Böbrek nakil hastasında metforminle ilişkili laktik asidoz (original) (raw)
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Lactic Asidosis after Metformin Use in a Chronic Hemodialysis Patient
DergiPark (Istanbul University), 2022
Objectives: Metformin is a biguanide and is used especially in metabolic syndrome where insulin resistance is at the forefront and in Type 2 diabetes mellitus, both by suppressing the endogenous glucose production in the liver and increasing the sensitivity of insulin in peripheral tissues such as fat and muscle tissue. 1 The most rare but life-threatening side effect of metformin is the development of lactic acidosis. Therefore, the glomerular filtration rate is 30 ml/min. its use is contraindicated in patients with chronic kidney disease. 2 Lactic acidosis is the cause of metabolic acidosis with increased anion gap; occurs when the plasma lactate concentration exceeds 4-5 millimol /Liter (mmol /L) (Normal range: 0.5-1.5 mmol /L). 3 Here, we present the development of lactic acidosis due to metformin use in an 84-year-old female patient who has been on chronic hemodialysis treatment for 4 months. The patient applied to the emergency department twice because of confusion. The patient, who was found to have acidosis in the blood gas, regained consciousness after he was taken to hemodialysis and was referred to the nephrology outpatient clinic, considering that she might have dialysis insufficiency. The patient, who learned that she used metformin in his anamnesis, did not recur after the drug was stopped. The use of metformin in advanced age and renal failure may cause fatal complications. Glomerular filtration rate 45 ml/ min. metformin should be used with caution in patients with should not be given to those below.
Toxicokinetics of metformin-associated lactic acidosis with continuous renal replacement therapy
European Journal of Drug Metabolism and Pharmacokinetics, 2012
A 70-year-old diabetic male patient with a baseline serum creatinine of 1.4 mg/dL presented with nausea and vomiting. He was diagnosed with metforminassociated lactic acidosis and acute kidney injury. He was managed with continuous veno-venous hemodiafiltration (CVVHDF). By measuring metformin concentration at different time intervals, we calculated the apparent volume of distribution of metformin at 34.7 L. The decline in serum metformin followed single-compartment first-order kinetics with an elimination rate constant of 0.0418/h and a serum half-life of 16.5 h; no metformin rebound was seen after discontinuation of CVVHDF. Using the previously calculated volume of distribution we calculated the expected serum metformin concentration 25 h post CVVHDF to be 3.0-3.7 lg/mL. The measured serum metformin of 3.4 lg/ml fell within the predicted range.
Metformin intoxication requiring dialysis
Hemodialysis International, 2011
Metformin (MTF) is one of the most common oral agents used to treat diabetes mellitus. Intoxication is associated with lactic acidosis and has significant clinical consequences. We report 12 cases requiring dialytic intervention. Twelve patients were analyzed from 2005 to 2010; 10 of these patients were treated with dialysis. Conventional hemodialysis (HD) and continuous veno-venous hemodialysis treatments with bicarbonate dialysis were used, and the results were presented as mean and standard deviation. The results are as follows: 33% of the patients were male, hospital stay was 9.3 (Ϯ12) days, average MTF dose 1.7 g/day, mortality was 25%. Baseline glomerular filtration rate for these patients was 51.5 mL/min, with an average age of 64 (Ϯ11) years. On presentation, all had acute kidney injury with blood urea nitrogen/creatinine 75 (Ϯ30)/8.1 (Ϯ3.7) mg/dL, lactic acid 12.4 (Ϯ8.1) mmol/L, pH 7.04 (Ϯ0.19), bicarbonate 7.2 (Ϯ4.5) mmol/L. Metformin level was 25 (Ϯ17) mg/mL; anion gap was 28 (Ϯ9), and serum potassium was 5.4 (Ϯ1.3) mEq/L. Seventy percent of patients were treated with conventional HD. Patients required 4 (Ϯ5) dialysis treatments at blood flow QB 330 (Ϯ53), dialysis flow QD 571 (Ϯ111) for 305 (Ϯ122) minutes. Postdialysis, the acidosis parameters improved: bicarbonate 19.2 (Ϯ4.1) mmol/L, lactic acid 6 (Ϯ4) mmol/L and MTF levels decreased 8.9 (Ϯ5.7) mg/mL. Metformin percentage removal was calculated to be 60% (Ϯ24). No difference was found between HD and continous veno-venous hemodialysis. The only difference between survivors was the age 53 (Ϯ7) vs. 78 (Ϯ10) (P < 0.05). Metformin toxicity is a serious clinical condition and causes severe lactic acidosis and significant mortality. Hemodialysis is an efficient method to treat MTF intoxication and correct the metabolic abnormalities.
Clinical Toxicology, 2019
Background: Metformin-associated lactic acidosis (MALA) and metformin-induced lactic acidosis (MILA) remain controversial entities. Metformin toxic effect depends on accumulation to lead to lactic acidosis (LA), particularly during an episode of acute kidney injury (AKI). In MILA, no other condition contributing to LA is found. The aims of this study were to describe the characteristics and prognosis of AKI associated with LA in metformin users and to clarify the role of this drug in the different types of LA. Methods: We performed a French multicenter retrospective study in diabetic patients treated by metformin presenting with LA in a context of AKI in 2015. 126 nephrology units (NU) and 23 intensive care units (ICU) were contacted. We individualized MILA and MALA patients in order to illustrate the role of metformin. Results: We included 173 patients (109 MILA, 64 MALA). 103 patients presented without hemodynamic instability (82 MILA and 21 MALA) whereas 70 patients were shocked including 27 MILA. The shock was associated with death with an odds ratio (OR) of 12.92 (p < .001). Digestive disorders (DD) were strongly associated with MILA (p ¼ .0001). MALA was significantly associated with shock (p < .0001). The mortality rate was higher in MALA (26%) when compared with MILA (7%). Dialysis performed in 133 patients was significantly associated with shock, kalemia, lactate and serum creatinine levels. In multivariate analysis, metformin level was independently associated with pH or lactate level only in MILA patients. Conclusions: MILA is associated with DD and death is due to severe refractory acidosis leading to cardiovascular collapse attributed to metformin accumulation mainly via AKI. MALA patients are more frequently shocked and death is related to their underlying condition, metformin accumulation increasing LA.
Metformin Toxicity: A Report of 204 Cases from Iran
Current Drug Safety, 2013
Objective: The aim of this study was to evaluate the frequency of metformin-associated lactic acidosis in our metformin-intoxicated patients, the general approach for their management, and determine the frequency of hypoglycemia and outcome in these patients. We also wanted to see if there was a significant difference in the course and outcome of metformin poisoning between our patients and those reported in the literature.
Metformin and Acute Kidney Injury: Recipe for Disaster
Indian Journal of Critical Care Case Report
Urine routine showed a specific gravity of 1.010, traces of glucose, 3-5 WBCs/HPF, no casts, and no bacteria detected. Her ABG showed severe metabolic acidosis with lactate levels of 7.8 mmol/L. She was resuscitated with crystalloids. ABG analysis after resuscitation showed an increase in lactate levels to 9.1 mmol/L, a base deficit of 25 mmol/L, and bicarbonate level of 4.6 mmol/L. In view of increasing lactate levels and respiratory distress, she was initiated on mechanical ventilation. The patient did not produce any urine after fluid resuscitation. The patient was initiated on hemodialysis immediately. Acidosis was corrected with dialysis, and the patient improved symptomatically within 12 hours. She was extubated the next day. She underwent three more cycles of dialysis; her kidney function improved. She did not require further hemodialysis. She was discharged after 5 days. Her renal function tests, and ABG values are tabulated in Table 2.
Journal of Nephrology, 2018
Background The choice of the specific modality and treatment duration of renal replacement therapy (RRT) to adopt in metformin-associated lactic acidosis (MALA) is still debated. We aimed to verify if sustained low-efficiency dialysis (SLED) is a rational choice in patients with MALA and acute kidney injury (AKI). Methods We collected serial serum metformin measurements, clinical parameters, and outcome data in ten consecutive patients (mean age 77 years [range 58-88], 5 males) admitted to our renal intensive care unit for suspected MALA associated with AKI and hemodynamic instability. Patients underwent a 16-h SLED session performed with either conventional dialysis machines or machines for continuous RRT (CRRT). A 2-compartment open-infusion pharmacokinetic model with first-order elimination was fitted to each subject's serum concentration-time data to model post-SLED rebound and predict the need for further treatments. Results Two patients died within 24 h after SLED start. Three patients needed one further dialysis session. Surviving patients (n = 8) were dialysis-free at discharge. Metformin levels were in the toxic range at baseline (median [range] 32.5 mg/l [13.6-75.6]) and decreased rapidly by the end of SLED (8.1 mg/l [4.5-15.8], p < 0.001 vs. baseline), without differences according to the dialysis machine used (p = 0.84). We observed a slight 4-h post-SLED rebound (9.7 mg/l [3.5-22.0]), which could be predicted by our pharmacokinetic model. Accordingly, we predicted that the majority of patients would need one additional dialysis session performed the following day to restore safe metformin levels. Conclusions A 16-h SLED session, performed with either conventional dialysis machines or CRRT machines, allows effective metformin removal in patients with MALA and AKI. However, due to possible post-SLED rebound in serum metformin levels, one additional dialysis treatment is required the following day in the majority of patients.