key: cord-0808645-9xtgwplc
authors: Parmar, Malvinder S.
title: COVID-19–Associated Acute Kidney Injury
date: 2020-11-21
journal: Kidney Med
DOI: 10.1016/j.xkme.2020.09.006
sha: 378fc62d95f7cffa92b4304088b40474863432bf
doc_id: 808645
cord_uid: 9xtgwplc

nan

To the Editor:

In their case series of acute kidney injury (AKI) associated with COVID-19, Patel et al 1 proposed that a hypercatabolic state with muscle breakdown was the cause of AKI as they presented 3 cases that typify hypercatabolic state, with rapid increase in serum urea nitrogen (SUN), hyperuricemia and hyperphosphatemia. However, in all three cases the urea to creatinine ratio (UCR) remained unchanged and was not elevated, as is observed in hypercatabolic state 2 . The SUN and creatinine levels (UCR Initial/peak ratios: case 1 -17.5/16.2; case 2 -12/13, case 3 -9.7/13) in all three cases remained essentially unchanged and was not in keeping with true hypercatabolic state 2 . In addition, the near normal levels of creatine kinase do not support significant muscle breakdown unless these patients had pre-existing cachexia. The hyperuricemia and hyperphosphatemia could very well be the effects of AKI rather than initiating factors; however, their role in perpetuation of acute kidney injury can not be excluded. The rapid drop in serum albumin is more consistent with a capillary leak syndrome as seen in severe sepsis -systemic inflammatory response syndrome (SIRS) that, I agree, results from the various inflammatory cytokines (interleukin 6, tumor necrosis factor etc.,). I agree with the authors that a better understanding of the factors associated with COVID-19 associated AKI and the role of cytokines is important.

Kidney Medicine Received Date

Please cite this article as: Parmar MS, COVID-19-Associated Acute Kidney Injury

COVID-19-Associated Acute Kidney Injury: A Case Series

Elevated urea-to-creatinine ratio provides a biochemical signature of muscle catabolism and persistent critical illness after major trauma