A randomized trial of captopril for microalbuminuria in normotensive adults with sickle cell anemia.
ABSTRACT Nephropathy is a common complication of sickle cell anemia and is often preceded by proteinurea. Our aim was to evaluate the effect of angiotensin-converting enzyme inhibition on microalbuminuria in sickle cell patients.
We performed a randomized, double-blind, placebo-controlled trial in 22 normotensive patients with sickle cell anemia and persistent microalbuminuria. Patients received captopril (25 mg/day) or placebo and were followed up for 6 months. Albuminuria, blood pressure, and serum creatinine and hemoglobin concentrations were measured at baseline and at 1, 3, and 6 months. The primary outcome variable was the 6-month change in albuminuria between the two groups.
Baseline albuminuria was 121 (SD 66) mg per 24 hours in the captopril group and 107 (SD 86) mg per 24 hours in the placebo group. Microalbuminuria decreased from baseline in the captopril group but increased in the placebo group. The mean absolute change and the mean percentage change in microalbuminuria were significantly different between the two groups at 6 months (absolute change -45 mg per 24 hours in the captopril group versus +18 mg per 24 hours in the placebo group, P <0.01; and percentage change -37% in the captopril group versus +17% in the placebo group, P <0.01). The 95% confidence intervals (CI) for the difference in albuminuria between the two groups were 63 (CI 40 to 86) mg per 24 hours for the mean absolute change and 54% (CI 22% to 85%) for the mean percentage change. Blood pressure decreased slightly from baseline in captopril-treated patients and did not change in the placebo group. The change was significantly different between the two groups only for diastolic blood pressure at 6 months (P <0.01).
Captopril reduces albuminuria and slightly decreases blood pressure in patients with sickle cell anemia. More studies are required to demonstrate the sustained benefit on protein excretion.
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ABSTRACT: Microalbuminuria is a pre-clinical marker of renal damage in children with sickle cell anaemia and can predict renal failure. Reported prevalence rates increased with age. In Nigeria, burden of disease and prevailing poor health facilities necessitate its screening, determination of prevalence and associated risk factors. It is a cross-sectional as well as descriptive study. Screening microalbuminuria used subjects' early morning urine. Socio-demographic as well as clinical details were ascertained using semi-structured questionnaires and case files. Associations and statistical relationship of prevalence rates and clinical/epidemiological data were ascertained using chi-squared and multivariate analysis (P < 0.05). Two hundred children with sickle cell anaemia (4-17 years) in steady state and 200 age/gender-matched controls were enrolled. Prevalence of microalbuminuria was ,respectively, 18.5% and 2.5% for subjects and controls (P = 0.001). Microalbuminuria was commoner in females (19.8%) than males (17.4%) P = 0.70, increased with age (P = 0.016), significantly associated with haemoglobin level (P = 0.002) and hospitalizations (0.001). Subjects had normal renal function. Hospitalizations and haemoglobin levels showed statistical significance on multivariate analysis. Prevalence of microalbuminuria is 18.5%. Age, haemoglobin concentrations, and higher hospitalizations influenced microalbuminuria among subjects. Screening for microalbuminuria should be incorporated in the case management of subjects with identified risk factors.01/2012; 2012:240173. DOI:10.1155/2012/240173
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ABSTRACT: The aim of this study was to identify possible risk factors for albuminuria, an early marker of sickle cell anemia (SCA) glomerulopathy, in a cohort of 189 SCA adult patients followed at the Sickle Cell Center of Guadeloupe, a French Caribbean island. Biological parameters obtained at baseline, alpha-globin gene status, and beta(S) haplotypes were compared in patients stratified accordingly to graded albuminuria. Abnormal albumin excretion rate was detected in half of the studied adult patients and macroalbuminuria occurred in 21.6%. Graded albuminuria was associated with advanced age (p=0.006), systolic blood pressure (p=0.031), and worsened anemia, i.e. low hemoglobin rate (p<0.0001) and red blood cell count (p<0.0001). Alpha-thalassemia frequency was lower in microalbuminuric and macroalbuminuric patients than in normoalbuminuric patients, 12.5%, 13.75% and 26%, respectively (p=0.0057). Comparison of albuminuria-free survival curves in SCA patients without and with alpha-thalassemia showed that the median time of albuminuria onset was delayed in the later ones (p=0.021). In contrast, no association of albuminuria was detected with the Bantou beta(S) haplotype. Our results strongly suggest a protective effect of alpha-thalassemia against glomerulopathy in SCA adult patients which could be related to a decreased hemolytic rate.Blood Cells Molecules and Diseases 08/2010; 45(2):154-8. DOI:10.1016/j.bcmd.2010.06.003 · 2.33 Impact Factor
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ABSTRACT: Sickle cell nephropathy is a common presentation in patients with sickle cell disease. End-stage kidney disease is the most severe presentation of sickle cell nephropathy in terms of morbidity and mortality. Sickle cell disease patients with end-stage kidney disease are amenable to renal replacement therapy including kidney transplant. Kidney transplant in these patients has been associated with variable outcome with recent studies reporting short- and long-term outcomes comparable to that of patients with HbAA. Sickle cell disease patients are predisposed to various haematological, cardiorespiratory, and immunological challenges. These challenges have the potential to limit, delay, or prevent kidney transplant in patients with sickle cell disease. There are few reports on the outcome and challenges of kidney transplant in this group of patients. The aim of this review is to highlight the outcome and challenges of kidney transplant in patients with sickle cell disease.Journal of Transplantation 04/2013; 2013:614610. DOI:10.1155/2013/614610