In Reply to 'COVID-19-Associated Kidney Injury'.

We thank Dr Parmar for his careful review of our article. We do not agree that the serum urea nitrogen–creatinine ratio, as cited in reference 2, should become the standard definition of a hypercatabolic state. In that reference, the ratio was a prespecified outcome, their patients had a different phenotype compared with ours, most did not have acute kidney injury (AKI), and their work did not account for the influence of total parenteral nutrition on urea levels. It is widely known that parenteral nutrition is extensively and intensively used in intensive care units and may contribute significantly to increased serum urea nitrogen levels out of proportion to serum creatinine levels. Moreover, we have other data quantifying in a more precise way the inordinate levels of urea generation in COVID-19–associated AKI among patients similar to our cohort, strongly supporting a hypercatabolic state. We also disagree with Dr Parmar’s interpretation of the meaning of near-normal creatinine kinase levels in our patients. We believe that these creatinine kinase values support our hypothesis that there was no actual loss of muscle cell integrity (rhabdomyolysis) but only increased muscle protein breakdown induced by the cytokine storm. We agree that there is much more to learn about the pathophysiology of this condition, both in COVID-19 and other critical illness.