137 New Thoughts, Old Problem: Lessons from Denervation and Phosphate Wasting in the Transplanted Kidney

NEW THOUGHTS, OLD PROBLEM: LESSONS FROM DENERVATION AND PHOSPHATE WASTING IN THE TRANSPLANTED KIDNEY Ali Kashkouli, Michael Zeigler, Robert Steiner UC San Diego Medical Center, Dept of Nephrology, San Diego, CA, USA While phosphate (PO4) homeostasis in CKD has attracted renewed interest, PO4 wasting has been observed for decades in kidney transplant (KT) populations, where hypotheses implicating only preexisting hyperparathyroidism (HPT) and recently FGF 23 have been unsatisfying. “Bench and bedside” observations suggest that persisting KT denervation may largely explain this enduring phenomenon. A normal kidney has a fractional excretion of catechols (FEC, epinephrine [E], and norepinephrine [NE]) of 300%, due to substantial contribution from renal nerves. FEC falls to 100% in KT’s reflecting excretion of only circulating catechols. (Ziegler et al (J. of HTN, 1990). In the longstanding KT’s from our own institution shown below, FEC, urinary E/Cr, and urinary NE/Cr are reduced by approximately 50%. Eplasma NEplasma UE/CR UNE/Cr FEE FENE C 88±11 pg/mL 516±91 pg/mL 32±3 μg/g 126±13 μg/gm 4.2±.5 3.4±.8