Glucocorticoids Induce Partial Remission of Focal Segmental Glomerulosclerosis but Not Interstitial Nephritis in COVID-19 Acute Kidney Injury in an APOL1 Low-Risk Genotype White Patient

Abstract

Patient: Male, 34-year-old Final Diagnosis: Focal segmental glomerulosclerosis Symptoms: Acute kidney injury • nephrotic syndrome Medication: — Clinical Procedure: Kidney biopsy Specialty: Nephrology Objective: Rare coexistence of disease or pathology Background: COVID-19 can be complicated by kidney disease, including focal segmental glomerulosclerosis (FSGS), interstitial nephritis, and acute kidney injury (AKI). Almost all known cases of COVID-19-associated glomerulonephritis have been in patients of African descent, with G1 or G2 apolipoprotein L1 (APOL1) risk alleles, and they presented collapsing type of FSGS. Case Report: We report a case of biopsy-confirmed non-collapsing FSGS with secondary acute interstitial nephritis and AKI in a young White man with APOL1 low-risk genotype, who had COVID-19 pneumonia. His past history included arterial hypertension, anabolic steroids, and high-protein diet. He fully recovered from type 1 respiratory failure and AKI after transfusion of COVID-19 convalescent plasma and intravenous treatment with dexamethasone administered for 16 days in a dose reduced from 16 to 2 mg/day. Due to progressing severe nephrotic proteinuria (22.6 g/24 h), intravenous methylprednisolone was administered (1500 mg divided in 3 pulses over 3 days) immediately followed by oral prednisone (0.6 mg/kg body weight), with dose reduced 19 weeks later and switched to cyclosporine A (4 mg/kg body weight). Kidney re-biopsy, at that time, showed a decrease in proportion of glomeruli affected with podocytopathy, but progression of interstitial lesions. After 23 weeks of therapy, partial remission of FSGS was attained and proteinuria dropped to 3.6 g/24 h. After 43 weeks, proteinuria decreased to 0.4 g/24 h and the serum creatinine concentration remained steady. Conclusions: High-dose glucocorticoid therapy was effective in the initial treatment of COVID-19-related non-collapsing FSGS, but had no effect on interstitial changes. Introduction of cyclosporine A to the therapy contributed to remission of disease.

Rheumatoid Arthritis With Focal Segmental Glomerulosclerosis: A Case Report and Literature Review

“…Despite that, our patient developed mild COVID a few months after her initial flare of proteinuria and did not require any treatment or hospitalization. FSGS in our patient was discovered with her flares of RA, unrelated to the time of her COVID infection, which makes COVID-19 less likely the culprit of her nephrotic syndrome compared to her RA diagnosis of 30 years [27].…”

Renal Histopathological Lesions Associated with SARS-CoV-2 Infection in Patients with no History of Kidney Disease: A Systematic Review

“…Nowak et.al. [40] demonstrate that an unproportional immune response to the virus antigens may lead to cytokine storm, interferon release and mononuclear cells activation resulting in kidney inflammatory injury.…”

“…ACE2 is widely expressed not only in the lungs, but also in other vital organs such as the kidney, and it interacts with viral spike protein [21]. However, it is still being questioned whether the kidney damage is directly mediated by presence of the virus or by a secondary to immune response [40]. Diao et al [21] showed that SARS-CoV-2 nucleocapsid protein and spike antigens were found binding the ACE2 protein in the kidney tubules.…”