Tanvi Gangal, Dallas Slack, Susan Blackburn, Andre Borisov, Ronak Patel, Guillermo A. Escobar
Surgery, Vascular Surgery Division, University of Michigan, Ann Arbor, MI.
OBJECTIVES: CIKI is a common etiology of renal dysfunction in hospitalized patients and affects the daily practice of vascular surgeons. It increases mortality, costs and LOS, yet no direct or specific marker exists. Indirect elevations of serum creatinine occur days later and, research into makers of early kidney injury has focused on various proteins with disappointing results. Our animal data revealed that even low-dose contrast leads to kidney injury and nephron-specific mRNA can be detected in the urine. We wished to evaluate if nephron-specific mRNA could be detected in patients after endovascular procedures as a new, specific marker for CIKI.
METHODS: Adults undergoing endovascular procedures requiring contrast were consented. Urine was collected over 24 hours. Urinalysis and mRNA extraction followed. rtPCR using nephron-specific (Nephrin, Podocin, Aquaporin-2) and a non-specific (TBF-Beta) probes. Clinical data was also collected.
RESULTS: Avg contrast: 116cc. Avg age: 69. Significant increases were found only in Nephrin mRNA at 6 hours, and returned to baseline (n=20, p=0.03 ¬– see Figure 1). Hematuria preceded this at 3 hours (p<0.02) after contrast exposure. There was no increase in the serum Cr (it decreased).
CONCLUSIONS: Consistent with our animal model, Nephrin mRNA and blood are detectable in the urine within hours after contrast exposure, regardless of serum creatinine. Urine mRNA is a potentially sensitive marker for CIN.
AUTHOR DISCLOSURES: S. Blackburn: Nothing to disclose; A. Borisov: Nothing to disclose; G. A. Escobar: Nothing to disclose; T. Gangal: Nothing to disclose; R. Patel: Nothing to disclose; D. Slack: Nothing to disclose.
Nephrin mRNA detected in urine (normalized to urine creatinine) prior to contrast exposure (time 0) or up to 24 hours after first contrast dose.
Posted April 2013