Nocturnal enuresis in children with sickle cell anemia

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Nocturnal enuresis in children with sickle cell anemia

Chapter

 

Abstract

 

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 occur-rence of nocturnal enuresis in children with SCA than in their non-SCA colleagues, its precise underlying mechanisms still remain controversial, with divergent conclu-sions 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.

Keywords: sickle cell anemia, nocturnal enuresis, hyposthenuria, multifactorial etiopathogenesis

 

  1. Introduction

 

Sickle cell anemia (SCA) is the commonest hemoglobin disorder among the black population worldwide [1, 2] . As a genetic defect with the Mendelian autosomal-recessive inheritance, children with the sickle cell hemoglobin genes

 

in the homozygous form have reversibly sickled and irreversibly sickled red blood cells. These abnormal red cells, which become rigid having lost their deformability, consequently block the microvasculature resulting in vasoocclusion. They are also prone to damage which leads to chronic hemolysis. Most of the clinical features of SCA are essentially related to these two events.

 

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 dys-function such as hyposthenuria and renal tubular acidosis [3] . As early as 3 years of age, 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 [4] . The symptomatic manifestation as nocturnal polyuria is thought to be the reason for the observed nocturnal enuresis in these children. In spite of the more prevalent occurrence of nocturnal enuresis in children with SCA than in their normal colleagues, the precise underlying mechanisms have not yet been resolved. Research on the subject has led to divergent conclusions about the pathogenesis; one report had earlier suggested that hyposthenuria was a major determinant of enuresis in the disease [5] , while other authors not only controverted this observa-tion but had reported disparate etiopathogenic factors [6–8] . In fact, a recent review of published evidence on the subject indicates similar determinants of nocturnal enuresis for both SCA and non-SCA patients [9] . Thus, the role of hyposthenuria as the exclusive determinant of nocturnal enuresis in children with SCA remains debatable although the consensus is now tilting towards a multifactorial etiopatho-genesis in affected children.

 

 

 

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