Malnutrition in pre-dialysis chronic kidney disease patients in a teaching hospital in Southern Nigeria.

Background: Malnutrition is a complication in chronic kidney disease (CKD) known to affect quality of life and prognosis although not often diagnosed. It is associated with rapid progression to end stage renal disease (ESRD) and mortality. Early identification and treatment will slow down progression to ESRD and mortality. Objective: To determine the prevalence and pattern of malnutrition in pre-dialysis CKD patients in Southern Nigeria. Methods: One hundred and twenty consecutive pre-dialysis CKD and 40 control subjects without CKD were studied. Data obtained from participants were demographics, body mass index (BMI), and aetiology of CKD. Indices used to assess presence of malnutrition were low BMI, hypocholesterolaemia and hypoalbuminaemia. Statistical significance was taken at 0.05 level. Results: The mean age of the CKD subjects was 48.8±16.6years with a male: female ratio of 1.7:1. Prevalence of malnutrition in the CKD subjects was 46.7%, higher than 27.5% observed in the controls (p=0.033). Prevalence of malnutrition increased significantly across CKD stages 2 to 5 (p=0.020). It was significantly commoner in elderly patients (p=0.047) but not significantly different between males and females(p=0.188). Conclusion: Malnutrition is common in pre-dialysis CKD patients even in early CKD stages. Prevalence of malnutrition increases with worsening kidney function and increasing age.

Expression and Role of CD166 in the Chronic Kidney Disease

Background: CD166, an adhesion molecule of the immunoglobulin superfamily, is one of the crucial effectors that traffic lymphocytes into tissues. Till now, the expression and role of CD166 in the chronic kidney disease remains unknown. Objectives: In the present study, we are to examine the expression of CD166 in the chronic kidney disease, and to explore its function with CD4+ T cells. Materials and Methods: CD166 expression was tested by Flow Cytometry (FACS) in the primary macrophages stimulated with LPS. In vivo, the expression of CD166 and CD4 were examined in the kidney tissues of adriamycin-induced nephropathy (AN) mice by immnohistochemistry. Macrophages and lymphocytes were co-cultured, the interaction between CD166 and CD4 was tested by immunofluorescent staining. Furthermore, the effects of CD166 on the activation and proliferation of T cells were explored. Results: In this study, CD166 expression was found to be upregulated on activated macrophages and glomerular endothelia in the adriamycin-induced nephropathy (AN) mice and CD4+ T cells were increased with CD166 expression in the AN mice. The interaction between macrophages and CD4+ T cells indicated that CD166 played a key role in the recruitment of lymphocytes in the chronic kidney disease, and neither proliferation nor activation of T cells was affected by CD166. Conclusions: CD166 expressed on macrophages and endothelia in AN kidney, and the function was related to the recruitment of CD4+ T cells into inflamed kidney, indicating that CD166 may be a potential target for reducing the inflammatory infiltrates in the chronic kidney disease.

Cardioprotective effects of Dan-Yang-Fu-Xin decoction on chronic heart failure in rats

Purpose: To evaluate the cardioprotective effects and possible mechanisms of Dan-Yang-Fu-Xin decoction (DYFX) in a rat chronic heart failure (CHF). Methods: A CHF rat model induced by ligation of the left anterior descending coronary artery was used to investigate the cardioprotective effects of DYFX. After intragastric administration for 8 weeks, several functional cardiac indices, including fractional shortening (FS), ejection fraction (EF), heart rate (HR) and cardiac output (CO) were assessed by ultrasound examination. Subsequently, inflammatory markers, viz, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), myocardial enzymes, namely, lactate dehydrogenase (LDH) and creatine kinase (CK), were also assessed by enzyme-linked immunosorbent assay (ELISA). Results: Intragastric administration of DYFX (200, 400 and 600 mg/kg) significantly reversed the decrease in body weight and increase in cardiac weight (p < 0.05) induced by CHF. Treatment with DYFX also significantly reversed EF, FS, HR, and CO changes in CHF rats. In addition, DYFX inhibited the two inflammatory cytokines (TNF-α and IL-6) and myocardial enzymes (CK and LDH), suggesting that these effects may include the mechanisms of cardioprotectiion involved in attenuation of CHF. Conclusion: DYFX possesses cardioprotective effects involving CHF. The protective mechanisms may include the suppression of expression of inflammatory mediators and myocardial enzymes.