diabetestalk.net

Metformin Acute Kidney Injury

A Case Of Metformin-induced Acute Kidney Injury Without Lactic Acidosis: A Case Report

A Case Of Metformin-induced Acute Kidney Injury Without Lactic Acidosis: A Case Report

A Case of Metformin-Induced Acute Kidney Injury without Lactic Acidosis: A Case Report *** A Case of Metformin-Induced Acute Kidney Injury without Lactic Acidosis: A Case Report 1Department of Internal Medicine, Hanyang University College of Medicine, Seoul, Korea. [email protected] 2Department of Internal Medicine, Hanyang University College of Medicine, Guri, Korea. Metformin is an oral antidiabetic drug in the biguanide class, which is used for type 2 diabetes. The side effects of metformin are mostly limited to digestive tract symptoms, such as diarrhea, flatulence and abdominal discomfort. The most serious potential adverse effect of metformin is lactic acidosis. A 51-year-old man was admitted due to hypoglycemia as a result of an overdose of antidiabetic drugs. He took massive dose of metformin. Conservative treatment failed for metabolic acidosis without lactic acidosis accompanied by acute kidney injury. Hemodialysis was executed to correct the high anion gap metabolic acidosis and acute kidney injury, and the patient recovered fully from metabolic acidosis. This case illustrates that the presence of clinical conditions, such as metformin-induced acute kidney injury and metabolic acidosis, can be developed without lactic acidosis. Prompt recognition of metabolic acidosis and early intervention with hemodialysis can result in a successful clinical outcome. Continue reading >>

Metformin-associated Acute Kidney Injury And Lactic Acidosis

Metformin-associated Acute Kidney Injury And Lactic Acidosis

Copyright © 2011 David Arroyo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Objectives. Metformin is the preferred oral antidiabetic agent for type 2 diabetes. Lactic acidosis is described as a rare complication, usually during an acute kidney injury (AKI). Material and Methods. We conducted a prospective observational study of metformin-associated AKI cases during four years. 29 cases were identified. Previous renal function, clinical data, and outcomes were recorded. Results. An episode of acute gastroenteritis precipitated the event in 26 cases. Three developed a septic shock. Three patients died, the only related factor being liver dysfunction. More severe metabolic acidosis hyperkalemia and anemia were associated with higher probabilities of RRT requirement. We could not find any relationship between previous renal dysfunction and the outcome of the AKI. Conclusions. AKI associated to an episode of volume depletion due to gastrointestinal losses is a serious complication in type 2 diabetic patients on metformin. Previous renal dysfunction (mild-to-moderate CKD) has no influence on the severity or outcome. 1. Introduction Metformin is the only biguanide extensively used these days, and has become the first-line oral drug in type 2 diabetes [1]. Metformin-associated lactic acidosis has not been thoroughly characterized. Meta-analyses and large studies have been unable to establish an epidemiological association, probably due to its low incidence rate. However, most cases have been reported associated with an episode of acute kidney injury (AKI), predominantly in intensive care units [ Continue reading >>

Pancreatitis And Metformin: Case-report And Review Of Literature

Pancreatitis And Metformin: Case-report And Review Of Literature

Received date: October 05, 2016; Accepted date: October 20, 2016; Published date: October 24, 2016 Citation: Gioia S, Lancia M, Persichini A, Tondi V, Bacci M, et al. (2016) Pancreatitis and Metformin: Case-Report and Review of Literature. JHepatol Gastroint Dis 2:138. doi:10.4172/2475-3181.1000138 Copyright: 2016 Gioia S, et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Metformin is the most used anti-hyperglycemic agent for the treatment of Type 2 Diabetes Mellitus. It is considered a very good drug, with low risk and high benefit. Metformin intoxication can be due to massive ingestion or to a progressive accumulation due to renal failure. Fatal cases due to metformin intoxication have been described. With regard to that we present a fatal case of a fifty-six-year-old patient with severe metformin intoxication (100 g/ml) who presented kidney failure, lactic acidosis, hyperglycemia and pancreatitis. He received alkalinization and hemodialysis therapy, afterwards which shortly hereby improved his condition, but the patient deceased after 7 days for a nosocomial pneumonia. Pancreatitis was confirmed by the post-mortem histopathological analysis. Acute pancreatitis as side effect of metformin is very rare, either in overdose or therapeutic dosage, and it has been attributed to an intrinsic toxicity mechanism. With regard to that, we performed a review of the literature of all cases in which pancreatitis was referred to metformin use in order to evaluate if this complication usually develops in presence of specific predisposing factors, or if it is unpredictable. From our review, a Continue reading >>

Use Of Metformin In The Setting Of Mild-to-moderate Renal Insufficiency

Use Of Metformin In The Setting Of Mild-to-moderate Renal Insufficiency

ADVANTAGES OF METFORMIN There is some evidence that early treatment with metformin is associated with reduced cardiovascular morbidity and total mortality in newly diagnosed type 2 diabetic patients (4). However, the data come from a small subgroup of a much larger trial. In contrast, despite multiple trials of intensive glucose control using a variety of glucose-lowering strategies, there is a paucity of data to support specific advantages with other agents on cardiovascular outcomes (5–7). In the original UK Prospective Diabetes Study (UKPDS), 342 overweight patients with newly diagnosed diabetes were randomly assigned to metformin therapy (8). After a median period of 10 years, this subgroup experienced a 39% (P = 0.010) risk reduction for myocardial infarction and a 36% reduction for total mortality (P = 0.011) compared with conventional diet treatment. Similar benefits were not observed in those randomly assigned to sulfonylurea or insulin. In an 8.5-year posttrial monitoring study, after participants no longer were randomly assigned to their treatments, individuals originally assigned to metformin (n = 279) continued to demonstrate a reduced risk for both myocardial infarction (relative risk 33%, P = 0.005) and total mortality (relative risk 27%, P = 0.002) (9). The latter results are even more impressive when one considers that HbA1c levels in all initially randomly assigned groups had converged within 1 year of follow-up. Unlike sulfonylureas, thiazolidinediones, and insulin, metformin is weight neutral (10), which makes it an attractive choice for obese patients. Furthermore, the management of type 2 diabetes can be complicated by hypoglycemia, which can seriously limit the pursuit of glycemic control. Here, too, metformin has advantages over insulin and some Continue reading >>

Metformin And Acute Kidney Injury: Is It The Culprit?

Metformin And Acute Kidney Injury: Is It The Culprit?

Endocrine Abstracts (2014) 34 P251 | DOI: 10.1530/endoabs.34.P251 Metformin and acute kidney injury: is it the culprit? Blackpool Victoria Hospital, Blackpool, UK. Three people (two males), with mean age (range) 65 (4975) years, presented as emergencies with acute renal failure (AKI). They had type 2 diabetes mellitus, with mean duration 7 (212) years. All three were taking anti-hypertensive therapy: two were on ramipril and one on losartan and indapamide. All three were taking metformin with mean daily dose 2.6 (1.73.0) g. All three patients had mild renal impairment (CKD stage 3), but renal function was stable 23 months before presentation with mean blood urea 8.1 (5.69.5) mmol/l, creatinine 118 (108133) mol/l and eGFR 49 (4359) ml/min per l. They presented with a 1 week history of symptoms including vomiting (2), diarrhoea (2), unsteadiness (3), confusion (1), and falls (2). On admission the mean blood glucose was 8.5 (4.913.0) mmol/l, urea 32 (22 42) mmol/l, and creatinine 763 (652978)mol/l. They were acidotic with mean pH 7.19 (7.157.23), bicarbonate 15.6 (10.321.2) mmol/l, and lactate 3.6 (2.05.9) mmol/l. The mean blood metformin level was raised at 12.2 (11.014.3) mg/l. The accepted therapeutic range is 0.52.0 mg/l). Metformin, ramipril, losartan and indapamide were discontinued. One patient required haemofiltration but in all three urine output soon improved with i.v. fluid therapy. Renal function was back to baseline 23 months later with mean blood urea 7.5 (6.88.4) mmol/l, creatinine 113 (104131) mol/l and eGFR 52 (4560) ml/min per l. Metformin is eliminated, unchanged, by renal excretion. We suggest that inappropriately high metfomin doses in these patients with mild renal impairment has led to escalating blood metformin levels, which in turn largely account Continue reading >>

Metformin-lactic Acidosis Risk Greater With Acute Kidney Injury

Metformin-lactic Acidosis Risk Greater With Acute Kidney Injury

Metformin-lactic acidosis risk greater with acute kidney injury Acute kidney injury severity associated with increased risk of 5-year readmission and mortality | STS Data provide strong evidence for current recommendation to omit metformin in any illness that may precipitate acute kidney injury (AKI), such as diarrhea or vomiting. Evidence supporting the recommendation has been lacking. Population-based case-control study including 1746 patientswith type 2 diabetes (T2D) and 846 people without diabetes, all with lactate measurements. Lactic acidosis was identified in 82 individuals, and of those, AKI was present in 79.3%. Lactic acidosis risk was higher in metformin users (OR, 2.3; P=.002), increasing with AKI severity (ORs ranging from 3.0 for stage 1 [P=.002] to 16.1 for stage 3 [P<.001]). In multivariate analysis of metformin users, development of lactic acidosis was associated with AKI stage 1 (OR, 3.8; P=.009), stage 2 (OR, 10.5; P<.001), stage 3 (OR, 24.6; P<.001), chronic kidney disease stages with estimated glomerular filtration rate <60 mL/min/1.73m2(OR, 2.7; P=.021), and HbA1c (OR, 1.2; P=.02). Metformin users more likely to have lactate measured. Several potential confounders could not be directly assessed (ie, admission reason, intravenous contrast medium use, or contributing comorbidities). Bicarbonate, not direct arterial pH, used to identify lactic acidosis. Only healthcare professionals with a Univadis account have access to this article. You have reached your limit of complementary articles Free Sign Up Available exclusively to healthcare professionals Continue reading >>

Metformin-associated Lactic Acidosis Following Acute Kidney Injury. Efficacious Treatment With Continuous Renal Replacement Therapy.

Metformin-associated Lactic Acidosis Following Acute Kidney Injury. Efficacious Treatment With Continuous Renal Replacement Therapy.

A comment on this article appears in " Type 2 diabetes, metformin and lactic acidosis-defining the risk and promoting safe practice. " Diabet Med. 2012 Feb;29(2):161-3. INTRODUCTION: Metformin is a biguanide anti-hyperglycaemic drug. Metformin-associated lactic acidosis may sometimes be life-threatening. Continuous renal replacement therapy has been suggested as a method for resolving this extremely dangerous metabolic state. We describe the history of six patients admitted to the intensive care unit over a 28-month period in pre-shock conditions because of severe lactic acidosis, attributed to metformin-associated lactic acidosis, and successfully treated. METHODS: We reviewed the charts of six patients admitted to our intensive care unit between January 2008 and May 2010. After initial assessment, all patients were treated with continuous renal replacement therapy. Admission serum lactate and creatinine levels, pH, need for ventilatory and cardiovascular support, as well as continuous renal replacement therapy details and length of stay were reviewed. RESULTS: Admission pH levels of the six patients ranged between pH 6.63 and 7.0 and their serum lactate levels ranged between 12 and 27 mmol/l; the estimated creatinine clearance ranged between 6 and 24 ml min(-1) 1.73 m(-2) . All patients required vasoactive support and five required ventilatory support. Lactate levels decreased to near zero with continuous renal replacement therapy within 7-19 h in five of the patients whose intensive care unit length of stay ranged between 1 and 5 days. One patient's length of stay reached 11 days because of pneumonia, one died from multi-organ failure and another suffered permanent neurological damage following prolonged cardiopulmonary resuscitation before continuous renal replacem Continue reading >>

Acute Kidney Injury: A Guide To Diagnosis And Management

Acute Kidney Injury: A Guide To Diagnosis And Management

Acute kidney injury is characterized by abrupt deterioration in kidney function, manifested by an increase in serum creatinine level with or without reduced urine output. The spectrum of injury ranges from mild to advanced, sometimes requiring renal replacement therapy. The diagnostic evaluation can be used to classify acute kidney injury as prerenal, intrinsic renal, or postrenal. The initial workup includes a patient history to identify the use of nephrotoxic medications or systemic illnesses that might cause poor renal perfusion or directly impair renal function. Physical examination should assess intravascular volume status and identify skin rashes indicative of systemic illness. The initial laboratory evaluation should include measurement of serum creatinine level, complete blood count, urinalysis, and fractional excretion of sodium. Ultrasonography of the kidneys should be performed in most patients, particularly in older men, to rule out obstruction. Management of acute kidney injury involves fluid resuscitation, avoidance of nephrotoxic medications and contrast media exposure, and correction of electrolyte imbalances. Renal replacement therapy (dialysis) is indicated for refractory hyperkalemia; volume overload; intractable acidosis; uremic encephalopathy, pericarditis, or pleuritis; and removal of certain toxins. Recognition of risk factors (e.g., older age, sepsis, hypovolemia/shock, cardiac surgery, infusion of contrast agents, diabetes mellitus, preexisting chronic kidney disease, cardiac failure, liver failure) is important. Team-based approaches for prevention, early diagnosis, and aggressive management are critical for improving outcomes. The incidence of acute kidney injury has increased in recent years, both in the community and in hospital settings.1,2 Continue reading >>

Post-contrast Acute Kidney Injury. Part 2: Risk Stratification, Role Of Hydration And Other Prophylactic Measures, Patients Taking Metformin And Chronic Dialysis Patients

Post-contrast Acute Kidney Injury. Part 2: Risk Stratification, Role Of Hydration And Other Prophylactic Measures, Patients Taking Metformin And Chronic Dialysis Patients

Post-contrast acute kidney injury. Part 2: risk stratification, role of hydration and other prophylactic measures, patients taking metformin and chronic dialysis patients Recommendations for updated ESUR Contrast Medium Safety Committee guidelines The Contrast Media Safety Committee (CMSC) of the European Society of Urogenital Radiology (ESUR) has updated its 2011 guidelines on the prevention of post-contrast acute kidney injury (PC-AKI). The results of the literature review and the recommendations based on it, which were used to prepare the new guidelines, are presented in two papers. Topics reviewed include stratification of PC-AKI risk, the need to withdraw nephrotoxic medication, PC-AKI prophylaxis with hydration or drugs, the use of metformin in diabetic patients receiving contrast medium and the need to alter dialysis schedules in patients receiving contrast medium. In CKD, hydration reduces the PC-AKI risk Intravenous normal saline and intravenous sodium bicarbonate provide equally effective prophylaxis No drugs have been consistently shown to reduce the risk of PC-AKI Stop metformin from the time of contrast medium administration if eGFR < 30 ml/min/1.73 m 2 Dialysis schedules need not change when intravascular contrast medium is given Contrast mediaAcute kidney injuryMetforminHaemodialysisPractice guidelines Appraisal of Guidelines for Research and Evaluation Agency for Healthcare Research and Quality Oxford Centre for Evidence Based Medicine The Contrast Media Safety Committee (CMSC) of the European Society of Urogenital Radiology (ESUR) produced their most recent guidelines on what was then termed contrast-induced nephropathy (CIN) in 2011 [ 1 ]. Guidelines on the use of contrast media (CM) in patients on dialysis and on the use of CM in diabetic patients us Continue reading >>

Metformin-associated Lactic Acidosis Precipitated By Zoledronic Acidinduced Acute Kidney Injury: A Case Of Polypharmacy In An Elderly Patient

Metformin-associated Lactic Acidosis Precipitated By Zoledronic Acidinduced Acute Kidney Injury: A Case Of Polypharmacy In An Elderly Patient

Metformin-Associated Lactic Acidosis Precipitated by Zoledronic AcidInduced Acute Kidney Injury: A Case of Polypharmacy in an Elderly Patient Sharon Leung, MD, Darlene LeFrancois, MD, and Lewis A. Eisen, MD Zoledronic acid, a third-generation aminobisphosphonate, was approved by the U.S. Food and Drug Administration (FDA) in August 2007 for the treatment of osteoporosis in postmenopausal women. Although it is generally safe, careful postmarketing surveillance of patients who are prescribed zoledronic acid and are taking other nephrotoxic medications, or medications that can result in kidney failure, appears to be warranted. It may be prudent to temporarily withhold metformin therapy in patients who are to undergo zoledronic acid infusion therapy. We report a case of metformin-associated lactic acidosis precipitated by zoledronic acidinduced acute kidney injury in a 78-year-old woman with several chronic medical conditions who presented with profound hemodynamic instability, lactic acidosis with a low pH level, and a low core body temperature 3 weeks after receiving a single intravenous dose of zoledronic acid for osteoporosis treatment. The patient was in oliguric renal failure, and her serum metformin levels were approximately tenfold higher than the therapeutic reference range. A 78-year-old woman with a history of hypertension, type 2 diabetes mellitus, hyperlipidemia, and osteoporosis was found lying on the floor in her home, not alert, and unresponsive to vocal stimuli. Initial assessment by an emergency medical technician showed that the patient responded to painful stimuli by making incomprehensible sounds. There was no sign of injury. The physical examination was significant for cold and dry skin, and her pupils were unreactive to light. Her blood pressure was Continue reading >>

Metformin Intoxication With Severe Lactic Acidosis And Acute Kidney Injury Treated With Sustained Low-efficiency Dialysis (sled)

Metformin Intoxication With Severe Lactic Acidosis And Acute Kidney Injury Treated With Sustained Low-efficiency Dialysis (sled)

Metformin intoxication with severe lactic acidosis and Acute Kidney Injury treated with sustained low-efficiency dialysis (SLED) We report here on a case of MALA due to metformin accumulation in a diabetic patient with AKI on CKD, focusing on relevant pharmacokinetic issues that should guide the choice of the most appropriate modality of emergency renal replacement therapy (RRT). A 76-year-old man with type 2 diabetes, CKD (usual serum creatinine [sCr] concentration 1.8 mg/dL, eGFR 36 mL/min/1.73 m2) and ischemic cardiomyopathy presented with a 48-hour history of vomiting, abdominal pain, hypotension and oliguria after uncomplicated day-surgery for inguinal hernia three days earlier. His usual medications included aspirin 100 mg, ramipril 7.5 mg, bisoprolol 2.5 mg, furosemide 25 mg bid, metformin 1000 mg tid, glimepiride 1 mg. Physical examination revealed an oliguric 72 Kg man in moderate respiratory distress, with cold extremities and a large hematoma of the abdominal wall (7 x 6 cm on CT scan, extending to the scrotum and left thigh). Blood pressure was 90/50 mmHg while on dopamine 8 mg/Kg/min, pulse rate 56 beats/min, respirations 32 breaths/min, peripheral oxygen saturation 98% on 50% O2, tympanic temperature 35.5 C. Initial laboratory workup showed a severe anion gap (AG) metabolic acidosis with hyperlactatemia and AKI on CKD (Fig.1). Other routine serum values and urine toxicology tests were unremarkable. RRT was started with an AK 200ultra machine (Gambro/Baxter, Mirandola, Italy) and a 1.8 m2 polysulfone F8 HPS filter (Fresenius, Palazzo Pignano, Italy). A 16-hour sustained low-efficiency dialysis (SLED) session with regional citrate anticoagulationwas planned (blood flow rate 200 mL/min, bicarbonate [32 mmol/L] dialysis fluid rate 300 mL/min, countercurrent f Continue reading >>

Metformin And Contrast-induced Acute Kidney Injury In Diabetic Patients Treated With Primary Percutaneous Coronary Intervention For St Segment Elevation Myocardial Infarction: Amulticenter Study

Metformin And Contrast-induced Acute Kidney Injury In Diabetic Patients Treated With Primary Percutaneous Coronary Intervention For St Segment Elevation Myocardial Infarction: Amulticenter Study

Volume 220 , 1 October 2016, Pages 137-142 Metformin and contrast-induced acute kidney injury in diabetic patients treated with primary percutaneous coronary intervention for ST segment elevation myocardial infarction: Amulticenter study Author links open overlay panel MarianneZellera To analyze the association between chronic metformin treatment and the development of contrast-induced acute kidney injury (CI-AKI) after primary percutaneous coronary intervention (PCI) for ST segment elevation myocardial infarction (STEMI). Patients with type 2 diabetes mellitus (T2DM) treated with PCI <24h in 2 coronary care units were included. Serum creatinine (Cr) was measured before and <48h after PCI. CI-AKI was defined as an increase in Cr>27mol/l (0.3mg/dl) or >50% over baseline after PCI. Since PCI was urgent, metformin could not be withheld prior to PCI but was usually stopped after PCI. Among the 372 patients included, 147 (40%) were using metformin, which had older diabetes, but had risk factors similar to patients without metformin. Baseline eGFR was better in patients under metformin therapy. After PCI, we observed an increase of 10% in Cr, for both groups. There was a trend toward a lower rate of CI-AKI in patients under metformin (16% vs 25%, p=0.051). In patients with chronic kidney disease, 31 (26%) were under metformin therapy, and the rate of CI-AKI was similar in both groups (41% vs 40%, p=0.915). By multivariate analysis, metformin showed a trend toward a reduced rate of CI-AKI, even when adjusted for confounding (OR (95% CI): 0.548 (0.2761.087)). No case of lactic acidosis was reported during the hospital stay. Moreover, there was no increased rate of cardiogenic shock or death with metformin treatment. In this multicenter observational study, chronic metformin tr Continue reading >>

Risk Of Acute Kidney Injury And Survival In Patients Treated With Metformin: An Observational Cohort Study

Risk Of Acute Kidney Injury And Survival In Patients Treated With Metformin: An Observational Cohort Study

Risk of acute kidney injury and survival in patients treated with Metformin: an observational cohort study Whether metformin precipitates lactic acidosis in patients with chronic kidney disease (CKD) remains under debate. We examined whether metformin use was associated with an increased risk of acute kidney injury (AKI) as a proxy for lactic acidosis and whether survival among those with AKI varied by metformin exposure. All individuals with type 2 diabetes and available prescribing data between 2004 and 2013 in Tayside, Scotland were included. The electronic health record for diabetes which includes issued prescriptions was linked to laboratory biochemistry, hospital admission, death register and Scottish Renal Registry data. AKI events were defined using the Kidney Disease Improving Global Outcomes criteria with a rise in serum creatinine of at least 26.5mol/l or a rise of greater than 150% from baseline for all hospital admissions. Cox Regression Analyses were used to examine whether person-time periods in which current metformin exposure occurred were associated with an increased rate of first AKI compared to unexposed periods. Cox regression was also used to compare 28day survival rates following first AKI events in those exposed to metformin versus those not exposed. Twenty-five thousand one-hundred fourty-eight patients were included with a total person-time of 126,904 person years. 4944 (19.7%) people had at least one episode of AKI during the study period. There were 32.4 cases of first AKI/1000pyrs in current metformin exposed person-time periods compared to 44.9 cases/1000pyrs in unexposed periods. After adjustment for age, sex, diabetes duration, calendar time, number of diabetes drugs and baseline renal function, current metformin use was not associated w Continue reading >>

Clarifying The Relationship Between Metformin, Acute Kidney Injury And Lactic Acidosis

Clarifying The Relationship Between Metformin, Acute Kidney Injury And Lactic Acidosis

Clarifying the relationship between metformin, acute kidney injury and lactic acidosis We read, with interest, the News & Views article by C. Rhee and K. Kalantar-Zadeh (Diabetes mellitus: Complex interplay between metformin, AKI and lactic acidosis. Nat. Rev. Nephrol. 13, 521522 (2017) ) 1 , which discusses our recent work looking at the relationship between metformin, acute kidney injury (AKI) and lactic acidosis 2 , 3 . In response to this discussion of some of our findings, we would like to highlight several points. First, Connelly et al. demonstrated that 80% of lactic acidosis within the study cohort occurred in the presence of AKI 3 . In view of the effectiveness of treatment and increasing evidence of the beneficial cardiovascular effects of metformin, we feel that metformin should be only temporarily discontinued in patients with a condition that predisposes them to acute AKI; this advice is similar to the advice given for angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers. Second, although we acknowledge the difficulties of accurately identifying metformin-associated lactic acidosis (MALA) cases in observational studies, we do not agree that the crude incidence rate of lactic acidosis observed in the study by Connelly et al. is biased because it differs from rates reported by others. Instead, we would like to emphasize that crude incidence rates disregard the structure of the population. Thus, comparing crude incidence rates alone can be misleading before standardization is carried out to remove the effect of differential structures in populations under comparison. Third, it was also suggested that the absence of a 'new-user' design in the study by Bell et al. 2 may not have accounted for patients who stopped using metformin or d Continue reading >>

Metabolic Effects Of Metformin In Patients With Acute Renal Failure

Metabolic Effects Of Metformin In Patients With Acute Renal Failure

Metformin use has been associated with significant disturbances in acid-base balance. Metformin remains the first-line therapy for majority of patients with type 2 diabetes mellitus. Its metabolic effects have provided great support for its use in diabetes management. However, risks of renal impairment and lactic acidosis have always warranted close monitoring in patients with predisposing factors to these events. In fact, lactic acidosis has been associated with renal impairment. Metformin is not metabolized in the liver and is excreted by active tubular secretion. The risk of developing lactic acidosis greatly depends on the magnitude of each patient’s renal impairment and their age. Nonetheless, these studies fail to take into consideration those patients with renal failure. The majority of trials out there exclude patients with renal defects due to its nephrotoxic potential. The nephrotoxicity of increased levels of metformin relies on its effect on renal mitochondrial activity. Previous studies have demonstrated that therapeutic doses of metformin are not associated with risk of lactic acidosis. Renal mitochondrial dysfunction can lead to tubular cell ischemia and increased lactic acid production. Hence, those patients with renal impairment will warrant closer monitoring and dose optimization strategies to prevent these complications while obtaining optimal glucose control. Recently, renal dose adjustments changed. Now patients are to be monitored based on glomerular filtration rate and not serum creatinine for metformin therapy. A recent study conducted by David Cucchiari and colleagues evaluated the dose-related effects of metformin on acid-base balance in patients with diabetes who develop acute renal failure. In this cross-sectional study, 126 patients were i Continue reading >>

More in diabetes