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)

We report a 59-year-old man who was found to have plasma cell dyscrasia and amyloid A protein (AA) amyloidosis during the follow-up period of chronic inactive hepatitis C. Clinical manifestations such as swallowing disturbance, proteinuria and leg edema were associated with AA amyloid deposits in his tongue and kidneys. Although the relationship between these two diseases remains to be determined, the ability of peripheral blood mononuclear cells to degradate serum amyloid A protein was apparently reduced in this patient, compared with normal volunteers. This would, in part, account for the AA amyloid deposition in this patient.
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PMID:Amyloid a protein amyloidosis in a patient with plasma cell dyscrasia. 1205 89

Membranoproliferative glomerulonephritis type 1 is an etiologically divergent disorder. Hepatitis C with or without cryoglobulinemia is considered one of the principal causes of de novo and post transplant membranoproliferative glomerulonephritis type 1. A 49-year-old male who underwent renal allograft for end stage renal disease developed proteinuria and positive hepatitis C serology during the post-transplant period. This was associated with moderate hepatic dysfunction, which necessitated both liver and renal biopsies. Features of both chronic active hepatitis and membranoproliferative glomerulonephritis type 1 were seen as a result of histological examination of both liver and renal biopsies. Ultra structural studies showing mesangial and membranous deposits which are characteristic of membranoproliferative glomerulonephritis have been observed. The case is reported with a review of pertinent medical literature.
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PMID:Membranoproliferative glomerulonephritis due to Hepatitis C in renal allograft. 1207 May 61

Available data suggest that hepatitis C virus positive (HCV+) renal transplant patients may be at an increased risk of morbidity and mortality compared with HCV- patients. Limited data are available regarding the impact of HCV status in pancreas transplant patients. We compared the outcomes of 10 HCV+ patients undergoing pancreas transplantation (seven simultaneous kidney-pancreas, one pancreas after kidney, two pancreas alone) between 1/96 and 10/99 with 20 HCV- recipients that were matched for age, race, gender, timing of transplant, type of pancreas transplant, and surgical technique. Length of follow-up was not significantly different between the HCV+ group compared with the HCV- group (24 +/- 14 vs. 20 +/- 13 months; p=0.45). There was a trend toward a higher incidence of all cause mortality in HCV+ recipients compared with HCV- recipients, 30 vs. 10%, respectively (p=0.17). Additionally, the HCV+ recipients had a trend toward a higher incidence of sepsis-related mortality compared with HCV- recipients, 20 vs. 5%, respectively (p=0.19). Renal allograft survival was 50% in the HCV+ group compared with 94% in the HCV- group (p=0.02). Pancreas allograft survival was not significantly different between the groups, 60 vs. 80%, respectively (p=0.24). At 3, 6, 12 months, and end of follow-up, there were no differences in serum creatinine, amylase, C-peptide, or fasting glucose levels. However, there was a significantly higher incidence of proteinuria at last follow-up in the HCV+ recipients with a renal allograft when compared with HCV- recipients, 50 vs. 12.5%, respectively (p=0.05). In order to maintain comparable glycemic control between the groups, there was a significant increase in oral hypoglycemic requirement in HCV+ recipients compared with HCV- recipients, 33 vs. 0%, respectively (p=0.01). These data suggest that HCV+ pancreas transplant patients may be at an increased risk of graft dysfunction and morbidity. Further studies with more patients and longer follow-up are needed to fully define the impact of HCV status on pancreas graft survival and function.
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PMID:Impact of hepatitis C virus status in pancreas transplantation: a case controlled study. 1209 79

Hepatitis C virus (HCV) infection is an important problem in the patient with end-stage renal disease. After transplantation, liver disease is more frequent in HCV-positive patients than in HCV-negative patients. In the long run, this leads to important liver complications. The patients have a higher risk for developing proteinuria and infections. Long-term patient and graft survival rates are lower in HCV-positive patients than in HCV-negative graft recipients. Mortality is higher, mainly as a result of liver disease and infections. Despite this, transplantation is the best option for the HCV-positive patient with end-stage renal disease. Transplantation of HCV-positive kidneys should be offered to HCV-positive recipients in whom HCV RNA is detected in the serum. Finally, several measures after transplantation minimize the consequences of HCV infection. Adjustment of immunosuppression and careful follow-up in the outpatient clinic for early detection of proteinuria, infection, or worsening of liver disease are mandatory.
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PMID:Hepatitis C virus infection and kidney transplantation. 1211 2

Three patients (one hepatitis C positive) presented with renal insufficiency and nephrotic-range proteinuria resulting from mixed cryoglobulinemia and glomerulonephritis. All three patients received two to four cycles of intravenous fludarabine (each cycle consisted of 25 to 50 mg/d for 4 to 5 days). All patients responded to therapy with a decrease in proteinuria, increase in serum albumin, and decrease in serum creatinine. This response was evident by 2 months and persisted for 2 to 5 years. In two patients, this response was accompanied by disappearance of cryoglobulins, at least transiently. One patient developed tuberculosis with neutropenia. Transient blindness and neutropenia were seen in another patient. These results suggest that fludarabine may be a useful treatment in cryoglobulinemia with glomerulonephritis, although its use may be accompanied by side effects.
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PMID:Fludarabine treatment of cryoglobulinemic glomerulonephritis. 1220 Aug 18

The purpose of this study was to examine the effect of pretransplant interferon administration on the occurrence of post-transplant de novo glomerulonephritis in hepatitis C virus (HCV)-positive renal allografts. From December 1992 to December 2000, 78 HCV-positive patients received a renal allograft in our unit. Fifteen out of 78 received pretransplant interferon for 1 year. Hepatitis C virus was investigated by serology and qualitative polymerase chain reaction (PCR). Hepatitis C virus-related de novo glomerulonephritis (membranoproliferative or membranous) was suggested by proteinuria (>1.5 g/24 h) and/or microhematuria and always diagnosed by renal biopsy. Of 15 HCV-positive recipients who received pretransplant interferon, 10 (67%) became HCV-RNA negative at the time of transplantation and only one out of the 15 (6.7%) developed de novo glomerulonephritis (this patient was HCV-RNA positive at transplantation). Among non-interferon-treated allograft recipients, 28.7% had negative HCV-RNA and 12 out of 63 (19%) developed de novo glomerulonephritis (9, membranoproliferative; 3 membranous), all 12 having positive HCV-RNA at transplantation (p < 0.0001). In conclusion, pretransplant interferon may reduce the occurrence of post-transplant HCV-related de novo glomerulonephritis. Our results suggest that the indication for pretransplant interferon should be extended to treat all HCV-RNA positive candidates for renal transplantation.
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PMID:Pretransplant interferon prevents hepatitis C virus-associated glomerulonephritis in renal allografts by HCV-RNA clearance. 1261 94

A 72-year-old female was admitted to our hospital for massive proteinuria. She had previously been diagnosed with hepatitis C virus (HCV) infection and macroglobulinemia. Renal histological examination demonstrated membranoproliferative glomerulonephritis (MPGN), and type 2 cryoglobulinemia was positive in her serum. It is generally recognized that MPGN is the most common nephritis associated with HCV infection and cryoglobulinemia, but this is the first report of an HCV-infected patient with macroglobulinemia associated with MPGN. After treatment with prednisolone and melphalan, proteinuria disappeared, but macroglobulinemia and cryoglobulinemia were not improved.
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PMID:Macroglobulinemia and membranoproliferative glomerulonephritis in a hepatitis C virus-positive patient. 1287 58

Cardiovascular diseases (CVD) have become the leading cause of mortality in renal transplant recipients. Well-known cardiovascular (CV) risk factors and graft dysfunction both play an important role in the development of the posttransplantation CV events. We studied 233 stable kidney transplant patients to establish the prevalence of CVD and to assess CV risk factors that can be evaluated (and modified) in daily clinical practice. While 6.2% of the patients had coronary heart disease (CHD) before the transplantation, 16% displayed at least 1 CV event posttransplantation. The most significant factors associated with CV events were as follows: gender, length of smoking, diabetes mellitus, hepatitis C virus antibodies (HCV), dyslipidemia, proteinuria, and serum creatinine levels.
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PMID:Risk factors for cardiovascular disease after renal transplantation. 1296 71

We describe a treatment made with interferon-alpha (IFN-alpha) plus ribavirin of two patients with membranoproliferative glomerulonephritis (MPGN) induced by hepatitis C virus (HCV): case # 1 was a 22-yr-old woman with leg and facial edema, hypertension and proteinuria, whose liver biopsy revealed chronic active hepatitis; and case # 2 was a 42-yr-old man with anasarca, hypertension and proteinuria, whose liver biopsy indicated cirrhosis. Both had anti-HCV, HCV-RNA and cryoglobulins. IFN-alpha (3 million units (MU), 3 times/week) and ribavirin (1 g/day) were administered for 12 months. The drugs were well tolerated by both patients. Serum alanine aminotransferase (ALT) levels normalized and HCV-RNA became negative. Cryoglobulins disappeared and an improvement in renal disease was seen after 6 months of therapy. However, after 9 months, case # 2 presented ALT elevation, and proteinuria was detected. Two years after the end of therapy, both patients were negative in repeated HCV-RNA and cryoglobulin tests. Case # 1 was asymptomatic, with normal liver and renal tests, and case # 2 had normal blood pressure, with mild edema of the ankles. Based on the evolution of these two cases, the association of IFN-alpha and ribavirin may be a therapeutic option for patients with MPGN related to HCV.
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PMID:Therapy with interferon-alpha plus ribavirin for membranoproliferative glomerulonephritis induced by hepatitis C virus. 1455 46

Recent epidemiological evidence suggests an association between HCV infections and immunologically mediated renal disease. A high seroprevalence of anti-HCV has been observed in patients with glomerulonephritis in several countries including, Japan, Italy, America and Spain. However, a study in France did not show such association but increased seroprevalence of anti-HCV has been reported in patients with end-stage renal disease (ESRD) on chronic haemodialysis when compared with normal population suggesting that dialysis patients might be at higher risk of acquiring this infection. Anti-HCV seroprevalence has been found to increase with the duration of dialysis and the number of units of blood transfused raising the possibility of both transfusion and nosocomial transmission of HCV. A greater seroprevalence of anti-HCV has also been reported in predialytic chronic renal failure (CRF) patients independent of blood transfusion when compared with patients without renal disease and the normal population. The mechanism underlying hepatitis C induced renal damage is not certain. However, most evidence suggests that glomerular injury results from the deposition of circulating immune complexes (CICs) containing hepatitis C antibodies, hepatitis C antigens and complement mainly C3 within the sub-endothelium and mesangium. The optimal treatment strategy for hepatitis C-associated renal diseases remains to be defined but treatment has been associated with improvement in the level of proteinuria and variable response in serum creatinine levels using some antiviral agents.
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PMID:Hepatitis C virus (HCV) and chronic renal disease. 1503 90


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