key: cord-0802071-geqkvkat
authors: Wan, Elizabeth R.; Woolfson, Robin G.; Greenwood, Richard; Walsh, Stephen B.
title: Transient Renal Tubular Syndromes Associated with Acute COVID-19 Disease
date: 2020-07-08
journal: Kidney Int Rep
DOI: 10.1016/j.ekir.2020.06.037
sha: 6acc0502633840c55e556307d539d56830e44703
doc_id: 802071
cord_uid: geqkvkat

nan

We report two transient renal tubular syndromes associated with COVID19 disease.

A 47-year old patient in a neurorehabilitation unit was diagnosed with COVID-19 following onset of respiratory symptoms and pyrexia, confirmed by RT-PCR. Ten days later, he developed hypernatraemia with an acute kidney injury (AKI). He was exclusively fed by percutaneous endoscopic gastrostomy (PEG) tube.

Investigations (Table 1 ) supported a diagnosis of nephrogenic diabetes insipidus.

He was managed with increased enteral water intake via the PEG and intravenous 5% dextrose over 24 hours. Biochemistry improved progressively, with serum sodium renal function returning to baseline by Day 23.

A 52-year-old lady with diabetic nephropathy and a kidney-pancreas transplant was recovering from a below-knee amputation. She developed fever and a cough; RT-PCR confirmed SARS-CoV-2 infection. Three days later, she developed a severe metabolic acidosis associated with profound hypophosphatemia, hyperphosphaturia and low molecular weight proteinuria, diagnostic of the renal Fanconi syndrome (Table 1) . She required aggressive intravenous potassium, bicarbonate and phosphate supplementation; she was weaned off all supplementation by day 18.

Kidney disease is widely recognized in COVID-19; there is evidence of direct viral invasion of the tubular epithelium 1,2 . ACE2, the ligand for viral cell invasion, is expressed on both proximal and distal tubular cells 3 . The first patient had a distal lesion (nephrogenic diabetes insipidus); the second had proximal tubular dysfunction.

These renal tubular syndromes support a direct toxic effect of the virus on the tubular epithelium. The prevalence and consequences of tubular dysfunction in COVID-19 is worthy of further study. 

Renal histopathological analysis of 26 postmortem findings of patients with COVID-19 in China

Ultrastructural Evidence for Direct Renal Infection with SARS-CoV-2

Renal ACE2 expression in human kidney disease