BACKGROUND: In patients with chronic renal disease, other lipid markers than total cholesterol or low density lipoprotein (LDL)-cholesterol are probably more appropriate to detect a potential lipid-related risk for progression to renal failure. Statin therapy might be protective. METHODS: From 1999 to 2001, 177 consecutive patients with renal disease from our out-patient clinic were included and 169 could be followed-up for a mean period of 4.1 years. Seventy-two progressive patients (end-stage chronic renal disease or >5 ml/min/year decrease of creatinine clearance) were compared in 97 patients with stable or slowly progressive disease (<5 ml/min/year decrease). Throughout the study all patients were treated according to nephrology guidelines. Atorvastatin was instituted in patients with elevated LDL-cholesterol (LDL-C) after the baseline determinations RESULTS: Proteinuria, mean arterial pressure and the type of underlying renal disease were independently associated with progressive renal disease. After adjustment for these factors and whether or not statin therapy was started, an increase in plasma apo B concentration was the most predictive lipid parameter for renal failure. An increase in apo B from 0.77 g/l (10th percentile) to 1.77 g/l (90th percentile) was associated with progressive loss of renal function, represented by an odds ratio of 2.63 (95% CI: 1.02-6.76; P = 0.045). Treatment with atorvastatin in the dyslipidaemic patients to lower LDL-C, was also accompanied by a reduction of proteinuria in this group (P < 0.001). The patients who reached the target level for LDL-C of <2.6 mmol/l in response to atorvastatin showed less often progression than patients with higher LDL-C (P = 0.010). CONCLUSIONS: A high apo B at baseline appeared to be the strongest risk factor among various lipid parameters for progression of renal failure during the following years. Atorvastatin, aimed at lowering LDL-C, reduced proteinuria. Renal outcome was better in patients with the lowest LDL-C on treatment.
BACKGROUND: In patients with chronic renal disease, other lipid markers than total cholesterol or low density lipoprotein (LDL)-cholesterol are probably more appropriate to detect a potential lipid-related risk for progression to renal failure. Statin therapy might be protective. METHODS: From 1999 to 2001, 177 consecutive patients with renal disease from our out-patient clinic were included and 169 could be followed-up for a mean period of 4.1 years. Seventy-two progressive patients (end-stage chronic renal disease or >5 ml/min/year decrease of creatinine clearance) were compared in 97 patients with stable or slowly progressive disease (<5 ml/min/year decrease). Throughout the study all patients were treated according to nephrology guidelines. Atorvastatin was instituted in patients with elevated LDL-cholesterol (LDL-C) after the baseline determinations RESULTS:Proteinuria, mean arterial pressure and the type of underlying renal disease were independently associated with progressive renal disease. After adjustment for these factors and whether or not statin therapy was started, an increase in plasma apo B concentration was the most predictive lipid parameter for renal failure. An increase in apo B from 0.77 g/l (10th percentile) to 1.77 g/l (90th percentile) was associated with progressive loss of renal function, represented by an odds ratio of 2.63 (95% CI: 1.02-6.76; P = 0.045). Treatment with atorvastatin in the dyslipidaemic patients to lower LDL-C, was also accompanied by a reduction of proteinuria in this group (P < 0.001). The patients who reached the target level for LDL-C of <2.6 mmol/l in response to atorvastatin showed less often progression than patients with higher LDL-C (P = 0.010). CONCLUSIONS: A high apo B at baseline appeared to be the strongest risk factor among various lipid parameters for progression of renal failure during the following years. Atorvastatin, aimed at lowering LDL-C, reduced proteinuria. Renal outcome was better in patients with the lowest LDL-C on treatment.
Authors: Vasilios G Athyros; Anna I Kakafika; Athanasios A Papageorgiou; Efstathios D Pagourelias; Savvas D Savvatianos; Moses Elisaf; Asterios Karagiannis; Konstantinos Tziomalos; Dimitri P Mikhailidis Journal: Open Cardiovasc Med J Date: 2007-07-28