Lipid profile in pre-dialysis chronic kidney disease patients attending University of Maiduguri Teaching Hospital, Maiduguri-Nigeria.

BACKGROUND/OBJECTIVES: Cardiovascular disease is a major cause of morbidity and mortality among patients with chronic kidney disease, and accounts for 50% of all deaths in them. Dyslipidaemia does not only accelerate atherosclerosis in these patients but also progresses the renal disease. This study therefore set to investigate the pattern of lipid profile in pre-dialysis chronic kidney disease patients. METHODS: This was case control study of 63 pre-dialysis chronic kidney disease patients attending University of Maiduguri teaching Hospital and 60 control subjects. All factors that may lead to dyslipidaemia were excluded in all subjects except hypertension. Lipid profiles were measured by standard methods. Data were analyzed using a statistical software SPSS version 11.0. Their observed differences in mean-SEM values were analyzed for statistical significance using Student's t-test andp-value <0.05 was considered significant. RESULTS: the mean+SEM of total cholesterol 4.50+0.14 mmol/L and triglycerides 2.18+0.10 mmol/L in patients were significantly higher than that of the controls 3.79+0.11 mmol/L and 1.19+0.06 mmol/L respectively, p<0.05. Similarly the mean+SEM of LDL 2.62+0.16 mmol/L and LDL/HDL ratio 3.53+0.12 in patients were significantly higher when compared to that of the controls 2.04+0.16 mmol/L and 2.04+0.08 respectively, p<0.05. However, although the mean+SEM HDL in patient 1.07+0.07 mmol/L, was lower than that of the controls 1.21+0.06 mmol/L, the difference was not statistically significant, p>0.05. The pattern of lipid profile did not change with severity of disease and dyslipidaemia in patients were more in triglycerides, 68.3% and HDL, 63.5% than in TC, 22.2% and LDL, 17.5%. CONCLUSION: Dyslipidaemia is common in pre-dialysis chronic kidney disease patients. It is pertinent to investigate and treat dyslipidaemia early in the course of the disease as it may prevent further progression of the renal damage.

Characterization of sialidase from bloodstream forms of Trypanosoma vivax.

Sialidase (EC: 3.2.1.18) from Trypanosoma vivax (Agari Strain) was isolated from bloodstream forms of the parasite and purified to apparent electrophoretic homogeneity. The enzyme was purified 77-fold with a yield of 32% and co-eluted as a 66-kDa protein from a Sephadex G 110 column. The T. vivax sialidase was optimally active at 37 degrees C with an activation energy (E(a)) of 26.2 kJ mole(-1). The pH activity profile was broad with optimal activity at 6.5. The enzyme was activated by dithiothreitol and strongly inhibited by para-hydroxy mercuricbenzoate thus implicating a sulfhydryl group as a possible active site residue of the enzyme. Theenzyme hydrolysed Neu5Ac2,3lac and fetuin. It was inactive towards Neu5Ac2,6lac, colomic acid and the gangliosides GM1, and GDI. Initial velocity studies, for the determination of kinetic constants with fetuin as substrate gave a V(max) of 142.86 micromol h(-1) mg(-1) and a K(M) of 0.45 mM. The K(M) and V(max) with Neu5Ac-2,3lac were 0.17 mM and 840 micromole h(-1) mg(-1) respectively. The T. vivax sialidase was inhibited competitively by both 2,3 dideoxy neuraminic acid (Neu5Ac2,3en) and para-hydroxy oxamic acid. When ghost RBCs were used as substrates, the enzyme desialylated the RBCs from camel, goat, and zebu bull. The RBCs from dog, mouse and ndama bull were resistant to hydrolysis.