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)

The authors report the case of a 38 year old man with horseshoe kidney who developed a severe nephroso-nephritis syndrome, caused by cryoglobulinemic membranoproliferative glomerulo-nephritis. A combination of steroid and cyclophosphamide treatment resulted in partial improvement, but was discontinued after 12 weeks due to adverse reactions, with a consequent early relapse. The 4 week course of cyclosporine monotherapy proved ineffective and signs of cryoglobulinemia appeared. The elevation of transaminase, manifested during the immunosuppressive therapy demonstrated the presence of underlying chronic C hepatitis. In the light of the liver biopsy result, interferon treatment was commenced at a dose of 3 million unit thrice weekly. After 4 months of interferon treatment the persistent nephrotic range proteinuria decreased to below 0.5 g/day. Four months later clinical signs of cryoglobulinemia disappeared, and after the 10th month of interferon treatment no cryoglobulin could be detected in the patient's sera. After one year, the interferon treatment was discontinued following a negative PCR result for HCV. However, one month later the proteinuria increased and the quantitative hepatitis C virus nucleic acid test in sera became positive again. Our case demonstrates that interferon therapy may be effective in the treatment of cryoglobulinemic glomerulonephritis responding poorly to the immunosuppressive therapy, though larger doses or longer periods of treatment may be required to prevent relapses.
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PMID:[Interferon therapy in cryoglobulinemic membranoproliferative glomerulonephritis associated with hepatitis C virus infection]. 902 71

To evaluate the therapeutic effect of recombinant human alpha-interferon (alpha-IFN) on hepatitis B virus associated glomerulonephritis (HBV-GN) and the relationship between the seroconversion of viral antigens and the change of proteinuria, the hepatitis B viral markers and urinary protein were monitored during alpha-IFN treatment in 8 male adult patients who (1) were positive in serum HBsAg and HBeAg, (2) had chronic hepatitis, (3) had persistent proteinuria > 1 g/day, and (4) showed glomerulonephritis on kidney biopsy. alpha-IFN was given at a dose of 3 million units, subcutaneously, three times a week for 6 months. Kidney biopsy specimens showed membranoproliferative glomerulonephritis (MPGN) in 4 patients, mesangial proliferative glomerulonephritis (MesPGN) in 2, and membranous glomerulonephritis (MGN) in 2 patients. Seven of the 8 patients received a 6-month course of alpha-IFN therapy; 1 patient with MGN quitted therapy 2 months after the initial dose because of side effects. In 5 of the 7 patients who received a 6-month therapy, serum HBeAg disappeared, and anti-HBe appeared during the therapy. In 2 of these 5 patients, HBeAg reappeared, in 1 during alpha-IFN therapy and in 1 9 months after the last dose of alpha-IFN. The hepatitis B viral markers of the patient who received a 2-month therapy did not change. HBs antigenemia persisted in all patients. In all 4 patients with MPGN, serum HBeAg was transiently or persistently converted to negative, but the proteinuria persisted. Both patients with MesPGN showed remission of proteinuria; however, only 1 patient had seroconversion of HBeAg. In 2 patients with MGN, proteinuria persisted. In conclusion, alpha-IFN at the doses given was not effective in MPGN type of HBV-GN. Improvement of proteinuria was achieved in MesPGN patients without disappearance of HBs antigenemia which is the finding against the possible role of HBsAg in the pathogenesis of this type of HBV-GN.
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PMID:Treatment of hepatitis B virus associated glomerulonephritis with recombinant human alpha interferon. 909 40

Glomerular abnormalities are frequent in patients undergoing liver transplantation; however, renal dysfunction following transplantation is mainly attributed to cyclosporine toxicity. Membranoproliferative glomerulonephritis (MPGN) is seen in patients infected with hepatitis C virus (HCV), the virus responsible for 30% of the end-stage liver disease leading to liver transplantation. To determine the incidence of renal abnormalities in liver transplant recipients and the association with HCV, we undertook a longitudinal study in HCV-positive (n=91) and HCV-negative (n=106) liver transplant recipients. Mean creatinine clearance before transplantation was 94 ml/min/1.73 m2 in HCV+ patients and 88 ml/min/1.73 m2 in HCV- patients. By 3 months after transplantation, the mean creatinine clearance decreased by approximately one third in both groups. A greater proportion of HCV+ patients excreted >2 g protein/day after transplantation (P=0.05) and had renal biopsies showing MPGN than did HCV- recipients (4/10 HCV+ patients vs. 0/7 HCV- patients; P=0.1). In the HCV+ group, proteinuria was not associated with recurrent HCV hepatitis, DQ matching, posttransplant diabetes, or hypertension. Treatment of HCV-related MPGN with interferon-alpha2b appeared to stabilize proteinuria and renal function but did not reverse renal dysfunction nor cause liver allograft rejection. After transplantation, HCV+ patients had similar renal function over 3 years after transplantation, compared with HCV- patients, but they had an increased risk of proteinuria and occurrence of MPGN that was only partially responsive to interferon.
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PMID:Renal disease in hepatitis C-positive liver transplant recipients. 915 23

According to previous reports, the prevalence of hepatitis B virus (HBV) infection in patients with systemic lupus erythematosus (SLE) is varied. There has been no report on Taiwan, a hyperendemic area for HBV infection. Furthermore, impaired production of interferon (IFN) in peripheral blood mononuclear cells (PBMC) has been reported to be potentially pathogenic to both chronic HBV infection and SLE. However, the production of IFN in patients with both diseases coexisting is unknown. The aims of this study were to evaluate the prevalence of HBV infection in lupus patients in Taiwan and to measure the production of IFN in patients with both diseases coexisting. One hundred and seventy-three consecutive lupus patients and a control group of 692 age- and sex-matched healthy subjects were included for evaluation of the prevalence of HBsAg. Four groups of subjects (patients with SLE and HbsAg, SLE, chronic hepatitis B and normal controls) were selected for evaluation of the in vitro production of IFN-alpha and -gamma. Six (3.5%) of the 173 SLE patients were positive for HBsAg, which was significantly lower than that of controls (14.7%; P < 0.0001). Patients with coexistent SLE and chronic HBV infection had less lupus activity, including less proteinuria (P = 0.02) and a lower serum titre of anti-double stranded DNA antibodies (anti-dsDNA; P = 0.04), than HBsAg-negative lupus patients. The in vitro production of IFN-alpha in patients with chronic hepatitis B was significantly lower than in those patients with SLE or in the normal control group (P < 0.01). The yields of IFN-alpha and -gamma in patients with coexistent SLE and chronic HBV infection were significantly different from those patients with SLE alone (P < 0.05), but close to those of patients with chronic HBV infection. In conclusion, the prevalence of HBsAg carriers is significantly lower in lupus patients in Taiwan. Patients with coexistent SLE and chronic HBV infection had less lupus activity. Interferon-alpha and -gamma may play a role in the above phenomenon.
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PMID:Hepatitis B infection and changes in interferon-alpha and -gamma production in patients with systemic lupus erythematosus in Taiwan. 919 65

A 31-year-old man diagnosed as having chronic myelocytic leukemia (CML) developed renal insufficiency with nephrotic-range proteinuria during alpha-interferon (IFN) therapy for CML. A renal biopsy specimen showed remarkable thrombotic microangiopathic lesions resembling those of hemolytic-uremic syndrome. The patient had papules on both lower legs, and a cutaneous biopsy showed similar microangiopathic lesions in dermal and subcutaneous vessels. Although discontinuation of IFN and initiation of prednisolone therapy resulted in resolution of proteinuria, renal insufficiency persisted. These findings suggest that long-term IFN therapy can induce late-onset thrombotic microangiopathy in systemic microvessels.
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PMID:Thrombotic microangiopathy associated with alpha-interferon therapy for chronic myelocytic leukemia. 921 12

Hepatitis C virus (HCV) infection may be associated with extrahepatic illness including renal disease. We investigated the clinical and virological characteristics of three patients who developed a mesangial proliferative and sclerosing glomerulopathy alone or in association with membranoproliferative glomerulonephritis after liver transplantation for end-stage liver disease secondary to HCV infection. Using polymerase chain reaction technology and the IgM RIBA assay, viral load, genotype and IgM antibody response to HCV in the setting of glomerulonephritis was evaluated. Within 1 year of transplantation, the patients showed decreased renal function, proteinuria and recurrent hepatitis C liver disease. Likewise, HCV viral load increased following transplantation, whereas the viral genotypes remained unchanged. Although the first patient presented with classic type II cryoglobulinemia in association with glomerulonephritis, the second patient developed an IgM directed specifically against the hepatitis C core antigen. The third patient developed a low-titered IgM directed against the hepatitis C core antigen with rheumatoid factor activity but without cryoglobulinemia. All of the patients show IgM in glomerular capillary walls by biopsy. One patient has shown a clinical response to interferon (IFN) alfa-2b therapy without evidence of hepatic allograft rejection. The second and third patients have not responded to IFN or developed hepatic rejection. This study suggests that HCV-associated glomerulonephritis may complicate liver transplantation in conjunction with the production of increased amounts of IgM of variable specificity. The posttransplant setting may provide a unique situation in which to investigate the specific requirements for the onset of renal disease.
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PMID:Hepatitis C--associated glomerular disease in liver transplant recipients. 934 60

Current therapy for primary systemic (AL) amyloidosis has only modest efficacy (response rate 25%) and because it includes alkylating agents, it has a significant leukemogenic potential (actuarial risk 21% at 3.5 years). We treated 9 consecutive patients with biopsy proven AL amyloidosis seen at our institution with pulse dexamethasone induction (40 mg on days 1-4, 9-12, 17-20 repeated q 35 days) for 3-6 cycles followed by maintenance alpha interferon 3-6 million units thrice weekly. Three patients also received maintenance dexamethasone (40 mg/day x 4 days q 4-8 weeks) for the first year. Improvement in > or = 1 AL organ involvement was seen in 8 of 9 patients. Of 7 patients with nephrotic range proteinuria, 6 had > or = 50% reduction in nonspecific proteinuria with a median time to response of 4 months (range 3-9 months). Marked improvement in organ function was also seen in 4 patients with gastrointestinal, hepatic and neuropathic involvement. However, none of the 2 patients with congestive heart failure improved. This dexamethasone plus alpha interferon regimen, devoid of leukemogenic potential, may lead to rapid and durable improvement in organ function in a significant proportion of patients with AL amyloidosis and deserves further evaluation as front line therapy.
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PMID:Treatment of AL-amyloidosis with dexamethasone plus alpha interferon. 940 33

Human recombinant interferon (IFN)-alpha (alpha)-2b was given to a 57-year-old man with hypereosinophilia syndrome refractory to prednisone and hydroxyurea. One year later, he developed progressive renal failure and nephrotic-range proteinuria. Percutaneous kidney biopsy showed focal and segmental glomerular and mesangial sclerosis, chronic interstitial nephritis, and focal tubular necrosis. Discontinuation of cytokine therapy led to marked improvement in renal function and significant reduction in proteinuria. The potential role of IFN-alpha as the cause of renal failure and nephrotic-range proteinuria is discussed. The spectrum of renal disease attributed to IFN-alpha and the proposed pathogenic mechanisms are reviewed.
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PMID:Reversible renal failure in a patient with the hypereosinophilia syndrome during therapy with alpha interferon. 942 62

T cells with T cell receptor (TCR) transgenes that recognized CD1 on syngeneic B cells stimulated B cells to secrete immunoglobulins in vitro. The CD4+, CD8+, or CD4-CD8- T cells from the spleen of the TCR transgenic BALB/c donors induced lupus with anti-double stranded DNA antibodies, proteinuria, and immune complex glomerulonephritis in irradiated BALB/c nude mice reconstituted with nude bone marrow. Injection of purified CD4-CD8- T cells from the marrow of transgenic donors prevented the induction of lupus by the transgenic T cells. Transgenic T cells that induced lupus secreted large amounts of interferon (IFN)-gamma and little interleukin (IL)-4, and those that prevented lupus secreted large amounts of IL-4 and little IFN-gamma or IL-10.
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PMID:Subsets of transgenic T cells that recognize CD1 induce or prevent murine lupus: role of cytokines. 946 3

Hepatitis C is an important cause of renal disease, and renal complications may be the presenting manifestation of hepatitis C infection. About half of patients present with evidence of renal insufficiency, and up to one quarter present with nephrotic syndrome. Others present with proteinuria or evidence of diminished renal function. The pathogenesis of hepatitis C-associated renal disease remains incompletely defined, but most evidence suggests that glomerular injury results from deposition of circulating immune complexes in the subendothelium and mesangium. Membranoproliferative glomerulonephritis, with or without cryoglobulinemia, is the most common renal lesion. Interferon alpha-2b is currently the treatment of choice. However, success is limited, with many patients failing to respond or suffering relapse upon discontinuation of therapy. Studies of newer treatment modalities, such as longer courses of interferon or the use of ribavirin or immunosuppressive agents, are underway. Hepatitis C-associated renal disease may progress to end-stage renal failure requiring dialysis in about 10% of patients.
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PMID:Renal manifestations of hepatitis C infection. 1019 Mar 85


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