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)

In order to investigate the role of hepatitis B virus (HBV) DNA in the pathogenesis of renal lesion in HBV-associated membranous nephropathy (HBVMN) patients, serial studies using an in situ hybridization technique at different time points were performed. Within 6 months after the onset of the disease, 7 of 8 (87.5%) HBVMN patients demonstrated HBV DNA in the glomeruli and tubular epithelia. In contrast to the 14 HBVMN specimens taken later than 6 months after the onset, HBV DNA was detectable in only 3 (21%) in the tubular epithelia but none in the glomerular region. Most of the glomeruli-associated HBV DNA seemed extracellular because they were also positive for both the accumulation of HB e antigen (HBeAg)-anti-HBe antibody (Ab) immune complex and immunoglobulin G. The finding suggested that glomeruli-associated viral DNA is joined with filtered HBeAg-anti-HBeAb immune complexes. In the analysis of follow-up biopsies, HBV DNA in tubular epithelia was detected more frequently in the progressive group (50%) than in the nonprogressive group (0%). HBV DNA was detectable in the tubular epithelia in 2 cases who were progressing to end-stage renal disease and had heavy proteinuria. However, in the cases with mild or no proteinuria, HBV DNA was no longer detectable in the kidney. These findings suggest that HBV disseminates in the kidney and its dynamic changes at different time points may implicate the important role of HBV in the pathogenesis of HBVMN. This needs further study to be clarified.
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PMID:Hepatitis B virus deoxyribonucleic acid in kidney cells probably leading to viral pathogenesis among hepatitis B virus associated membranous nephropathy patients. 844 53

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

We undertook this study to determine the clinical, biologic, immunologic, and therapeutic factors associated with the prognoses of polyarteritis nodosa (PAN) and Churg-Strauss syndrome (CSS). Three hundred forty-two patients (260 with PAN, 82 with CSS) followed from 1980 to 1993 were included in a prospective study on prognostic factors. Two hundred eighty-eight of these patients were included in the prospective studies on PAN and CSS. Items to be considered for analysis were collected at the time of diagnosis, during the acute phase of the disease. A survival curve was plotted for each clinical and biologic symptom observed in PAN or CSS. Each treatment arm of the prospective therapeutic trials was also tested: 1) prednisone (CS) + oral cyclophosphamide (CYC) + plasma exchanges (PE) versus CS E, 2) CS + PE versus CS, 3) CS + oral CY versus CS + pulse CY, 4) CS + pulse CY + PE versus CS + pulse CY in severe PAN and CSS, and 5) PE + antiviral agents after short-term CS in hepatitis B virus-related PAN. Of the parameters thus evaluated, the following had significant prognostic value and were responsible for higher mortality: proteinuria > 1 g/d (p < 0.0001; relative risk [RR] 3.6), renal insufficiency with serum creatinine > 1.58 mg/DL (p < 0.02; RR 1.86), GI tract involvement (p < 0.008. RR 2.83 for surgery). Cardiomyopathy and CNS involvement were associated with a RR of mortality of 2.18 and 1.76, respectively; these were not statistically significant. Similar survival rates were obtained with the prospectively tested therapies. The five-factors score (FFS) we established considered the prognostic factors creatinemia, proteinuria, cardiomyopathy, GI tract involvement, and CNS signs. Multivariate analysis showed that proteinuria (due to vascular or glomerular disease) and GI tract involvement were independent prognostic factors. When FFS = 0 (none of the 5 prognostic factors present), mortality at 5 years was 11.9%; when FFS = 1 (1 of the 5 factors present), mortality was 25.9% (p < 0.005); when FFS > 2 (3 or more of the 5 factors present), mortality was 45.95% (p < 0.0001 between 0 and 2, p < 0.05 between 1 and 2). We conclude that an initial assessment of PAN or CSS severity enables outcome and mortality to be predicted. The FFS is a good predictor of death and can be used to help the clinician choose the most adequate treatment. Renal and GI signs are the most serious prognostic factors.
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PMID:Prognostic factors in polyarteritis nodosa and Churg-Strauss syndrome. A prospective study in 342 patients. 856 67

In children with hepatitis B-associated membranous glomerulonephritis, the time of onset of the infection and the duration of the carrier state before diagnosis of the renal disease are always unknown. Moreover, follow-up is usually short. We report the unique observation of a French girl who was infected with hepatitis B virus by her mother who had acute hepatitis during the immediate postpartum period; the girl developed proteinuria at 6 years of age. The onset of the infection in the perinatal period, the mild liver abnormalities, and the absence of nephrotic syndrome did not justify any treatment. Spontaneous seroconversion to anti-HBe antibody positive occurred at 12 years of age. Proteinuria gradually diminished and was absent at 18 years. However, HBs antigenemia persists.
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PMID:Membranous nephropathy following perinatal transmission of hepatitis B virus infection--long-term follow-up study. 861 64

We studied direct and indirect methods of measuring membrane charge by detecting fixed anionic sites with polyethylenimine (PEI) on the glomerular basement membrane (GBM) and Alcian blue on red blood cell (RBC) membrane (ABRBC), respectively, in 40 children with nephrotic syndrome (NS). Size selectivity of the GBM was measured indirectly by fine analysis of urinary proteins with sodium dodecyl sulfate-polyacrylamide gel electrophoresis in 22 of these children. Correlation between ABRBC and PEI was strongest (r = 0.79; p = 0.0037) in 11 children with steroid-responsive NS (SRNS), moderate (r = 0.31) in 10 children with focal glomerulosclerosis (FGS), and absent in 14 children with hepatitis B antigen membranous nephropathy (MGN) and 5 with mesangioproliferative glomerulonephritis (MPGN). ABRBC and PEI were reduced in the group as a whole as compared with their controls (ABRBC: 44.53 +/- 9.81 vs 71.54 +/- 12.14, p < 0.05; PEI: 16.31 +/- 4.34 vs 33.3 +/- 1.09, p < 0.005). This reduction was greater in SRNS (26.35 +/- 7.15 p = 0.004) but was also detected in the remainder of the group taken together (52.31 +/- 26.07, p < 0.001). Excretion of glomerular proteins was restricted by size (< or = 80 kd) in SRNS but unrestricted (< or = 80 kd plus > 80 kd) in FGS, MGN, and MPGN. The main cause of proteinuria is likely to be depletion of negative charge on the GBM in SRNS, and distortion of capillary pore size in MGN and MPGN, with probable overlap of these mechanisms in each disease, especially in FGS. Basement membrane injury appears widespread in SRNS but confined to the kidney in MGN and MPGN.
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PMID:Direct and indirect tests of pore size and charge selectivity in nephrotic syndrome. 863 48

Two siblings (case 1 and case 2) with homozygous C1q deficiency are described. Both presented with a photosensitive rash, and during follow-up case one developed SLE with nephrotic range proteinuria. Case 2 had microscopic hematuria with a past history of macroscopic hematuria. Renal biopsies revealed mesangioproliferative glomerulonephritis in case 1 and IgA nephropathy in case 2, a new finding in association with C1q deficiency. Since the classical pathway of complement plays a role in the development of antibody responses, the family was also evaluated for the immune response to hepatitis B vaccine. Antibody response to hepatitis B vaccine was normal in both affected members and the rest of the family. The A-, B- and C- chain genes of C1q were amplified by PCR and directly sequenced. A homozygous C to T point mutation was identified in genomic DNA isolated from the patients at codon 186 in the A chain that resulted in a premature stop codon. This mutation was present in both parents and both unaffected sibs in the heterozygous state. This mutation was identical to that previously described in a Slovakian family with C1q deficiency. Because of this finding, a series of 92 genomic DNA samples was screened from ethnically distinct patient groups with SLE to test the hypothesis that this mutation of C1q may be a widespread disease susceptibility gene. No further examples of this mutation were found.
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PMID:Molecular basis of hereditary C1q deficiency associated with SLE and IgA nephropathy in a Turkish family. 884 Feb 96

A patient with a history of drug abuse and histologically diagnosed hepatitis B-related polyarteritis nodosa was admitted for severe hypertension. After a cesarean section because of worsening of her clinical status with severe proteinuria and edema, she improved dramatically. No sign of acute polyarteritis nodosa occurred.
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PMID:Severe preeclampsia superimposed on polyarteritis nodosa. 906 53

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

Human immunodeficiency virus-associated nephropathy (HIVAN), characterized by heavy proteinuria, rapidly progressive renal failure, "collapsing" glomerulopathy, and tubulointerstitial abnormalities, is the most common finding in HIV-infected patients undergoing a renal biopsy and predominantly affects blacks. We describe the clinical features and renal pathologic findings of 12 intravenous drug users (IVDUs) coinfected with HIV and hepatitis C virus (HCV) who were selected for renal biopsy because they presented with features different from typical HIVAN, including hypertension, microscopic hematuria, and cryoglobulinemia. There were seven black and five Hispanic patients. Eleven patients had immune complex glomerulonephritis (ICGN); one had glomerulosclerosis with immune complex deposits. Ten individuals had evidence of past hepatitis B viral infection, but none had persistent hepatitis B surface antigenemia. No other underlying cause for immune complex glomerulonephritis was identified. Renal biopsy showed membranoproliferative glomerulonephritis in five patients, mesangial proliferative glomerulonephritis in five, membranous nephropathy in one, and "collapsing" glomerulopathy with immune complex deposits in one. Hepatitis C virus RNA was detected by reverse transcription-polymerase chain reaction (RT-PCR) in the renal tissue and/or serum of nine of the 11 patients tested, and also in the renal biopsy tissue of four of eight patients with clinical and pathologic features of typical HIVAN without immunofluorescence evidence of immune complex deposits. One patient presented with renal failure, five patients developed end-stage renal disease (ESRD) requiring hemodialysis (mean time, 6.5 months), and six had stable renal function after a mean follow-up of 29.1 months (range, 2 to 72 months). Liver function abnormalities were present in seven of the 12 individuals, including four of the six patients who developed renal failure. These findings indicate that in some patients coinfected with HIV and HCV, the development of ICGN may dominate the clinical course of the disease. The occurrence of ICGN among black patients at risk for HIVAN may be related to the relatively high prevalence of HCV infection among IVDUs in this group.
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PMID:Immune complex glomerulonephritis in patients coinfected with human immunodeficiency virus and hepatitis C virus. 910 39

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


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