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Kidney disease is a major complication of viral infection, which can cause both acute and chronic kidney diseases via different mechanisms such as immune-mediated injury, kidney cell injury from a direct viral infection, systemic effects, and antiviral drug-induced nephrotoxicity. HIV-associated nephropathy (HIVAN), characterized by collapsing focal segmental glomerulosclerosis (cFSGS), has been described 2 decades ago as a major complication of acquired-immunodeficiency syndrome. The pathogenesis of HIVAN has been well studied, including viral entry, host response, and genetic factors. The incidence of this disease has been dramatically dropped with current antiretroviral therapy. In the recent severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) pandemic, acute kidney injury was also found to be a major complication in patients with (coronavirus disease) COVID-19. These patients also developed glomerular disease such as cFSGS in African Americans with apolipoprotein L1 risk alleles, similar to HIVAN. Whether SARS-CoV-2 can infect kidney cells locally remains controversial, but both local infection and systemic effects are likely involved in the pathogenesis of this disease. In this review, we present a comparison of the clinical presentations, pathological findings, disease mechanisms, and potential treatments between HIVAN and COVID-19. Leveraging the knowledge in HIVAN and experimental approaches used to study HIVAN will facilitate the exploration in the pathogenesis of COVID-19-associated kidney disease and improve our management of COVID-19 patients.

Sheena Pramod, Murad Kheetan, Iheanyichukwu Ogu, Ahlim Alsanani, Zeid Khitan Division of Nephrology, Department of Internal Medicine, Joan C Edwards Marshall University School of Medicine, Huntington, WV, USACorrespondence: Sheena PramodJoan C Edwards Marshall University School of Medicine, 1690 Medical Center Drive, Huntington, WV, 25701, USATel + 1 3045262532Email surindran@marshall.eduAbstract: Viral infections in the immunocompetent host can cause both acute and chronic kidney disease either as a direct damage to the infected kidney cells or as a consequence of systemic immune responses that impact kidney function. Since identifying these entities in the 1970s and 80s, major breakthroughs in the understanding of the viral mechanisms have occurred. Viruses have evolved mechanisms to hijack signaling pathways of infected cells to evade antiviral immune responses by the host. Over time, the clinical presentations and management of these diseases have evolved along with our in-depth understanding of the various pathophysiological mechanisms causing these conditions. Similarly, both at the cellular and systemic levels, the host has evolved mechanisms to counter viral subversion strategies for mutual survival. Since the start of the current COVID-19 pandemic, numerous cases of acute kidney injury have been reported in the literature with various possible pathophysiological mechanisms. In this review, we summarize lessons learned from prior viral pandemics related to viral mechanisms utilized in the pathogenesis of numerous renal manifestations to attempt to utilize this knowledge in predicting post-COVID-19 kidney disease.Keywords: viral nephropathy, COVID-19, viral immunogenicity, hepatitis B, hepatitis C, HIV, SARS-CoV-2

The article focuses on hepatitis C virus (HCV) and its association with a large spectrum of histopathological lesions and clinical sequelae, in both native and transplanted kidneys. According to the author, several studies reveal that the majority of patients with type II mixed essential cryoglobulinaemia were victims of HCV infection. A table that offers information on renal lesions associated with HCV infection is presented.

Type I interferon (IFN-I) mediates tissue damage in a wide range of kidney disorders, directly affecting the biology and function of several renal cell types including podocytes, mesangial, endothelial, and parietal epithelial cells. Enhanced IFN-I signaling is observed in the context of viral infections, autoimmunity (e.g., systemic lupus erythematosus), and type 1 interferonopathies, rare monogenic disorders characterized by constitutive activation of the IFN-I pathway. All these IFN-I-related disorders can cause renal dysfunction and share pathogenic and histopathological features. Collapsing glomerulopathy, a histopathological lesion characterized by podocyte loss, collapse of the vascular tuft, and parietal epithelial cell proliferation, is commonly associated with viral infections, has been described in type 1 interferonopathies such as Aicardi-Goutières syndrome and stimulator of IFN genes-associated vasculopathy with onset in infancy, and can also be induced by recombinant IFN therapy. In all these conditions, podocytes and parietal epithelial cells seem to be the primary target of IFN-I-mediated damage. Additionally, immune-mediated glomerular injury is common to viral infections, systemic lupus erythematosus, and type 1 interferonopathies such as coatomer subunit-α syndrome (COPA) and DNASE1L3 deficiency, diseases in which IFN-I apparently promotes immune-mediated kidney injury. Finally, kidney pathology primarily characterized by vascular lesions (e.g., thrombotic microangiopathy and vasculitis) is a hallmark of type 1 interferonopathy adenosine deaminase 2 deficiency as well as of systemic lupus erythematosus, viral infections, and IFN therapy. Defining the nosology, pathogenic mechanisms, and histopathological patterns of IFN-I-related kidney disorders has diagnostic and therapeutic implications, especially considering the likely near-term availability of novel drugs targeting the IFN-I pathway., (Copyright © 2022 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.)

Kidney disease is a major complication of viral infection, which can cause both acute and chronic kidney diseases via different mechanisms such as immune-mediated injury, kidney cell injury from a direct viral infection, systemic effects, and antiviral drug-induced nephrotoxicity. HIV-associated nephropathy (HIVAN), characterized by collapsing focal segmental glomerulosclerosis (cFSGS), has been described 2 decades ago as a major complication of acquired-immunodeficiency syndrome. The pathogenesis of HIVAN has been well studied, including viral entry, host response, and genetic factors. The incidence of this disease has been dramatically dropped with current antiretroviral therapy. In the recent severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) pandemic, acute kidney injury was also found to be a major complication in patients with (coronavirus disease) COVID-19. These patients also developed glomerular disease such as cFSGS in African Americans with apolipoprotein L1 risk alleles, similar to HIVAN. Whether SARS-CoV-2 can infect kidney cells locally remains controversial, but both local infection and systemic effects are likely involved in the pathogenesis of this disease. In this review, we present a comparison of the clinical presentations, pathological findings, disease mechanisms, and potential treatments between HIVAN and COVID-19. Leveraging the knowledge in HIVAN and experimental approaches used to study HIVAN will facilitate the exploration in the pathogenesis of COVID-19-associated kidney disease and improve our management of COVID-19 patients., Competing Interests: All authors in this article declare that they have no competing financial interests. J.C.H. is currently an associate editor of this journal., (Copyright © 2021 by S. Karger AG, Basel.)

Evolving BK polyomavirus–associated nephropathy (BKPyVAN) is characterized by tubulointerstitial inflammation that closely resembles acute T‐cell–mediated allograft rejection if tubulitis is significant. The cellular composition of the inflammation varies during the course of BKPyVAN, and clusters of plasma cells may herald resolution of the infection. Less commonly, BKPyVAN can present with a predominance of histiocytes and granuloma formation. Granulomatous interstitial nephritis is uncommon in biopsies of either native or transplant kidneys. In both settings, this distinctive type of inflammatory response requires a systematic approach with careful clinicopathological assessment to determine its etiology. We present three patients with granulomatous BKPyVAN in the first year post‐transplantation. These allograft biopsies at 4, 6, and 12 months post‐transplant exemplify spontaneously resolving BKPyVAN, resolving infection after immunosuppression reduction, and early BKPyVAN, respectively. In immunosuppressed patients, BKPyVAN should be added to the relatively broad differential diagnosis of granulomatous tubulointerstitial nephritis. [ABSTRACT FROM AUTHOR]