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    Rev Electron Biomed / Electron J Biomed 2020;1:2-6.



    1Victoria P. Musso-Enz, 2Guido M. Musso-Enz, 1Carlos G. Musso, MD. PhD.

    1Instituto Universitario. Hospital Italiano de Buenos Aires,
    2Facultad de Medicina, Pontificia Universidad Católica Argentina Santa María de los Buenos Aires.

    carlos.musso @

    Version en español

      It is known that renal physiology is classically constituted by five main functions; glomerular filtration, tubular reabsorption, tubular secretion, as well as renal endocrine and exocrine activities1.

      Acute renal injury (AKI) is one of the main renal alterations, as well as one of the most frequent complications associated with non-renal medical problems that require hospitalization2-3.

      AKI is defined, according to the KDIGO guidelines, by the following criteria4:

      • increase in serum creatinine > 0.3 mg/dl within 48 hours, or
      • increase > of 1.5 times of baseline serum creatinine presumed to occur within 7 previous days, or
      • urine volume reduction <0.5 ml/kg/hour for 6 hours.

      Therefore, since the current AKI definition is only based on renal filtering or urine excretory reduction, it cannot allow physicians to detect renal damages expressed by tubular dysfunction.

      AKI affects about 20% of hospitalized patients, regardless of the hospitalization cause, and is associated with high rates of in-hospital morbidity, mortality and costs5-6. Thus, it would be crucial to better recognize this entity to install an early treatment and consequently reduce its associated mortality, morbidity and hospitalization costs.

      For this purpose, it would be very useful to newly conceptualize AKI to include renal tubule dysfunction criteria in its definition. In this sense, simple tubular dysfunction markers should be investigated with the objective of applying this new concept to clinical setting7.

      In conclusion, the current AKI definition seems to be incomplete, and would be very important to incorporate tubular dysfunction criteria to its clinical screening.


        1.- Beker BM, Corleto MG, Fieiras C, Musso CG. Novel acute kidney injury biomarkers: Their characteristics, utility and concerns. Int Urol Nephrol 2018;50:705?13

        2.- Shlipak M, Stehman-Breen C. Observational research databases in renal disease. J Am Soc Nephrol. 2005;16:3477-3484.

        3.- Musso CG, Rosell C, Gonzalez-Torres H, Ordonez J, Aroca-Martinez G. Primary prevention for acute kidney injury in ambulatory patients. Postgraduate Medicine.2020; 132: 746-748

        4.- KDIGO Clinical practice guidelline for acute kidney injury Kidney Int Suppl 2012;2:1-38.

        5.- Córdova-Villalobos JA, Barriguete-Meléndez JA, Lara-Esqueda A, Barquera S, Rosas-Peralta M, Hernández-Avila M, de León-May ME, Aguilar-Salinas CA. Las enfermedades crónicas no transmisibles en México: sinopsis epidemiológica y prevención integral. Salud Publica Mex. 2008;50:419-427.

        6.- Musso CG, Terrasa S, Ciocchini M, González-Torres H, Aroca-Martínez G. Looking for a better definition and diagnostic strategy for acute kidney injury: A new proposal. Arch Argent Pediatr 2019;117:4-5.

        7.- Risso MA, Sallustio S, Sueiro V, Bertoni V, Gonzalez-Torres H, Musso CG. The Importance of Tubular Function in Chronic Kidney Disease. International Journal of Nephrology and Renovascular Disease. 2019:12 257-262.

    Carlos G. Musso, MD. PhD.
    Instituto Universitario.
    Hospital Italiano de Buenos Aires,
    Buenos Aires. Argentina
    Email: carlos.musso @