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Year : 2019  |  Volume : 22  |  Issue : 2  |  Page : 201-207

Study of association between sickle cell trait and renal dysfunction among young adults in South-west Nigeria

1 Department of Medicine, University of Medical Sciences Teaching Hospital, Ondo, Nigeria
2 Department of Medical Laboratory Services, University of Medical Sciences Teaching Hospital, Ondo, Nigeria
3 Renal Unit, Obafemi Awolowo University Teaching Hospital, Ile Ife, Nigeria
4 Department of Haematology, University of Medical Sciences Teaching Hospital, Ondo, Nigeria
5 Department of Dietetics, University of Medical Sciences Teaching Hospital, Ondo, Nigeria
6 Department of Nursing Science, University of Medical Sciences Teaching Hospital, Ondo, Nigeria

Date of Acceptance15-Oct-2018
Date of Web Publication7-Feb-2019

Correspondence Address:
Dr. A A Akinbodewa
PMB 542, Medical Village, 23434 Ondo Township, Ondo State
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/njcp.njcp_253_18

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Background: Although sickle cell disease has become a recognized etiology of chronic kidney disease (CKD), the sickle cell trait (SCT) variant was until recently believed to be a benign carrier state with little or no effect on the health of affected individuals. However, recent studies now appear to suggest an association between SCT and CKD. Objective: The objective of the study is to determine the association between SCT (hemoglobin AS) and renal dysfunction among young Nigerian adults. Methodology: This was a cross-sectional, descriptive study among apparently healthy undergraduates of Adeyemi College of Education, Ondo, southwest Nigeria. Their hemoglobin genotypes were determined using standard alkaline electrophoresis; their blood pressure, anthropometry, serum total cholesterol (TC), creatinine, and estimated glomerular filtration rate (eGFR) were determined. Data analyzed using Statistical Package for Social Sciences (SPSS) 20 were significant at P < 0.05. Results: Six hundred and two subjects with HbAS (SCT, n = 465) and HbAA (non-SCT, n = 137) were studied. Their age range was 18–30 years with male-to-female ratio 1:3.8. There was no difference in the prevalence of renal dysfunction between SCT and non-SCT subjects (5.1% vs. 5.2%, P = 0.591). There was no increased risk of CKD among subjects with SCT (PR, 0.99 at 95% CI [0.417–2.348]). Conclusion: SCT was not associated with increased risk of renal dysfunction among young adults in Nigeria. Further studies are needed to clarify the controversy, especially in Nigeria, with a relatively higher prevalence of SCT.

Keywords: Nigeria, renal dysfunction, risk, sickle cell trait, young

How to cite this article:
Akinbodewa A A, Ogunleye A, Adejumo O A, Daomi V O, Okunola O, Oluwafemi T T, Alli E O, Olalusi V O, Osho P O, Lamidi O A, Fadipe F, Falekulo O K. Study of association between sickle cell trait and renal dysfunction among young adults in South-west Nigeria. Niger J Clin Pract 2019;22:201-7

How to cite this URL:
Akinbodewa A A, Ogunleye A, Adejumo O A, Daomi V O, Okunola O, Oluwafemi T T, Alli E O, Olalusi V O, Osho P O, Lamidi O A, Fadipe F, Falekulo O K. Study of association between sickle cell trait and renal dysfunction among young adults in South-west Nigeria. Niger J Clin Pract [serial online] 2019 [cited 2019 Oct 14];22:201-7. Available from:

   Introduction Top

The sickle cell trait (SCT) is one of the heterozygous forms of sickle cell disease (SCD). It is defined by the presence of an abnormal allele of the hemoglobin beta-globin gene on chromosome 11 due to a single point mutation, thereby manifesting as the hemoglobin genotype AS. Although SCD, marked by presence of two sickle cell genes, is associated with cardiovascular disorders and has become a recognized etiology of chronic kidney disease (CKD),[1] SCT was until recently believed to be a benign carrier state with little or no effect on the health of affected individuals.

Despite ongoing controversies of whether SCT should be considered as a benign carrier state or as an intermediate disease phenotype, newer research outcomes seem to indicate that SCT portends risks for CKD unlike otherwise thought previously.[2],[3] However, evidence linking SCT to CKD are yet to be fully elucidated. For instance, even though there seems to be a higher prevalence of SCT among African-Americans with ADPKD who had ESRD, and higher incidence of microalbuminuria among diabetics with coexisting SCT, there has not been any study to show a direct cause and effect between only SCT and CKD.[4],[5]

SCT is estimated to have a prevalence of 300 million worldwide, mostly concentrated in Africa, Middle East, and Mediterranean region with the reported prevalence of 10–45% in sub-Saharan Africa far outweighing 7–9% quoted among African-Americans.[6],[7],[8] Nigeria, the most populous black nation in Africa, has the largest number of sickle cell anemia patients in the world with the highest prevalence of 20–26% in southwest Nigeria.[9],[10],[11],[12]

Though SCT is usually not regarded as a disease state, individuals with SCT do have 30–40% of their hemoglobin as the sickle variant and this may confer a risk for certain medical conditions. With certain metabolic or environmental changes, the silent SCT may be transformed into a syndrome resembling SCD associated with vaso-occlusive crisis due to an accumulation of low deformable red blood cells in the microcirculation.[13] Such conditions include hypoxia, acidosis, dehydration, hyperosmolality, or hyperthermia as demonstrated during strenuous exercise among individuals with SCT.[14] Microangiopathic studies demonstrated damaged intra-renal medullary blood vessels in SCT, similar to SCD though to a lesser degree.[15]

Renal abnormalities are among the most widely acknowledged complications of SCT. It has been shown to be associated with impaired urinary concentration,[12] microalbuminuria and proteinuria among diabetics, autosomal dominant polycystic kidney disease (ADPKD) in African–Americans, and macroscopic hematuria.[4],[5],[14] HbAS has also been associated with renal microvascular obstruction which most often presents as asymptomatic hematuria and renal papillary necrosis.[16]

Renal medullary carcinoma, a universally fatal and aggressive tumor that is almost always metastatic at presentation, has also been observed rarely but almost exclusively among HbAS patients.[3],[17],[18] It has also been linked with a more rapid progression of CKD to ESRD. The mechanism by which SCT contributes to the pathogenesis and progression of CKD is not fully understood. It was postulated that SCT may directly lead to loss of renal function through episodic sickling leading to chronic parenchymal ischemia. Low oxygen content of the renal medulla as a result of extreme stress or physical exercise may provide an enabling setting for intravascular sickling. Repeated localized areas of sickling and venous occlusion lead to chronic microvascular damage and, as a consequence, to chronic hypoxia and tubulointerstitial fibrosis.[19]

It has been suggested that SCT acts synergistically when coexisting with other conditions such as hypertension or diabetes that equally affect the renal microvasculature to accelerate renal damage. This possibility supports the association of microalbuminuria and proteinuria found to be more prevalent in diabetics with SCT than those with normal hemoglobin.[19] In fact, the two studies that showed a link between SCT and CKD used subjects with older age range. Naik et al. analyzed data of 15,975 African-Americans from 5 large cohort studies with a wide age range of 18–84 years; interestingly, the Coronary Artery Risk Development in Young Adults (18–30, n = 848) study contributed the lowest number of subjects.[2] Dueker et al. on their part used subjects with mean age of 67 ± 8 years and stated in their report that “SCT carriers were slightly older and more likely to have diabetes compared with non-carriers.”[3]

The import of this is that the influence of age, hypertension, obesity, hypercholesterolemia, diabetes, and other age-associated risk factors for CKD on the outcome of these studies cannot be completely set aside. For instance, the age prevalence of obesity in United States (US) is about 35–40% among those of 40–65 years and above compared to 10–20% in the young.[20] In 2008, the World Health Organization (WHO) global prevalence of hypercholesterolemia was 39% with Europe (54%) and the Americas (48%) having the highest.[21] Between 1999 and 2014, the unadjusted hypertension prevalence was 7.3% in those aged 18–39 years compared to 32.7% in those aged 40–59 years, and 65.6% in those aged ≥60 years in US.[22]

Moreover, it has been well established that age above 30 years is an independent risk factor for CKD and advancement in age has been associated with further reduction in renal function.[23],[24]

Our literature search showed that in the natural course of sickle cell nephropathy, among children who were followed up from early childhood, renal failure developed below the age of 30 years.[25] We therefore set out to evaluate the prevalence of renal dysfunction among young SCT carriers in southwest Nigeria and its association (if any) with SCT on the hypothesis that recruiting the younger age group eliminates, to a large extent, the effect of some confounding variables such as older age, primary hypertension, type 2 diabetes, obesity, long-term cigarette smoking, and significant alcoholic use.

   Methodology Top

This was a multistage, case-controlled, cross-sectional study of undergraduates in a tertiary institution in southwest Nigeria. The participants were volunteers who were students of Adeyemi College of Education, Ondo City, Ondo State, Nigeria. It is a federal tertiary institution, which receives studentship from the 6 geo-political zones in Nigeria with a student population of about 15,000.

In the first stage of this study, we determined the hemoglobin genotype of the volunteers. Seven hundred and fifty two students presented at this stage. A total of 602 subjects were found to fall within the two hemoglobin genotype of interest (AA and AS) for our study. These were recruited for the next stage of the study.

Inclusion and exclusion criteria

Consecutive students whose hemoglobin genotype was either AA or AS were recruited for the final phase of the study. Individuals with acute infection, heart failure, and pregnancy or those who declined further testing were excluded.

Blood pressure

Blood pressure was measured using their right arms in the sitting position after 5 min of rest with the adult cuffed mercury sphygmomanometer (Accosons, Germany). The systolic blood pressure (SBP) and diastolic blood pressure were taken as the first and fifth Korotkoff sounds, respectively. Subjects with elevated blood pressure at first reading were instructed to rest for 30 min and the blood pressure was repeated. Systemic hypertension was defined as consistent blood pressure reading ≥140/90 mmHg or if the subject is a known hypertensive or normal blood pressure reading but currently on antihypertensive medications. Prehypertension was defined by SBP of 120–139 mmHg and DBP of 80–89 mmHg.[26]


Their waist and hip circumferences (WC and HC), weight, and height were measured without shoes and with light clothing by trained personnel. During the measurement, participants stood in an upright position, with arms relaxed at the side, feet evenly spread apart, and body weight evenly distributed in accordance with the WHO expert consultation report on waist circumference and waist–hip ratio. Abdominal obesity was determined as a waist–hip ratio >0.94 in men and >0.88 cm in women according to the WHO definitions.[27] Weight was measured to the nearest 0.1 kg using a standard stadiometer (RGZ 160 Lincon Mark Medical, England). Height was measured to nearest 0.5 cm using a wall-mounted microtoise. Body mass index (BMI) was calculated as BMI (kg/m 2) = [weight (kg)/height (m 2)]. General overweight and obesity were defined using the current WHO definitions: underweight: BMI <18.5 kg/m 2, normal weight: BMI 18.5–24.9 kg/m 2, overweight (preobese): BMI 25–29.9 kg/m 2, and obese: BMI >30 kg/m 2.[28]

Blood sampling procedure

Aside radiological abnormalities (cysts, kidney stones) within the kidneys, individuals with persistently elevated or progressively rising serum creatinine, raised urine protein–creatinine ratio, hypertension, hyperlipidaemia, abnormally elevated blood glucose, and presence of apolipoprotein-1 gene are among those at risk of developing CKD. However, we excluded non-fasting blood glucose estimation because of its low sensitivity and variability.[29]

Non-fasting venous blood sample for analysis was collected at the media-cubital fossa from each participant. Two milliliters (ml) of blood was dispensed into the ethylene diamine tetra-acetate blood collection tubes for determination of hemoglobin genotype using the standard hemoglobin electrophoresis machine (alkaline medium, MICROFIELD, England). Assessment of serum creatinine was performed using 5 ml of venous blood dispensed in lithium heparin collection tubes. Samples were centrifuged in the laboratory to separate the serum which was then analyzed by the modified kinetic Jaffe method using the RANDOX, UK commercially prepared reagent.[30] The serum TC was determined using a commercially prepared reagent (BIOSYSTEM, Spain). Serum TC of 5.2–6.2 mol/l was taken as “borderline high,” whereas serum of TC of greater than 6.2 mmol/l was taken as “high.”

The eGFR was calculated using the modification of diet in renal diseases formula which has been previously validated in Nigeria.[31] Renal dysfunction was defined by reduced eGFR below 60 ml/min/1.73 m 2.[32]

Statistical analysis

Data were analyzed using SPSS version 20. Quantitative variables normally distributed were presented as mean ± standard deviation. Categorical variables were presented as absolute (n) and relative (in percent) frequencies. Comparison of means and percentages was done using the Student's t-test and Chi square test, respectively. P value < 0.05 was taken to be significant. Prevalence ratio (PR) was determined at confidence interval of 95%.

Ethical approval

Approval to conduct the study was obtained from the Management of Adeyemi College of Education. Each participant received verbal and written information on the study prior to commencement. Each participant gave a written consent to participate before being recruited into the study. Ethical clearance was obtained from the Health Research Committee of the State Specialist Hospital, Akure, Ondo State.

   Results Top

[Table 1] shows that 602 subjects (SCT, n = 465) and HbAA (non-SCT, n = 137) with complete data were eligible for the study after filtering out subjects with hemoglobin genotype other than AS and AA. Their age range was 18–30 years with male-to-female ratio 1:3.8.
Table 1: Hemoglobin genotypes of participants

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[Table 2] shows that the proportion of individuals with hypertension (11.7% vs. 8.2%), obesity (10.2% vs. 8.2%), and hypercholesterolemia (29.1% vs. 26.2%) was higher among individuals with SCT than non-SCT subjects. There was no difference in the proportion of subjects, with prehypertension between the two groups, nor gender variation. [Table 3] shows that there was a significantly higher mean diastolic blood pressure among subjects with SCT; however, their mean BMI was lower. The proportion of subjects with renal dysfunction was similar between the groups (SCT, 5.1% vs. non-SCT 5.2%). [Table 4] showed that there was no increased risk of CKD among subjects with SCT (PR, 0.99 at 95% CI [0.417–2.348]).
Table 2: Proportion of subjects with risk factors for CKD among SCT and non-SCT groups

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Table 3: Comparison of clinical and laboratory parameters of participants between SCT and non-SCT subjects

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Table 4: Test of association between hemoglobin genotype and renal dysfunction

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   Discussion Top

The prevalence of SCT of 21.4% obtained in our study falls within the established range earlier documented in Nigeria.[9],[11] There was a high prevalence of risk factors/comorbidities among our SCT subjects. Of particular note is that the proportion of SCT subjects with hypertension, obesity, and hypercholesterolemia was higher than those with normal hemoglobin genotype, even though the difference in their mean values was not statistically significant, aside DBP and BMI. Nonetheless, this observation is worthy of note as recent observations suggest that there may be a synergistic relationship between SCT and these risk factors in causing CKD and/or its progression to ESRD. For instance, Mukendi et al. showed that hypertension, diabetes, metabolic syndrome, and proteinuria were the determinants of CKD among adult Congolese with SCT; in that study, SCT was not found to be an independent determinant of CKD.[33]

This is probably due to the fact that diabetes, obesity, and hypertension can independently impair microvascular function within the nephrons, thereby leading to accelerated progression of CKD to ESRD in the presence of SCT. In one study among type 2 diabetics in Nigeria, Ajayi et al. demonstrated a significantly greater proportion of proteinuria among those with SCT than in diabetics with normal hemoglobin genotype.[5] In the landmark study by Naik et al., it was demonstrated that the presence of comorbidities resulted in a higher rate of progression to ESRD among SCT than in noncarriers.[2]

The prevalence of SCT subjects with reduced renal function was 5.1% in our study even though it was not significantly different from what was obtained among the group with normal hemoglobin. There has not been previous attempt in Nigeria to quantify the burden of CKD among individuals with SCT. However, this prevalence is lower when compared to the global prevalence of 15–18% reported for renal disease among SCD patients.[31] In Nigeria, 22.5% of subjects with SCD were found to have subnormal creatinine clearance.[34]

Our study indicates that SCT may not directly induce reduced renal function. A similar pattern was demonstrated in earlier studies among blacks in Congo and African-American subjects where no association was found between SCT and CKD.[14],[33] It is only recently that it was shown in a large scale study by Naik et al. that SCT may be independently associated with a higher prevalence of CKD among African-Americans with SCT but the authors, apart from using largely older subjects from five large studies with different study designs, did not set out to demonstrate a direct cause–effect relationship between SCT and CKD.[3] More so, similar studies from the same geographical location yielded contrary results.[35],[36] Among 376 African-American diabetics, Bleyer et al. found that there was no difference in the values of eGFR and microalbuminuria in subjects with and without SCT.[35]

This difference in the outcome of studies from Africa (Nigeria and Congo) and that conducted by Naik et al. in the US calls for further studies in the African continent and other geographical locations where SCT is prevalent. There may be need to consider whether genetics, environmental, or cultural differences can account for the varying relationship of SCT to CKD between African and Afro-American subjects. Indeed, our postulation may not be so far-fetched as contrary to the findings of the Naik study group; Hicks et al. were able to demonstrate that there is no genetic association between SCT and ESRD in a large sample (1085) of African-Americans with CKD as far back as 2011.[36] They also could not demonstrate any interaction between APOL 1 or MYH9 with the SCT.[36]

It is also possible that extreme cold in the temperate regions may contribute to the rate of red cell sickling and invariably the higher degree of renal damage among subjects in such environments.[37] Perhaps, there may also be need to explore the presence of undetected coexisting renal pathologies and their behavioral pattern in the presence of SCT in different population groups across the globe. For instance, the coexistence of ADPKD with SCT has long been shown to lead to earlier onset of CKD and progression to ESRD.[5] There has also been case reports on the cooccurrence of SCT and lupus nephritis.[38],[39] One of the earliest cases of immune deposit glomerulonephritis in SCT patients was first demonstrated by Ozawa et al. over 50 decades ago.[40]

This study considered young adults aged 30 years and below, thus eliminating age as a risk factor. It also demonstrated a low prevalence of the other risk factors (hypertension, obesity, and hypercholesterolemia) and potentially their low influence as confounders. It is a well-established fact that age above 30 years is an independent risk factor for CKD and further deterioration in renal function.[23],[24] It is also worthy of note that the separate studies by Naik et al. and Dueker et al., which suggested association between SCT and CKD, included large number of older adults as subjects.[2],[3]

Perhaps the age restriction in our study (although having the potential advantage of eliminating age among other traditional risk factor for CKD) may be a reason for the relatively low prevalence of renal dysfunction in our study. This is because of the glomerular hyperfiltration, which can give a falsely normal or high eGFR despite the presence of kidney damage. Studies have shown that hyperfi ltration status among hemoglobin SS patients was significantly associated with younger age.[41],[42] The same factor, alongside lower muscular mass in individuals with SCT, may be responsible for the apparent similarity in the prevalence of renal dysfunction between SCT and non-SCT subjects in this study.[41],[42]

   Conclusion Top

SCT alone was not found to be an independent risk factor for CKD among young adult Nigerians. Further studies are needed to clarify this controversial topic, especially in Nigeria with a relatively higher prevalence of SCT. We recommend a larger scale multiethnic, case-controlled, prospective study that will include urine albumin, urine microscopy, APOL 1, and MYH9 genetic mapping in association to SCT among Nigerian subjects. The important role of male gender in determining the prevalence and progression of CKD [43] could not be sufficiently discussed in our study as the number of SCT subjects with renal dysfunction was too small to make any conclusive statement.

This study was limited by its cross-sectional design, sample size, omission of other important risk factors for CKD such as diabetes mellitus and cigarette smoking, and single values for serum creatinine.

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Conflicts of interest

There are no conflicts of interest.

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  [Table 1], [Table 2], [Table 3], [Table 4]


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