Use of metformin in patients who require intravascular administration of a contrast agent

Abstract

ExpErt opinionas well as MATE1 and MATE2-K located in the renal tubular cells. Polymorphism of genes encoding metformin transport membrane proteins or the influence of other drugs on these proteins (e.g. inhibition of the MATE protein by cimetidine) may have a direct impact on the pharmacokinetics of metformin, the variability of the drug response, and the toxic effect of the drug in a particular patient [2,3]. In impaired renal function with decreased creatinine clearance, renal clearance of metformin is also decreased, leading to a prolonged metformin half-life and increased plasma levels. This mechanism may lead to the development of lactic acidosis in patients taking metformin and suffering from acute or chronic kidney disease with significantly reduced glomerular filtration rates [1,3].One of the mechanisms of action of metformin is to inhibit hepatic gluconeogenesis by blocking mitochondrial glycerophosphate dehydrogenase (mGDP), an enzyme that links carbohydrate and lipid metabolic pathways. The action of metformin on the mGDP enzyme hinders the conversion of glycerol-3-phosphate to dihydroxyacetone phosphate (DHAP) and thus blocks gluconeogenesis from glycerol. Due to the influence of metformin on this part of the metabolic pathway, the concentration of oxidized nicotine adenine dinucleotide (NAD+) is decreased, which leads to impaired