Abstract
Abstract Background and Aims Chronic kidney disease (CKD) is a cardiovascular risk factor per sé and enhances the risk of cardiovascular events. Dyslipidemia is one of the most studied risk factors and current guidelines recommend the universal treatment in CKD patients (not in dialysis) irrespective of low density lipoprotein (LDL) cholesterol level. However, the latest European Cardiology guidelines recommend monitoring LDL cholesterol to achieve levels lower than 70 mg/dl in CKD stage 3 and lower than 55 mg/dl in stages 4 and 5. Proprotein convertase subtilisin-kexin type 9 inhibitors (PCSK9i) have opened a new era leading greater reduction of LDL cholesterol and subsequently cardiovascular events but real-life data is not available in CKD patients. The aim of the present study is analysing the evolution of renal function and proteinuria in a cohort of patients with PCSK9i. Method This is a retrospective study that included all the patients treated with PCSK9i in our centre. Inclusion criteria were the presence of CKD and dyslipidemia with indication of the use of PCSK9i (not reaching LDL target with maximum tolerated statin dose or intolerance for the use of statins). At baseline, epidemiological data and comorbidities were collected, as well as renal function using glomerular filtration rate (GFR) estimation with CKD-EPI equation, proteinuria (mg/g of creatinine) and lipid profile. During a one-year follow up, renal function, proteinuria, lipid profile and adverse events were collected and analysed. Results: . Forty-one patients were included with a mean age of 70±10 years and 26 men (62%). Thirty-four patients (83%) had hypertension, 11 (27%) were diabetic, 19 (44%) had coronary disease, 8 (20%) history of heart failure, 3 (7%) peripheral vascular disease and 6 (15%) history of stroke. Regarding renal function, at baseline mean of creatinine was 1.3±0.5 mg/dl, GFR 54±19 ml/min/1.73m2 and proteinuria 456±215 mg/g. Lipid profile at baseline demonstrated an LDL cholesterol value of 163±58 mg/dl, triglycerides of 255±389 mg/dl and high density lipoprotein (HDL) of 53±14mg/dl. During follow up, total cholesterol, LDL-cholesterol and triglycerides improved significantly (p<0.001 for all in comparison to baseline values). GFR remained stable during the first year of follow up (CKD-EPI at 1 year 52±20 ml/min/1.73m2). Proteinuria improved at first month (235±71 mg/g), achieving stability at 3 months (124±44 mg/g), 6 months (176±94 mg/g) and 1 year (163±83 mg/g) (p for trend 0.02) (figure 1). No adverse events were registered during follow up, and two patients required hospitalization due to cardiovascular events. Conclusion The treatment of dyslipidemia with PCSK9i could decrease proteinuria in CKD patients via controlling lipoid nephrotoxicity. Clinical trials are needed to further investigate this effect.
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