MO411: SGLT2 Inhibitors Use in Chronic Kidney Disease-Better Cardiometabolic Profile

Abstract

Abstract BACKGROUND AND AIMS SGLT2 inhibitors have been shown to reduce kidney and cardiovascular events and slowing the decline of renal function in chronic kidney disease. We have examined the effect of SGLT2 inhibition in our cohort of ambulatory patients METHOD We have included patients with chronic kidney disease, with or without diabetes, fulfilling the criteria for SGLT2 prescription (dapagliflozin and empagliflozin). Eligible patients were started on SGLT2 inhibitors from January to August 2021. Blood pressure, estimated pulse wave velocity, kidney function according to KDIGO; estimated glomerular filtration rate (GFR), chronic kidney disease (CKD) EPI and albuminuria, as well as metabolic profile (lipids, HbA1C, uric acid) measurements were done at the beginning and follow-up. Exclusion criteria were recurrent urinary infection, CKD stage 4 and more, immunosuppressive therapy, diabetes mellitus type 1. Non-parametric statistical tests were used due to sample size, median, 25 and 75 percentile were stated for continuous variables and number and percentage for categorical variables. RESULTS A total of 49 patients were enrolled, the average age of 66 years (min-max ranging from 25–75 years), with male predominance (N = 32, 65%). 48% of them completed the follow-up of 4 months (ranging from 3 to 6). A total of 22% had a history of myocardial infarction and/or cerebrovascular incident. Two patients were excluded due to intolerance, one due to non-adherence and one patient was transferred to another hospital. Patients mostly had chronic kidney disease accompanied by diabetes mellitus (DM) type II (N = 31, 63%), 5 (10%) had glomerulonephritis and others (N = 4) had CKD of other origins. There was expected fall in eGFR (median 58 versus median 53 mL/min/1.73m²; P = 0.036) and rise in creatinine values (median 111 versus median 119 umol/L; P = 0.045). No significant change in proteinuria [median 0.71 (interquartile range, IQR 0.20–1.23) versus median 0.30 (IQR 0.13–0.59); P = 0.060] nor albuminuria (median 72, IQR 19–720 mg/dU versus median 76 IQR 9–334 mg/dU; P = 0.327) was observed. A total of 35 (92.5%) patients were on RAAS blockade and doses of antihypertensive therapy were not upscaled. There was a statistically significant decline in systolic blood pressure (median 136 versus median 132 mmHg; P = .047) and diastolic blood pressure (median 83 versus median 80.9 mmHg; P = 0.041). There was a significant increase in mean arterial pressure (median 99 versus median 101; P = 0.006) and estimated pulse wave velocity (median 7.65 versus median 8.62; P < .001). There was a trend toward reduction of serum uric acid levels (median 334 mmol/L versus median 265mmol/L; P = 0.182). Glycaemic control was improved with significant change in blood glucose levels (median 6.9 mmol/L versus median 6.1 mmol/L; P = 0.03) as well as Hba1c (median 7.2 versus 6.1, P = 0.013). There were no significant adverse effects in our cohort. CONCLUSION SGLT2 inhibitors can be safely used in patients with chronic kidney disease with benefits on blood pressure and metabolic profile which is of utmost importance in this population of very high risk for cardiovascular, as well as, cerebrovascular events. There was a slight decline in kidney function in our cohort which is expected after the initiation of therapy. The effect on estimated pulse wave velocity was not established in our cohort, probably due to the short period of follow-up. Further follow-up of our cohort is needed to establish the lasting effect of SGLT2 inhibitors.