Viral-Associated GN: Hepatitis C and HIV

Abstract

Viruses are capable of inducing a wide spectrum of glomerular disorders that can be categorized on the basis of the duration of active viremia: acute, subacute, or chronic. The variable responses of the adaptive immune system to each time period of viral infection results mechanistically in different histologic forms of glomerular injury. The unique presence of a chronic viremic carrier state with either hepatitis C (HCV) or HIV has led to the opportunity to study in detail various pathogenic mechanisms of viral-induced glomerular injury, including direct viral infection of renal tissue and the development of circulating immune complexes composed of viral antigens that deposit along the glomerular basement membrane. Epidemiologic data show that approximately 25%-30% of all HIV patients are coinfected with HCV and 5%-10% of all HCV patients are coinfected with HIV. This situation can often lead to a challenging differential diagnosis when glomerular disease occurs in this dual-infected population and requires the clinician to be familiar with the clinical presentation, laboratory workup, and pathophysiology behind the development of renal disease for both HCV and HIV. Both of these viruses can be categorized under the new classification of infection-associated GN as opposed to being listed as causes of postinfectious GN as has previously been applied to them. Neither of these viruses lead to renal injury after a latent period of controlled and inactive viremia. The geneses of HCV- and HIV-associated glomerular diseases share a total dependence on the presence of active viral replication to sustain renal injury so the renal disease cannot be listed under "postinfectious" GN. With the new availability of direct-acting antivirals for HCV and more effective combined antiretroviral therapy for HIV, successful remission and even regression of glomerular lesions can be achieved if initiated at an early stage.

Successful recovery of associated interstitial nephritis and focal segmental glomerulosclerosis in patients with HCV and HIV treated with sofosbuvir and daclatasvir and revision of literature

“…Current guidelines suggest the correction of risk factors in case of secondary disease [ 14 ], but in our case, the patient had already stopped intravenous drugs abuse and achieved HIV-RNA suppression with ART when symptoms appeared. Additionally, steroid treatment is recommended as the first-line regimen for autoimmune renal diseases, and it may be withdrawn after a period of clinical stability, as it can lead to remission [ 15 ].…”

Clinical and pathological findings of SARS-CoV-2 infection and concurrent IgA nephropathy: A case report

“…Viral infections may exacerbate glomerular disease, such as immune-complex-mediated glomerulopathies related to HCV infection and collapsing glomerulopathy (CG) related to HIV infection (18). Importantly, recent studies show that African American patients with COVID-19 who carried the APOL1 gene risk variant developed CG, which raise the possibility that COVID-19 can induce glomerular disease (19,20).…”

APOL1 variant-expressing endothelial cells exhibit autophagic dysfunction and mitochondrial stress

“…However, exaggerated APOL1 expression beyond that expected in native cells poses a limitation on the clinical interpretation of these results. Moreover, viruses themselves can not only induce APOL1 expression but also engage other autophagy pathways, making it difficult to assign risk variant-mediated effects [45] Therefore, HUVECs naturally expressing the variants were utilized acknowledging shortcomings inherent in this approach as well.…”