P274 Renal failure in children with inflammatory bowel disease

Abstract

Abstract Background Renal manifestations may occur in children with inflammatory bowel disease (IBD). The cause of renal manifestations is often unclear, but may occur as an extra-intestinal manifestation or due to IBD treatment. Renal complications can lead to acute renal failure, a severe complication and associated with a risk of developing chronic kidney disease (CKD). Current paediatric ECCO/ESPGHAN guidelines recommended to regular monitor renal function with calcineurin inhibitors. However, these recommendations are based on limited knowledge of renal manifestations in paediatric IBD. The aim of this study was to investigate the diagnosis and underlying causes of renal failure in children with IBD. Methods Cases of renal failure in children <19 years with IBD were collected from the international, prospective PIBDSETQuality Safety Registry1. A monthly survey was sent to participating paediatric gastroenterologists throughout the world asking to report cases of renal failure within their clinical practice. Renal failure was defined as an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73m2 based on the Schwartz formula. Upon reporting a case of renal failure, a follow-up form was automatically sent to obtain more information about renal failure, IBD characteristics and outcomes (including CKD, defined as an eGFR <60 for >3 months). Results From November 2016 until August 2023, 220 gastroenterologists from 36 countries participated in the Safety Registry and 38 cases of renal failure were included. Characteristics at time of renal failure are reported in Table 1. Reported causes and diagnoses of renal failure are represented in Figure 1. Most frequently reported causes were IBD medication (n=12) and IBD itself (n=10). IBD medication included 5-ASA (n=5), tacrolimus (n=2) and one case of azathioprine or ibuprofen, vedolizumab, adalimumab, cyclosporine A and ciprofloxacin. Of the cases most likely caused by IBD itself, disease activity was remission (n=4), mild (n=2), moderate (n=3) or severe (n=1). In the majority of cases (n=26, 68%) creatinine was measured during routine follow-up, and not due to kidney-related symptoms. In 13/37 patients creatinine remained elevated after a median follow-up of 82 weeks [41-136 weeks]. Nine patients developed CKD, two patients required renal replacement therapy. Conclusion This is the first prospective study to report cases of renal failure in children with IBD. Renal failure can occur without symptoms, and may lead to CKD. Timely identification of cases of renal failure is important to adequately treat and monitor patients. We recommend to monitor creatinine in all children with IBD, independent of drug use, every 6 months.