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)

There is considerable circumstantial evidence relating neoplasia to glomerular injury. Recently, more convincing evidence has been derived from the demonstration of tumor-associated antigen or antibody to such antigen, in relation to glomerular basement membranes in four patients with glomerular injury and cancer. The most common form of glomerulopathy reported in patients with carcinoma has been membranous glomerulonephritis. However, increased mesangial cells and matrix have also been found in some patients with hematuria and progressive renal failure. In contrast, most patients with Hodgkin's disease and glomerulopathy have had the minimal lesion-type nephrotic syndrome, which has usually responded to successful treatment of the Hodgkin's disease. Glomerular abnormalities have also been reported with chronic lymphocytic leukemia, lymphosarcoma, Waldenstrom's macroglobulinemia, and benign tumors. When there is no apparent cause, proteinuria with or without hematuria or impaired renal function should suggest the possibility of associated neoplasia, particularly in elderly patients.
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PMID:Glomerular injury in patients with neoplasia. 18 Aug 69

In 51 patients with type 1 and 9 patients with type 2 membranoproliferative glomerulonephritis, we found a male predominance in both types, a wide age range but with younger patients having predominantly type 2 disease, and clinical presentations that varied and included the nephrotic syndrome, an abnormal urinalysis only, acute nephritis, and recurrent hematuria. Hypertension and impaired renal function at the time of first evaluation, which were present in more than one-third of the patients, presaged a poor prognosis; in most of these patients end-stage renal failure or worsening of renal function occurred. Acute nephritis at onset was also related to a deteriorating course and was especially frequent in patients with type 2 membranoproliferative glomerulonephritis. Retrospective analysis of treatment regimens, in which patients were given an average of 1 year of therapy with prednisone alone or combined with cytotoxic agents, showed no effect in patients who had progressive forms of the glomerulopathy.
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PMID:Idiopathic membranoproliferative (mesangiocapillary) glomerulonephritis: a clinicopathologic study. 43 Nov 20

Severe renal failure associated with proteinuria occurred in a 21-year patient, who had massive rheumatic aortic regurgitation. There was no sign of congestive heart failure or extra-cellular dehydration. Subacute bacterial endocarditis was ruled out by appropriate laboratory investigations. Prosthetic aortic valve replacement resulted in normalization of the renal function and marked reduction of proteinuria. Renal histology showed severe sclerotic endarteritis involving predominantly the large arteries, and membrano-proliferative-like glomerulopathy without immune deposits. The role of the massive aortic regurgitation in the production of renal failure and histologic alterations is suggested.
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PMID:Reversible renal failure secondary to severe compensated aortic regurgitation. 65 89

Exacerbation of focal sclerosing glomerulopathy (FSGN) during pregnancy was noted in the three patients. All had antecedent asymptomatic proteinuria. Toxemia developed in two of the women during pregnancy and progressed rapidly to renal failure. Severe nephrotic syndrome developed in one patient with pregnancy and remitted after delivery. These cases suggest a deleterious effect of pregnancy on the course of FSGN and indicate the necessity for doing renal biopsy in women of childbearing age with asymptomatic fixed proteinuria or nephrotic syndrome so that those patients with FSGN can be properly counseled about future pregnancies.
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PMID:Focal sclerosing glomerulopathy with adverse effects during pregnancy. 71 21

Antireflux surgery was performed in five patients with vesicoureteral reflux at a time when renal insufficiency was present. Notable proteinuria was present in four of the patients, and a kidney biopsy specimen showed glomerular lesions in one. Despite the eradication of reflux and of infection, all five patients continued to have progressive renal insufficiency culminating in renal failure. Vesicoureteral reflux nephropathy may include a glomerulopathy leading to progressive glomerular sclerosis. Antireflux surgery would not alter this ongoing process and therefore would not halt progressive renal failure.
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PMID:Irreversible renal failure following vesicoureteral reflux. 75 14

An idiopathic nephrotic syndrome associated with membranous glomerulopathy antedated the subsequent emergence of systemic lupus erythematosus in two patients (7-year-old and 14-year-old girls). At the onset of INS, there was neither clinical evidence of multisystem disease nor unequivocal serologic evidence of SLE. The only early possible indication of SLE was the presence of microtubular inclusions in glomerular endothelial cells on electron microscopy. In each instance (one year and three years after onset of INS), a second renal biopsy showed transformation of the membranous glomerular lesion to a more florid type with glomerular subendothelial dense deposits. One patient died of overwhelming pulmonary infection while she was receiving prednisone and cyclophosphamide; the other developed progressive renal failure despite steroid treatment. SLE should be considered in patients presenting with apparent idiopathic MG, in whom nephrotic syndrome persists. Intraendothelial cell microtubular inclusions may be an early clue to later emergence of SLE.
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PMID:Idiopathic membranous glomerulopathy preceding the emergence of systemic lupus erythematosus in two children. 83 Aug 97

Complementuria is a common finding in patients with heavy proteinuria from a variety of causes, and was detected in 23 out of 34 nephrotic subjects. Mean excretion of C3 and C4 in these patients was 49 +/- 22 and 14 +/- 3 mg/24h, respectively. The renal handling of complement appears to be largely molecular weight (MW) dependent, an inverse relationship between the sieving coefficient and MW of transferrin, IgG, C3, and C4 obtaining, in nephrotic patients irrespective of the nature of their glomerulopathy or degree of renal function. Furthermore, glomerular sieving of C3 and C4 was not significantly different in patients with immune glomerular injury associated with extensive glomerular complement deposition, from that in patients with non-immune glomerulopathy, suggesting that no unique mechanism exists for the transglomerular passage of complement from serum into the urine of the former group. The finding of a large increase of sieving of C3 and C4 in nephrotic patients with end-stage renal failure may indicate a failure by atrophic tubules to reabsorb and catabolize filtered complement.
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PMID:Renal handling of the third (C3) and fourth (C4) components of the complement system in the nephrotic syndrome. 126 8

Several authors described a high incidence of proteinuria with frequent progression to nephrotic syndrome and/or renal failure in patients with HIV infection. Though renal histological changes were rather non-specific, the existence of a specific, HIV-associated glomerulopathy was postulated. We repeatedly investigated proteinuria and serum creatinine in 203 HIV-infected patients. One hundred and twenty-two patients (group 1) had early stages of the disease without opportunistic infections, 81 suffered from acute opportunistic infections (group 2). In patients with a positive qualitative test (Combistix), quantitative measurement (Biuret) for proteinuria was carried out; when proteinuria was greater than 0.5 g/24 h, SDS gel electrophoresis was performed. None of the patients of group 1 had a proteinuria greater than 0.5 g/24 h or an elevated serum creatinine. Eleven of 81 patients from group 2 had a proteinuria between 0.5 and 3 g/24 h; one further patient of group 2 developed a transient proteinuria of 7.7 g/24 h. Only three of the proteinuric patients showed a glomerular pattern in SDS gel electrophoresis, all three during acute CMV or EBV infections. Fourteen of 81 group 2 patients showed a transient elevation of serum creatinine (x +/- SD of the maximum serum creatinines: 225.3 +/- 163 mumol/l), most during pentamidine therapy for Pneumocystis carinii infection; one patient treated with high-dose acyclovir had to be temporarily dialysed. In the investigated 203 HIV patients no nephrotic syndrome and no sustained elevation of serum creatinine greater than 200 mumol/l was observed. All cases of proteinuria and elevation of serum creatinine were associated with severe opportunistic infections and the administration of potentially nephrotoxic antibiotics.
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PMID:Lack of clinical evidence for a specific HIV-associated glomerulopathy in 203 patients with HIV infection. 131 85

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

We administered a 12-week course of cyclosporine (CsA) (4 to 6 mg/kg/24 h) to nephrotic patients with membranous glomerulopathy (MG). Nephrotic patients with minimal change nephropathy (MCN) served as a comparison group. We evaluated the effects of CsA on proteinuria, glomerular function, and the release of cytokines by peripheral blood mononuclear cells in culture. Proteinuria was restored to normal levels within 2 to 4 weeks in MCN. Proteinuria declined from nephrotic to subnephrotic levels (< 3,500 mg/24 h) in 10 of 14 patients with MG, also within 2 to 4 weeks of onset of therapy. The four nonresponders exhibited a rapidly progressive and presumably irreversible form of MG culminating in renal failure. On average, fractional clearances of albumin and IgG declined by 59% and 73% in MG (P < 0.005); corresponding declines in MCN were by 99% (P < .0001). Corresponding rates of glomerular filtration in each glomerular injury remained unchanged. A strong trend for proteinuria to relapse after CsA was withdrawn was evident in both disorders. The release of tumor necrosis factor (TNF)-alpha by mononuclear cells in culture was enhanced in each glomerular injury, both before and after the course of CsA. We conclude that the proteinuria in most cases of MG exhibits a responsiveness to CsA that is qualitatively similar to, but less complete than, that in MCN. The rapidity with which barrier function improves suggests a possible role for cell-mediated immune injury in MG.
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PMID:Short-term responsiveness of membranous glomerulopathy to cyclosporine. 848 28


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