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)

Eighty-six renal biopsies were under-taken in the Nephrology Service of the Yaounde Central Hospital (Cameroon, Central Africa) during a 4 year period (1st January 1986 to 31st of December 1989). Fifty of them (58%) were done in case of nephrotic syndrome associated or not with hypertension, renal failure. Only 42 of these 50 biopsies were valid and concerned 9 patients aged 8 to 15 years, 22 aged 16 to 30 years and 11 above 30 years. On the whole, 3 main lesions were noted: minimal changes (16 cases: 38.4%), membranous glomerulonephritis (13 cases: 31.2%) and proliferative glomerulonephritis (10 cases: 24%). From the analysis of lesions observed in each age group, it was found that the histopathologic profile of renal biopsies during nephrotic syndrome is practically identical in cameroonian children, young and adults with a relative predominance of minimal change and various glomerular lesions regardless of the age group.
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PMID:[Renal puncture biopsy in nephrotic syndrome in Cameroonian children, adolescent and adults: histopathologic profile according to age]. 236 88

In a retrospective study of 82 adults with idiopathic membranous nephropathy, we have studied the predictive factors of renal death. Thirty one patients developed renal failure, sixteen of them progressed to end-stage renal failure (ESRF) (13 males and 3 females). Nine patients developed ESRF in the first 5 years following the renal biopsy. The males and the patients with a nephrotic syndrome have a high risk of ESRF. The age is not a predictive factor of poor outcome. Hypertension seems to be more frequent in patients who developed early but slowly progressive renal failure. Extensive renal interstitial lesions are indicative of poor renal prognosis.
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PMID:[Long term course of idiopathic extramembranous glomerulonephritis. Study of predictive factors of terminal renal insufficiency in 82 untreated patients]. 239 7

We report a case of renal failure in a newborn infant due to membranous glomerulonephritis. The patient was anuric in the first 3 weeks of life, after which renal function recovered. The serum of the mother contained IgG antibodies which reacted with tubular brush borders and glomeruli of adult and fetal human kidneys. Reactivity with renal epithelium from human kidneys was detected. We suggest that a transplacental, passive Heymann nephritis-like mechanism was the pathogenesis of the neonate's symptoms, although the antigen(s) involved was shown not to be gp 330 or any of the renal antigens known to be involved in experimental nephropathies.
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PMID:Transplacental induction of membranous nephropathy in a neonate. 239 75

We studied the clinical features, pathologic findings, and course of 18 patients who were found to have glomerular disease at the time of hospitalization with manifestations of acquired immunodeficiency syndrome or acquired immunodeficiency syndrome-related complex at New York University Medical Center, New York, NY, during 1984 through 1987. Focal glomerulosclerosis, characterized by segmental and/or global collapse of capillary walls, was observed in 15 of these patients; mesangial proliferation in 2, and membranous nephropathy in 1. Those with focal glomerulosclerosis typically demonstrated heavy proteinuria without edema or hypertension and progressed rapidly to renal failure in less than 1 year from the time of discovery. This form of focal glomerulosclerosis is characterized by a fulminant course, the collapse type of sclerosis, and the frequent occurrence of uremia without advanced glomerular obliteration. The absence of widespread glomerular sclerosis and the rapid course suggest that unique renal hemodynamic mechanisms may be responsible for the progression.
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PMID:Rapid renal failure in AIDS-associated focal glomerulosclerosis. 240 96

The effect of pulse intravenous methylprednisolone therapy followed by oral immunosuppression was evaluated in ten patients with idiopathic membranous glomerulonephritis who had developed progressive renal failure--a group generally considered to have a poor prognosis. The patients (six male, four female, mean age 50 years) were monitored over 9-30 months during which time creatinine clearance reduced from (mean +/- SEM) 83 +/- 10 to 29 +/- 6 ml/min, and plasma creatinine increased from 135 +/- 22 to 297 +/- 35 mumol/l. All patient were nephrotic with mean 24-h urinary protein excretion ranging from 5.8 to 19.6 g. Treatment administered was pulse intravenous methyl-prednisolone 1 g X 3 then oral prednisolone 30 mg and azathioprine 50 mg (nine patients) or cyclophosphamide 50 mg (one patient). Mean prednisolone dosage was 25 mg at 3 months, 16 mg at 6, and 10 mg at 12 months. Patients have been followed up for between 12 and 57 months on therapy. Creatinine clearance increased to 39 +/- 6, 47 +/- 5 and 48 +/- 18 ml/min after 3, 6 and 12 months treatment with a fall in proteinuria to 6.2 +/- 1.7, 5.7 +/- 1.4, and 3.1 +/- 1.1 g/24h. The deterioration of renal function was reversed in six patients (associated with a reduction in proteinuria to less than 1 g/24 hours in five), slowed in three (with a significant reduction in proteinuria in two), and only one patient with more advanced renal failure before treatment progressed to end-stage failure without any retardation of the rate of deterioration or change in proteinuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunosuppression can arrest progressive renal failure due to idiopathic membranous glomerulonephritis. 249 75

We report on a case of Wilms tumor associated with segmental, focal membranous glomerulonephritis in the contralateral kidney of a 4-year-old boy. The possible etiopathogenesis and outcome of this rare disease entity are discussed. Except for rare cases, this condition usually progresses to end-stage renal failure.
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PMID:[Wilms' tumor associated with membranous glomerulonephritis]. 254 54

We conducted a prospective randomized study in which patients with biopsy-confirmed idiopathic membranous nephropathy were assigned to receive either a six-month course of prednisone given on alternate days (45 mg per square meter of body-surface area; n = 81) or no specific treatment (n = 77). The mean duration of follow-up was 48 months. Patients in the prednisone group (median age, 46 years) entered with a mean disease duration of 15 months, a median creatinine clearance of 1.2 ml per second per 1.73 m2 (range, 0.25 to 2.6), and a median rate of urinary protein excretion of 6.8 g per day (0.3 to 26). The annual change in the corrected creatinine clearance at six months did not differ between the prednisone group and the control group (0.10 vs. 0.06 ml per second; P = 0.8), or at the last follow-up evaluation (-0.07 vs. -0.02 ml per second; P = 0.2; 95 percent confidence interval on the difference, -0.03 to 0.13). The proportion of patients with complete remission of proteinuria was also similar in the groups at 6 and 12 months and after a mean of 48 months. Outcomes were similar in the two groups with respect to progression to renal failure (3 vs. 4 patients), death (3 vs. 1 patient), complete remission of proteinuria at 36 months (16 vs. 19 patients), and a decline of 25 percent or more in the creatinine clearance at 60 months (32 vs. 25 percent of patients). A multivariate analysis, which adjusted for differences at entry in sex distribution, urinary protein excretion, and creatinine concentration, as well as other prognostic variables, failed to provide an explanation for the lack of effect of prednisone. We conclude that a six-month course of therapy in which prednisone is given on alternate days is of no benefit to patients with idiopathic membranous nephropathy.
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PMID:A randomized controlled trial of prednisone in patients with idiopathic membranous nephropathy. 264 46

All patients 14 years and older seen between July 1972 and June 1983 in four of the five nephrological centers in New Zealand with biopsy-proven primary glomerulonephritis (GN), were enrolled in a central register. This study included 803 patients from 84% of the total New Zealand population in this age group. Polynesians (predominantly Maoris) were found to have a higher overall incidence of GN than New Zealanders of European descent, a higher incidence of postinfectious GN, mesangio-capillary GN and focal glomerulosclerosis and a reduced incidence of IgA nephropathy. The racial difference in the incidence of GN may account in part for the known higher rate of end-stage renal failure in Polynesians. Overall the incidence of GN in men was more than twice that in women, and this was particularly so for postinfectious GN, IgA nephropathy, antiglomerular basement membrane initiated GN and membranous nephropathy. An adverse outcome (entry into a dialysis-transplant program, death from renal failure, non-renal death), was more frequent for Polynesians than Europeans. Follow-up is continuing to define the long-term survival of patients with each histological category of GN and any potential prognostic factors.
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PMID:The New Zealand Glomerulonephritis Study: introductory report. 273 13

Mononuclear inflammatory cells in renal biopsies from 36 patients with membranous nephropathy (MN) were analyzed, using monoclonal antibodies. In the interstitium, monocytes/macrophages and T cells were the predominant cell types (210 +/- 27 and 171 +/- 25/mm2, respectively); in contrast, very few intraglomerular leucocytes, mostly macrophages (1.0 +/- 0.7 cell/glomerular cross-section), were found. Among the interstitial T-cell population, helper/inducer cells (CD4+) predominated (CD4:CD8 ratio, 2.2 +/- 1.5). Natural killer (NK) cells and B lymphocytes were a minor component of the interstitial infiltrates and were almost absent in the glomeruli. Significantly higher numbers of DR-expressing cells were found in the interstitium (322 +/- 20/mm2) than in controls (109 +/- 30), but tubular DR expression was similar to controls (17 +/- 12 mm2). The numbers of total leukocytes and their subsets CD4+, CD8+, monocytes/macrophages, and B cells all correlated with the degree of renal impairment at the time of biopsy, but surprisingly there was no correlation between interstitial cell numbers and the histological severity of tubulointerstitial lesions. Progressive renal impairment over 5 years was associated with many interstitial T cells and monocytes/macrophages in the initial biopsy. Our results suggest that interstitial mononuclear cells may be important determinants in the pathogenesis of MN. Both cellular and humoral immune mechanisms may play a major role in the initiation of the disease, whereas progression toward renal failure seems to be determined mainly by cell-mediated immunity.
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PMID:Immune mechanisms in idiopathic membranous nephropathy: the role of the interstitial infiltrates. 278 56

Camostat mesilate, a developed derivative of gabexate mesilate for oral use, was administered in a daily dose of 600 mg for 4 weeks to 17 patients with heavy proteinuria due to various nephropathies. Five patients had glomerulonephritis (3 patients with IgA nephropathy, one each with membranoproliferative GN and membranous nephropathy) and 3 had systemic vasculitis. These patients had been treated with glucocorticoid, cyclophosphamide, anticoagulants, and dipyridamole. Five patients had diabetic nephropathy and had been treated with conventional therapy including angiotensin converting enzyme inhibitors. Two cases with benign nephrosclerosis, one with Alport syndrome, and the rest with end-stage renal failure of undetermined cause were also included in this study. Urinary protein decreased promptly within 2 weeks (from 5.2 +/- 0.7 to 3.5 +/- 0.5, mean +/- SE, p less than 0.005), and serum total protein and albumin levels increased significantly. Serum creatinine levels did not change. Decreases in urinary protein excretion of more than 50% were observed in five out of eight patients with glomerulonephritis or systemic vasculitis, two out of five with diabetic nephropathy, and one with chronic renal failure. However, urinary protein excretion values remained at the same level in two patients with benign nephrosclerosis and a patient with Alport syndrome. We suggest that camostat mesilate caused a change in glomerular capillary permeability for macromolecules through its inhibitory effects on the kallikrein-kinin system, complement system, coagulation system, and platelet function, which contributed to the treatment of the various nephropathies.
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PMID:Effect of camostat mesilate on heavy proteinuria in various nephropathies. 279 62


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