Editorial High prevalence of renal dysfunction also after small bowel transplantation Renal dysfunction after pediatric solid organ transplantation Solid organ transplantation is the therapy of choice for end-stage solid organ disease, espe- cially in children. As rejection rates are improv- ing, much of the focus after pediatric solid organ transplantation is shifting toward the identifica- tion 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 trans- plant recipients (3, 4). CKD is a major cause of morbidity and mortality after non-renal trans- plantation (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 indepen- dent 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. Progres- sive worsening of GFR was demonstrated in heart-transplanted children (12). Bharat’s manu- script also demonstrated a high degree of under- estimation 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 moni- toring 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 2 ) 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 preva- lence of CKD after orthotopic liver trans- plantation in children with cyclosporin immunosuppression (17). A recent longitudinal study from Geneva of 24 pediatric liver trans- plant 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 2 at the time of transplantation. The particular strength of Stelle’s study is its longitu- dinal nature and the inclusion of other nephro- logical parameters such as proteinuria and hypertension (19). Interestingly, albeit that ta- crolimus-related nephrotoxicity is considered as the etiological factor for the development of pro- gressive 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. CKD in small bowel transplant patients Olivia Boyer et al.’s (21) study now adds to the literature and describes renal function and even renal histology in pediatric small bowel trans- plant recipients in this issue of Pediatric Trans- plantation. Boyer et al. studied 15 combined liver/small bowel transplant recipients and 12 8 Pediatr Transplantation 2013: 17: 8–11 © 2012 John Wiley & Sons A/S. Pediatric Transplantation DOI: 10.1111/petr.12025