Acute kidney injury assessed by cystatin C after transcatheter aortic valve implantation and late renal dysfunction.

The aim of the present study was to evaluate acute kidney injury (AKI) with cystatin C following transcatheter aortic valve implantation (TAVI) and to assess the impact of postoperative AKI on outcome and late renal function. A prospective study. Single, tertiary referral center. Sixty-eight consecutive patients with severe aortic stenosis and advanced comorbidity. Blood samples were collected on 4 occasions pre- and postoperatively to determine levels of s-creatinine and cystatin C. Additionally, a sample was collected at followup 12 months postoperatively for the determination of s-creatinine. The mean preoperative eGFR (s-creatinine) was 67±24 mL/min/1.73 m² compared to 45±21 mL/min/1.73 m² with eGFR (cystatin C) (p<0.001). Postoperative AKI was diagnosed in 25 patients (39%) with eGFR (cystatin C), compared to 21 patients (33%) with GFR (s-creatinine) and the RIFLE criteria. The 90-day mortality was 14.3% for the AKI+group and 2.3% for the AKI-group (p = 0.099). At 12 months followup, renal function remained impaired in patients with postoperative AKI and deteriorated in patients without. The risk of postoperative AKI is considerable following TAVI, with an increased risk of early mortality for AKI+patients. Cystatin C may be a valuable adjunct to the established biomarker s-creatinine for preoperative risk assessment and for early postoperative diagnosis of AKI. The acute postoperative renal impairment in patients with AKI does not fully recover in the long term. There is a progressive renal impairment in both groups postoperatively, the etiology probably being multifactorial.