Erschienen in:
21.04.2016 | Nephrology - Original Paper
Retrospective analysis of lactic acidosis-related parameters upon and after metformin discontinuation in patients with diabetes and chronic kidney disease
verfasst von:
Savas Sipahi, Yalcin Solak, Seyyid Bilal Acikgoz, Ahmed Bilal Genc, Mehmet Yildirim, Ulku Yilmaz, Ahmet Nalbant, Ali Tamer
Erschienen in:
International Urology and Nephrology
|
Ausgabe 8/2016
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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.