Viral Nephropathies: Core Curriculum 2024

Abstract

Viral-associated nephropathy is when kidney disease results from active viral replication. Because of the high global burden of viral infections, clinicians should be aware of their incidence, kidney manifestations, mechanism of injury, and management. Some viruses, such as hepatitis B, hepatitis C, human immunodeficiency virus (HIV), and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), can lead to nephropathy more commonly than other endemic viruses, such as Epstein-Barr virus, cytomegalovirus, and polyoma virus which are more important causes of nephropathy in the immunosuppressed patient. Other viruses, such as hantavirus and dengue virus, have a high global infectivity rate with rare but severe kidney manifestations. Advances over the past decades have offered us a better understanding of the pathogenesis of viral-associated nephropathies and antiviral therapy options. The patterns of kidney injury include glomerular and tubulointerstitial lesions in the setting of acute and chronic infection. Direct viral infection of kidney parenchymal cells may drive pathologic findings, but kidney pathology may also result from indirect mechanisms due to activation of the innate and adaptive immune system. Some viruses can cause kidney injury due to altered hemodynamics from liver dysfunction or shock. More information about the role of genetics, specifically APOL1 polymorphisms, has come to light in regard to HIV-associated nephropathy and SARS-CoV-2–associated nephropathy. Advances in antiviral therapy help reduce nephrotoxicity and improve morbidity and mortality. In this Core Curriculum, we review common viruses responsible for kidney disease worldwide, discuss mechanisms of pathogenesis, and highlight specific management principles of viral nephropathies. We also discuss other viruses with high endemicity despite low incidence of kidney disease in the immunocompetent and immunosuppressed host.