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)

A 60-year-old man with long-standing chronic myelogenous leukemia presented with renal insufficiency and proteinuria after more than 6 years of therapy with daily interferon alpha injections. He also manifested unusual skin lesions and a low-titer antinuclear antibody (ANA). Percutaneous renal biopsy disclosed an unusual glomerular lesion characterized by global, diffuse, and marked widening of the lamina rara interna, and focal segmental mesangial proliferation. Discontinuation of the drug resulted in resolution of the proteinuria, but not the renal insufficiency. These glomerular changes have not been reported previously as a complication of this form of malignancy and are similar to lesions reported in newborn rats and mice receiving interferon alpha. The potential role of interferon alpha in the development of this glomerular disease is discussed.
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PMID:Unusual glomerular lesion in a patient receiving long-term interferon alpha. 144 66

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

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

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

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

A retrospective review was undertaken on all renal biopsies performed in Chinese children under 13 years of age in Queen Mary Hospital, Hong Kong from 1980 to 1990. Of 172 renal biopsies, 18 cases were diagnosed to be membranous glomerulonephritis. All were associated with hepatitis B virus infection. Fourteen patients presented with, and 3 others developed later nephrotic syndrome. Hematuria was a common feature (83%). Complement C3 was low in 5 cases and they became normal later. At last observation, 10 patients (59%) remitted, usually within 3 years. One had persistent proteinuria and 5 had nephrotic syndrome. One patient developed end-stage renal failure 12 years after onset of illness. All three female patients completely remitted. Of the 15 boys, 50% remitted whether they received steroid treatment or not. Two patients received interferon alpha-2a therapy. One achieved remission but HBsAg and HBeAg persisted. The other had transient seroconversion and clinical improvement but nephrotic syndrome returned after stopping treatment.
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PMID:Hepatitis B virus associated membranous glomerulonephritis in children--experience in Hong Kong. 840 68

A 31-year-old male patient with an asymptomatic HIV infection but with a hepatitis B (HBV) related membraneous glomerulonephritis with nephrotic syndrome was given interferon alpha-2b subcutaneously 3 times weekly for 7.5 months. Zidovudine was added at the 10th week due to low CD4+ cell counts. Before the 6th week of treatment the patient reported a reduced need for diuretics to keep his lower limb edemas at a minimum. This response was partially sustained even after the 7.5 months interferon treatment course. The titers of HBV-DNA decreased markedly during the treatment with interferon but rose to pretreatment levels after discontinuation of the interferon treatment. The serum albumin increased but the proteinuria and hematuria were unaffected. Adverse reactions like fever, myalgias and anemia were tolerable and did not require dose reduction of either interferon or zidovudine. This treatment regimen, at least temporarily, improved the situation for the patient and can be worthwhile to try in HIV-infected patients with HBV related nephritis with nephrotic syndrome.
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PMID:Interferon alpha-2b treatment in an HIV-infected patient with hepatitis B virus induced nephrotic syndrome. 846 Mar 37

Three patients suffering from IgD myeloma, which a rare variant of multiple myeloma which often has an aggressive course, were studied retrospectively in order to elucidate the existence of clinical or laboratory features in relationship to survival time. The patients were monitored in follow-up for a time variable for 8 to 52 months. All patients received courses of chemotherapy using an association of Melphalan and Prednisone (MP); one patient also received recombinant interferon alpha in association. Response to chemotherapy, with a > 50% reduction of serum M component, disappearance of Bence Jones proteinuria and permanent control of the disease was achieved in all patients. The median duration of survival in IgD myeloma is shorter than that currently observed in patients with other myeloma types: in our series one patient died 8 months after diagnosis but other two patients are still alive 8 and 52 months after diagnosis, respectively. Great difficulty was encountered in analysis of unfavourable prognostic clinical and laboratory data: in our series, in spite of the small number of cases, the Authors observe that only the relief of increased serum levels of Lactate Dehydrogenase (LDH) seem to be in relationship with a trend of shorter survival. The authors, confirming the particular clinical and laboratory aspects of this myeloma, stress that there may coexist cases in which standard chemotherapy failed to control the diseases: these seem to indicate neoplasia with fast growth kinetics. Further studies are necessary in order to identify new prognostic index which allows the identification of selected groups of patients who can profit from a combination chemotherapy regimen other than the standard MP association.
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PMID:IgD multiple myeloma. A report of three cases. 866 86

Immunoglobulin (Ig) class switch from alpha1 to gamma2 associated with kappa-type Bence Jones proteinuria was evident in the escape phase of an IgA1 myeloma patient treated with interferon alpha (IFN alpha). The additional M-protein, IgG2-kappa, level rapidly increased and was associated with Bence Jones proteinuria, whereas monoclonal IgA1-kappa progressively declined. The N-terminal 21 amino acid sequences of the kappa-chains of monoclonal IgA1, IgG2 and the Bence Jones protein were the same. The N-terminal 15 amino acid sequence of the gamma2-chain was identical to that of the alpha1-chain. Based on these findings, the IgA1 myeloma cells underwent a class switch in CH gene expression from alpha1 to gamma2 with cell differentiation in vivo. The mechanism of the Ig class switching is discussed from three points of view: (1) Increase in immature and plasmablastic myeloma cells in the escape phase is susceptible to Ig class switching by the T-cell-derived cytokines. (2) We presumed that administered IFN alpha increased the amounts of secreted IFN gamma from the Th1 cells. (3) Due to a large quantity of IFN gamma, an inducer of Cgamma2 germline transcript, Ig class switching occurred stepwise from the alpha1 constant region gene to the next 3'CH gamma2 gene.
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PMID:Immunoglobulin class switch from IgA1 to IgG2 and simultaneous association with Bence Jones proteinuria in the escape phase in a myeloma patient treated with interferon alpha. 923 73


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