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COVID-19–Associated Acute Kidney Injury

Open AccessPublished:November 20, 2020DOI:https://doi.org/10.1016/j.xkme.2020.09.006
      To the Editor:
      In their case series of acute kidney injury (AKI) associated with coronavirus disease 2019 (COVID-19), Patel et al
      • Patel N.
      • Rein J.L.
      • Sanchez-Russo L.
      • Winston J.
      • Uribarri J.
      COVID-19-associated acute kidney injury: a case series.
      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.
      • 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.
      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.
      • 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 addition, the near-normal creatine kinase levels 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 AKI can not be excluded. The rapid decrease in serum albumin level is more consistent with a capillary leak syndrome, as seen in severe sepsis-systemic inflammatory response syndrome that I agree results from the various inflammatory cytokines (interleukin 6, tumor necrosis factor, etc). I agree with the authors that better understanding of the factors associated with COVID-19–associated AKI and the role of cytokines is important.

      Article Information

      Financial Disclosure

      The author declares that he has no relevant financial interests.

      Peer Review

      Received August 29, 2020. Accepted September 10, 2020, after editorial review by the Editor-in-Chief.

      References

        • 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

      Linked Article

      • In Reply to ‘COVID-19–Associated Kidney Injury’
        Kidney MedicineVol. 3Issue 1
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          We thank Dr Parmar1 for his careful review of our article.2 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.3 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.
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