Savas Sipahi1, Yalcin Solak2, Seyyid Bilal Acikgoz3, Ahmed Bilal Genc3, Mehmet Yildirim3, Ulku Yilmaz3, Ahmet Nalbant3, Ali Tamer3. 1. Division of Nephrology, Department of Internal Medicine, Sakarya University Faculty of Medicine, Adnan Menderes Cd. Saglik Sok. No: 195, 54100, Adapazari/Sakarya, Turkey. ssipahi@sakarya.edu.tr. 2. Division of Nephrology, Department of Internal Medicine, Sakarya University Faculty of Medicine, Adnan Menderes Cd. Saglik Sok. No: 195, 54100, Adapazari/Sakarya, Turkey. 3. Department of Internal Medicine, Sakarya University Faculty of Medicine, Sakarya, Turkey.
Abstract
PURPOSE: To investigate association between renal functions, lactic acid levels and acid-base balance in type 2 diabetes patients with chronic kidney disease under metformin treatment and after metformin discontinuation in a real-life setting. METHODS: A total of 65 patients with diabetes (mean age 68.5 ± 8.9 years, 56.9 % females) in whom metformin treatment was discontinued due to reduced glomerular filtration rate (GFR) were included in this retrospective study. Data on patient demographics, metformin treatment and laboratory findings on the last day of metformin treatment and 2-3 weeks after metformin discontinuation including blood lactate and creatinine, estimated glomerular filtration rate (eGFR) and acid-base balance measurements in blood [pH, bicarbonate, base excess] were collected from medical records. The correlation of lactate levels with eGFR, blood pH and creatinine levels and changes in laboratory findings after metformin discontinuation were evaluated. RESULTS: Before metformin discontinuation, hyperlactatemia was observed in 78.5 % of patients and metabolic acidosis in 36.9 % of patients, but none had lactic acidosis. Patients with normolactatemia and hyperlactatemia were similar in terms of metformin dosage and laboratory parameters. Lactate levels were not significantly correlated with serum creatinine (r = -0.14; p = 0.263) and eGFR (r = 0.11, p = 0.374). After metformin discontinuation, a significant decrease was observed in median lactate levels (from 2.20 to 1.85 mmol/L; p = 0.002). CONCLUSION: In conclusion, our findings support the low risk of MALA among patients with mild-to-moderate renal impairment and the likelihood of metformin to be an innocent bystander without a pathogenic role in the lactic acidosis in most cases.
PURPOSE: To investigate association between renal functions, lactic acid levels and acid-base balance in type 2 diabetespatients with chronic kidney disease under metformin treatment and after metformin discontinuation in a real-life setting. METHODS: A total of 65 patients with diabetes (mean age 68.5 ± 8.9 years, 56.9 % females) in whom metformin treatment was discontinued due to reduced glomerular filtration rate (GFR) were included in this retrospective study. Data on patient demographics, metformin treatment and laboratory findings on the last day of metformin treatment and 2-3 weeks after metformin discontinuation including blood lactate and creatinine, estimated glomerular filtration rate (eGFR) and acid-base balance measurements in blood [pH, bicarbonate, base excess] were collected from medical records. The correlation of lactate levels with eGFR, blood pH and creatinine levels and changes in laboratory findings after metformin discontinuation were evaluated. RESULTS: Before metformin discontinuation, hyperlactatemia was observed in 78.5 % of patients and metabolic acidosis in 36.9 % of patients, but none had lactic acidosis. Patients with normolactatemia and hyperlactatemia were similar in terms of metformin dosage and laboratory parameters. Lactate levels were not significantly correlated with serum creatinine (r = -0.14; p = 0.263) and eGFR (r = 0.11, p = 0.374). After metformin discontinuation, a significant decrease was observed in median lactate levels (from 2.20 to 1.85 mmol/L; p = 0.002). CONCLUSION: In conclusion, our findings support the low risk of MALA among patients with mild-to-moderate renal impairment and the likelihood of metformin to be an innocent bystander without a pathogenic role in the lactic acidosis in most cases.
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