Abstract
Hepatitis C virus (HCV) infection is frequently associated with extrahepatic disorders, among which renal diseases are frequent. This article highlights the most frequent HCV-associated renal disorders, the impact of HCV infection on chronic renal disease and renal transplantation, and the role of current direct-acting antiviral therapies. HCV is associated with membranoproliferative glomerulonephritis, acceleration of end-stage renal diseases in patients with glomerulopathies, and a higher risk of death in patients affected by chronic kidney disease. Before the introduction of direct-acting antiviral drugs as treatment modality, renal transplantation was a challenging clinical problem because the drugs available until 2011 obtained a poor sustained virologic response, had several side effects, and caused acute rejection when used after transplantation. The knowledge of the viral structure and its replication allowed the discovery of new classes of direct-acting antiviral drugs that revolutionized this scenario. These new drugs are comparatively more effective and safer. Accumulating evidence suggests that it is possible to cure HCV-related glomerulonephritis, and obtain a sustained virologic response in patients with renal failure, or on dialysis, before commencing transplantation. Finally, it became possible to transplant HCV-positive kidneys into HCV-positive or HCV-negative recipients.
Highlights
Hepatitis C virus (HCV) infection is a relevant health issue with 150–170 million people chronically infected worldwide [1]
HCV may cause chronic kidney disease (CKD) via specific forms of glomerulonephritis (GN), primarily membranoproliferative GN (MPGN) which is associated with mixed cryoglobulinemia (MC)
The use of sofosbuvir is only recommended for patients with an estimated glomerular filtration rate (eGFR) >30/mL/min, and investigations on the use of sofosbuvir in patients with end-stage renal disease (ESRD) are underway
Summary
Hepatitis C virus (HCV) infection is a relevant health issue with 150–170 million people chronically infected worldwide [1]. HCV may cause chronic kidney disease (CKD) via specific forms of glomerulonephritis (GN), primarily membranoproliferative GN (MPGN) which is associated with mixed cryoglobulinemia (MC) In such cases, MC represents HCV/anti-HCV immune complex in association with rheumatoid factor (RF) and complement [8]. A study by Lai et al [24] demonstrated that chronic HCV infection is an independent risk factor for the development of ESRD in patients with genotype 1. In another study [51], tubulointerstitial changes were frequently observed in HCV-infected patients, and the viral antigens and HCV-RNA were detected in the tubulointerstitium of these patients. The most frequently reported HCV-related adverse events after kidney transplantation are acute and chronic graft dysfunction, infections, posttransplant diabetes mellitus (PTDM), posttransplant lymphoproliferative disease, and GN [57]. There are four classes of DAA agents based on their mechanisms of action (Table 3)
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