Sickle cell anemia (SCA) is the commonest hemoglobin disorder among the black population worldwide. Children with SCA may eventually end up with end-organ complications: the kidneys being one of the most frequently affected organs. The renal complications arise from medullary ischemia and infarction leading to features of tubular dysfunction such as hyposthenuria and renal tubular acidosis. Early in life, children with SCA may present with hyposthenuria: one of the earliest renal defects in the disease which results in an obligatory urine output of more than 2 l in a day. The symptomatic manifestation as nocturnal polyuria is thought to be the reason for nocturnal enuresis observed in these children. In spite of the more prevalent occurrence of nocturnal enuresis in children with SCA than in their non-SCA colleagues, its precise underlying mechanisms still remain controversial, with divergent conclusions regarding its pathogenesis. However, the consensus is now tilting towards a multifactorial etiopathogenesis in affected children. This book chapter aims to discuss the epidemiologic perspectives of nocturnal enuresis in SCA, as well as the current hypotheses on the etiopathogenesis of this complication.
Part of the book: Contemporary Pediatric Hematology and Oncology