Devaki R. Nair

We comment on the role of dyslipidaemia in cardiovascular disease (CVD) in HIV-infected patients. We have discussed various risk factors, including traditional CVD risk factors, HIV-related risk factors and antiretroviral therapy (ART)-induced dyslipidaemia. HIV-infected individuals are prone to lipid and lipoprotein abnormalities as a result of the infection itself and the effect of ART. The older drugs used for the treatment of HIV were associated with an increased risk of these abnormalities. New therapies used to treat HIV are lipid friendly. Calculating CVD risk in the HIV population is complex due to the infection itself and the ART-related factors. The advancement in ART has helped to increase the life expectancy of HIV patients. As a result, a growing number of patients die of non-HIV related complications such as CVD, hepatic and renal disease. Outcome studies with intervention for dyslipidaemia in HIV are underway. The implications of the above findings suggest that all patients with HIV should undergo a CVD risk assessment before starting ART. Appropriate lipid-friendly ART regimen should be initiated along with intervention for associated CVD risk factors (e.g. lipids, hypertension and smoking).

Background: Chronic kidney disease (CKD) is associated with increased vascular risk. Some studies suggested that considering markers of CKD might improve the predictive accuracy of the Framingham risk equation. Aim: To evaluate the links between kidney function and risk stratification in patients with primary dyslipidemia. Methods: Dyslipidemic patients (n = 156; 83 men) who were non-smokers, did not have diabetes mellitus or evident vascular disease and were not on lipid-lowering or antihypertensive agents were recruited. Creatinine clearance (CrCl) was estimated using the Cockcroft-Gault equation. Estimated glomerular filtration rate (eGFR) was calculated using the Modification of Diet in Renal Disease (MDRD) equation. We estimated vascular risk using the Framingham equation. Results: In both men and women, there was a significant negative correlation between estimated Framingham risk and both eGFR and CrCl (p < 0.001 for all correlations). When men were divided according to creatinine tertiles, there were no significant differences in any parameter between groups. When men were divided according to either eGFR or CrCl tertiles, all estimated Framingham risks significantly increased as renal function declined (p<0.001 for all trends). When women were divided according to creatinine tertiles, all estimated Framingham risks except for stroke significantly increased as creatinine levels increased. When women were divided according to either eGFR or CrCl tertiles, all estimated Framingham risks significantly increased as renal function declined. Conclusions: Estimated vascular risk increases as renal function declines. The possibility that incorporating kidney function in the Framingham equation will improve risk stratification requires further evaluation.