Purpose of reviewIn this paper, we seek to review coronavirus disease 2019 (COVID-19) associated kidney injury with a focus on what is known about pathophysiology.Recent findingsKidney injury is a common complication of SARS-CoV-2 infection and is associated with increased morbidity and mortality. Acute tubular necrosis and glomerular injury are two common findings. Direct viral effect, endothelial dysfunction, and podocyte and tubular epithelial injury have been described. COVID-19-related glomerular injury may also be associated with high-risk APOL1 genotype.SummaryData on COVID-19 renal involvement have suggested novel mechanisms of kidney injury that need to be further elucidated. More data are needed on renal involvement in milder disease, renal-specific therapeutic interventions, and long-term sequelae.

Iron is a key element for normal cellular function and plays a role in many cellular processes including mitochondrial respiration. The role of iron deficiency (ID) in heart failure (HF) has been a subject of debate amid increasing advocacy for intravenous (IV) supplementation. Both the definition and the approach to treatment of ID in HF have been adapted from the experience in patients with chronic kidney disease (CKD). In this review, we highlight the differences in regulatory mechanisms as well as pathophysiology of ID in CKD and HF population both at the systemic and cellular levels. We will review the major clinical trials in HF patients that have shown symptomatic benefit from IV iron supplementation but without effect on clinical outcomes. Intravenous iron loading bypasses the mechanisms that tightly regulate iron uptake and can potentially cause myocardial and endothelial damage by releasing reactive oxygen species. By contrast, newer oral iron preparations do not have similar toxicity concerns and might have a role in heart failure.

BackgroundIt is well established that the incidence of focal segmental glomerular sclerosis (FSGS) increased from 1970–1990 to become the leading primary glomerular disease in patients of African descent.MethodsTo determine whether this trend has continued in the past years in Chicago, adult, native kidney biopsies from January 2001 to December 2011 at our hospital were reviewed and collected relevant clinical information in patients with a primary glomerular disease including FSGS, membranous nephropathy (MN), minimal change disease (MCD), membranoproliferative glomerulonephritis (MPGN), and IgA nephropathy (IgAN).ResultsIn the 204 patients analyzed, MN was the most prevalent (32.7%), followed by FSGS (29.7%), IgAN (15.8%), MCD (14.4%), and MPGN (4.5%). Patients with MN had the highest proteinuria (7.9 gms/d) and were significantly older, more edematous, hypoalbuminemic, and hypercholesterolemic than those with FSGS. In both African Americans and Hispanics, MN was the most prevalent primary glomerular lesion at 39.2% and 34% respectively.ConclusionsComparable in size to prior cohorts of African Americans and Hispanics, our report demonstrates a reversal in the incidence of FSGS and MN in both ethnic groups where MN is now more prevalent. To our knowledge, this is the first demonstration of a reverse in the upward trend of the prevalence of FSGS in African Americans.

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