Should dialysis be offered in all cases of metformin-associated lactic acidosis 英文参考文献.docVIP

Should dialysis be offered in all cases of metformin-associated lactic acidosis 英文参考文献.doc

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Should dialysis be offered in all cases of metformin-associated lactic acidosis 英文参考文献

Available online /content/13/1/110 Commentary Should dialysis be offered in all cases of metformin-associated lactic acidosis? S Neil Finkle Capital Health, 5089 Dickson Centre, 5820 University Avenue, Halifax, Nova Scotia, Canada, B3H 1V8 Corresponding author: S Neil Finkle, neil.finkle@cdha.nshealth.ca Published: 9 January 2009 Critical Care 2009, 13:110 (doi:10.1186/cc7161) This article is online at /content/13/1/110 ? 2009 BioMed Central Ltd See related research by Peters et al., /content/12/6/R149 Abstract filtration rates (eGFRs) of less than 60 mL/minute and not at all in eGFRs of less than 30 mL/minute [5]. Identified risk factors for MALA include acute kidney injury (AKI), hypoxe- mia, sepsis, alcohol abuse, liver failure, myocardial infarction, and shock [6]. Medications that interfere with renal hemo- Metformin is commonly used in diabetes mellitus type 2, with lactic acidosis being a rare but potentially fatal complication of this therapy. The management of metformin-associated lactic acidosis (MALA) is controversial. Treatment may include supportive care, activated charcoal, bicarbonate infusion, hemodialysis, or continuous venovenous hemofiltration. In the previous issue of Critical Care, Peters and colleagues systematically evaluated outcomes in MALA patients admitted to their intensive care unit. The mortality rate of patients who received dialysis was similar to that of patients who were not dialyzed. However, it was the more acutely and chronically ill patients who actually received dialysis. This suggests that hemodialysis was beneficial in preventing a higher mortality rate in those who required renal replacement therapy. dynamic autoregulation (that is, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and non- steroidal anti-inflammatory drugs) and volume depletion are frequently implicated in generating the AKI leading

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