High prevalence of renal dysfunction also after small bowel transplantation

Solid organ transplantation is the therapy of choice for end-stage solid organ disease, especially in children. As rejection rates are improving, much of the focus after pediatric solid organ transplantation is shifting toward the identification and prevention of collateral damage such as nephrotoxicity (1, 2). Ojo et al. taught us about the high prevalence of chronic kidney disease (CKD) in all non-renal adult solid organ transplant recipients (3, 4). CKD is a major cause of morbidity and mortality after non-renal transplantation (5). Renal damage is best studied by monitoring glomerular filtration rate (GFR, 6). GFR should be measured using appropriate clearance studies or at least using cystatin C (7, 8). Cystatin C is a low molecular weight protein that measures GFR reliably and independent of body composition (9). Using calculated GFR such as the Schwartz formula, creatinine clearance or the serum creatinine level will lead to an overestimation of GFR (10, 11). Pediatric Transplantation recently published a number of studies on the prevalence of CKD in solid organ transplantation in children. Progressive worsening of GFR was demonstrated in heart-transplanted children (12). Bharat’s manuscript also demonstrated a high degree of underestimation of the degree of CKD when using the Schwartz formula. Feingold et al. (13) provided additional insights from a multi-institutional database of pediatric heart transplant recipients by carefully analyzing risk factors for late renal dysfunction after pediatric heart transplantation. The study highlighted the importance of monitoring and managing low GFR after one yr of transplantation (13, 14). In Feingold’s study, 1.4% of heart transplant children became dialysis dependent after a median follow-up of only 4.1 yr, and most certainly that number will increase with longer follow-up. Clearly, identifying and managing CKD is of high importance as identifying and managing CKD early may help to reduce morbidity (1), and if done well, decline of GFR can be slowed significantly (15). In 2010, there also was a report on large liver transplant registry, which reported on a large data set with a cross-sectional study of 397 patients (16). In that study, 11% of patients had CKD stage 2 or worse (GFR below 90 mL/min/ 1.73 m) at the time of transplantation (16). Among the remaining 333 patients, 52 (15.6)% with initially normal renal function developed abnormally low GFR at a mean follow-up of 5.2 yr (16). Kivela also reported a high prevalence of CKD after orthotopic liver transplantation in children with cyclosporin immunosuppression (17). A recent longitudinal study from Geneva of 24 pediatric liver transplant recipients on tacrolimus suggests that the prevalence of CKD may not be related to the choice of the calcineurin inhibitor (18). In this cohort, 39% of patients had a GFR <90 mL/ min/1.73 m at the time of transplantation. The particular strength of Stelle’s study is its longitudinal nature and the inclusion of other nephrological parameters such as proteinuria and hypertension (19). Interestingly, albeit that tacrolimus-related nephrotoxicity is considered as the etiological factor for the development of progressive CKD (20), there was no correlation between the tacrolimus exposure (measured as trough level) and the measured GFR in the study from Geneva (18). The etiology of the CKD is probably multifactorial.