Glomerular disease during HCV infection in renal transplantation

Hammoud, Hacene; Haem, J.; Laurent, B.; Alamartine, Éric; Diab, Nabil; Defilippis, J. P.; Berthoux, P; Berthoux, F

doi:10.1093/ndt/11.supp4.54

Cited by 53 publications

(30 citation statements)

References 5 publications

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“…Altogether, our findings clearly show that a HCV-positive status is associated with an adverse outcome in renal transplant patients, as well as for renal survival after renal transplant. Our findings are in agreement with the findings of earlier similar studies [4, 5, 8, 13, 15, 29,31,32,33,34,35,36]. …”

Section: Discussionsupporting

confidence: 94%

“…In recent years, tremendous improvement has taken place in the short-term, 1-year survival of renal allograft due, mainly, to improved medical care and advanced therapeutic strategies. Apart from other risk factors, hepatitis virus infection is one of the important risk factors for the long-term deterioration of kidney function, reduced long-term graft and patient survival [2, 6, 8, 13, 29,31,32,33,34] and an increased incidence of graft rejection [5, 13, 15]. In contrast, several studies have shown no significant difference regarding graft and patient survival in HCV-positive and HCV-negative patients [10, 19, 35] and recommended renal transplant from/or to the HCV-positive patients.…”

Section: Discussionmentioning

confidence: 99%

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Effect of Chronic Viral Hepatitis on Graft Survival in Saudi Renal Transplant Patients

Mitwalli¹,

Alam

Al-Wakeel³

et al. 2005

Nephron Clin Pract

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Background: In Saudi Arabia the prevalence of hepatitis C among hemodialysis patients is very high ranging from 60 to 80%. A large number of these dialysis patients go for renal transplant, resulting into a higher prevalence of hepatitis C virus (HCV) infection in renal transplant patients. Yet no current systematic report is available on the influence of hepatitis C status on patient and graft survival. The present study was therefore undertaken to address this objective. Methods: Retrospective analysis of data of 448 renal transplantation subjects was undertaken. The mean follow-up period was 5.85 ± 2.7 (median 5.3) years. The factors associated with renal graft survival were reviewed and these include: age, sex, and type of donor, immunosuppressive medication, episodes of infection, blood pressure, serum creatinine, and status of hepatitis. The primary end-points were renal graft function and patient survival. Logistic regression, COX regression analysis, and Kaplan-Meier survival estimates were used to evaluate the influence of hepatitis C on the above parameters. Results: Among 448 recipients of first kidney transplant patients, 286 (63.8%) were positive for HCV infection. In the HCV-positive group, 204 (71.32%) were males. Kaplan-Meier survival analysis showed a significantly better graft survival for HCV-negative patients than HCV-positive patients (p < 0.001; log-rank test). Logistic regression analysis and COX regression analysis have shown different grades of graft dysfunction were present in HCV-positive patients after adjustment for covariates: age, sex, blood pressure, type of donor, and immunosuppressive medication; the presence of HCV was a major predictor of bad outcome and significantly influenced graft survival (odds ratio = 4.37; 95% Cl = 1.81–4.77). Significant deterioration of liver function was noted in HCV-positive patients at the last follow-up, taking ALT as a marker (ALT level 80.6 ± 5.8 U/l at the last follow-up versus 49.5 ± 32 U/l at baseline p ≤ 0.0001). Sixteen patients had a chronic active course and 1 patient developed biopsy-proven liver cirrhosis and portal hypertension. A serious and significantly greater incidence of fatal chest infections was seen in HCV-positive patients. Although mortality was greater in HCV-positive versus HCV-negative patients (20 vs. 7), the difference did not attain statistical significance (p = 0.23) and none of the patients died as a result of hepatic failure. Conclusion: The presence of HCV infection greatly influenced graft survival in renal transplant patients and a higher proportion of infected patients had renal and hepatic dysfunction. A significant increase in fatal chest infections was noted in HCV-positive patients. Overall mortality was higher in HCV-positive patients, but it was not statistically significant. All measures should be taken to prevent HCV transmission in the dialysis population. Renal transplant recipients with HCV infection need close monitoring for both graft and liver function.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Effect of Chronic Viral Hepatitis on Graft Survival in Saudi Renal Transplant Patients

Mitwalli¹,

Alam

Al-Wakeel³

et al. 2005

Nephron Clin Pract

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“…De novo Ig-mediated MPGN develops uncommonly after transplantation and is associated with HCV in about one half of cases (34). In a French series, only 13 of 399 renal transplant recipients developed a de novo MPGN (35). Renal biopsy showed the typical MPGN pattern of mesangial hypercellularity accompanied by broadening of the peripheral capillary loops caused by reduplication of the GBM.…”

Section: Membranoproliferative Gnmentioning

confidence: 99%

De Novo Glomerular Diseases after Renal Transplantation

Ponticelli

Moroni

Glassock

2014

Clinical Journal of the American Society of Nephrology

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Glomerular diseases developing in the kidney allograft are more often recurrences of the original disease affecting the native kidneys. However, in an undefined number of cases de novo, glomerular diseases unrelated to the original disease in the native kidneys can develop in the transplanted kidney. The clinical presentation and histologic features of de novo diseases are often similar to those features observed in patients with primary or secondary GN in the native kidneys. However, in transplanted kidneys, the glomerular, vascular, and tubulointerstitial changes are often intertwined with structural abnormalities already present at the time of transplant or caused by antibody-or cell-mediated allograft rejection, immunosuppressive drugs, or superimposed infection (most often of a viral nature). The pathophysiology of de novo glomerular diseases is quite variable. In rare cases of de novo minimal change disease, circulating factors increasing the glomerular permeability likely participate. Maladaptive hemodynamic changes and tissue fibrosis caused by calcineurin inhibitors or other factors may be involved in the pathogenesis of de novo FSGS. The exposure of cryptic podocyte antigens may favor the development of de novo membranous nephropathy. Many cases of de novo membranoproliferative GN are related to hepatitis C virus infection. Patients with Alport syndrome lacking antigenic epitopes in their glomerular basement membrane may develop antibodies against these glomerular basement membrane antigens expressed in the transplanted kidney. Infection may cause acute GN to have a heterogeneous clinical presentation and outcome. De novo pauci-immune GN in renal transplant is rare. Preexisting or acquired intolerance to glucose may, in the long term, cause diabetic nephropathy. The prognosis of de novo diseases depends on the type of GN, the severity of lesions caused by the alloimmune response, or the efficacy of immunosuppressive therapy. In most cases, the management of de novo glomerular diseases is empirical or elusive.

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“…Types II and III cryoglobulinemias are systemic vasculitides, and nearly half of the HCV-infected patients who have type II or III cryoglobulinemia develop renal complications, including membranoproliferative glomerulonephritis and membranous nephropathy (42). Therefore, in addition to its direct effects on the liver, HCV infection increases posttransplantation morbidity by enhancing the risk for de novo or recurrent HCV-associated glomerulopathies (43)(44)(45)(46)(47). Recurrence of HCV-associated kidney disease has the potential to adversely affect graft survival and has been linked to higher serum creatinine levels (44,48).…”

Section: Hcv-associated Posttransplantation Glomerulopathiesmentioning

confidence: 99%

The Kidney Transplant Recipient with Hepatitis C Infection

Terrault

Adey

2007

Clinical Journal of the American Society of Nephrology

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Liver disease secondary to chronic hepatitis C virus (HCV) infection is an important cause of morbidity and mortality in dialysis patients and kidney transplant recipients. Evaluation of patients with chronic HCV infection is warranted to determine stage of disease and the need for HCV therapy. Although combination therapy with interferon (IFN) plus ribavirin is the standard of care for chronic HCV infection, IFN monotherapy is recommended in dialysis patients because ribavirin is contraindicated in the presence of renal failure. The goals of pretransplantation HCV therapy are to decrease the risk for progression of HCV-associated liver disease, stabilize renal function in patients with HCV-related glomerulopathy, and prevent development of HCV-associated renal disease after transplantation. Posttransplantation HCV therapy is generally not recommended because of concerns regarding risk for precipitating acute rejection; however, antiviral therapy may be indicated to treat HCV-related glomerulopathy or prevent progression of chronic hepatitis C in patients with more advanced stages of fibrosis. When treatment is required, restored renal function allows use of combination therapy with IFN and ribavirin. Limitations of current HCV therapy include lack of tolerability and suboptimal response rates. New antiviral agents that can be used in dialysis patients (e.g., ribavirin alternatives) and in the posttransplantation setting (e.g., IFN alternatives) are needed to improve outcomes in these populations.

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Glomerular disease during HCV infection in renal transplantation

Cited by 53 publications

References 5 publications

Effect of Chronic Viral Hepatitis on Graft Survival in Saudi Renal Transplant Patients

Effect of Chronic Viral Hepatitis on Graft Survival in Saudi Renal Transplant Patients

De Novo Glomerular Diseases after Renal Transplantation

The Kidney Transplant Recipient with Hepatitis C Infection

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