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In Reply to ‘COVID-19–Associated Kidney Injury’

Open AccessPublished:November 22, 2020DOI:https://doi.org/10.1016/j.xkme.2020.10.003
      We thank Dr Parmar
      • Parmar M.S.
      COVID-19–associated acute kidney injury [letter].
      for his careful review of our article.
      • Patel N.
      • Rein J.L.
      • Sanchez-Russo L.
      • Winston J.
      • Uribarri J.
      COVID-19-associated acute kidney injury: a case series.
      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.
      • Haines R.W.
      • Zolfaghari P.
      • Wan Y.
      • Pearse R.M.
      • Puthucheary Z.
      • Prowle J.R.
      Elevated urea-to-creatinine ratio provides a biochemical signature of muscle catabolism and persistent critical illness after major trauma.
      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.
      • Gunst J.
      • Vanhorebeek I.
      • Casaer M.P.
      • et al.
      Impact of early parenteral nutrition on metabolism and kidney injury.
      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,
      • Uribarri J.
      • El Shamy O.
      • Sharma S.
      • Winston J.
      COVID-19 associated AKI and quantified protein catabolic rate: a likely effect of cytokine storm on muscle protein breakdown.
      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.

      Article Information

      Financial Disclosure

      The authors declare that they have no relevant financial interests.

      Peer Review

      Received October 14, 2020. Accepted October 25, 2020, after editorial review by the Editor-in-Chief.

      References

        • Parmar M.S.
        COVID-19–associated acute kidney injury [letter].
        Kidney Med. 2020; 3: 128
        • Patel N.
        • Rein J.L.
        • Sanchez-Russo L.
        • Winston J.
        • Uribarri J.
        COVID-19-associated acute kidney injury: a case series.
        Kidney Med. 2020; 2: 668-669
        • Haines R.W.
        • Zolfaghari P.
        • Wan Y.
        • Pearse R.M.
        • Puthucheary Z.
        • Prowle J.R.
        Elevated urea-to-creatinine ratio provides a biochemical signature of muscle catabolism and persistent critical illness after major trauma.
        Intensive Care Med. 2019; 45: 1718-1731
        • Gunst J.
        • Vanhorebeek I.
        • Casaer M.P.
        • et al.
        Impact of early parenteral nutrition on metabolism and kidney injury.
        J Am Soc Nephrol. 2013; 24: 995-1005
        • Uribarri J.
        • El Shamy O.
        • Sharma S.
        • Winston J.
        COVID-19 associated AKI and quantified protein catabolic rate: a likely effect of cytokine storm on muscle protein breakdown.
        Kidney Med. 2021; 3: 60-63

      Linked Article

      • COVID-19–Associated Acute Kidney Injury
        Kidney MedicineVol. 3Issue 1
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          In their case series of acute kidney injury (AKI) associated with coronavirus disease 2019 (COVID-19), Patel et al1 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 levels, hyperuricemia, and hyperphosphatemia. However, in all 3 cases, the urea-creatinine ratio (UCR) was unchanged and was not elevated, as is observed in a hypercatabolic state.2 Serum urea nitrogen and creatinine levels (UCR initial/peak: case 1, 17.5/16.2; case 2, 12/13; case 3, 9.7/13) in all 3 cases were essentially unchanged and were not in keeping with a true hypercatabolic state.
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