher than the pretreatment value (p < 0.05). The decrease in proteinuria did not coincide with a fall in blood pressure or any changes in creatinine clearance. We conclude that captopril does have a significant antiproteinuric effect in patients excreting heavy proteinuria with various glomerular diseases. However, the long term therapeutic efficacy and any renal protective effect of this drug remain to be proven.
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PMID:Effect of captopril on heavy proteinuria in patients with various glomerular diseases. 129 47

In order to analyze urinary proteins from patients with various renal diseases, a reversed-phase high performance liquid chromatography (HPLC) with IPG PACK ODS column packed with polyporous glass was used. The reproducibility of standard proteins was good. The results by this method correlated well with those by radioimmunoassay or laser nephelometry, precolumn procedure needed the centrifugation only. The reversed-phase HPLC was superior to the other HPLC methods in the analysis of urinary proteins for its simplicity and high sensitivity. The peaks of both alpha 1-acid glycoprotein (alpha 1-AGP) and human serum albumin (HSA) in the chromatogram was regarded as the marker of renal damage. Urinary alpha 1-AGP/HSA ratio was calculated after measuring these two peak areas. As a result, it was significantly higher in the urine from patients with various glomerulonephritis (GN) than in those from healthy children. In the patients with postural proteinuria, it was the same level as that in healthy children. These date suggest that the urinary alpha 1-AGP/HSA ratio would be a beneficial indicator to find out the patients with GN from among children with proteinuria. Furthermore, it seems that this method is suitable for use in routine screening of renal diseases for its simplicity and speed.
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PMID:[Studies of the analysis of urinary proteins from children with renal diseases by reversed-phase high performance liquid chromatography]. 129 75

We studied the effects of symptomatic, antiproteinuric treatment with NSAID's (n = 28) and ACE-inhibitors (n = 14) in patients with proteinuria due to idiopathic membranous glomerulopathy (MGP). These two treatment groups were compared with a group of patients who did not receive antiproteinuric medication (n = 14). Urinary protein loss was effectively lowered by NSAID and ACE inhibitor therapy from 9.5 +/- 1.0 to 4.5 +/- 0.5 g/day (mean +/- SEM) and from 9.8 +/- 1.4 to 3.9 +/- 0.7 g/day respectively, whereas the control group showed a slight fall in proteinuria from 6.9 +/- 0.8 to 5.5 +/- 0.8 g/day. As a result of this treatment hypoalbuminaemia and hypercholesterolaemia improved significantly: serum albumin rose in the NSAID group from 25.4 +/- 1.2 to 29.0 +/- 1.0, and in the ACEi group from 29.9 +/- 1.8 to 32.7 +/- 1.2 g/l (control group from 27.4 +/- 1.6 to 27.8 +/- 1.6 g/l, while cholesterol was lowered in the NSAID group from 8.5 +/- 0.5 to 7.5 +/- 0.4 and in the ACEi group from 8.7 +/- 0.5 to 7.6 +/- 0.4 mmol/l (control group from 9.7 +/- 1.1 to 8.5 +/- 1.0 mmol/l). The antiproteinuric effect of both drugs was well maintained during an 18-month follow-up. Progression towards end-stage renal failure was observed especially in patients with impaired renal function at entry. Remission of proteinuria occurred particularly in patients with lower baseline values of proteinuria, irrespective of the treatment modality.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antiproteinuric drugs in patients with idiopathic membranous glomerulopathy. 133 89

Clinical episodes of IgA nephropathy coincide recurrently with microbial infections. Cytokines produced during such infections may play a role in the pathogenesis of IgA-associated glomerulonephritis. To test this hypothesis, we examined the influence of passively administered proinflammatory cytokines (IL-1, IFN-gamma and IL-6) on the development of glomerulonephritis in an experimental model of IgA nephropathy. Glomerular IgA immune deposits were induced in mice by administration of IgA anti-phosphorylcholine (PC) with either a PC-containing carbohydrate antigen of Pneumococcal C polysaccharide (PnC) or a protein antigen of PC-conjugated bovine serum albumin (PC-BSA). The effect of IL-1 on the IgA-PC-BSA induced glomerular changes resulted in an increase of mesangial hypercellularity that was associated with mild proteinuria and hematuria. Mice treated with IL-1 and IgA-PnC developed diffuse proliferative glomerulonephritis with proteinuria and hematuria. In contrast, IL-6 treatment with IgA-PC-BSA of IgA-PnC failed to exert any significant renal effect. The combination of IL-6 and IL-1, however, intensified the mesangial hypercellularity of the IgA-PC-BSA, and induced severe proliferative glomerulonephritis with inflammatory monocytes and neutrophils infiltrates in the IgA-PnC treated mice. These glomerular changes were also accompanied by increased proteinuria and hematuria. Similarly, the combination of IFN with IL-1 produced histologic changes and compromised renal function more than IFN or IL-1 exerted independently. These results suggest that extrarenal cytokines influence the renal response to IgA immune deposits. We also conclude that a synergy of multiple cytokines and nephritogenic antigens immobilized in glomerular IgA immune deposits may lead to rapid progression of IgA-associated glomerulonephritis.
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PMID:Extrarenal cytokines modulate the glomerular response to IgA immune complexes. 140 17

We developed an approach in quantifying the risk of developing chronic renal insufficiency (CRI) based on a cohort of 184 patients with idiopathic membranous glomerulonephritis (IMGN), prospectively followed by the Toronto Glomerulonephritis Registry between 1974 and 1988. After a mean follow-up period of 5.8 years, 26% of patients developed CRI (defined as persistent reduction of creatinine clearance (CCr) less than or equal to 60 ml/min/1.73 m2 for greater than or equal to 12 months). We found that when compared to the baseline probability of the unselected patients, the severity of proteinuria at kidney biopsy added only marginally to the prediction of CRI. We introduced a special test condition: persistent proteinuria (PP) (that is, duration of proteinuria, g/day, above different cut-off levels). We examined the positive predictive value (PPV) and sensitivity (SEN) of 15 arbitrarily chosen levels of PP (that is, proteinuria greater than or equal to 4, 6 or 8 g/day persisting for greater than or equal to 6, 9, 12, 18 or 24 months) to select levels with optimal predictive characteristics. We found that PP greater than or equal to 8 g/day for greater than or equal to six months was a simple and useful predictor of CRI with a PPV and SEN of 66%. To further improve our prediction, we tested the following parameters: age, sex, initial SCr and CCr, proteinuria, serum albumin, hypertension, rate of change of CCr over time, and therapy (steroids +/- immunosuppressive drugs) in a multivariate analysis. Proteinuria, initial CCr, and rate of change of CCr were most important in predicting CRI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Predicting chronic renal insufficiency in idiopathic membranous glomerulonephritis. 145 88

We performed two trials. The former was a multicentric trial on 24 untreated patients with nephrotic syndrome due to membranous nephropathy to ascertain whether or not a long-term reduction of protein intake reduces urinary protein loss. In a randomized cross-over design the patients ate sequentially each for 3 months a normal protein diet (1.1 +/- 0.3 g/kg/day of proteins) and a low-protein diet (0.7 +/- 0.1 g/kg/day). Both diets were low in fat (< 30% of total calories). Neither urinary protein excretion nor serum albumin concentration were significantly different at the end of the low protein diet period or the normal protein diet period. We found that after 6 months of dietary manipulation serum total and LDL-cholesterol were reduced by 24 and 27% from the values at the beginning of the run-in period, also the mean 24 h proteinuria was significantly lower. In the later trial, after a baseline control period of 2 months on free diet, 20 untreated nephrotic patients were fed for two months a vegetarian soy diet, low in fat (28% of total calories) and in proteins (0.71 +/- 0.36 g/kg ideal body weight/day). At the end of the diet period all patients ate the same free diet as in the baseline period for 2 more months. The soy diet induced highly significant decreases in total serum cholesterol (28%). LDL-cholesterol (33%), apolipoprotein B (19%), urinary protein excretion (32%), that reversed on discontinuation of the diet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of dietary manipulation on the lipid abnormalities and urinary protein loss in nephrotic patients. 146 59

One of the most prominent manifestations of the nephrotic syndrome is hyperlipidemia. Lipoprotein synthesis is increased and catabolism is reduced in nephrotic patients and animals. The observation that infusion of either albumin or dextran reduces lipid levels suggests that oncotic pressure (pi) may regulate lipogenesis. It has been postulated that prolonged plasma half-life of lipoproteins in nephrosis is a consequence of saturation of catabolic sites and is secondary to the hyperlipidemia that results from increased lipogenesis. However, the absolute rate of triglyceride catabolism is reduced in nephrotic rats in comparison to normal suggesting that defective lipid catabolism may be a cause rather than a consequence of hyperlipidemia. Furthermore, chylomicrons (CM) and very-low-density lipoproteins (VLDL) are cleared normally in rats with hereditary analbuminemia despite increased lipid synthesis. When we cause proteinuria in analbuminemic rats, the clearance of CM and VLDL becomes greatly prolonged, suggesting that proteinuria, and not reduced serum albumin or pi, is responsible for defective lipoprotein catabolism. Maneuvers that reduce proteinuria, such as administration of an angiotensin-converting enzyme inhibitor, reduce lipid levels in nephrotic patients and animals even when plasma albumin concentration is unchanged supporting a hypothesis that proteinuria may lead to reduced catabolism of lipoproteins.
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PMID:Nephrotic hyperlipidemia: primary abnormalities in both lipoprotein catabolism and synthesis. 146 61

The Medical Research Council's Glomerulonephritis Registry was used to study clinicopathological correlations and renal survival in patients with IgA nephropathy reported between 1978 and 1985. IgA nephropathy was the histological diagnosis in 9.3 per cent of all renal biopsies reported to the registry during this period, and in 18.1 per cent of those with a primary glomerulonephritis. The 10-year cumulative renal survival rate accounting for censored data (Kaplan-Meier) was 83.3 per cent. Univariate analysis of survival curves (log-rank test) found the following parameters to be significantly correlated with poor renal survival: serum creatinine > 120 mumol/l (p < 0.001), hypertension (p < 0.001), serum albumin < 40 g/l (p < 0.005), proteinuria > 1 g (p < 0.025), age > 30 years (p < 0.025), and focal mesangial proliferation (p < 0.05). There was no significant difference in renal survival between males and females. Multivariate analysis (Cox's proportional hazards model) revealed that only a serum creatinine of > 120 mumol/l and a serum albumin of < 40 g/l were independently predictive of outcome. These findings indicate marked similarities between the UK experience of IgA nephropathy and the published European experience. IgA nephropathy is not a benign condition in the UK and patients with impaired renal function and/or those with a reduced serum albumin are significantly more likely to progress to end-stage renal failure within 10 years.
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PMID:Clinico-pathological correlations and long-term follow-up of 253 United Kingdom patients with IgA nephropathy. A report from the MRC Glomerulonephritis Registry. 148 40

B700 is a murine melanoma antigen that is closely related to, but distinct from, serum albumin. The present study examined the metabolic fate and anatomic distribution of radioiodinated B700 and mouse serum albumin (MSA) administered s.c. to mice. In blood, both proteins were associated with the plasma fraction where the halflife of B700, a glycoprotein, was 0.5 days, compared to 2.7 days for MSA. Of particular interest was the observation that B700, a 67 kD anionic protein, was excreted primarily in urine. The selective B700-proteinuria did not alter urinary volumes or produce hematuria or edema. SDS-polyacrylamide gel electrophoresis and western blot analysis using the H-2-3-3 B700-specific monoclonal antibody revealed that B700 proteinuria occurred in B-16 murine melanoma bearing animals but not in control mice. These studies demonstrate that the tumor-bearing host readily distinguishes between very similar normal protein (MSA) and tumor-associated antigen (B700) molecules and processes them differently.
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PMID:Proteinuria of B700, a 67 kD albumin-like melanoma-specific antigen. 149 72

Cross-linking glomerular basement membrane (GBM) has been shown to render it more permeable to protein. Isolated pig GBM was cross-linked with dimethylmalonimidate which reacts selectively with lysine epsilon-NH2 groups or with glutaraldehyde, a less selective cross-linking agent. Studies of the ultrafiltration properties of these materials in vitro using cytochrome c, myoglobin, bovine serum albumin and immunoglobulin showed that cross-linking had markedly increased solvent and protein fluxes as compared with native membranes particularly at higher pressures. Filtration studies with serum demonstrated that the cross-linked membranes were more permeable to serum proteins. Thickness measurements under pressure indicated that cross-linked membrane was less compressed than native membrane as pressure was increased. Pore theory did not provide a suitable model for analysis of the results, but analysis of the results using the fibre-matrix hypothesis indicated that cross-linking had the effect of bundling together the fibres (type IV collagen) in the GBM matrix. The effect of cross-linking on filtration could be explained by a combination of contraction of the membrane, fibre bundling and increased rigidity compared with native membrane. Cross-linking of GBM might lead to long-term damage of the glomerular capillary wall in nephritis, so promoting proteinuria.
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PMID:Studies of the permeation properties of glomerular basement membrane: cross-linking renders glomerular basement membrane permeable to protein. 154 78


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