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 4 patients with glomerulonephritis (GN) associated with hepatitis C virus (HCV) infection seen between August 1993 and July 1996. Two of them were male and median age was 41 years. Anti-HCV was detected by enzyme-immunoassay and HCV-RNA by PCR. Serum cryoglobulins, 24-hour proteinuria, and erythrocyte dismorphism were also determined. Viremia, cryoglobulinemia, hematuria and proteinuria were observed in all patients. Liver biopsies revealed inflammatory activity in 3 cases, and renal biopsies revealed membranoproliferative glomerulonephritis in 3 patients and mesangial proliferative glomerulonephritis in 1 patient. Two patients are on specific therapy for HCV infection (IFN in combination with ribavirin) and have presented clinical and laboratory improvement. The occurrence of active liver disease and viremia concurrent with urinary alterations suggests viral involvement in renal disease, a conclusion supported by the by improvement of urinary alterations observed after treatment for HCV. We conclude that the search for viral markers in patients with GN is important since their detection could change the therapeutic approach.
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PMID:[Glomerulonephritis associated with hepatitis c virus infection]. 992 17

There is an increasing recognition of the association between chronic hepatitis C virus infection and glomerular diseases. Renal complications may be the presenting manifestation of hepatitis C virus infection. Patients may present with signs and symptoms of cryoglobulinemic systemic vasculitis, proteinuria, microscopic hematuria, acute renal failure, or nephrotic syndrome. The pathogenesis of hepatitis C virus associated with renal disease remains incompletely understood; however, deposition of circulating immune complexes in the subendothelial space and mesangium in the glomeruli seems to play a major role. The most common renal pathology associated with hepatitis C virus infection is type I membranoproliferative glomerulonephritis with or without cryoglobulinemia. In patents who do not have significant renal impairment, combination therapy with interferon alfa (IFN-alpha) and ribavirin seems to be the treatment of choice, although the experience with this combination is quite limited in patients with renal involvement. A prolonged course of high-dose IFN-alpha has been most commonly used for these patients with significant success, but relapse of hepatitis C viremia and renal disease after discontinuation of therapy have frequently occurred.
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PMID:Kidney disease in patients with chronic hepatitis C. 1117 99

It currently is thought that human immunodeficiency virus-associated nephropathy (HIVAN) occurs late in the course of HIV infection. Although HIVAN may be the presenting manifestation of acquired immunodeficiency syndrome (AIDS), it usually occurs after a prolonged period of viral infection often associated with high levels of HIV viremia. The patient described here developed HIVAN as a manifestation of acute retroviral syndrome. A 41-year-old black man presented with nephrotic range proteinuria, renal insufficiency, and acute gastrointestinal and pulmonary symptoms. He recently had been treated for primary syphilis. Two HIV serologic tests, performed 3 months apart, were negative. Renal biopsy was consistent with HIVAN. After the biopsy, the patient was discovered to have more than 700,000 viral copies per mL in his blood. CD4(+) count was greater than 500/mm(3). Six weeks later, enzyme-linked immunosorbent assay and Western blot analyses for HIV antibody became positive. HIVAN can occur early in the course of HIV infection, even during acute infection before seroconversion, and prolonged exposure to virus is not necessary for this renal involvement to occur in the susceptible host.
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PMID:Hiv-associated nephropathy occurring before HIV antibody seroconversion. 1132 4

We report a urinary tract infection (UTI) with erythrovirus B19 in an HIV-1-positive homosexual man persisting for more than 7 months after the decline of viremia after a primary infection. During the course of the UTI, the patient complained of soreness in the kidney region and suffered from transient episodes of edema and hematuria. Proteinuria and elevated serum concentrations of creatinine further substantiated the hypothesis of a renal focus of a persistent erythrovirus B19 infection.
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PMID:Persistent erythrovirus B19 urinary tract infection in an HIV-positive patient. 1167 36

Mixed cryoglobulinemia (MC) and glomerulonephritis are the most important extrahepatic manifestations of chronic hepatitis C virus (HCV) infection. In HCV-infected patients with MC, renal involvement worsens the overall prognosis because of a high incidence of infection or cardiovascular disease. The relationship between MC and HCV infection has prompted the use of antiviral therapy. Two patients with chronic HCV infection, type-II MC and membranoproliferative glomerulonephritis (MPGN), presenting as nephrotic syndrome were treated with interferon (IFN)-alpha (3 MU 3 times per week) and ribavirin (15 mg/kg daily) for 6 months. Laboratory tests included measurement of anti-HCV antibodies, HCV RNA, and HCV genotyping, and characterization of circulating cryoglobulins. A pretreatment renal biopsy was performed, and the histopathologic lesions were scored according to the index of disease activity. Viremia and cryoglobulinemia were suppressed in both patients. However, a complete remission of proteinuria was observed in 1 patient only. The evaluation of the renal biopsy specimens revealed a mild MPGN (activity score: 5/24) in the patient with remission of proteinuria and a severe MPGN (activity score: 15/24) in the patient who maintained a nephrotic-range proteinuria. Although a fully satisfactory treatment is not yet available, we feel that a reasonable therapeutic strategy for HCV-infected patients with MC nephritis could be as follows: (1) antiviral treatment alone for patients with a low-grade kidney involvement, and (2) a short-term course of steroids and cytotoxic drugs followed by antiviral therapy for acute exacerbations and/or rapidly progressive GN.
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PMID:Interferon-alpha in combination with ribavirin as initial treatment for hepatitis C virus-associated cryoglobulinemic membranoproliferative glomerulonephritis. 1172 95

Treatment of chronic hepatitis C in renal-transplant (RT) recipients with alpha-interferon is associated with a high rate of acute rejection. We therefore evaluated the biochemical, virological, histological efficacies, as well as the safety of one year ribavirin monotherapy in 16 HCV-(+) RNA (+) RT patients (group A) matched to 32 HCV-(+) RNA (+) RT patients (group B) who did not receive ribavirin. Ribavirin was initially started at a daily dose of 1000 mg and then adapted to hemoglobin level. Ribavirin monotherapy was associated with a significant decrease in AST, ALT and gamma glutamyl transpeptidase levels. Serum creatinine decreased as well. When proteinuria was present (n = 5), this decreased or disappeared. There was no significant changes in HCV viremia. The histological analysis of liver biopsies revealed a significant progression in liver fibrosis with no improvement in inflammation scores. There was a significant decrease in hemoglobin levels, despite an important support by recombinant erythropoeitin. However, in three cases, ribavirin therapy had to be stopped. In group B, after 1 year of follow up, there was a significant increase in serum ALT and creatinine values. Proteinuria decreased in only 2 of 12 patients. In conclusion, one year ribavirin therapy in HCV-(+) RNA (+)ve RT has no impact upon liver histology, although it improves liver enzyme levels. It impact upon renal function remains unknown. Nevertheless when proteinuria is present it disappears.
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PMID:[Is there a place for ribavirin in the treatment for renal transplant patients infected by hepatitis C virus?]. 1272 14

Type C liver cirrhosis is often associated with a nephrotic syndrome secondary to membranoproliferative glomerulonephritis. Liver transplantation in such patients may sometimes worsen viremia, causing renal dysfunction upon the introduction of immunosuppressive drugs. We present a case of a patient whose proteinuria decreased after liver transplantation. The patient was a 49-year-old male who had been followed due to chronic hepatitis type C from 1984. From 1999 he was diagnosed as having nephrotic syndrome. We performed a living related liver transplant on August 21, 2001. An intraoperative renal biopsy revealed the histology to show membranoproliferative glomerulonephritis. The volume of proteinuria was 2 to 11 g/day before surgery. After surgery it varied from 6 to 10 g/day, gradually decreasing to 1 to 2 g/day. One of the causes of reduced proteinuria may be alleviation of membranoproliferative glomerulonephritis by immunosuppression. But from the view that the recovery of the renal function followed the recovery of liver function, the major effect may have been alleviated hepatorenal syndrome.
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PMID:Decreased proteinuria following liver transplantation in a patient with type C liver cirrhosis complicated with nephrotic syndrome: a case report. 1556 Dec 37

Mixed cryoglobulinemia (MC) and glomerulonephritis are the most important extrahepatic manifestations of chronic hepatitis C virus (HCV) infection. MC is a non-neoplastic B cell lymphoproliferative process induced by HCV in an antigen-driven mechanism. The clinical expression of cryoglobulinemia varies from an indolent course to the development of systemic vasculitis. Glomerulonephritis is predominantly associated with MC, and almost always takes the form of membranoproliferative glomerulonephritis. The renal manifestations may range from isolated proteinuria to overt nephritic or nephrotic syndrome with variable progression towards chronic renal insufficiency. The treatment of these virus-related diseases must be individualized on the basis of the severity of clinical symptoms. Antiviral therapy with interferon alpha and ribavirin (the currently recommended treatment of HCV infection) may be successful in patients with mild-to-moderate disease, but sustained responses are uncommon. In case of severe and rapidly progressive disease, although it is capable of suppressing viremia and cryoglobulinemia, antiviral therapy is not fully effective in controlling the inflammatory and self-perpetuating reaction consequent to the deposition of cryoglobulins in the glomeruli and vessel walls. In such cases, a short course of steroids and cytotoxic drugs (with or without plasmapheresis) may be needed to improve the vascular manifestations and decrease the production of cryoglobulins. Once the acute disease flare has been controlled, antiviral therapy may be administered to eradicate HCV, the causative agent of the cryoglobulinemic syndrome. In patients in whom antiviral therapy is ineffective, contraindicated or not tolerated, rituximab, a monoclonal anti-CD20 antibody, may be an alternative to standard immunosuppression.
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PMID:Hepatitis C virus-related cryoglobulinemia and glomerulonephritis: pathogenesis and therapeutic strategies. 1605 39

Patient survival is significantly lower in hepatitis C virus (HCV)-positive compared to HCV-negative dialysis patients. After renal transplantation, immunosuppressive therapy can result in an increased burden of HCV viremia. Both patient and graft survivals are lower in HCV-positive compared to matched HCV-negative renal-transplant patients. Therefore, it is important to treat HCV infection. At present, after renal transplantation, there is no current safe and efficient therapy. Alpha-interferon (alpha-IFN) does not give a sustained virological response, and is associated with a high rate of renal failure. Ribavirin and amantadine monotherapies are associated with a significant improvement in liver enzymes, but have no impact upon HCV viremia. Ribavirin, however, may be indicated in cases of HCV-related glomerulopathy because it can significantly decrease proteinuria. The combined use of alpha-IFN and ribavirin should only be given to those patients who have developed posttransplant fibrosing cholestatic hepatitis. Therefore, HCV infection needs to be treated pretransplant. In dialysis patients, the only recommended therapy, as yet, is alpha-IFN monotherapy. Pegylated alpha-IFN is under evaluation and ribavirin is contraindicated because it results in severe hemolytic anemia. Twelve months of alpha-IFN therapy results in sustained virological clearance in approximately 40% of patients, regardless of their genotype. HCV RNA, after three months of alpha-IFN therapy, is a predictive factor for a long-term sustained response. Finally, when HCV-positive dialysis patients with a sustained virological response undergo successful renal transplantation, very few suffer a virological relapse, thus emphasizing that these patients were cured.
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PMID:Treatment of hepatitis C virus infection (HCV) after renal transplantation: implications for HCV-positive dialysis patients awaiting a kidney transplant. 1703 97

Polyomavirus BK (BKV) reactivation can occur in immunodeficient patients. Few studies on BKV infection in patients with systemic lupus erytematosus (SLE) nephritis are available. Aim of this study was to analyse the prevalence of BKV infection by quantifying viral load and to investigate the association with clinical and histological parameters indicating duration, type and activity of SLE.BKV-DNA was evaluated by polymerase chain reaction in serum (sBKV) and urine (uBKV) specimens from 40 patients with SLE nephritis and 29 healthy controls. Renal function, urinary activity, clinical index of SLE activity [SLE Disease Activity Index (SLEDAI) score], CD4+/CD8+ ratio, histological classes and duration of SLE nephritis were compared according to the BKV-DNA-positivity.sBKV was present in 15% of SLE patients and in 13.8% of controls; uBKV in 32% of SLE patients and in 17.2% of controls. There was no significant difference in terms of kidney function, urinary activity, SLEDAI score, presence of anti-dsDNA antibodies, CD4+/CD8+ ratio and BKV viremia and/viruria, as well as there was no significant correlation between SLEDAI score, anti-dsDNA antibodies titers and median viral load. Duration of nephropathy tended to be shorter in patients with BKV viremia and/or viruria; proteinuria/creatininuria ratio tended to be higher in patients with positive sBKV and uBKV. BKV-DNA-positivity tended to be more frequent in patients treated with an immunosuppressive agent versus those on steroid treatment. Reactivation of BKV infection can occur in patients with SLE, although prevalence data do not significantly differ from those obtained in the control group. The trend toward an association between BKV infection and degree of proteinuria and less duration of SLE nephritis could indicate a major susceptibility to develop BKV infection in more active phases of the disease. The role of BKV reactivation in terms of clinical parameters and histological pattern, as well as the role of therapeutic protocols in the onset of BKV reactivation and, conversely, the therapeutic implication of BKV reactivation in SLE patients remain to be defined and should be addressed in further studies on a larger number of patients.
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PMID:Human polyomavirus BK in patients with lupus nephritis: clinical and histological correlations. 1797 61


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