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Lipid profile in sickle cell disease patients with chronic kidney disease


MA Emokpae
A Abdu
PO Uadia
MM Borodo

Abstract

Background: Dyslipidaemia is reported to occur in patients with sickle cell disease as well as patients with chronic kidney disease irrespective of the haemoglobin genotype. This study aimed at evaluating lipid profile in subjects with sickle cell anaemia (HbSS), sickle cell trait (HbAS) and normal haemoglobin genotype (HbAA), and comparing the lipid parameters between sickle cell disease patients with and those without chronic kidney disease.
Methods: A total of 66 patients with chronic kidney disease: 26 HbAA, 24 HbAS and 16 HbSS and 60 apparently healthy controls were recruited for the study. Lipoproteins, urea, creatinine, estimated glomerular filtration rate and electrolytes were determined using standard procedures in both patients and controls.
Results: The mean total cholesterol, low density lipoproten cholesterol and high density lipoproten cholesterol in stable HbSS subjects were significantly lower (p<0.001) than those of the HbAS and HbAA controls, while mean triglyceride was significantly higher (p<0.001) in sickle cell disease subjects. The mean total cholesterol in sickle cell disease patients with chronic kidney disease was higher (p<0.001) than sickle cell disease without chronic kidney disease. The potential atherogenic effects of lipids as measured by the artherogenic index were higher in sickle cell disease patients with chronic kidney disease compared with HbAS and HbAA subjects with chronic kidney disease, although lipoprotein changes occurred in all patients with chronic kidney disease irrespective of the haemoglobin genotypes.
Conclusion: Dyslipidaemia is present in patients with sickle cell disease and patients with chronic kidney disease irrespective of the haemoglobin genotype. The potential effects of lipids on cardiovascular disease
risk as measured by three predictor ratios were higher in HbSS compared to HbAA and HbAS chronic kidney disease patients.

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eISSN: 1118-8561