Sickle cell anemia (SCA) is caused by a single point variation in the β-globin gene (HBB): c.20A> T (p.Glu7Val), in homozygous state. SCA is characterized by sickling of red blood cells in small blood vessels which leads to a range of multiorgan complications, including kidney dysfunction. This case-control study aims at identifying sickle cell nephropathy biomarkers in a group of patients living with SCA from Senegal. A total of 163 patients living with SCA and 177 ethnic matched controls were investigated. Biological phenotyping included evaluation of glycemia, glucosuria, albuminuria, proteinuria, tubular proteinuria, serum creatinine, urine creatinine, urine specific gravity and glomerular filtration rate. Descriptive statistics of biomarkers were performed using the χ2 –test, with the significance level set at p<0.05. Patients living with SCA had a median age of 20 years (range 4 to 57) with a female sex frequency of 53.21%. The median age of the control participants was 29 years (range: 4–77) with a female sex frequency of 66.09%. The following proportions of abnormal biological indices were observed in SCA patients versus (vs.) controls, as follows: hyposthenuria: 35.3%vs.5.2% (p<0.001); glomerular hyperfiltration: 47.66%vs.19.75% (p<0.001), renal insufficiency: 5.47%vs.3.82% (p = 0.182); microalbuminuria: 42.38%vs.5.78% (p<0.001); proteinuria: 39.33%vs.4.62% (p<0.001); tubular proteinuria: 40.97%vs.4.73% (p<0.001) and microglucosuria: 22.5%vs.5.1% (p<0.001). This study shows a relatively high proportion of SCA nephropathy among patients living with SCA in Senegal. Microglucosuria, proteinuria, tubular proteinuria, microalbuminuria, hyposthenuria and glomerular hyperfiltration are the most prevalent biomarkers of nephropathy in this group of Senegalese patients with SCA.
This protocol describes how to determine microglucosuria in patients living with sickle cell disease in order to diagnose a nephropathy as a result of proximal convoluted tubule damaged by heme catabolites.
The aim of our research was to evaluate the cardiovascular risk factors on epileptic patients treated at the Fann University Hospital and to study the influence of haptoglobin (Hp) polymorphism on disease progression. In order to do that, eighty-six (86) patients followed in neurology for at least 2 years were recruited. Each patient was matched to a control according to age and sex. Hp phenotyping was performed by electrophoresis on polyacrylamide gel, and lipid peroxidation was quantified by the dosage of the thiobarbituric acid reacting substances (TBARS). The determination of a number of biochemical parameters was performed in both patients and controls. The evaluation of lipid parameters showed significant differences in total cholesterol levels, triglycerides, low-density lipoprotein (LDL) cholesterol and atherogenic index between patients and controls. For C-Reactive Protein-ultra sensible (CRP-us) values greater than 3 mg / L, a statistically significant difference was found (p = 0.009). The frequencies of the three major phenotypes of patients compared to controls has shown significant difference only for Hp2-2 phenotype (p = 0.042). The significant increase of TBARS for patients compared to controls suggested an oxidative mechanism. Results have shown a risk of developing cardiovascular diseases during the progression of epilepsy. The influence of Hp polymorphism in modulating oxidative stress suggests that taking antioxidants may have a beneficial effect, especially in patients of phenotype Hp2-2.
The association between hyperuricemia and metabolic syndrome (MS) has been reported in many studies. The authors performed this cross-sectional study to determine the association between hyperuricemia and the MS among diabetic patients in Dakar. Type 2 diabetic patients received as part of their follow-up at the Marc Sankalé Center of Abass Ndao Hospital in Dakar were enrolled. For each patient, blood samples and 24 h urine collection were performed. Hyperuricemia was defined for uric acid concentrations > 416 µmol/l in men and > 357 µmol/l in women and the MS was evaluated according to WHO criteria. Statistical analysis was done using the XLSTAT 2019 software. A total of 153 type 2 diabetic patients were included with an average age of 56.63 years. Thirty-one percent (31%) of patients had metabolic syndrome and 32% of them had hyperuricemia. Significant correlations were found between serum uric acid and some components of the MS including triglyceride levels (r = 0.25, p = 0.002), microalbuminuria (r = 0.19, p = 0.018), and fasting glucose (r = -0.22, p = 0.005). The authors found that hyperuricemia is frequent in patients with MS and this could be considered as a biomarker associated with the presence of this syndrome.
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