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Abstract: PO0040

Urinary Findings Reveal Dominant Tubular Injury in Hospitalized Patients with COVID-19

Session Information

Category: Coronavirus (COVID-19)

  • 000 Coronavirus (COVID-19)


  • Angel-Korman, Avital, Samson Assuta University Hospital, Ashdod, Israel
  • Leiba, Adi, Samson Assuta University Hospital, Ashdod, Israel

Renal manifestations during infection with SARS-CoV-2 are prevalent and include proteinuria and hematuria as well as acute kidney injury (AKI). Possible mechanisms of renal involvement with COVID-19 are acute tubular injury (ATI) due to cytokine storm, direct virus-induced tubulopathy or glomerular injury related to podocytopathy. However, a kidney biopsy or urine studies including direct urine microscopy have rarely been performed.
Our aim was to examine the urinalysis, level of protein excretion and microscopy findings in urine collected from hospitalized COVID-19 patients in order to better elucidate the nature of COVID-19 related kidney involvement.


We collected fresh urine samples from 92 patients admitted to the COVID-19 ward at Samson Assuta University Hospital in Israel. Urine samples were collected randomly, regardless of renal function or prior medical history. Urinalysis and urine chemistry were performed in addition to direct urine microscopy analyzed by an experienced nephrologist.


Urine samples were collected from 55 men and 37 women, most of whom (64%) had severe COVID-19 at the time urine samples were obtained. AKI at different levels of severity was diagnosed in 37 patients (40%). Proteinuria and hematuria were present in 43% and 38% of urinalysis samples, respectively, suggesting glomerular involvement. Urine protein to creatinine and albumin to creatinine ratios were measured in 76 patients (83%). Median urinary albumin to protein ratio (UATPR) was very low –0.16, indicating a tubular origin of the proteinuria. Direct urine microscopy was performed on 58 samples, of which granular casts were detected in 43% (25 samples) and in 5 of them granular casts were spotted without evidence of AKI. Additionally, uric acid crystals and amorphous urate were found in 19 (33%) of microscopy samples. Median urine pH was 5.5 which likely contributed to precipitation of uric acid.Notably, urine sediment clues of either nephrotic or nephritic syndrome were absent in all examinees.


Urinary sediment findings and a very low UATPR support ATI as the main mechanism for kidney injury in COVID-19 patients. Acidic urine and uric acid crystals may have resulted from viral related ACE2 down regulation, enhanced angiotensin II and aldosterone mediated urinary acidification. Further studies are needed to shed light on COVID-19 related kidney involvement.