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)

Recent experimental and clinical data have suggested that angiotension converting enzyme (ACE) inhibitors may decrease glomerular proteinuria by specific effects on the glomerulus. We studied a group of 15 adult patients with chronic renal failure and proteinuria due to various glomerulopathies. These patients had mild to moderate hypertension which was effectively controlled with conventional antihypertensive therapy. We then treated the patients with captopril, maintaining a similar dietary protein and salt intake. After 6 months of study, proteinuria was reduced significantly without reduction in inulin or para-aminohippurate clearance. This supports the concept that captopril may have salutary effects on the glomerulus, independently of its effect on systemic blood pressure.
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PMID:Control of hypertension with the angiotensin converting enzyme inhibitor captopril reduces glomerular proteinuria. 307 87

To elucidate the role of the kidneys in the development of hypertension in Dahl salt-sensitive (S), as compared to resistant (R) rats of the JR strain, we analyzed functional and morphological changes before and after the administration of an 8% NaCl diet and the onset of hypertension. The diet was begun at six weeks of age and was continued until 12 weeks of age. At six weeks, blood pressure was not different between S and R rats. Hypertension occurred in S rats receiving the 8% NaCl diet at week 8, and in S rats receiving 0.9% NaCl at week 10. Albuminuria and proteinuria were found in S rats prior to the 8% NaCl diet and progressed regardless of diet. Electron microscopy of glomeruli revealed segmental loss of epithelial foot processes in S rats at six weeks prior to the 8% NaCl diet. Mesangial widening, arteriolar myo-intimal cell hyperplasia and interstitial fibrosis occurred in all S rats. Inulin and PAH clearances in S rats decreased with time, the changes being accelerated by the 8% NaCl diet. Micropuncture of S and R rats prior to the 8% NaCl diet revealed no glomerular hypertension in S rats. The number of glomeruli in S and R rats were not different. We conclude that prehypertensive S rats of the JR strain already have albuminuric glomerular disease not associated with reduced number of glomeruli or glomerular hypertension. The renal pathology is accelerated once hypertension develops. A lower NaCl intake delays, but does not prevent renal disease in S rats.
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PMID:Renal disease and the development of hypertension in salt-sensitive Dahl rats. 340 12

Seven salt depleted patients with the idiopathic nephrotic syndrome were treated with various non-steroidal anti-inflammatory drugs. Indomethacin, diclofenac-sodium and flurbiprofen decreased proteinuria, glomerular filtration rate, plasma renin activity and renal prostaglandin E2 excretion by 59%, 19%, 55% and 68% respectively. Sulindac induced no major changes in proteinuria, glomerular filtration rate, plasma renin activity and renal prostaglandin E2 excretion. The relative change in proteinuria and glomerular filtration rate during non-steroidal anti-inflammatory drug treatment correlated strongly with that of the renal prostaglandin E2 excretion (r = 0.89 and r = 0.70, respectively p less than 0.05). It is likely that the anti-proteinuric effect of non-steroidal anti-inflammatory drugs is dependent on their potency to inhibit renal prostaglandin synthesis and it is suggested that this effect is mediated by lowering transcapillary glomerular hydraulic pressure.
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PMID:Reduction of urinary protein and prostaglandin E2 excretion in the nephrotic syndrome by non-steroidal anti-inflammatory drugs. 351 75

An epidemic of renal disease is occurring among the Zuni Indians in western New Mexico. In 1985, 1.6% of Zunis had clinically recognized renal disease and 1% had renal insufficiency. The incidence of end-stage renal disease (ESRD) in 1984 and 1985 was 14 times the rate for US whites, and three times the rates of other Indians in ESRD network 6. One third of the cases of renal disease and ESRD is due to type 2 diabetes, but the etiology of disease in most of the remainder is unknown. Affected subjects range from early childhood to old age. Early signs are hematuria, mild to moderate proteinuria, normal BP, and low total hemolytic complement, normal or low C3 and C4 levels, in about 40% of the cases. The clinical course varies from benign to rapidly progressive renal failure. Biopsies usually reflect an immune-complex mediated mesangiopathic glomerulonephritis, with IgA, IgG, IgM, and C3 variably present in the mesangium. In some cases, there is a very strong familial pattern suggesting autosomal dominant inheritance or a marked communal exposure effect. This may be a genetic disease educed by the consanguinity in the ethnically homogeneous Zuni population. Mesangiopathic renal disease is common in some Oriental populations, and this phenomenon may reflect the American Indians' Oriental ancestry. This disease may also be due to toxic exposures related to jewelry-making, potting, Zuni water, Zuni salt, or herbal or other products used for medicinal or religious purposes. This epidemic is much morbidity and generating huge costs for ESRD treatment. Further study is needed to better understand its etiology.
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PMID:Epidemic renal disease of unknown etiology in the Zuni Indians. 359 94

The polycation hexadimethrine (HDM) binds to anionic sites in the glomerular basement membrane (GBM) and causes heavy proteinuria when infused in vivo. An in vitro assay of 3H-HDM binding to isolated dog GBM was developed, to permit further analysis of the GBM components binding HDM. 3H-HDM binding to isolated GBM was saturable, reversible in dose-dependent fashion by competing polycations, and inhibited by increasing salt concentration and low pH. The pH dependence of binding suggested that most of the HDM binds to carboxyl groups rather than to the sulfate groups of proteoglycans. Removal of heparan sulfate by heparinase or purified heparatinase had no detectable effect on HDM binding. Treatment of GBM with neuraminidase, hyaluronidase, or chondroitinase reduced binding of HDM by a maximum of 20 to 38%. However, substitution of carboxyl anions with nonionizable glycine methyl ester residues resulted in complete elimination of HDM binding. Parallel results were obtained in studies of glomerular localization of cationized ferritin (CatF), pI 8.5. After carboxyl substitution, GBM did not bind CatF; heparinase-treated GBM bound CatF in a distribution not demonstrably different from normal. Cellulose acetate electrophoresis of glycosaminoglycan fractions prepared from treated GBM confirmed that carboxyl modification did not alter the content or charge of the heparan sulfate of GBM, but heparinase treatment removed at least 90% of heparan sulfate. The results indicate that carboxyl groups are quantitatively more important than heparan sulfate for binding of HDM in vitro. Since HDM causes proteinuria in vivo, carboxyl groups may be important for maintenance of normal permselectivity.
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PMID:Polycation binding to glomerular basement membrane. Effect of biochemical modification. 380 16

In a double-blind crossover study in 10 salt-depleted nephrotic patients the reduction of proteinuria was significantly larger during indomethacin 50 mg three times daily than during naproxen 250 or 500 mg three times daily (72 vs. 44%, p less than 0.05; 77 vs. 46%, p less than 0.05, respectively). Both drugs induced similar reversible intrarenal hemodynamic changes, but indomethacin had more pronounced effects than naproxen. A common pathway, such as the reduction of the glomerular filtration rate and a reduction of the glomerular transcapillary hydraulic pressure, is likely to explain the observed phenomena and is most probably mediated by inhibition of intrarenal prostaglandin synthesis. If treatment with a nonsteroidal anti-inflammatory drug is considered in patients with the idiopathic nephrotic syndrome, indomethacin appears up to now the most effective agent in reducing urinary protein loss.
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PMID:Antiproteinuric effect of naproxen and indomethacin. A double-blind crossover study. 390 56

As part of an on-going longitudinal study, 7895 men of Japanese ancestry living on the island of Oahu, aged 45-68 and free of evidence of prior stroke at entry examination, have been followed by re-examinations and surveillance. During ten years of follow-up 154 men developed thromboembolic stroke, 65 developed intracranial hemorrhage, and 19 developed stroke of unknown type. There were 79 deaths attributed to stroke. The independent risk factors for thrombo-embolic stroke were elevated blood pressure, glucose intolerance, age, electrocardiographic evidence of left ventricular hypertrophy or strain, cigarette smoking and proteinuria. Attributes associated with increased risk of intracranial hemorrhage were age, elevated blood pressure, cigarette smoking, serum uric acid and, inversely, serum cholesterol level. Electrocardiographic evidence of left ventricular hypertrophy or strain significantly increased the risk of cerebral hemorrhage, but was not associated with subarachnoid hemorrhage. In univariate analysis, there was an inverse relation between dietary fat intake and thrombo-embolic and total stroke incidence. An inverse relation was also shown between protein intake and total stroke incidence. These dietary relations became statistically not significant in multivariate analysis. No relation was found between salt intake and the incidence of stroke.
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PMID:Dietary and other risk factors for stroke in Hawaiian Japanese men. 400 55

A 23-year-old male whose uncle died of nephronophthisis, and whose pathology is also discussed, presented with 5 g of protein in a 24-hour urine collection. Nephrogenic diabetes insipidus and salt wasting were present in addition to azotemia. Characterization of the proteinuria, including elevated alpha globulins by electrophoresis and markedly elevated urinary beta-microglobulins by radioimmunoassay (49.55 mg/L) indicated predominantly tubular proteinuria. A percutaneous renal biopsy showed normal glomeruli, interstitial inflammation and fibrosis, and tubular atrophy. Electron microscopy revealed notable alterations of the tubular basement membrane.
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PMID:Nephronophthisis with massive proteinuria. 618 93

For over 50 years, gold therapy has played an important role in the treatment of rheumatoid arthritis. Since 1932, many clinicians and investigators have confirmed the beneficial effects of the water-soluble gold salts, aurothioglucose and gold sodium thiomalate. Gold therapy is indicated for patients with active disease who are not responsive to conservative therapy. To minimize patient risks, contraindications must be considered, and careful clinical and laboratory monitoring must be performed under close supervision by the physician during therapy. Side effects may include vasomotor reactions, dermatitis, stomatitis, leukopenia, proteinuria, nephrosis, and thrombocytopenia. During therapy, one of six patients may have an adverse reaction requiring suspension or termination of therapy. Of the five tolerating gold, one will not benefit, three may have marked improvement, and one may have a remission. The usual recommended dosage schedule is intramuscular injection of 25 to 50 mg of gold salt at weekly intervals until a total of 1,000 mg has been achieved. At this level, gold injections may be spaced biweekly, triweekly, and then monthly for an indefinite period.
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PMID:Parenteral gold in the treatment of rheumatoid arthritis. 622 81

Hypertension frequently accompanies chronic glomerulonephritis. Mesangial injury and glomerulosclerosis are common in glomerulonephritis and are often harbingers of progressive glomerular destruction. Thus, in a model of mesangial immune injury we studied the relationship between hypertension, mesangial injury, and glomerulosclerosis. We induced mesangial ferritin-antiferritin immune complex disease (FIC) in Dahl salt-sensitive (S) and salt-resistant (R) rats. S and R rats with FIC were fed chow containing 0.3% NaCl until 14 weeks of age and then switched to 8.0% NaCl chow until 28 weeks of age. Groups of control S and R rats (no FIC) were either fed 0.3% NaCl for 28 weeks or switched to 8.0% NaCl chow at 14 weeks of age. Blood pressure, serum creatinine, urinary protein, and glomerular injury (assessed by semiquantitative morphometric analysis) were determined at 14 and 28 weeks of age. R rats with or without FIC did not develop hypertension; mesangial injury was minimal. At 14 weeks of age, only S FIC rats developed hypertension, proteinuria, significant mesangial expansion and early glomerulosclerosis. At 28 weeks of age, proteinuria, mesangial expansion, and glomerulosclerosis were significantly more severe in hypertensive S rats with FIC than in those without FIC. These studies show that despite a normal salt intake, mesangial injury hastened the onset of hypertension, but only in rats genetically predisposed to hypertension (S FIC at 14 weeks). High dietary salt further aggravated hypertension, which, in turn, magnified both mesangial injury and glomerulosclerosis. Clinically, the different rates of progression of human glomerulonephritis associated with hypertension may be in part dependent on similar mechanisms.
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PMID:Mesangial immune injury, hypertension, and progressive glomerular damage in Dahl rats. 623 58


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