RPS Case of the Month
Shreeram Akilesh, MD PhD
University of Washington
Seattle, United States of America
CLINICAL HISTORYThe patient is a 72-year-old female who had baseline normal serum creatinine of approximately 0.5 mg/dL. In the setting of only mild COVID-19 bronchopneumonia, she presented with acute kidney injury with creatinine up to 4.5 mg/dL, requiring initiation of hemodialysis. At the time of kidney biopsy, a repeat COVID-19 PCR was negative. The patient is a recent immigrant from West Africa.
KIDNEY BIOPSY FINDINGS
Figure 1. Collapsing glomerulopathy with prominence of podocytes overlying the collapsing capillary loops. Jones stain.
Figure 2. Three different patterns of acute tubular injury: epithelial attenuation (A), tubules engorged with lysosomes/reabsorption droplets (B) and microcystic tubular changes (C). Jones stain.
The immunofluorescence studies were negative.
Figure 3. Diffuse podocyte foot process effacement seen by electron microscopy. Some capillary loops also show subepithelial electron lucency as can be seen with severe podocyte injury.
The SARS-CoV-2 pandemic has infected millions of individuals in the US and caused hundreds of thousands of deaths. Individuals with kidney disease are at increased risk of morbidity and mortality (1, 2). Three pathologies have frequently been detected in autopsy and biopsy-based studies of kidney impairment in COVID-19 patients. These include acute tubular injury (“acute tubular necrosis”), collapsing glomerulopathy and acute endothelial cell injury/acute thrombotic microangiopathy (Figure 4). The association of COVID-19 with collapsing glomerulopathy, a usually rare and devastating kidney disease is particularly striking and has been termed COVAN (COVID-19 Associated Nephropathy) (3-6). As seen with HIV associated nephropathy (HIVAN), COVAN is strongly associated with high-risk APOL1 genotypes (6, 7), which have increased prevalence in Black and some Hispanic populations (8, 9). In addition, most of COVAN patients had mild COVID-19 symptoms and did not require intensive care (3, 4, 6, 10, 11), suggesting that the development of COVAN is independent of severe lung manifestations and other life-threatening complications. COVAN does appear to be devastating for the kidney, and the majority of reported COVAN patients progressed to end stage kidney disease and are dialysis-dependent (3, 4, 6, 10, 11). Though she was not genotyped, this patient was from West Africa, which has high prevalence of high risk APOL1 genotypes (12). At the time of this writing, she is dialysis-dependent and has been listed for transplant.
Figure 4.The three most common histologic patterns of kidney injury seen in COVID-19 patients.
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