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)

Lovastatin, a 3-hydroxy-3-methylglutaryl coenzyme A inhibitor, was given to 14 patients with unremittent nephrotic syndrome (heavy proteinuria with hyperlipidaemia) for 6 months. Treatment was started at an initial dose of 20 mg/day, increasing to a maximum of 80 mg/day. Treatment was well tolerated except in two patients: one developed rhabdomyolysis and one severe hypertriglyceridaemia requiring an additional antihyperlipidaemic agent. Lovastatin was effective in reducing serum cholesterol, LDL-C and apolipoprotein B in the remaining 12 patients. Cholesterol was reduced by 31% from 8.24 +/- 0.49 mmol/l (mean +/- SEM) to 5.7 +/- 0.18 mmol/l after 6 months (P less than 0.001). LDL-C was normalized to 3.26 +/- 0.21 mmol/l from a pretreatment value of 5.76 +/- 0.48 mmol/l (P less than 0.001), a decrease of 43%. Serum apolipoprotein B was also normalized to 1.11 +/- 0.09 g/l from a basal level of 1.51 +/- 0.10 g/l (P less than 0.05). Triglyceride, HDL-C and apolipoprotein A1 concentrations were unchanged. Proteinuria as well as renal albumin clearance were unchanged. GFR by plasma radioisotope Cr-EDTA clearance for the whole group was unaltered by treatment. However, among those with relatively good pretreatment renal function (GFR greater than 70 ml/min per 1.73 m2), GFR increased at the end of 6 months' treatment (118.2 +/- 15 ml/min per 1.73 m2 versus 77.6 +/- 8.4 ml/min per 1.73 m2 in wash-out phase).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lovastatin in glomerulonephritis patients with hyperlipidaemia and heavy proteinuria. 131 86

1. To elucidate the mechanisms by which cyclosporin A diminishes proteinuria, we studied 20 patients with severe nephrotic syndrome. Biopsy-established pathologies included minimal change disease (n = 5), membranous glomerulopathy (n = 6), membranoproliferative glomerulonephritis (n = 5) and focal segmental glomerulosclerosis (n = 4). Before, at the end of a 90 day course of cyclosporin A, and finally 1 month after stopping cyclosporin A we determined 24 h protein excretion. Measurements of glomerular filtration rate, effective renal plasma flow, fractional clearance rates of albumin and immunoglobulins with different charges and the transglomerular sieving of uncharged dextrans of broad size distribution were used to study the effects of cyclosporin A on renal perfusion and the glomerular filtration barrier. The findings were analysed with a theoretical model of solute transport. 2. Among the different forms of glomerulopathy the response to low-dose cyclosporin A (trough levels 32.0-36.9 ng/ml) varied markedly. In minimal change disease, proteinuria decreased from 9.5 +/- 3.1 to 1.3 +/- 0.2 g/24 h (mean +/- SEM, P less than 0.01). This response was due to restoration of the charge selectivity of the glomerular barrier. The depressed value of the glomerular permeability coefficient also returned to normal. Glomerular filtration rate, effective renal plasma flow and renal vascular resistance did not change. Proteinuria returned after stopping cyclosporin A, although it did not reach pretreatment levels. In membranous glomerulopathy, proteinuria fell from 9.9 +/- 1.5 to 1.8 +/- 0.3 g/24 h (P less than 0.01). Changes in protein excretion and dextran sieving were compatible with an increase in glomerular permselectivity and a decrease in filtrate flow through the 'shunt' pathway. Glomerular filtration rate was maintained, although effective renal plasma flow fell significantly. Proteinuria relapsed after stopping cyclosporin A. In membranoproliferative glomerulonephritis and focal segmental glomerulosclerosis proteinuria did not respond to cyclosporin A, although cyclosporin A exerted important haemodynamic effects. 3. In minimal change disease and membranous glomerulopathy cyclosporin A exerts its beneficial effects on proteinuria through changes in the properties of the glomerular barrier, resulting in increased charge and size selectivity, respectively.
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PMID:Effects of cyclosporin A on glomerular barrier function in the nephrotic syndrome. 132 May 44

From 1983 to 1990, 32 patients with hemorrhagic fever with renal syndrome (HFRS) were admitted to our hospital. The diagnosis was confirmed by high IgM type titers of antibodies to Hantaan virus. All patients presented with serum and urine abnormalities suggesting renal involvement. Serum creatinine was elevated and ranged between 1.8 and 14.3 mg/dl. Proteinuria ranged between 0.5 and 6.4 g/24 h. Seven patients died due to shock or hemorrhage, while 6 patients were supported by hemodialysis or peritoneal dialysis. Five of them had a complete recovery. Two patients were discharged with some degree of renal impairment which remained stable 12-15 months later. Kidney biopsy in the first patient performed 1 year after his discharge revealed some degree of interstitial fibrosis and tubular atrophy as well as an area with ischemic and sclerosed glomeruli. We conclude that HFRS in Greece is a severe disease with a high mortality rate. The disease may cause chronic renal failure in a limited number of patients.
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PMID:Hemorrhagic fever with renal syndrome in an endemic area of Greece. 135 72

A MoAb 1-22-3 (IgG3) was produced in mice immunized with rat glomeruli. A blotting study indicated the antigen molecule recognized by this MoAb has a molecular weight of about 25 kD, which is the same as that of the Thy 1.1 molecule. This MoAb is capable of inducing the morphological changes similar to those induced by anti-thymocyte serum or the anti-Thy 1.1 MoAb, ER4 and massive proteinuria in rats by a single i.v. injection. Proteinuria started immediately after MoAb 1-22-3 injection and peaked on day 5. Reaction products were detected by immunoelectron microscopy in vitro on the limited mesangial cell surface facing endothelial cells and in vivo in partially lysed mesangial cells 30 min after injection. Unlike the proteinuria-inducing MoAb ER4, reactivity of MoAb 1-22-3 was detected neither on endothelial cells, epithelial cells, nor along the glomerular basement membrane in vivo and in vitro. There is a difference in reactivity toward guinea-pig and rabbit materials between MoAb 1-22-3 and the commercial anti-Thy 1.1 MoAb (OX7). The antigenic determinant of MoAb 1-22-3 is concluded to be a new epitope and only the binding of MoAb 1-22-3 to this epitope proved to lead to an abnormal increase of glomerular capillary wall permeability.
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PMID:Epitope-specific induction of mesangial lesions with proteinuria by a MoAb against mesangial cell surface antigen. 137 51

Alterations of the anionic charge and/or sites of the glomerular basement membrane (GBM) in the heterologous phase of passive Heymann nephritis (PHN) were studied. Rats with PHN induced by a single injection of anti-Fx1A IgG were examined at days 1, 2, 3 and 4. The left kidney was perfused with ruthenium red (RR) solution as a cationic probe. The RR particles (= anionic sites) in the GBM were counted and expressed as the number of RR particles per unit length of GBM. For quantitative determination of the total anionic charge of the GBM, the GBM-bound ruthenium (= anionic charge) was measured with an atomic absorption spectrophotometer (AAS). Abnormal proteinuria corresponding to a decrease in anionic charge was detected at days 3 and 4. The anionic sites in the lamina rara externa (LRE) adjacent to immune complex (IC) deposits were found to have diminished earlier from day 1 onwards. This diminution was largely confined to areas adjacent to the IC deposits and was significantly correlated with the amount of urinary albumin excretion. Proteinuria in the heterologous phase of PHN would thus appear to be causally related to a decrease in the number of anionic sites in the LRE adjacent to IC deposits.
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PMID:Alterations of anionic charge and/or sites of the glomerular basement membrane in the heterologous phase of passive Heymann nephritis. 137 13

Hypertension and diabetes mellitus are strongly associated conditions from epidemiologic, genetic, and pathophysiologic points of view. The prevalence of hypertension is high in patients with diabetes, and, conversely, many patients with essential hypertension are glucose intolerant. Proteinuria appears in 40-50% of patients with insulin-dependent diabetes mellitus and 20-30% of patients with non-insulin-dependent diabetes mellitus. Progressive renal failure occurs in 30-40 and 3-8% of patients, respectively, hypertension being a leading factor in its rate of progression. In various animal experiments, ACE inhibitors are able to prevent proteinuria and glomerular sclerosis, presumably by lowering transglomerular capillary pressure. In the diabetic human, ACE inhibitors are powerful antihypertensive drugs, devoid of metabolic side effects. Clinical studies indicate that ACE inhibitors reduce proteinuria and possibly slow the rate of decline in renal function. Such an effect is not observed with beta-blockers. Large-scale studies are needed to confirm this very important hypothesis.
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PMID:Angiotensin-converting enzyme inhibition and diabetic nephropathy. 138 63

A case of ulcerative colitis associated with secondary amyloidosis in a 62-year-old man who died from septic shock and pneumonia complicating head injury is reported. Amyloid deposition was incidentally found at autopsy. Proteinuria and hepatomegaly discovered a few days before his death were the only signs of amyloidosis. The postmortem examination showed chronic ulcerative colitis (remitting form) with pseudo-polyps and amyloid deposition in the liver, spleen, pancreas, rectum, adrenals and kidneys. Although secondary amyloidosis complicating with Crohn's disease has been frequently reported, amyloidosis associated with ulcerative colitis has been exceptionally described and only 10 cases have been collected from the literature.
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PMID:[Ulcerative colitis and amyloidosis. Presentation of a case and review of the literature]. 138 45

Irreversible mesangial changes with persistent proteinuria were induced in rats given two consecutive injections 2 weeks apart of a MoAb 1-22-3 to rat mesangial cell. The characteristics of the resulting lesions were investigated and compared with those of the reversible change induced by a single injection. At 24 h after the second injection, mesangiolytic changes similar to those after a single injection were evident. The accumulation of macrophage-like cells in glomeruli observed at 1 week after the first injection was not evident during the experimental period after the second injection. Hypercellularity with the characteristics of intrinsic mesangial cell and increased mesangial matrix were already present 1 week after the second injection. And mesangial sclerotic change progressed up to 6 months. Deposition of collagen type I and type III and accumulation of collagen fibril at the ultrastructural level were evident in rats 6 months after the second injection. Proteinuria started immediately and continued for more than 6 months after the second injection. The mesangial sclerotic change with persistent proteinuria described here is considered to be a better model for investigating the mechanism of chronic progression of human mesangial proliferative glomerulonephritis.
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PMID:Mesangial sclerotic change with persistent proteinuria in rats after two consecutive injections of monoclonal antibody 1-22-3. 139 93

A 58-year-old fisherman was admitted because of an abnormal chest X-ray shadow on the right side. Bronchoscopic examination revealed tumor of right B7. Transbronchial biopsy showed squamous cell carcinoma. He was treated with four courses of CDDP and PEP. Two years later, he developed nephrotic syndrome and relapse of lung cancer. Proteinuria and pedal edema continued. Renal biopsy revealed the characteristic light and immunofluorescent microscopic features of membranous nephropathy. Oral administration of low dose etoposide resulted in reduction of the carcinomatous lung lesion and a decrease in proteinuria as well as pedal edema.
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PMID:[A case of nephrotic syndrome associated with bronchogenic carcinoma]. 140 14

To ascertain the contribution of systemic hypertension in the progression of renal failure, we have studied the effects of pharmacological treatment of hypertension in rats with the remnant kidney model of renal insufficiency, streptozotocin diabetes, or nephrotoxic serum nephritis. Treatment with the angiotensin converting enzyme (ACE) inhibitor enalapril lowered systemic blood pressure in the remnant kidney and diabetic animals, but did not lower blood pressure in rats with nephrotoxic serum nephritis. Proteinuria was reduced in all three models, and creatinine clearance improved in the remnant kidney and diabetic animals, when compared with untreated controls. In the remnant kidney and diabetic models systemic blood pressure was lowered to a similar degree by treatments with a calcium blocker, with no improvement in either proteinuria, or glomerular filtration rate. Further studies of the long-term effects of enalapril have been undertaken in rats with the two kidney one clip model of hypertension. Rats treated with enalapril had a lower blood pressure and improved survival over one year of treatment, compared with untreated rats. After 1 year of treatment however the clipped kidney was small and fibrotic, and non functional. Following withdrawal of enalapril therapy there was no functional improvement of the clipped kidney. The possibility that ACE inhibitors have a specific intra-renal effect reducing the rate of progression of renal disease now needs confirmation in human studies. In renovascular hypertension however, intra-renal changes induced by ACE inhibitors may cause irreversible renal damage.
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PMID:Systemic and renovascular hypertension. 141 41


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