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The handwriting is on the wall: there will soon be a drug for AKI

Nature Reviews Nephrologyvolume 15pages6566 (2019) | Download Citation

With many failures, a sense of helplessness has overshadowed the field of acute kidney injury (AKI). Publications in 2018 offer new hope: better drug targets, better end points and improved understanding of conditions that cause AKI and its complications bring promise that a drug will soon be available.

Key advances

  • The risk of acute kidney injury (AKI) and adverse kidney events in hospitalized patients can be reduced by using physiological solutions instead of saline for intravenous fluid therapy1,2.

  • Strategies for the enrichment and subcategorization of patients with AKI who are most likely to benefit from specific treatments are now available5,8.

  • New mechanisms and related drug targets, most notably related to mitochondrial dysfunction, have transformed the therapeutic landscape of AKI7,8,9.

  • End points for use in trials of AKI therapies are now well defined1,2,5,10.

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    Semler, M. W. et al. Balanced crystalloids versus saline in critically ill adults. N. Engl. J. Med. 378, 829–839 (2018).

  2. 2.

    Self, W. H. et al. Balanced crystalloids versus saline in noncritically ill adults. N. Engl. J. Med. 378, 819–828 (2018).

  3. 3.

    Kidney Disease: Improving Global Outcomes (KDIGO) Work Group. KDIGO clinical practice guildeline for acute kidney injury. Kidney Int. Suppl. 2, 1–138 (2012).

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    Kellum, J. A. Acute kidney injury: AKI: the myth of inevitability is finally shattered. Nat. Rev. Nephrol. 13, 140–141 (2017).

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    Husain-Syed, F. et al. Preoperative renal functional reserve predicts risk of acute kidney injury after cardiac operation. Ann. Thorac. Surg. 105, 1094–1101 (2018).

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    Husain-Syed, F. et al. Persistent decrease of renal functional reserve in patients after cardiac surgery-associated acute kidney injury despite clinical recovery. Nephrol. Dial.Transplant. (2018).

  7. 7.

    Guo, Y. et al. MicroRNA-709 mediates acute tubular injury through effects on mitochondrial function. J. Am. Soc. Nephrol. 29, 449–461 (2018).

  8. 8.

    Poyan Mehr, A. et al. De novo NAD+ biosynthetic impairment in acute kidney injury in humans. Nat. Med. 24, 1351–1359 (2018).

  9. 9.

    Katsyuba, E. et al. De novo NAD+ synthesis enhances mitochondrial function and improves health. Nature 563, 354–359 (2018).

  10. 10.

    Alobaidi, R. et al. Association between fluid balance and outcomes in critically ill children: a systematic review and meta-analysis. JAMA Pediatr. 172, 257–268 (2018).

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Author information


  1. Center for Critical Care Nephrology, University of Pittsburgh, Pittsburgh, PA, USA

    • John A. Kellum
    •  & Dana Y. Fuhrman
  2. Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA, USA

    • John A. Kellum
    •  & Dana Y. Fuhrman
  3. Children’s Hospital of Pittsburgh, Pittsburgh, PA, USA

    • Dana Y. Fuhrman


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Competing interests

J.A.K. has received grant support and consulting fees from Astute Medical and TES Pharma. D.Y.F. declares no competing interests.

Corresponding author

Correspondence to John A. Kellum.

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