**2. Sickle cell nephropathy**

Renal involvement in SCD is a complex phenomenon resulting from an increased tendency of sickling in the renal medulla due to hypoxia, acidosis and hyperosmolar conditions [13]. Abnormally, high hemodynamic renal blood flow leads to early onset hypertrophic and impaired urinary concentrating ability, distal nephron dysfunction and progressive glomerulopathy. The combination of cortical hyperperfusion, medullary hypoperfusion and vasoconstriction leads to further vasculopathy in the kidney. Sickle cell nephropathy (SCN) is a spectrum of changes resulting from a cascade of events occurring in the kidney. This is triggered by RBC vascular occlusion, infarction and reperfusion injury occurring within the renal medullar, cortex and collecting system. These may present as hyperfiltration, microalbuminuria, impaired urinary concentrating ability complicated by episodes of acute kidney disease (AKD) features early in childhood. In young adults, there is progressive increase in albuminuria and regression of the glomerular filtration rate (GFR). Further deterioration of renal function with the development of chronic kidney disease (CKD) (defined as estimated GFR of less than 90 ml/min/1.73 m2 ) eventually leads to end-stage renal disease (ESRD) in adulthood (**Figure 1**).
