J.I. Roodnat, A.M.E. Mik-van Egmond, J.W. Visser, S.P. Berger, W.A.G. van der Meijden, F. Knauf, M. van Agteren, M.G.H. Betjes, E.J. Hoorn
Chair(s): prof. dr. Hans de Frijter, neuroloog, LUMC
Thursday 10 march 2016
13:00 - 13:30h at Foyer
Parallel session: Postersessies XI - Opgesplitst in 3 tijdblokken en 3 categoriëen (klinisch, basaal, donatie)
Chronic oxalate nephropathy is observed secondary to enteric hyperoxaluria that is associated with malabsorption e.g. in short bowel syndrome. It may lead to end-stage renal disease. Kidney transplantation in patients with chronic oxalate nephropathy can be challenging given the risk of recurrent calcium-oxalate nephrolithiasis and crystal-induced kidney injury resulting in graft dysfunction in the peri-transplant setting. Therefore, we studied whether a strategy to decrease serum oxalic acid prior to transplantation may allow successful kidney transplantation.
Patients and methods:
We established a protocol to reduce serum oxalic acid levels prior to and shortly after kidney transplantation based on reduced intake and increased removal of oxalic acid via intensified hemodialysis (HD). Months before transplantation a low oxalic acid diet (40 mg/day), cholestyramine, potassium citrate, and calcium carbonate were started. One week before transplantation (living donor transplantation) or immediately after surgery (deceased donor transplantation), an oxalic-acid free drip-feed and daily 6h HD session were started. When a urine output>2L was reached HD was stopped and 40mg oxalic acid diet was re-started. Patients were instructed to maintain diuresis > 2L/day.
We report three patients with short bowel syndrome following surgery for Crohn’s disease who presented as potential kidney transplant recipients. All three patients had elevated serum oxalic acid levels and biopsy-proven calcium oxalate depositions in their native or transplanted kidney. The protocol reduced serum oxalic acid levels from 102, 112, and 48 to 23, 13, and 11 μmol/l. Patients 1 and 2 received a living donor kidney and had immediate functioning grafts. Patient 3 received a deceased donor kidney and achieved urine output >2L/day after 3 weeks. The post-transplantation periods were complicated by sepsis in Patient 1 and symptomatic native kidney stones in Patient 2 requiring temporary re-institution of the protocol. The patients are currently 12, 11, and 7 months after transplantation with stable estimated glomerular filtration rates of 40, 46, and 50 ml/min/1.73 m2, respectively.
We conclude that successful kidney transplantation in patients with secondary hyperoxaluria is feasible by implementing a strategy aimed at reducing serum oxalic acid levels in the peri-transplantation period.