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 purpose of the present paper was to study clinical, morphological and immunological aspects of late rejection of renal allotransplants. We have, therefore, analyzed the occurrence and nature of renal transplant disease and graft failure among 125 recipients surviving for 1 to more than 8 years after transplantation. In this population transplant disease as defined by the appearance of heavy proteinuria and/or steadily declining graft function occurred in 22 patients. At the closure date of the study on December 31, 1972 complete graft failure had occurred in 12 of these 22 patients and 4 of these have died. In addition two patients died in the presence of normal graft function, due to chronic hepatitis and metastatic cancer respectively. As based on clinical findings, pathophysiological features and renal lesions the patients with late transplant disease were classified into two groups and described accordingly. Group A, termed glomerular transplant disease, included a majority of 16 patients, constituting a rather homogenous idsease entity in relation to course of disease, clinical findings and renal lesions as studied by light-, immunofluorescence- and electron microscopy. All these patients presented with heavy proteinuria, which was non-selective in all but two, resulting eventually in complete loss of graft function in eight cases. All these patients developed hypoalbuminemia and hypercholesterolemia, and one half manifested a classical nephrotic syndrome. Arterial hypertension occurred in all patients except two. Glomerular structure as studied by light microscopy revealed a number of lesions of a rather polymorphous pattern in all patients in group A. Endomesangial proliferation, hyperplasia and segmental proliferation of epithelial cells and thickening of capillary walls were prominent features, although the degree of severity, extension and type of lesion occurred in such varying proportions that classification into any well characterized category of glomerulonephritis was not possible. All cases in group A revealed immune deposits, most frequently containing IgG, IgM, complement and fibrinogen. IgA, IgD and IgE were also demonstrated in a lesser proportion of cases in this group. The immunofluorescent pattern was a mixed granular and linear, and in no case strictly linear or granular alone. The ultrastructural investigation contains a detailed analysis of the
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PMID:Late failure or human renal transplants. An analysis of transplant disease and graft failure among 125 recipients surviving for one to eight years. 23 63

We report 6 cases with membranous glomerulonephritis associated with chronic hepatitis B virus infection, who came under our observation for microscopic haematuria in 2 cases, haematuria and proteinuria in 1 case, and nephrotic syndrome in the others. At the examination all 6 children were found to have hepatomegaly with raised serum transaminase activity. All the patients were positive in the serum for HBsAg and anti-HBc, 3 were HBeAg and anti-HBe negative. Liver biopsy showed features of chronic hepatitis with moderate signs of activity. Renal biopsy was consistent with membranous glomerulonephritis in all patients. With a fluorescent antibody technic HBeAg was found to be deposited in diffuse granular fashion, along glomerular capillary walls, together with IgG, in 2 out of 3 cases stained, but no deposition of HBsAg was detected in all the patients. Steroid therapy was started from 18 to 33 months. Urine analysis became negative in 4 cases and persisted normal in the follow-up. One patient with haematuria developed nephrotic syndrome and one died from miliary tuberculosis. Our findings suggest that the clinical outcome is favourable in children with membranous glomerulonephritis and chronic active hepatitis and that the pathogenesis probably is not unique.
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PMID:[Membranous nephropathy associated with chronic hepatitis caused by B virus]. 294 50

The nature of circulating immune complexes (CIC) which appear in patients with type B hepatitis was investigated using a method of Raji cell fluorescent immunoassay. CIC were found in seventeen of thirty-five cases (48.6%) with HBs antigen (HBsAg)-positive liver diseases (4/8 cases with acute hepatitis, 9/18 cases with chronic hepatitis, and 4/9 cases with liver cirrhosis), whereas no CIC were detectable in sera of ten asymptomatic, healthy carriers with HB virus. Among the seventeen cases with CIC-positive liver diseases, HBs antigen-antibody immune complexes (HBsIC) were demonstrated in eleven (65%). A high incidence (54%) of proteinuria was observed in patients with CIC-positive liver disease compared to those without them (10%). Moreover, 83% of patients with HBsIC were associated with proteinuria. A case of fulminant type B hepatitis showed high titers of both CIC and HBsIC during the acute phase of the disease; in the recovery stage, the titers decreased to within normal ranges. These results demonstrate that HBsAg is a possible antigen in CIC during type B hepatitis. Determination of serum HBsIC is significant for the clinical evaluation of HB virus-related liver diseases.
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PMID:Significance of circulating HBs antigen-antibody immune complexes in patients with HBs antigen-positive liver disease. 711 81

We reported a case of type II cryoglobulinemia involving glomerulopathy associated with HCV-induced liver cirrhosis. The patient was a 57-year-old woman. Her past history included chronic hepatitis at 51 years and rheumatoid arthritis at 53 years of age. At 46 years, an erythematous lesion appeared on her legs, which was diagnosed as allergic vasculitis by skin biopsy. At 50 years, proteinuria, hematuria and hypertension were recognized. The next year, the first renal biopsy was performed and showed membranoproliferative glomerulonephritis (MPGN). Recently, the edema of her legs has progressed, and the laboratory data showed proteinuria, hematuria, hypocomplementemia, rheumatoid factor positivity, and increase of monoclonal IgG kappa chain. The second renal biopsy revealed an endocapillary proliferative glomerulonephritis-like lesion with marked infiltration of monocytes and macrophages. The subendothelial deposit showed a fine fibril-like pattern. She was treated with steroids and double filtration plasmapheresis (DFPP) therapy, but the treatment was not very effective. She died of liver cirrhosis, which was probably induced by hepatitis C virus (HCV), and sepsis. Generally, the patients of type II cryoglobulinemia often showed HCV antibody positivity, pointing to HCV as an etiological factor. In this case, renal biopsy was performed twice in the same patient, and the histologic findings suggest the clinicopathological course of cryoglobulinemia.
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PMID:[A case of type II cryoglobulinemia involving glomerulopathy associated with hepatitis C antibody]. 750 47

Type 2 mixed cryoglobulinemia is a relatively common although rarely recognized consequence of chronic hepatitis C virus infection. Its detection should be pursued in individuals with lower extremity vasculitis which occurs in association with other signs of systemic disease such as proteinuria or a peripheral neuropathy. Importantly, HCV-associated cryoglobulinemia can occur in individuals with clinical evidence for cryoglobulinemia but without any evidence of detectable liver injury. Two cases recently seen in Oklahoma demonstrating these points are reported.
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PMID:Type 2 cryoglobulinemia and hepatitis C virus: its recognition and treatment. 779 10

In recent years, several laboratories have suggested that chronic hepatitis C virus (HCV) infection is strongly associated with type II cryoglobulinemia (CG) and/or membranoproliferative glomerulonephritis (MPGN). We report here a case of MPGN due to type II CG probably associated with chronic HCV infection, and discuss the pathogenesis and treatment of such cases. A 60-year-old-female was referred to us from a local hospital because of progressive peripheral edema, purpura on the lower limbs, pleural effusion, ascites, hypertension, and renal failure. Laboratory findings indicated proteinuria, abnormal urinary sediments, normochromic normocytic anemia and azotemia. Other laboratory findings included positive rheumatoid factor, elevated serum IgM, hypocomplementemia and elevated circulating immune complexes. Cryoglobulin was detected and found to consist of a mixture of a monoclonal IgM kappa with polyclonal IgG. Renal biopsy showed MPGN. These observations suggested a close association between MPGN and type II CG. We did not find any causes of type II CG except for positive HCV antibody and HCV RNA. Therefore, we made the diagnosis of type II CG associated with chronic HCV infection. Symptoms related to CG was responsiveness to steroid, but development of liver dysfunction developed. Treatment with alfa-interferon (alpha IFN) was added and thereafter, the liver dysfunction improved. However, the serum Cryo level was not reproducibly lowered. While in this case it was unclear whether IFN therapy was beneficial, several reports in addition to the findings of this case suggest a close relation between HCV infection and type II CG and MPGN.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of membranoproliferative glomerulonephritis due to type II cryoglobulinemia probably associated with hepatitis C virus infection]. 819 26

The outcome of kidney transplantation was evaluated in 246 nondiabetic, CsA-treated recipients of primary cadaver transplant, divided into 4 groups according to length of time on dialysis: group < or = 2, 0-24 months; group 2-5, 25-60 months; group 5-15, 61-180 months; group > 15, over 180 months. The 4 groups did not differ in graft survival, proteinuria (g/die), or estimated GFR values at 1, 2, 3, 4, and 5 years after grafting. They did not differ in the frequency of cataract, hip osteonecrosis, tumors, or posttransplant diabetes mellitus at 3 years after grafting. Ocular hypertone (p < 0.02), tendon ruptures (p < 0.001), arterial occlusive disease of lower limbs (p < 0.01), cholelithiasis (p < 0.05), and chronic hepatitis--which occurred only in anti-HCV and/or HBs Ag-positive patients--(p < 0.001), were more frequent in group > 15, and in all these cases but ocular hypertone a linear trend of increasing frequencies with increasing dialytic age was statistically significant. Group 5-15 had the lowest patient survival (p < 0.02). Moreover, a progressive decline of patient survival with increasing dialytic age was noted in groups < or = 2, 2-5, and 5-15. Unexpectedly, group > 15 had remarkably good survival, and this finding denies the hypothesis of a purely linear decline of patient survival after transplantation with increasing dialytic age.
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PMID:Influence of length of time on dialysis before grafting on kidney transplant results. 872 66

Sixteen renal transplant (RT) patients (10 men, 6 women, aged 49 +/- 10 years) with chronic hepatitis C received alpha interferon (IFN alpha) therapy (Intron A, Schering Plough) at a dose of 3 x 10(6) units s.c. 3 times a week, scheduled for 24 consecutive weeks. At the beginning of the study all had a stable renal function since at least 12 months (mean serum creatinine -SCr- 121 +/- 38 mmol/l). Fourteen patients were receiving cyclosporin A (CsA) either alone (1) or in combination with steroids and/or azathioprine -AZA- (double therapy: 8; triple therapy: 5); two patients were on conventional therapy. The mean daily doses of CsA were 2.6 mg/kd i.e. a mean whole blood trough level of 104 ng/ml. Six patients experienced renal failure either acute (5) or subacute (1) within 7 to 24 weeks after the start of IFN alpha therapy. Their mean SCr increased from 105 +/- 31 mmol/l to 207 +/- 63 mmol/l (p = 0.02) with de-novo proteinuria in one case (1 g/d) and an increase in pre-existing proteinuria in 2; 3 remained without proteinuria. The histological study showed in all cases a diffuse interstitial edema associated with dilatation of peritubular capillaries; mild inflammatory infiltrates were present in only 3 cases; mild glomerular lesions were not always found (glomerular ischemia, mesangial hypertrophy). There was no vascular lesions IFN alpha was withdrawn in these 6 patients, associated with methylprednisolone pulses in 5 cases. Renal function improved in two cases, stabilized in one and progressed to end stage renal failure in 3 within 4 to 12 months. Four patients had iterative renal biopsies showing in all cases diffuse interstitial fibrosis. This subgroup of patients did not statistically differ at the start of the study from those who did not develop renal failure according to baseline immunosuppression, HLA matching, total peripheral blood lymphocyte (PBL) count. PBL subtypes. INF alpha therapy was associated with acute or subacute renal failure in 37% of patients. The most prominent histological finding was a diffuse interstitial edema of rapid onset, without signs of cellular or vascular rejection. Thus we do not recommend to use IFN alpha therapy in RT patients with chronic hepatitis C, until the mechanisms of the subsequent renal failure be more understood.
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PMID:[Acute renal insufficiency in renal transplants treated with interferon-alpha for chronic hepatitis C]. 876 57

Sixteen kidney transplant (KT) patients (10 men, 6 women, aged 49 +/- 10 years) with chronic hepatitis C alpha-interferon (IFN-alpha) therapy (Intron A, Schering Plough) at a dose of 3 x 10(6) units subcutaneously 3 times a week. The treatment was scheduled for 24 consecutive weeks. Each patient had had stable renal function for at least 12 months prior to IFN-alpha therapy (mean serum creatinine, SCr, 121 +/- 38 mmol/l). Fourteen patients were receiving cyclosporin-A (CsA)-based immunosuppression and 2 patients were on conventional therapy. The patients' SCr was checked every 2 weeks while on IFN-alpha, or weekly if it increased more than 15% from baseline. IFN-alpha was withdrawn if SCr increased more than 25% from baseline, in which case a kidney biopsy was performed. Six patients experienced either acute (n = 5) or subacute (n = 1) renal failure within 7-24 weeks after the onset of IFN-alpha therapy. Their mean SCr increased from 105 +/- 31 to 207 +/- 63 mmol/l (p = 0.02) with de novo proteinuria in 1 case (1 g/day) and an increase in preexisting proteinuria in 2. The other 3 patients did not develop proteinuria. In each case, histological study showed diffuse interstitial edema associated with dilation of the peritubular capillaries, whereas mild inflammatory infiltrates were present in only 3 cases and mild glomerular lesions were not always found (glomerular ischemia, mesangial hypertrophy). There were no vascular lesions. IFN-alpha was withdrawn in these 6 patients, in association with methylprednisolone pulses in 5 cases. Renal function improved in 2 cases, stabilized in 1 and progressed to end-stage renal failure in 3 within 4-12 months. Four of these patients had iterative renal biopsies which showed diffuse interstitial fibrosis in each case. The patients who developed renal failure did not statistically differ at the start of the study from those who did not, with respect to the following: baseline immunosuppression, HLA matching, total peripheral blood lymphocyte count or peripheral blood lymphocyte subtypes. IFN-alpha therapy was associated with acute or subacute renal failure in 37% of the patients. The most prominent histological finding was diffuse interstitial edema of rapid onset, without signs of cellular or vascular rejection. In conclusion, we do not recommend IFN-alpha therapy for KT patients with chronic hepatitis C, until the mechanisms of the subsequent renal failure are better understood.
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PMID:Acute renal failure in kidney transplant patients treated with interferon alpha 2b for chronic hepatitis C. 893 73

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


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