Abstract
Sickle cell disease (SCD), the commonest single gene disorder amongst Nigerian children, may present as sickle cell nephropathy (SCN). SCN is detectable by persistent proteinuria, a “nephrotoxin” that contributes to progression of SCN to end stage renal disease. Unfortunately, screening for persistent proteinuria is an uncommon practice among Nigerian children with SCD, even when reduction of proteinuria is a proven renoprotective therapy. Dipstick urinalysis was done to detect persistent proteinuria (proteinuria of trace and above, on first contact and a month on follow-up in the same subject) among consecutive steady state sickle cell anaemia (haemoglobin SS confirmed using cellulose acetate paper electrophoresis) children attending sickle cell clinic at the University of Ilorin Teaching Hospital between October, 2004 and July, 2005. Subjects with persistent proteinuria were also assessed for estimated glomerular filtration rate (eGFR) using the method described by Schwartz et al. A total of 75 children aged between 1 to 17 years, comprising 35 males and 40 females, were studie. Proteinuria was found in 6 (8%) subjects (5 males, 1 female) and in 5 (6.7%) subjects (3 males, 2 females) on first contact and one month on follow-up, respectively. Persistent proteinuria was only seen in 3 (4%) male subjects (older than 10 years age) whose eGFR was not impaired. Although proteinuria occurred more commonly among male subjects than females on first contact and at follow-up, this observation was not statistically significant (p = 0.175 at first contact, p = 0.224 at follow-up). Proteinuria also occurred more among subjects older than 10 years of age at both contacts, this association was also not significant (p = 0. 071 on first contact, p value = 0.10 at follow-up). Although, a low prevalence of persistent proteinuria was found among the sickle cell anaemia children studied, its screening should become a routine to identify children who will benefit from antiproteinuric treatment. Key words: Persistent proteinuria, steady state sickle cell anaemia, children, Ilorin, Nigeria.
Highlights
The prevalence of persistent proteinuria in this study was lower than 12.3% reported by Morgan among 407 Jamaican sickle cell anaemia (SCA) patients and the 7% reported by Ugwu and Eke among 72 SCA children in Port Harcourt, Nigeria (Morgan, 1982; Ugwu and Eke, 2002)
We are very careful in comparing our study with those of other Nigerian researchers (Solarin et al, 2014; Yaguo-Ide et al, 2010; Abhulimhen-Iyoha et al, 2009) as these researchers measured microalbuminuria in Nigerian children with SCA in contrast to dipstick proteinuria measured in this study
The study reveals that the prevalence of persistent haematuria is low in this cohort of SCA children in steady state
Summary
The cause of the SCD is the substitution of valine for glutamic acid at the sixth position of the β-goblin chain of the haemoglobin (Nath and Hebbel, 2015). Sickled haemoglobin causes oxidative damage of the erythrocyte membrane, cellular dehydration, abnormal phospholipid asymmetry and increased adherence to endothelial cells (Francis and Johnson, 1991; Hebbel, 1991). The net result of these alterations is a shortened erythrocyte life span from chronic haemolysis and episodic microvascular occlusion that cause tissue ischaemia and acute and chronic dysfunction of virtually all the organs of the body including the kidney (Oral and George , 1993; Alhwiesh, 2014). The kidney’s microvasculature is vulnerable because of absence of collateral circulation and the characteristic sickling promoting features of the renal medulla including the low oxygen tension, acidosis and hypertonicity (Alhwiesh, 2014)
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