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Abstract: TH-PO030

Insights Into Urinary Renin in AKI

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical‚ Outcomes‚ and Trials


  • Flannery, Alexander H., University of Kentucky College of Pharmacy, Lexington, Kentucky, United States
  • Ortiz-Soriano, Victor M., University of Kentucky College of Medicine, Lexington, Kentucky, United States
  • Devarajan, Prasad, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, United States
  • Neyra, Javier A., The University of Alabama at Birmingham School of Medicine, Birmingham, Alabama, United States

An activated intra-renal renin-angiotensin system (RAS), reflected by urinary markers including renin, is hypothesized to contribute to and serve as a biomarker of AKI. However, methodologic limitations with urinary renin immunoassay have been noted, including whether the standard is prorenin and not renin. Furthermore, it is unknown if urine renin is elevated simply due to elevations in plasma concentrations. Using a validated direct renin assay with a low cross-reactivity for prorenin, we sought to evaluate concurrent concentrations of urinary and serum renin in patients with and without AKI.


Biospecimens for this study were obtained from a previous cohort study investigating serum renin in critically ill patients. We identified 19 patients with AKI (KDIGO stage 2 or higher) due to sepsis and 19 matched control patients (i.e. critical illness without AKI). The biospecimens under study were obtained within the first 3 days of intensive care unit admission. Urine and serum renin were measured in duplicate with a renin (active) ELISA and normalized to urine creatinine (Cr).


Patients were well-matched with demographics, although AKI patients were more critically ill. Urine renin and urine renin normalized to Cr were significantly (p<0.001 for both) higher in AKI patients versus controls (Fig. 1A-B). Serum renin was higher in AKI patients than controls (p=0.014). Urine renin: serum and urine renin (normalized to urine Cr): serum renin ratios were numerically higher in AKI patients versus controls (Fig. 1C-D): p=0.300 and 0.226, respectively. Scatterplots (Fig. 1E-F) support the concept of a differential relationship of urine to serum renin in AKI and that an elevated serum renin is not a requirement for elevated urinary renin.


Urine renin is higher in AKI patients vs. controls, is not solely explained by high circulatory concentrations, and may represent a biomarker of intra-renal RAS activation in AKI.

Fig. 1. Urine Renin in AKI vs. Controls


  • NIDDK Support