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)

We report a case of renal allograft rejection induced by the administration of interferon-alpha for hepatitis type C in a 36-year-old male. In September 1986, renal transplantation from his brother was performed after a 6-month delay because of his liver dysfunction. In October 1992, under the diagnosis of chronic active hepatitis type C, interferon alpha therapy was administered. Although his liver function was normalized during the treatment, proteinuria turned positive after 8 weeks of the therapy. Fourteen weeks after the start of interferon alpha therapy, the serum creatinine level was elevated, which was diagnosed clinically as a rejection reaction. We first discontinued the medication of interferon alpha and administered steroid pulse injection. As the renal disfunction did not respond to our first treatment, we changed mizoribine to azathioprine and added horse antilymphocyte immunoglobulin. Two weeks later, the creatinine level improved from 2.5 mg/dl to 2.0 mg/dl. The pathological findings of the transplanted kidney were acute on chronic type rejection.
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PMID:[A case of allograft rejection induced by the interferon-alpha therapy to hepatitis type C after renal transplantation]. 807 63

Hepatitis C virus infection has been associated with a variety of extrahepatic disorders. We report four patients with membranous glomerulonephritis and hepatitis C virus infection. In contrast to patients previously reported with HCV infection and membranoproliferative glomerulonephritis, these patients have normal or minimally reduced complement levels and no evidence of rheumatoid factor or cryoglobulinemia. A liver biopsy in one patient was consistent with chronic active hepatitis although liver enzymes were only minimally elevated and coagulation studies normal. Three patients were treated with alpha-interferon with some success. Treatment with alpha-interferon may have a beneficial effect in reducing proteinuria and improving liver function and may be related to the ability of interferon to suppress viremia. Future studies need to focus on clarifying the role of the virus in causing glomerular disease and improving dosing strategies for alpha-interferon. Randomized, controlled studies need to be performed to determine whether the beneficial effect of alpha interferon is significant, and if so, if it is superior to conventional therapies.
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PMID:Hepatitis C virus associated membranous glomerulonephritis. 855 29

A 68-year-old male patient with chronic active hepatitis C was treated with interferon-alpha (IFN-alpha) for a period of 5 months. The patient responded well to the IFN therapy showing substantial improvement in liver function and disappearance of HCV-RNA. However, one year after the treatment he was found to have developed proteinuria and showed a reduction in Ccr. Renal biopsy findings were as follows: Light microscopy showed diffuse expansion of mesangial cells with a focal/local increase in cellularity accompanied by capillary loop thickening. Splitting of the basement membrane was also present. An immunofluorescent study showed that IgA was localized predominantly in the peripheral capillary wall. Electron microscopy showed that there was mesangial cell interposition between the peripheral capillary wall and endothelial cells. Furthermore, endothelial cells were expanded and numerous platelets were seen in the capillary lumen. These findings were compatible with focal MPGN accompanied by activation of endothelial cells. These histological data suggest two clinical disease entities: late-onset renal damage induced by IFN-alpha alone, and HCV-induced renal damage possibly modified by the direct effect of IFN-alpha on the endothelium. The present case suggests that IFN therapy for HCV may produce a particular type of renal damage, under the influence of either IFN or HCV infection, and/or both.
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PMID:[Renal damage in a chronic active hepatitis C patient receiving interferon-alpha therapy]. 956 71

A 59-year-old woman with hepatitis B surface antigen (HBsAg) and hepatitis C viral (HCV) antibody presented with proteinuria and hematuria. The patient was treated with interferon-alpha (INF-alpha) because plasma aminotransferase levels had been elevated and a liver biopsy had showed chronic active hepatitis. Her urinary protein excretion decreased as liver function normalized and her serum HCV-RNA was negative during treatment. Eleven weeks after completion of INF-alpha treatment, she suddenly presented with nephrotic-range proteinuria, although an improvement in the hepatic function was maintained. Renal pathologic findings were consistent with membranous glomerulonephritis (MGN), and HBsAg was detected in the glomeruli but not HCV. After treatment with prednisolone, her 24-hour protein excretion was below 0.7 g/day. To our knowledge this is the first report on hepatitis B virus MGN with nephrotic syndrome following IFN-alpha therapy for HCV. This suggests that treatment with INF-alpha might affect the immune processes and may be associated with the pathogenic mechanism in this patient.
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PMID:Appearance of nephrotic syndrome following interferon-alpha therapy in a patient with hepatitis B virus and hepatitis C virus coinfection. 973 May 72

We report a case of hepatitis C virus-associated glomerulonephropathy presenting with MPO-ANCA-positive, rapidly progressive glomerulonephritis(RPGN). A 60-year-old woman was admitted to our hospital for evaluation of RPGN. Laboratory evaluation revealed microhematuria, proteinuria(800 mg/day), anemia, renal failure(blood urea nitrogen 27 mg/dl, serum creatinine 2.2 mg/dl), cryoglobulinemia, hypocomplementemia, positive MPO-ANCA(232 EU), and hepatitis C virus infection(GOT 58 IU/l, GPT 38IU/l, HCV-RNA(PCR) 1,200 kcopy/ml, serotype 1). After admission, the patient's renal function and anemia deteriorated rapidly, then prednisolone(30 mg/day) was started. After treatment her renal function gradually improved, then a renal and liver biopsy was performed. The renal biopsy revealed six sclerosing fibrous crescentic glomeruli in twelve glomeruli. Immunofluorescent examination revealed granular deposits of IgG, C3, and fibrinogen along the glomerular basement membrane and mesangial matrix. The pathogenesis of RPGN in this case may relate to the deposition of immune complexes in the glomeruli because immunofluorescent examination was revealed to be the immune-complex type, but not pauci immune type nephritis. Liver histology revealed chronic active hepatitis with mild piecemeal necrosis and did not reveal vasculitis. Although her renal function was improved after treatment with prednisolone, she suffered from pulmonary manifestations(dry cough etc.) on the 120th hospital day. Suddenly she died because of pulmonary hemorrhage on the 180th hospital day. These findings suggest that various HCV-induced immunological abnormalities, such as positive MPO-ANCA, cryoglobulinemia and hypocomplementemia, play an important role in the pathogenesis of this RPGN, although we could not demonstrate deposition within glomeruli of immune complexes containing HCV. The effect of interferon therapy on such immunological abnormalities remains to be documented. Since interferon is known to have immunomodulatory effects, we selected corticosteroid therapy. Future studies need to focus on the optimal treatment strategy for hepatitis C virus-associated glomerulonephritis.
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PMID:[A case of hepatitis C virus-associated glomerulonephropathy presenting with MPO-ANCA-positive rapidly progressive glomerulonephritis]. 1089 95

We report a patient, a 23-year-old man, who was a hepatitis B virus(HBV) carrier complicated with nephrotic syndrome. He was admitted to our hospital because of generalized edema and massive ascites. Laboratory data on admission were as follows: proteinuria 9,850 mg/day, Cr 2.7 mg/dl, BUN 73 mg/dl, albumin 1.9 g/dl, cholesterol 501 mg/dl, GOT 23 IU/l, GPT 19 IU/l, HBsAg(+), and HBeAg(222.7). Since his nephrotic symptoms were seriously complicated with renal failure, we selected steroid therapy for nephrosis preference. His renal function was improved and the urinary protein decreased immediately, but his liver function deteriorated. The renal biopsy revealed focal mesangial proliferative glomerulonephritis. Immunofluorescent examination revealed slight deposits of IgG, IgM, and C3 along the glomerular basement membrane and mesangial matrix. He was not compliant and often stopped taking the steroid therapy, thereby causing nephrosis to recur each time. After all, nephrotic symptoms have been well-controlled with cyclosporin and steroid. In spite of the seroconversion of HB virus by formation of HBe antibody, mutant HBV infection continued. The fact that liver biopsy revealed severe lymphoid infiltration at the portal area suggested chronic active hepatitis. His clinicopathologic course suggests that HBV-associated nephropathy does not always remit as there are some cases in whom hepatitis remains in an active state even after seroconversion, due to its mutant status. In these cases, the long-term prognosis of HBV nephropathy has not been defined. Further study is necessary to establish the optimal treatment for HB nephropathy in adults.
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PMID:[A case of hepatitis B virus carrier complicated with nephrotic syndrome]. 1099 20

We report on a case of autoimmune hepatitis (AIH) associated with membranous glomerulonephritis. A 61-year-old woman was admitted because of peripheral edema, proteinuria and abnormal liver function test findings. A diagnosis of AIH was made on the basis of an elevation of aminotransferase and serum IgG levels, the presence of positive antinuclear antibody and the characteristic histological features of chronic active hepatitis. Histological examination of a renal biopsy specimen disclosed membranous glomerulonephritis with granular deposits of IgG, IgM, C3 and C1q along the capillary walls. This condition is rare in AIH and should be carefully distinguished from systemic lupus erythematosus.
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PMID:Autoimmune hepatitis with membranous glomerulonephritis. 1133 33

We treated a 67-year-old Japanese woman with membranoproliferative glomerulonephritis (MPGN) and chronic active hepatitis associated with hepatitis C virus (HCV) infection. Treatment commenced with a daily dose of 6 MU IFN alpha-2b for 2 weeks, which was changed to three times weekly thereafter. After 2 weeks, HCV RNA in the serum was undetectable and there was a concomitant reduction in proteinuria. Treatment with IFN alpha-2b was discontinued because of severe headache and fever. Five weeks after the discontinuation of IFN alpha-2b, the patient experienced the sudden onset of visual loss due to retinal hemorrhage. Subsequently, proteinuria and renal function progressively deteriorated though HCV RNA was undetectable. This case exemplifies the need for careful monitoring of renal function and retinal lesions not only in patients receiving IFN but also in those following the discontinuation of IFN treatment.
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PMID:Progressive renal failure and blindness due to retinal hemorrhage after interferon therapy for hepatitis C virus-associated membranoproliferative glomerulonephritis. 1151 7

Membranoproliferative glomerulonephritis type 1 is an etiologically divergent disorder. Hepatitis C with or without cryoglobulinemia is considered one of the principal causes of de novo and post transplant membranoproliferative glomerulonephritis type 1. A 49-year-old male who underwent renal allograft for end stage renal disease developed proteinuria and positive hepatitis C serology during the post-transplant period. This was associated with moderate hepatic dysfunction, which necessitated both liver and renal biopsies. Features of both chronic active hepatitis and membranoproliferative glomerulonephritis type 1 were seen as a result of histological examination of both liver and renal biopsies. Ultra structural studies showing mesangial and membranous deposits which are characteristic of membranoproliferative glomerulonephritis have been observed. The case is reported with a review of pertinent medical literature.
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PMID:Membranoproliferative glomerulonephritis due to Hepatitis C in renal allograft. 1207 May 61

A 65-year-old-woman presented with edema, ascites, proteinuria and abnormal liver function tests. A small amount of mixed cryoglobulin was detected in her serum. Liver biopsy revealed mild chronic active hepatitis, but tests for hepatotropic viral infection were negative. Electron microscopy of the renal biopsy revealed glomerular electron-dense deposits that contained numerous tubular structures. Renal amyloidosis and light chain deposition disease were ruled out by appropriate histological techniques. The ultrastructural findings of renal biopsy suggested either cryoglobulinemic glomerulonephritis or immunotactoid glomerulopathy. Although the exact interrelationship among the peculiar glomerulopathy, cryoglobulinemia and chronic active hepatitis in the present case remains undetermined, this report enlarges the spectrum of glomerulopathy characterized by extracellular deposition of microtubules.
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PMID:Glomerulonephritis with microtubular deposits associated with cryoglobulinemia and chronic active hepatitis. 1216 8


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