Background: Recent publications have described an increasing incidence of end stage renal disease amongst kidney donors. This highlights the paucity of knowledge which exists in the understanding of postoperative renal physiology and thus the determinants of residual renal function. We investigated the impact of donor nephrectomy on the physiology of the residual kidney through the measurement of validated markers of ATP depletion / tubular dysfunction, glomerular filtration rate (GFR), and hyperfiltration.

Methods: 48 patients undergoing hand assisted laparoscopic donor nephrectomy consented to the collection of urine and plasma samples pre and postoperatively (immediate, day1, day2, day3, day30). Urinary retinol binding protein (RBP: a marker of ATP depletion and mitochondrial stress), urinary albumin creatinine ratio (UAC) and plasma cystatin C calculated GFR were measured with colorimetric nephelometry. RBP was corrected for concentration effect by urinary creatnine ratio.

Results: The cohort mean age was 46yrs (SD11.7) and 31 patients were female. RBP levels were normal preoperatively (mean 9.5 mg/mol SD 5) and peaked on day 3 (mean 2969mg/mol, min 31 max 12004) on day 3 before normalising again at day 30 (mean 14.1, SD 5). UAC was normal preoperatively (mean2.2 g/mol SD 5) and peaked postoperatively (20g/mol SD 4) before reaching a steady state at Day 3 5.6g/mol (SD13). Peak RBP levels demonstrated a positive correlation with post/preoperative Cystatin C ratio (r=0.56 p=0.04) and UAC (r=0.44 p=0.04) ratio. In a linear regression model {F(4,34) =13.10, R2 0.61 p=0.00} adjusted for preoperative GFR, day 3 GFR, age and sex); day3 RBP was an independent negative predictor (beta = -2.39 p=0.022) of Day 30 GFR.

Discussion: Our results indicate the existence of a mitochondrial stress environment with a lasting negative impact on residual kidney function at 30 days postoperatively. This likely reflects renal tubular dysfunction in the remaining kidney following donor nephrectomy. Further biochemical analyses are ongoing to confirm the nature of this dysfunction. This will allow the targeting of timely interventions to mitigate the effect of such dysfunction and thus optimise residual renal function.

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