MO166AUTOPTIC KIDNEY FINDINGS IN HOSPITALIZED PATIENTS WITH COVID-19

Abstract

BACKGROUND AND AIMS: SARS-CoV-2, isolated for the first time at the end of 2019, is the third human infecting Coronavirus found so far. Acute kidney injury (AKI) is the most common presentation when kidney is involved. There is evidence that kidney damage is determined through different pathological mechanisms. Has been observed that pathological kidney lesions can be due to the direct cytopathic effect of the virus on tubular cells or by pro-inflammatory cytokine storm. Aim of this observation is to evaluate the clinical and pathological patterns of kidney damage mediated by Coronavirus. METHOD: We analysed kidney autopsies of 4 patients with COVID-19 infection, hospitalized between March and April 2020, admitted to the Intensive Care Unit. The tissue samples have been observed by light microscopy and immunofluorescence. RTPCR SARS-CoV-2 was performed in all cases. RESULTS: CASE 1: female, 69 y; affected by obesity, previous ictus; smoking habit. Admitted for COVID-related pneumonia. At onset creatinine 0.45 mg/dl. Progression of lung failure and exitus after 3 days. Autopsy: diffuse alveolar damage. Renal autopsy: acute tubular necrosis; mild glomerular ischemia, lymphocyte T CD4+ parenchyma infiltration. CASE2: male, 66 y; affected by hypertension with cardiac involvement. Admitted for persistent fever. At onset creatinine 0.98 mg/dl. Nasopharingeal swab COVID-19 positive. Progression of lung failure and oligoanuric AKIn 3 (creatinine 4.5 mg/dl, urea 239 mg/dl), dialysis dependent. Exitus after one week for diffuse alveolar damage and sepsis. Renal autopsy: proximal and distal acute tubular moderate injury, mild diffuse glomerular ischemia, glomerular capillaritis, overlap chronic nephropathy. CASE 3: male 45 y; affected by obesity and diabetes. Admitted for COVID-related pneumonia with acute lung failure requiring ECMO. After one week developed AKIn 3 dialysis dependent. Exitus for cardio-respiratory arrest. Renal autopsy: diffuse acute tubular necrosis, glomerular capillaritis, overlap chronic diabetic nephropathy. CASE 4: male, 51 y; affected by CKD grade IV, hypertension, previous ictus; drug abuser. Admitted for AKIn 2 and COVID-related pneumonia. After 3 days progression of lung and renal failure requiring intubation and dialysis treatment. Exitus the day after for diffusive alveolar damage and lymphocytic myocarditis. Renal autopsy: diffused acute tubular necrosis, glomerular ischemia with mild tuft collapsing, diffuse infiltration of lymphocytes CD4+. In all cases light microscopy examination showed diffuse proximal tubular injury, with isomeric and non-isomeric vacuolar degeneration; collapsing tuft, and interstitial inflammation. Virus RNA performed by RT-PCR on kidney tissue was positive in all patients. Moreover in some cases our patients showed multi-systemic organ involvement: lung in 4 cases, heart in 1, liver in 1. CONCLUSION: Our observations show that the main pathological effect caused by Coronavirus is a direct cytopathic effect on the proximal tubules with variable degree of damage until acute tubular necrosis (ATN). In addition to this pathway, other factors contributing to kidney damage include systemic hypoxia, microvascular capillaritis. Associated sepsis can worse overall and renal survival. Previous comorbidities, especially obesity, diabetes, systemic hypertension and preexisting chronic renal failure, are significant negative prognostic factors.