Comparison between serum nephrin and microalbuminuria as biomarkers for sickle cell nephropathy

Abstract

Sickle cell anemia is the most common monogenic blood disorder. The most common genotype is homozygous hemoglobin SS. Damage to red blood cells occurs due to changes in shape and function of the hemoglobin molecule inside it. This results in hemolytic anemia and the blockade of small blood vessels, which lead to vaso-occlusion and end organ failure. Sickle cell disease significantly alters renal structure and function and causes diverse renal diseases. To evaluate the validity of serum nephrin as a biomarker of sickle nephropathy and compare its sensitivity versus urinary microalbuminuria in the early detection of sickle cell nephropathy. This case control study was conducted on sixty patients suffering from sickle cell disease, 10 of them were diagnosed as sickle nephropathy, in addition to sixty apparently healthy children as a control group. Laboratory tests were hemoglobin electrophoresis, urinary microalbumin, serum ferritin, urea and creatinine. The glomerular filtration rate was estimated and serum nephrin was measured using enzymelinked immunosorbent assay. Among children with sickle cell anemia, 16.6% (10 patients) had sickle nephropathy diagnosed with elevated kidney function and low glomerular filtration rate. Liver and kidney function were significantly higher in cases with nephropathy than cases without nephropathy, while glomerular filtration rate was significantly lower in cases with nephropathy than cases without nephropathy. Serum nephrin was significantly higher in patients with nephropathy than patients without nephropathy versus non-significant difference regarding microalbuminuria level. The cutoff point for nephrin to diagnose sickle cell nephropathy was > 13 ng/mL versus 29.5 mg/dL for urinary microalbumin. Serum nephrin could be a valuable biomarker in early diagnosis of nephropathy in patients with sickle cell anemia.