TO029EPIDEMIOLOGY OF PAEDIATRIC UROLITHIASIS IN A LARGE COHORT IN UK

Abstract

Introduction and Aims: The epidemiology of both adult and childhood renal stone disease has evolved over the last 50 years but whilst dietary and lifestyle factors are important for older patients, their relevance to the causation of paediatric stones is still unclear. We set up a dedicated renal stone service for children combining medical and surgical expertise in a joint clinic in 1997 and now have a large case series of children to investigate the epidemiology. Method(s): All children were reviewed in a dedicated paediatric stone clinic and demographic and clinical data were collected. A retrospective hospital note review of children presenting with kidney stones during the last eighteen years (1997-2015) was conducted. All patients had a comprehensive infective and metabolic screen and were classified as metabolic, infective or idiopathic (defined as the absence of UTIs or metabolic abnormalities) stone disease. Result(s): 511 patients (322 male) were reviewed. The median age of presentation was 4.4y for males (0-16.6y) and 7.3y (1-18.5y) for females. Median centile for weight was 33th and 25th for male and female, respectively. 183 (36%) presented with UTI, 163 (32%) with abdominal pain, 137 (27%) with macroscopic haematuria and 7 (1.4%) with acute renal failure. 67 (13%) patients were asymptomatic. 30% had a positive family history. 175 (34%) had an underlying metabolic abnormality, 112 (22%) had infective stones and 224 (44%) were classified as idiopathic. The majority of stones analysed were composed of calcium oxalate or calcium phosphate. Of the 175 patients with a metabolic abnormality: 91 (52%) had hypercalciuria (76 persistent and 15 transient), 37 (21%) hyperoxaluria, 38 (22%) cystinuria, 3 (2%) abnormalities in the purine metabolism and the remainder had other metabolic abnormalities. Within the 76 patients with persistent hypercalciuria, 3 (4%) had a diagnosis of Familial hypomagnesaemia with hypercalciuria and nephrocalcinosis and the remainder had idiopathic hypercalciuria. The hyperoxaluria group included 19 (51.4%) patients with primary hyperoxaluria (12 with type 1, 2 with type 2 and 5 with type 3). In 11 children the mutation could not be identified and 7 patients had enteral hyperoxaluria. There was a significant increased risk of bilateral stones within the metabolic group (OR 2.0, p < 0.05). Conclusion(s): In this large cohort of paediatric stone disease in a developed country, more than half of the patients had metabolic or infective stones. Hypercalciuria was the most common metabolic cause of paediatric urolithiasis. Children with renal stones presented with reduced weight in contrast to the adult experience. Nearly thirty percent of the children had a positive family history for stone disease, indicating the importance of future genetic work up of paediatric renal stone disease.