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)

Although IgA nephropathy (IgA N) is reportedly the most common form of primary glomerulonephritis worldwide, there is a very low incidence of IgA N in Black Americans, and IgA N in Black patients with renal allografts has not been reported. In this report, we present the case of a Black patient with endstage renal disease presumed secondary to hypertensive nephrosclerosis who developed nephrotic range proteinuria due to IgA N in a cadaveric renal allograft 2 years following transplantation. Biopsy of the allograft in the immediate post-transplantation period had revealed no evidence of IgA N. Chronic active hepatitis related to hepatitis C preceded the development of proteinuria by approximately 1 year, raising the possibility that IgA N in the renal allograft was secondary to the liver disease. The clinical and histological features of primary IgA N and IgA N secondary to liver diseases are discussed.
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PMID:Immunoglobulin A nephropathy in a renal allograft of a black transplant recipient. 141 57

We report here two cases of mixed cryoglobulinemia showing renal involvement associated with hepatitis C virus (HCV) infection. The subjects were 62- and 63-year-old males. Both patients presented with purpura on the legs, which was diagnosed as allergic vasculitis by skin biopsy. Case 1 followed a clinical course of progressive nephrotic syndrome with mild hematuria. He also had diabetes mellitus and hypertension. In contrast, case 2 showed only mild hematuria without proteinuria at the time of the renal biopsy. Both cases had immunological disarrangements, such as severe hypocomplimentemia and seropositive rheumatic factor. Recently, it was reported that patients with type II mixed cryoglobulinemia had HCV seropositivity, and revealed membranoproliferative glomerulonephritis. These facts strongly suggested that renal lesions are the result of direct damage mediated by cryoglobulinemia and an activated complement pathway through an immune complex mechanism related to HCV.
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PMID:[Glomerular lesion in patients with type II mixed cryoglobulinemia having antibodies to hepatitis C virus]. 747 12

To determine the prevalence and type of glomerulonephritis (GN) associated with hepatitis C virus (HCV) cirrhosis, we prospectively evaluated 28 consecutive Saudi patients with HCV cirrhosis for liver transplantation. Six patients (21%) underwent kidney biopsies for proteinuria, unexplained elevated serum creatinine or both. All 6 had GN, 4 had membranoproliferative, one focal segmental and one membranous GN. Immunologic and electron microscopic studies demonstrated immune complex deposition in the glomeruli. Two patients with significant proteinuria were treated with interferon alpha for 3 months with improvement in kidney and liver function. To our knowledge, this is the first report of focal segmental GN associated with HCV. This high prevalence of HCV associated GN is alarming and warrants further studies in cirrhotic and noncirrhotic patients, particularly as an indication for therapeutic intervention.
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PMID:Hepatitis C associated glomerulonephritis. 750 40

We reported a case of type II cryoglobulinemia involving glomerulopathy associated with HCV-induced liver cirrhosis. The patient was a 57-year-old woman. Her past history included chronic hepatitis at 51 years and rheumatoid arthritis at 53 years of age. At 46 years, an erythematous lesion appeared on her legs, which was diagnosed as allergic vasculitis by skin biopsy. At 50 years, proteinuria, hematuria and hypertension were recognized. The next year, the first renal biopsy was performed and showed membranoproliferative glomerulonephritis (MPGN). Recently, the edema of her legs has progressed, and the laboratory data showed proteinuria, hematuria, hypocomplementemia, rheumatoid factor positivity, and increase of monoclonal IgG kappa chain. The second renal biopsy revealed an endocapillary proliferative glomerulonephritis-like lesion with marked infiltration of monocytes and macrophages. The subendothelial deposit showed a fine fibril-like pattern. She was treated with steroids and double filtration plasmapheresis (DFPP) therapy, but the treatment was not very effective. She died of liver cirrhosis, which was probably induced by hepatitis C virus (HCV), and sepsis. Generally, the patients of type II cryoglobulinemia often showed HCV antibody positivity, pointing to HCV as an etiological factor. In this case, renal biopsy was performed twice in the same patient, and the histologic findings suggest the clinicopathological course of cryoglobulinemia.
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PMID:[A case of type II cryoglobulinemia involving glomerulopathy associated with hepatitis C antibody]. 750 47

Hepatitis C virus (HCV) infection is one of the important causes of chronic and severe hepatitis in China. In an attempt to understand if there is any relationship between HCV infection and glomerulonephritis (GN), serum samples from 570 GN patients and 100 normal volunteers were screened for anti-HCV antibody (HCV-Ab) with ELISA method. Among the cases with positive HCV-Ab, serum HCV-RNA was tested with nested RT-PCR method. The incidence of serum HCV-Ab was 2 in 100 normal volunteers (2%) and 34 in 570 GN patients (6%). The incidence of positive serum HCV-RNA was 0 in normal volunteers whereas 21 in GN patients. The main clinical manifestation of GN patients with serum positive HCV-Ab was an unique proteinuria with/without nephrotic syndrome or renal failure, whereas the pathologic lesions in GN patients with serum positive HCV-Ab or HCV-RNA consisted of different disease entities. There was no close link between MPGN and active HCV infection. From the data observed, it seems that there is a coincidence between glomerular diseases and HCV infection rather than a matter of cause and consequence.
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PMID:[Is there hepatitis C virus associated glomerulonephritis?]. 753 65

Hepatitis C virus (HCV) infection may present as a primary glomerular disease. We report 34 adult patients who presented with proteinuria and had circulating anti-HCV antibodies. Primary risk factors included a history of intravenous drug abuse (56%) or blood transfusion (18%). Patients presented with nephrotic syndrome (71%) or with non-nephrotic proteinuria (29%) and had membranoproliferative or acute proliferative glomerulonephritis on renal biopsy. Signs of clinical liver disease were infrequent (18%), though elevated liver function tests were common (66%) and liver biopsy in 16 of 18 patients showed chronic active hepatitis. Cryoglobulinemia was frequent (59%), but only 44% had extrarenal manifestations. In 100% of cases tested, HCV RNA could be found in the serum or cryoprecipitates. Fourteen patients received interferon alpha for 6 to 12 months with a significant reduction in proteinuria but no improvement in renal function. A good clinical response correlated with disappearance of HCV RNA from the serum during treatment; however, relapse of viremia and renal disease was common after completing therapy. Evidence for HCV infection should be sought in all patients with primary glomerular disease. The optimal treatment strategy, however, remains to be defined.
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PMID:Hepatitis C virus-associated glomerulonephritis. Effect of alpha-interferon therapy. 753 69

Hepatitis C virus (HCV) is the leading cause of non-A, non-B hepatitis among renal allograft recipients. We sought to identify and describe a proteinuric renal disease occurring in our HCV-infected renal transplant patients. Patients with proteinuria exceeding 1 g/day were identified from a cohort of 98 HCV-infected kidney recipients. Qualitative and quantitative reverse transcriptase polymerase chain reaction (RT-PCR) and restriction fragment-length polymorphism of the amplified RT-PCR product was performed to detect circulating HCV RNA, viral titer, and strain type, respectively. An immune complex nephritis (ICN) of the membranoproliferative pattern (MPGN) was found on five of eight biopsies. Two patients infected with the Hutch strain-type developed nephrotic-range proteinuria within three months posttransplant while the remaining three MPGN patients had been transplanted greater than 5 years prior to the onset of proteinuria. Testing for rheumatoid factors, cryoglobulins, hypocomplementemia, and circulating immune complexes failed to show a consistent pattern. Sucrose density gradient (SDG) equilibrium centrifugation was used to determine the buoyant-density of HCV virions from control (HCV-infected nonproteinuric recipients; n = 5) and nephrotic patients (n = 5). Whereas HCV virions from the control patients had a low buoyant density on sucrose gradients, a substantial percentage of the circulating HCV RNA from the MPGN patients was present in the high-density fractions in association with IgM and IgG. Treatment of the pooled high-density layers with NP40 followed by recentrifugation resulted in a shift of the HCV RNA to the medium-density layers. In conclusion, MPGN developed in five HCV-infected kidney recipients despite pharmacologic immunosuppression. Both the physicochemical properties of the HCV virions on SDG and their association with IgG and IgM in the high-density layers provide indirect evidence for the presence of circulating complexes of anti-HCV antibody and HCV antigen(s).
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PMID:De novo membranoproliferative glomerulonephritis in hepatitis C virus-infected renal allograft recipients. 754 75

Hepatitis C virus (HCV) infection is a major cause of chronic liver disease and is associated with a variety of extrahepatic manifestations, including cryoglobulinemia and glomerulonephritis. Epidemiologic evidence suggests that HCV infection may be a major risk factor for both cryoglobulinemic and type I membranoproliferative glomerulonephritis (MPGN). Clinical symptoms and laboratory data may or may not reflect the presence of chronic liver disease. Most patients have evidence of hypocomplementemia, circulating rheumatoid factors, and cryoglobulinemia. The pathogenesis of HCV-associated MPGN is probably a result of glomerular deposition of circulating HCV and anti-HCV antibodies. Treatment with interferon-alpha has been shown to improve proteinuria, suppress viremia, and stabilize renal function. However, patients often relapse after therapy is stopped. The optimal therapy remains to be defined but may involve different dosage regimens of interferon-alpha or the combination of several antiviral agents.
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PMID:Hepatitis C virus-associated glomerulonephritis. 764 27

The last 4 years have been a period of rapid expansion in our understanding of both the molecular biology and clinical significance of hepatitis C virus (HCV) infection. Initial studies using first-generation enzyme-linked immunosorbent assays suggested that the end-stage renal disease population had an exceptionally high prevalence of anti-HCV compared with asymptomatic healthy blood donors. Subsequent analyses with second-generation assays and polymerase chain reaction techniques to detect viremia confirmed these earlier studies. Considering the prevalence of HCV within the dialysis population, it comes as no surprise that several studies confirmed HCV as the leading cause of non-A, non-B hepatitis among renal allograft recipients. Furthermore, transmission of HCV by transplantation of a kidney from an HCV-infected organ donor has been unequivocally demonstrated. The natural history of HCV infection in the immunosuppressed allograft recipient and its impact on long-term patient outcome are still being analyzed. Finally, HCV has been associated with essential mixed cryoglobulinemia and several histologic patterns of immune complex glomerulonephritis, including membranous and membrano-proliferative glomerulonephritis. Although HCV antigen-antibody complexes have not been demonstrated in the kidney, the marked decrease in proteinuria following clearance of HCV RNA with interferon alpha-2b therapy suggests an etiologic role for HCV in these glomerular diseases. Furthermore, the demonstration of HCV RNA in the cryoprecipitate of patients with essential mixed cryoglobulinemia and a beneficial response to treatment with interferon alpha-2b also suggest a role for HCV in the pathogenesis of these clinical syndromes.
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PMID:Hepatitis C virus: the nephrologist's view. 757 29

Although the occasional occurrence of glomerulonephritis associated with hepatitis C virus (HCV) infection has been reported recently in the literature, the type described has been mainly membranoproliferative glomerulonephritis (MPGN); membranous glomerulonephritis (MGN) is very rare. In this paper, two cases of MGN associated with HCV infection are reported. Case 1 was a 56-year-old male who had positive HCV Ab and HCV RNA. The diagnosis of chronic active hepatitis was verified by liver biopsy. Laboratory data showed proteinuria (5g per day), hematuria and hypocomplementemia by hemolytic assay. Renal biopsy led to the diagnosis of MGN in stage II. The patient was treated with interferon alpha for 6 months, resulting in improvement of hypocomplementemia, transient reduction of GOT and GPT during the course of treatment. The GOT and GPT were aggravated again after the completion of therapy. No improvement was seen in proteinuria and hematuria, and HCV Ab remained positive. Case 2 was a 69-year-old male who had positive HCV Ab and HCV RNA, and had normal liver function. Subsequently, his GOT value was slightly elevated. Proteinuria (2g per day) was demonstrated. The diagnosis of MGN in stage II was made on the basis of renal biopsy. The clinical characteristics of these two cases suggest that MGN is a type of glomerulonephritis associated with HCV infection.
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PMID:[Two cases of membranous glomerulonephritis associated with hepatitis C virus infection]. 781 54


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