Hepatitis C (HCV) can cause kidney injury through immune complexes, cryoglobulins, and direct viral effects, leading to acute kidney injury (AKI) and accelerating chronic kidney disease (CKD). HCV increases cardiovascular and liver-related mortality in dialysis patients and raises the risk of acute post-transplant complications, compromising long-term graft survival. Direct-acting antivirals (DAAs) are effective treatments for HCV at various stages of kidney disease, but limited availability in endemic regions necessitates treatment prioritization.
HCV leads to kidney disease via immune complex deposition, direct viral invasion, and renal complications from extrarenal manifestations. Acute kidney disease often progresses to AKI, especially in patients with cryoglobulinemic vasculitis or undergoing treatment. Chronic HCV infection significantly raises the risk of AKI, particularly in patients with other complications. In dialysis settings, HCV spreads mainly through inadequate hygienic measures, affecting patient survival. In kidney transplant recipients, HCV increases the risk of acute transplant glomerulopathy, vascular rejection, and long-term complications such as lymphoproliferative disease, diabetes, and liver failure. Effective use of DAAs can improve outcomes for dialysis and transplant patients in HCV-endemic areas.
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