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.

Anaemia affects ~15.4% of patients with chronic kidney disease (CKD) in the US, an estimated 5.7 million people. 1,2 Anaemia prevalence increases with CKD stage, ranging from 8% at stage 1 to 53% at stage 5, 1 and with age, with 28% in patients aged 18-63 years and 50% in patients aged 66-85 years. 3 Race/ethnicity and sex also impact the prevalence of anaemia of CKD with increased risk in Black, Hispanic and female patients. 4

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Complement deposition is detected in kidney biopsies of various types of kidney disease. The type of complement fragments and the location along with other deposited materials describe mechanistically the pattern of glomerular injury encountered and point toward a specific type of glomerular disease. Glomerular disorders, where complement mediated glomerular injury has been documented, include immune complex (IC) mediated kidney disease as seen in lupus nephritis and certain types of membranoproliferative glomerulonephritis (MPGN), where the classic complement pathway is being activated. Other disorders can result from activation of the alternative pathway as in C3 glomerulopathy (C3G) and atypical hemolytic uremic syndrome (aHUS) where dysregulation of the alternative pathway is prominent, or the mannose-binding lectin pathway as in IgA nephropathy. Moreover, the complement system is involved directly and indirectly in several other glomerular disorders as in membranous nephropathy (MN) and ANCA associated vasculitis.Complement activation through any of the pathways leads to the proteolytic cleavage and activation of C3 to C3b. The full activation of any of the complement pathways generates C5b-9 (the membrane attack complex), a multimeric structure that form pores in the mem- branes of target cells causing injury and lysis. 1The renin-angiotensin-aldosterone system (RAAS) plays an important role in the pathogenesis of chronic kidney disease. Aliskerin is the first orally active, nonpeptide direct renin inhibitor approved for clinical use. 2 Interestingly, Aliskerin has been shown to attenuate tubulo-interstitial fibrosis suggesting significant renal tissue distribution of the drug. 3In addition, Aliskiren is known to have long half-life of 34-41 hours compared to other agents which provides an additional benefit of less frequent dosing. 4 In patients with diabetic nephropathy, this drug has been shown to have significant anti-proteinuric effect that was sustained for 2 weeks after withdrawal of the drug which cannot be explained by the plasma half-life or by the pharmacokinetics of this agent. 5,6 Recently, Bekassy et al 7 demonstrated a novel property of renin to cleave C3 in vitro into its physiological cleavage products C3b and C3a in a manner identical to C3 convertase activating the alternate complement pathway. They then demonstrated that this cleavage reaction by renin was specifically blocked by the renin inhibitor Aliskerin. In order to further test their theory in clinical practice, the authors demonstrated a favorable effects of Aliskiren in three patients with dense deposit disease (DDD) on levels of C3 and glomerular C3 deposition. 7 This brings to attention a possible mechanism by which Aliskiren and possibly other renin inhibitors can explain additional benefits in complement mediated renal disease apart from its established antiproteinuric and antifibrotic effects. Let's also keep in mind that the other members of the RAAS blockade family, the angiotensine converting enzyme inhibitors (ACEI's) a...