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)

A 32-year-old female was suffering from intractable lupus nephritis (LN). Prednisolone at 30 mg per day had been prescribed for two months because of massive proteinuria and edema. After that, anasarca and orthopnea were induced, and hypoproteinemia, hypercholesteremia, and anti-cardiolipin antibody were observed. Prednisolone at a dose of 60 mg per day was necessary. However, there was no improvement of the nephrotic state and renal pathological changes shown as diffuse proliferative lupus nephritis were followed by moderate crescent formation as determined by serial needle biopsy. Cyclophosphamide (CYP) pulse therapy was started and marked improvement of LN was obtained clinically and serologically without significant adverse effects.
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PMID:Effect of cyclophosphamide pulse therapy in a patient with intractable lupus nephritis. 227 25

Spontaneous nephrotic mice (ICGN mice), a new mutant strain of mouse from outbred ICR, were clinically, macroscopically, histologically and immunohistochemically studied to establish their value as a model for human nephrotic syndrome. Most of the affected mice developed proteinuria, hypoproteinaemia and hypercholesterolaemia, and some of them developed systemic oedema. A high concentration of blood urea nitrogen (BUN) and a low haematocrit value were also observed. The kidneys of severe cases showed a decrease in size and had a yellowish granular surface. These findings indicated that the mice were terminally affected by chronic renal insufficiency. Histopathology demonstrated glomerular lesions consisting of thickened basement membranes of the capillary loops with irregular spike-like protrusions and enlargement of the mesangium unaccompanied by cellular proliferation. The immunofluorescence technique revealed positive granular staining for IgA, IgG and IgM and to a lesser extent for C3 along the capillary loops in affected mice. The similarity between this spontaneous disease and human nephrotic syndrome caused by idiopathic glomerular lesions is discussed. ICGN mice may be a useful animal model for this human disease.
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PMID:Characteristics of mutant mice (ICGN) with spontaneous renal lesions: a new model for human nephrotic syndrome. 252 1

The efficacy and safety of lovastatin as a hypolipidemic agent were evaluated in ten adult patients with secondary hypercholesterolemia due to proteinuria (greater than 2 g/d) and (in seven patients) concurrent corticosteroid therapy. Patients were on a low-cholesterol diet throughout the study. After a 4-week baseline period, patients were randomized to receive either placebo or 10 mg lovastatin twice daily for a period of 6 weeks. The dose of lovastatin was increased to 20 mg twice daily for 6 weeks, and 40 mg twice daily for 6 weeks in the latter group. Those patients who received placebo for the first 6 weeks subsequently received 10, 20, and 40 mg of lovastatin twice daily in a stepped dose regimen, with each dose given for 6 weeks. Lovastatin was well tolerated by all patients and none withdrew from the study. Baseline plasma cholesterol concentrations (390 +/- 20 mg/dL; mean +/- SEM) decreased 22% (P less than 0.003) at the lowest dose of 10 mg twice daily, 27% at 20 mg twice daily, and 33% at 40 mg twice daily. Baseline plasma triglycerides decreased by 25% (P less than 0.05) at the highest dosage. Concentrations of low-density lipoprotein (LDL) cholesterol fell by 29%, 34%, and 45% on doses of 10, 20, and 40 mg of lovastatin twice daily. Concentrations of high-density lipoprotein (HDL) cholesterol increased slightly. Serum creatinine concentrations and proteinuria were not affected by lovastatin therapy. We conclude that lovastatin was a well-tolerated and extremely effective hypocholesterolemic agent in patients with persistent secondary hypercholesterolemia associated with proteinuria or proteinuria and concurrent corticosteroid therapy.
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PMID:Lovastatin in the treatment of multifactorial hyperlipidemia associated with proteinuria. 265 May 39

Progressive passive Heymann nephritis (group II) was induced in rats by i.v. injections of rabbit antiserum against an antigen from the brush border of the proximal tubules of rat kidney following immunization with rabbit gamma-globulin in Freund's complete adjuvant, and the process of the disease was compared with that of rats that received the antiserum alone (group I). The rats of group I showed proteinuria (30-50 mg/day) and plasma cholesterol content (80-90 mg/dl) slightly higher than the normal level from the 17th or the 22nd day after antiserum injection to the 90th day. The rats of group II revealed a heavy proteinuria (300-400 mg/day) and hypercholesterolemia (approx. 200 mg/dl) during the same period. In group II, there were the thickening of glomerular basement membrane (GBM) and spike formation. Moreover, granular deposits of rat IgG, rabbit IgG and rat C3 were observed along the GBM. These changes were weaker in group I. When given orally, daily, azathioprine (20 mg/kg) and prednisolone (1 and 3 mg/kg) showed a beneficial effect on the nephritis in group II. The group II model closely resembles human glomerulonephropathy and may be useful for studying the effect of medication on glomerulonephropathy.
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PMID:Accelerated passive Heymann nephritis in rats as an experimental model for membranous glomerulonephritis and effects of azathioprine and prednisolone on the nephritis. 272 71

It is known that chronic alcoholics and type II diabetics show hyperlipidemia, characterized by hypertriglyceridemia and in a minor degree by hypercholesterolemia. The mechanisms underlying the effect of ethanol and carbohydrates on plasma lipids seem to be different; therefore in diabetic subjects chronic alcohol consumption could produce a more severe hyperlipidemia and so accelerate atherosclerotic events. In order to verify it we have measured plasma cholesterol, HDL-cholesterol, and triglycerides and investigated the presence of micro- and macroangiopathy in two groups of non-insulin-dependent diabetics, differing each other for daily alcohol intake (18 chronic male alcoholics and 30 male subjects consuming respectively more than 150 g and less than 50 g of alcohol daily). In alcoholics, no clinical features, laboratory and echographic findings of cirrhosis and pancreatic disease were present. In order to avoid a possible interference of other factors on the metabolism of plasma lipids, in our study patients were selected with the following criteria: 1) only male subjects; 2) age 40-60 years; 3) nonsmokers; 4) moderate coffee drinkers; 5) average physical activity; 6) with BMI less than 28; 7) in good diabetic control (HbA1c less than 6%, n.v. 4.4%-5.6%); 8) normal kidney function (plasma creatinine less than 1.3 mg%) and 24 hr proteinuria absent;) 9) in treatment with diet alone or diet plus low doses of sulphonylureas or biguanides. The data were analyzed by Student's "t" and chi-squared tests. No significant differences could be detected (alcoholics/occasional drinkers, means +/- 1 SD) either in the plasma levels of cholesterol (181.7 +2- 39.3/198.2 +/- 32.5), HDL-cholesterol (43.4 +/- 12.7/38.5 +/- 11.9), and triglycerides (105.5 +/- 56.4/159.7 +/- 114.8) and in the frequency of micro (22.2%/16.6%) and macroangiopathy (16.6%/26.6%) between the two studied groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of chronic alcohol consumption on blood lipid levels and angiopathy in diabetics]. 274 71

The medical records of 59 dogs with renal amyloidosis were reviewed. Most dogs with amyloidosis were greater than 6 years old, and females were affected more often than males. Beagles, Collies, and Walker Hounds were at increased risk, whereas German Shepherd Dogs and mixed-breed dogs were at decreased risk. Common historical findings were anorexia, polyuria, polydipsia, lethargy, vomiting, and weight loss. Common laboratory findings were leukocytosis, lymphopenia, nonregenerative anemia, hypercholesterolemia, azotemia, hyperphosphatemia, metabolic acidosis, isosthenuria, cylindruria, and proteinuria. Proteinuria was moderate to severe in most dogs, as assessed by qualitative determination of urine protein concentration, urine protein/urine creatinine ratio, and 24-hour urine protein excretion. Conservative medical management was of little value, and survival ranged from 3 to 20 months in 12 dogs for which this information was available. Moderate to severe diffuse global glomerular amyloidosis was detected in all dogs. Medullary amyloid deposition was multifocal and less severe, but was evident in most dogs. Secondary tubulointerstitial and glomerular lesions were mild or absent in most dogs. Thromboembolism was identified in approximately 14% of affected dogs, underlying inflammatory disease in 37%, and neoplasia in 20%. Laboratory indicators of renal function correlated poorly with histologic lesions, with the exception of glomerular amyloid deposition and "chronic renal disease" index with endogenous creatinine clearance.
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PMID:Clinicopathologic findings in dogs with renal amyloidosis: 59 cases (1976-1986). 276 63

Hypercholesterolemia is a known complication of the nephrotic syndrome. Patients with persistent proteinuria and prolonged hypercholesterolemia are probably at increased risk for cardiovascular disease. Until recently there has been no safe and effective treatment for this disorder. The effects of gemfibrozil on plasma lipids and lipoproteins in hypercholesterolemic patients with the nephrotic syndrome were therefore studied. Eleven patients with the nephrotic syndrome were studied in a randomized, double-blind placebo-controlled trial with six-week treatment periods. Gemfibrozil 600 mg or placebo was administered twice a day. There was a third unblinded period in which seven patients received gemfibrozil plus the bile acid-binding resin, colestipol, 10 grams twice a day. Gemfibrozil treatment produced a marked reduction in plasma triglyceride (51%, P = 0.001) and a 15% decrease in plasma total cholesterol (P = 0.003). Low density lipoprotein cholesterol decreased 13% (P greater than 0.05), high density lipoprotein cholesterol increased 18% (P = 0.006) and the ratio of low density lipoprotein to high density lipoprotein cholesterol fell 26% (P = 0.01). Apolipoprotein A-l was unchanged while apolipoprotein B decreased 26% (P = 0.006). Four patients were unable to complete period 3 because of gastrointestinal symptoms. The remaining patients had further improvement in plasma lipids and lipoproteins with the combined therapy: total cholesterol further decreased 26%, triglycerides decreased 17%, low-density lipoprotein cholesterol decreased 36%, high-density lipoprotein to high-density lipoprotein cholesterol fell 33%. Gemfibrozil improved lipid and lipoprotein cardiovascular risk factors without major toxicity. Persistent elevations in total plasma and low-density lipoprotein cholesterol during gemfibrozil treatment, however, indicate the need for individualized drug therapy.
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PMID:Treatment of nephrotic hyperlipoproteinemia with gemfibrozil. 277 95

1. Daily intravenous administration of bovine serum albumin (BSA) to rats produces chronic serum sickness glomerulonephritis, an immune-complex-mediated renal disease that is eventually always fatal. We have performed a detailed study of the onset of proteinuria in chronic serum sickness in order to assess the long-term consequences of discontinuing daily BSA injections precisely at that very early and well-defined stage of disease. 2. Urine and plasma samples from rats receiving daily BSA injections were collected and analysed daily before the onset of proteinuria, at which time the rats were divided into three groups. Group 1 continued to receive daily BSA injections, in group 2 injections were stopped on the first, and in group 3 on the third, day of proteinuria. Proteinuria began suddenly and was not preceded either by microalbuminuria or abnormalities of plasma composition. The sudden expression of proteinuria was accompanied by an equally rapid development of hypoalbuminaemia and hypercholesterolaemia. Development of the characteristic glomerular histopathology of serum sickness coincided with, but did not precede, the onset of proteinuria. Despite the discontinuation of antigen injections at the onset of proteinuria, basement membrane thickening was evident 8 weeks later; proteinuria persisted and hypercholesterolaemia increased. 3. In this model of immune complex glomerulonephritis, changes in kidney function and immunopathology were abrupt and closely linked, precluding the use of those criteria to predict when proteinuria would begin. Furthermore, extremely brief periods of active immunological injury to the peripheral capillary wall were sufficient to produce persistent abnormalities of glomerular structure and function.
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PMID:Sudden onset of proteinuria in chronic serum sickness in rats. 278 84

The nephrotic syndrome is characterized by proteinuria, hypoalbuminemia, and hypercholesterolemia. Hypertriglyceridemia often is present as well. In this study, the kinetics of plasma lipoproteins were investigated in four patients with nephrotic hyperlipidemia, and repeat studies were carried out in three of these patients during therapy with lovastatin. Before lovastatin therapy, the patients had an extremely delayed catabolism of very low density lipoproteins (VLDL) without evidence of overproduction of lipoproteins in this fraction. Three of four patients had elevated levels of low density lipoprotein (LDL) that were due mainly to increased production rates for LDL. In the three patients treated with lovastatin, the drug therapy lowered plasma concentrations of total cholesterol, triglycerides, VLDL-cholesterol, and LDL-cholesterol, and raised high density lipoprotein (HDL)-cholesterol. Lovastatin therapy decreased VLDL-triglycerides primarily by enhancing their catabolism, and lowered LDL-cholesterol levels mainly by reducing input rates for LDL. Overall, lovastatin appears to be an effective drug for the treatment of hyperlipidemia in the nephrotic syndrome.
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PMID:Lovastatin therapy in nephrotic hyperlipidemia: effects on lipoprotein metabolism. 316 83

Recent evidence suggests a role for lipid deposition in the pathogenesis of some forms of glomerular disease. To gain further insight into this phenomenon guinea pigs (GP) were fed a 2% cholesterol (HC) diet and compared to GP on a normal diet (C). Serial observations were made 5, 10, 30 and 70 days after the initiation of the experiment. HC gained less weight than C (P less than 0.001) and developed hemolytic anemia after 30 days. At all time periods serum total cholesterol (TC) was significantly elevated in HC (P less than 0.001). High density lipoprotein-cholesterol and total phospholipids (PL) were significantly higher in HC at days 30 and 70. Lipoprotein-X was detected in HC serum. The relative proportion (%) of cholesteryl ester (CE) at day 70 was significantly higher in HC than in C when renal cortical lipids were analyzed (P less than 0.017). Renal function was normal in both groups throughout the 70 days. The HC group developed proteinuria and hematuria (proteinuria, HC = 22.1 +/- 7.2 mg/24 hr; C, 6.4 +/- 2.3 mg/24 hr), which was detected at day 70 but not at day 30. HC developed significant progressive mesangial expansion which was first evident at day 30. In HC only oil red 0 material was first detected in glomeruli at day 5 and was very conspicuous at day 70. Increased intraglomerular monocyte numbers were detected at day 70 (P less than 0.017) but not at day 30 in HC. No glomerulosclerosis was observed in GP's with drug-induced hemolysis on a normal diet. To see the effect of high protein intake on HC GP's, a group of GP's was put on a HC diet for 30 days followed by a 2% cholesterol-high protein (HCHP) diet for 40 days. Compared to HC GP's, the HCHP group showed significantly higher serum TC and PL (P less than 0.017), mesangial expansion (P less than 0.01) and proteinuria (P less than 0.01). The results indicate that hypercholesterolemia plays an important role in the pathogenesis of glomerulosclerosis in this model and that the process appears to be mediated, at least in part in the later stages, by monocytes. The addition of protein to the HC diet augments these effects.
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PMID:Glomerular disease in hypercholesterolemic guinea pigs: a pathogenetic study. 336 51


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