TABLE 1.

Summary of the type of reported kidney involvement during SARS-CoV-2 infection according to the underlying site of kidney damage.

Renal involvement	Features	Underlying condition	References	Commentaries
Prerenal azotemia	AKI Signs of ECV decrease FeNa <1% RBF decrease Favorable outcome after volume repletion	Hemodynamic changes Hypovolemia Venous congestion Mechanical ventilation	Chand et al., 2020,Xia et al., 2020,Watchorn et al., 2020,Mohamed et al., 2020
Tubular	AKI Low-range proteinuria Low molecular weight proteinuria ±Hypouricemia ±Hypophosphatemia ±Aminoaciduria	Ischemic ATI Sepsis-associated ATI Rhabdomyolysis	Werion et al., 2020,Kormann et al., 2020,Mohamed et al., 2020,Kudose et al., 2020,Santoriello et al., 2020,Sharma et al., 2020	No direct identification of SARS-CoV-2 (ISH, IHC, and PCR) (Unspecific microvesicular bodies on electron microscopy)
Glomerular	AKI Nephrotic-range proteinuria Albuminuria ±Hematuria	Collapsing glomerulopathy Membranous nephropathy Minimal change disease Anti-GBM GN Pauci-immune crescentic GN Chronic glomerulosclerosis	Kudose et al., 2020,Santoriello et al., 2020,Sharma et al., 2020,Wu et al., 2020,Gaillard et al., 2020	APOL-1 variant–associated collapsing glomerulopathy Role of interferon?
Vascular	AKI Hematuria ±Low-range proteinuria Severe COVID-19	Microvascular 6 cases of TMA Focal fibrin thrombi in 6/42 Macrovascular 2 cases of renal infarction Chronic vascular lesions	Jhaveri et al., 2020,Akilesh et al., 2020,Santoriello et al., 2020,Post et al., 2020	Evidence of complement activation in one case of TMA Evidence of multiple thrombosis in one case of renal infarction

In bold the most frequently reported lesions. AKI, acute kidney injury; ECV, extracellular volume; ATI, acute tubular injury; ISH, in situ hybridization; IHC, immunohistochemistry; GBM, glomerular basal membrane; GN, glomerulonephritis; TMA, thrombotic microangiopathy.