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 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 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

We report a case of a patient with hepatitis B virus (HBV)-related membranous glomerulonephritis (MGN) who showed improvement after interferon-alpha (IFN-alpha) therapy. A 35-year-old man with nephrotic syndrome and HBV antigens received a 24-week course of IFN-alpha. At the end of therapy there was an elevation in the level of plasma aminotransferase and an increase in proteinuria, which were followed by antigen/antibody seroconversion. This "flare-up" before seroconversion suggests an increase in disease activity in the liver and kidney, demonstrating in vivo HBV involvement in MGN.
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PMID:alpha-Interferon therapy for HBV-related glomerulonephritis. 1003 Jan 9

Interferon-alpha (IFN-alpha) is a naturally occurring cytokine. It was the first cytokine used with clinical benefit in the treatment of viral hepatitis and malignancies. Patients with viral hepatitis B or C may have complications with glomerulonephritis (GN). Improvement in proteinuria with or without clearing of viral markers after IFN-alpha therapy has been reported. This encouraged us to offer IFN-alpha therapy to four patients with GN. These patients refused treatment with steroids and/or cyclophosphamide because of concerns about side effects. One patient with membranous GN and two patients with mesangial GN (MesGN) had a remission of nephrotic syndrome. In one patient with type II diabetes and MesGN, renal insufficiency and proteinuria did not subside; however, renal function remained stable. The mechanism of action of IFN-alpha is discussed, with its possible role in the treatment of primary GN.
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PMID:Role of interferon-alpha in the treatment of primary glomerulonephritis. 1035 11

Most human nephritis is due to glomerular deposition and/or formation of immune complexes (IC). In cultured mesangial cells, Fc receptor stimulation induces proliferation, matrix synthesis, and release of several mediators implicated in the initiation and progression of glomerular injury. Since Ig Fc fragments in vitro modified these phenomena, we studied the effects of systemic administration of IgG Fc fragments on the evolution of experimental IC nephritis. Fc fragment injection (1 mg/day i.p.) to rats with ongoing nephritis (proteinuria 20-50 mg/24 h vs 9 +/- 0.2 mg/24 h in controls) markedly ameliorates proteinuria, renal function, and morphological renal lesions. This was accompanied by a reduction in the renal synthesis of chemokines (monocyte chemoattractant protein-1, IFN-inducible protein-10, and cytokine-induced neutrophil chemoattractant-1), matrix proteins, and growth factors (platelet-derived growth factor, and TGF-beta), and in the activity of transcription factors. The treatment did not affect the glomerular deposition of IgG IC and complement C1q. In contrast, a decrease in the renal expression and production of C3 was observed without changes in serum complement levels. In vitro, very low complement consumption and no C3b covalent interaction were observed with Fc fragments, confirming that they did not modify systemic complement activity. These results indicate that the administration of Fc fragments prevents the development of glomerular damage in an aggressive model of proliferative glomerulonephritis through mechanisms involving a reduced local generation of complement, chemokines and growth factors. Modulation of IC-mesangial cell interaction by Fc fragment administration could represent a new approach to the treatment of severe immune nephritis.
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PMID:Administration of IgG Fc fragments prevents glomerular injury in experimental immune complex nephritis. 1065 63

Systemic lupus erythematosus (SLE)-prone female MRL-lpr / lpr (MRL-lpr) mice were treated with mouse or rat IFN-gamma under different experimental conditions, both prophylactically in 6- to 8 week-old animals and therapeutically in 12- to 18-week-old SLE-affected mice. It was found that IFN-gamma heterogeneously modulated the course of the disease in MRL-lpr mice. When administered prophylactically, IFN-gamma favorably modulated the histological, serological and clinical signs of the disease. Relative to untreated or PBS-treated control animals, the MRL-lpr mice which received IFN gamma were virtually free of inflammatory infiltration of the kidneys and the lungs, had lower levels of azotemia with reduction of both circulating IgG1, IgG2a and IgG3 and anti-double strand (ds) and single strand (ss) DNA antibodies, milder skin vasculitis, significantly reduced enlargement of their lymph nodes and lower weight of the spleens. IFN-gamma also lowered the rate of mortality of MRL-lpr mice. In contrast to these findings, therapeutically administered IFN-gamma worsened the course of the disease in MRL-lpr mice, which exhibited increased proteinuria, higher levels of IgG2a and IgG3 and anti-ds and -ss DNA antibodies, more aggressive nephritis and died at an earlier age than PBS-treated control mice. The dichotomic effect of IFN-gamma on disease manifestation in MRL-lpr mice offers new insights into the complex role of this cytokine in the regulation of systemic autoimmunity such as SLE.
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PMID:Dichotomic effects of IFN-gamma on the development of systemic lupus erythematosus-like syndrome in MRL-lpr / lpr mice. 1067 Nov 99

There is evidence that crescentic glomerulonephritis initiated in rodents by heterologous antibodies against the glomerular basement membrane (anti-GBM glomerulonephritis) depends on a Th1-type immune reaction. Interleukin 12 (IL-12) is crucial for the development of Th1 helper cells, and interferon gamma (IFN-gamma) is a major proinflammatory product of these cells. In order to test the role of the two cytokines in anti-GBM glomerulonephritis we used mice lacking either the p40 chain of IL-12 (IL-12-/-) or the IFN-gamma receptor (IFN-gammaR-/-). Glomerulonephritis was induced by injecting a rabbit anti-GBM serum in mice preimmunized against rabbit IgG. Glomerulonephritis was assessed on the basis of proteinuria, immunofluorescence findings and histology. IL-12-/- mice were completely protected against glomerulonephritis. In contrast, IFN-gammaR-/- mice were more severely affected than wild-type mice. Similarly, cutaneous delayed-type hypersensitivity, a typical Th1 response, was abolished in the IL-12-/-, mice but increased in the IFN-gammaR-/- mice. The data obtained in IL-12-/- mice support the view that crescentic glomerulonephritis in this model represents a Th1 response. Since IFN-gamma is not required, other products of Th1 cells are likely to mediate glomerulonephritis.
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PMID:IL-12-dependent, INF-gamma-independent experimental glomerulonephritis. 1117 3

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

Bilaterally nephrectomized Lewis recipients of Fisher 344 (F344) kidney allografts, treated with CyA (1.5 mg/kg/day x 10), develop progressive changes of chronic rejection. Treated F344-to-F344 acted as isograft controls. Proteinuria was determined sequentially. Grafts were harvested 8, 12 and 16 weeks after transplantation (n = 9/group/time period). Infiltrating host cells and their products were assessed in chronically rejecting grafts by histology and immunostaining using mAbs for monocyte/macrophages, T-cells, ICAM-1, LFA-1 and cytokines. For in vitro binding studies, snap-frozen sections of transplanted kidneys were incubated with monocytes/macrophages and lymphocytes isolated from peripheral blood (PBL) of naive animals. For in vivo migration studies, naive cell populations were labeled with Bis-Benzamide and transferred i.v. to grafted animals at weeks 8, 12 and 16 (n = 3/group); grafts were harvested 24 h later and cell localization assessed under immunofluorescence. Increasing numbers of ED1 + monocytes/macrophages in allografted kidneys peaked at 16 weeks, localizing preferentially in glomeruli, where IL-1, IL-6 and TNF-alpha expression had also become intense and correlated with progressive glomerulosclerosis. Binding studies corroborated these results. In vitro, a few monocytes/macrophages bound to glomeruli and vessels at 8 weeks; by 12 weeks, binding to glomeruli was high (72% of cells). In vivo, large numbers of transferred labelled monocytes/macrophages were found in kidney allografts at 12 weeks (23%, isografts; < 7%, P < 0.01). In contrast T cells (primarily CD4+) were a consistent feature in allografts elevated as compared to isografts and correlating with in vitro and in vivo binding patterns; associated cytokines included IL-2, IFN- and TNF-alpha. Functional data followed these results: urine protein excretion by allograft recipients increased from baseline at 8 weeks (12 mg/day) to > 50 mg/day at 16 weeks at which point animals were beginning to die of renal failure; proteinuria in isografted rats did not increase during this time period. These results suggest that monocyte/macrophage and CD4+ T cells and their products are important in chronic kidney allograft rejection, contributing to the progressive sclerosis and fibrosis.
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PMID:Host leukocytes and their products in chronic kidney allograft rejection in rats. 1127 Dec 42

Focal segmental glomerulosclerosis (FSGS) is a renal disease characterized by sclerotic segmentary lesions, involving a few glomeruli. Male-female ratio is >1 and, in the majority of cases, the patients are aged between 25 to 35 years. The clinical picture is similar to a nephrotic syndrome with non-selective proteinuria poorly sensitive to steroids and often associated with microhematuria. The etiology is still unknown, even in a prevalence in drug addicts, patients with AIDS and subjects with recurrent urological infections with vesico-ureteral reflux was observed. Recent reports showed that chronic infection Hepatitis C Virus (HCV)-related may be associate with or responsible for onset of some syndrome involving the kidney but not the liver. We report the case of a young woman with HCV-Ab positive chronic hepatitis that, during the disease, showed clinical findings of renal involvement, histologically related to a FSGS. We administered to her alpha-IFN at doses of 3 Mega Units thrice-a-week for six months. Serum HCV-RNA, proteinuria and hematuria disappeared simultaneously after the treatment. We underline that the lack of finding of HCV antigens or HCV-RNA in glomerular lesions (as occurred in our patient) does not rule out the virus role in pathogenesis of immunological nephritis. The recovery of our patient as well as the disappearance of proteinuria and hematuria during IFNalpha treatment may be further evidence that FSGS and chronic hepatitis HCV-related are not associated by chance. Further observations and perfectioning of diagnostic techniques are required to clarify the pathogenetic relationship between HCV and renal immunological syndromes.
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PMID:Focal segmental glomerulosclerosis and hepatitis C virus: a case report. 1131 19


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