Metformin-induced lactic acidosis: usefulness of measuring levels and therapy with high-flux haemodialysis
Acidosis láctica grave por metformina: utilidad de la medición de niveles y terapia con hemodiálisis de alto flujo
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García Marcos, J.L. Serrano Carrillo de Albornoz" "autores" => array:4 [ 0 => array:4 [ "Iniciales" => "M.A." "apellidos" => "Martin Gómez" "email" => array:1 [ 0 => "doritamg@gmail.com" ] "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 1 => array:3 [ "Iniciales" => "M.D." "apellidos" => "Sánchez Martos" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 2 => array:3 [ "Iniciales" => "S.A." "apellidos" => "García Marcos" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 3 => array:3 [ "Iniciales" => "J.L." 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Metformin is a widely-used oral antidiabetic agent, which is eliminated by active tubular secretion, but accumulates in patients with kidney failure.<span class="elsevierStyleSup">1</span> Clinically, metformin-associated lactic acidosis (MALA) develops abruptly and is accompanied by overbreathing, abdominal pain, drowsiness and coma. Abnormal laboratory MALA indicators are a high anion gap, base excess in the arterial blood gas and high plasma lactate levels (prognostic value) and metformin plasma levels. Monitoring the lactate and metformin levels is a very useful way of evaluating the evolution and the possible modifications in the treatment. MALA treatment is controversial; using bicarbonate is usual although there is no scientific evidence associating it with a better prognosis. Low metformin binding to plasma proteins allows haemodialysis techniques with bicarbonate solutions to be used when it has been overdosed. This technique has proven to be effective in eliminating plasma metformin and also allows acidosis to be corrected.<span class="elsevierStyleSup">2,3</span> Dialysis seems to contribute significantly to treating this severe pathology and improving results where MALA is associated with acute renal failure.<span class="elsevierStyleSup">4</span> If we were to compare MALA to severe lactic acidosis located elsewhere, MALA prognosis is significantly better. Its diagnosis should be considered in all metformin-treated patients that present with lactic acidosis.<span class="elsevierStyleSup">5</span></p><p class="elsevierStylePara">Eighty-one year old patient with high blood pressure, dyslipidaemia, type 2 diabetes and dilated myocardiopathy (ejection fraction [EF] 30%). Usual treatment: telmisartan, torsemide, metformin 850mg/8hrs, atorvastatin, carvedilol and omeprazole. She arrived at the emergency department with diarrhoea with mucus and blood, and vomiting, which had lasted for one week, as well as oligoanuria for 24 hours.</p><p class="elsevierStylePara">Physical examination: blood pressure: 120/70mm Hg, heart rate (HR): 95bpm, temperature (T): 36ºC.</p><p class="elsevierStylePara">Neurological examination: Glasgow score 12, time/space disorientation and bradypsychia, with no signs of focusing. Rhythmic heart beat, no murmur, crackling until the middle field. No signs in the abdomen and lower limbs.</p><p class="elsevierStylePara">Biochemical tests showed: haemoglobin: 11.7g/dl; leukocytes: 18 030 (78.9% neutrophils); platelets: 307 000; glucose: 68mg/dl; urea: 133mg/dl; creatinine: 6.89mg/dl; sodium: 134mEq/l; potassium: 4.4mEq/l; pH: 6.89; pCO<span class="elsevierStyleInf">2</span>: 29mm Hg; bicarbonate: 6.9mmol/l; ionic calcium: 3.85mg/dl; anion gap: 28. Normal coagulation. Urine: pH: 6; creatinine: 71mg/dl; proteinuria: 400mg/dl; 100 red blood cells/field; 60 leukocytes/field; positive ketone bodies and negative drugs (benzodiazepines, barbiturates). Normal abdominal ultrasound with symmetrical kidneys (12cm); good corticomedullary delimitation.</p><p class="elsevierStylePara">Electrocardiogram: left bundle branch block (LBBB) at 93bpm. Chest X-ray: cardiomegaly and normal cranial computerised tomography (CT). She was diagnosed with stage 2 chronic kidney failure secondary to acute prerenal hypertensive and diabetic nephropathy in a tubular necrosis phase and high anion gap lactic metabolic acidosis. Repletion treatment with physiological saline solution (PSS) at 0.9%, and dextrose solution at 5%, loop diuretics and 1M sodium bicarbonate. Despite this treatment, she continued with anuria and her cognitive function continued to deteriorate. We therefore decided to perform her first 2-hour haemodialysis session without ultrafiltration. Having confirmed hyperlactacidaemia (10.7mmol/l), high metformin levels (34.4mg/l; therapeutic levels 1.3-5) and symptoms of heart overload with haemodynamic disorder, we decided to perform dialysis for four days and then every 48 hours until reaching a constant lactate decrease and non-toxic levels of metformin (Table 1). She received 7 sessions in total. She received empirical antibiotic therapy with third-generation cephalosporin; the urine and faecal cultures were negative.</p><p class="elsevierStylePara">She was discharged without any neurological and renal symptoms, with creatinine at 1.6mg/dl and the following treatment: carvedilol at a dosage of 6.25mg/24hrs, repaglinide at a dosage of 1.5mg/8hrs, telmisartan, atorvastatin, torsemide at a dosage of 10mg/24hrs and omeprazole at 20mg/24hours.</p><p class="elsevierStylePara">She currently presents with 1.26mg/dl creatinine and is neurologically stable.</p><p class="elsevierStylePara"><a href="grande/10899_108_21722_en_t110899.jpg" class="elsevierStyleCrossRefs"><img src="10899_108_21722_en_t110899.jpg" alt="Evolution of metformin levels"></img></a></p><p class="elsevierStylePara">Table 1. Evolution of metformin levels</p>" "pdfFichero" => "P1-E524-S3361-A10899-EN.pdf" "tienePdf" => true "multimedia" => array:1 [ 0 => array:8 [ "identificador" => "fig1" "etiqueta" => "Tab. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "10899_108_21722_en_t110899.jpg" "Alto" => 138 "Ancho" => 600 "Tamanyo" => 62604 ] ] "descripcion" => array:1 [ "en" => "Evolution of metformin levels" ] ] ] "bibliografia" => array:2 [ "titulo" => "Bibliography" "seccion" => array:1 [ 0 => array:1 [ "bibliografiaReferencia" => array:5 [ 0 => array:3 [ "identificador" => "bib1" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Gainza FJ, Jimeno I, Muñiz R. Acidosis láctica asociada con la utilización de metformina: Papel de la hemodiálisis en el tratamiento. Nefrologia 1998;18(5):427-30." "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 1 => array:3 [ "identificador" => "bib2" "etiqueta" => "2" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Solano M, González C, Álvarez M. Acidosis láctica en paciente diabético tratado con metformina. An Med Interna (Madrid) 2004;21(6):288-90." "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 2 => array:3 [ "identificador" => "bib3" "etiqueta" => "3" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Holanda MS, Suberviola B, González A. Acidosis láctica grave asociada a intoxicación por metformina. Nutr Hosp 2007;22(1):124-5. <a href="http://www.ncbi.nlm.nih.gov/pubmed/17260541" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 3 => array:3 [ "identificador" => "bib4" "etiqueta" => "4" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Devetzis V, Passadakis P, Panagoutsos S. Metformin-related lactic acidosis in patients with acute kidney injury. Int Urol Nephrol 2010. doi: 10. 1007/s11255-010-9845-1." "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 4 => array:3 [ "identificador" => "bib5" "etiqueta" => "5" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Friesecke S, Abel P, Roser M. Outcome of severe lactic acidosis associated with metformin accumulation. Critical Care 2010;14:R226. doi: 10.1186/cc9376." "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] ] ] ] ] ] "idiomaDefecto" => "en" "url" => "/20132514/0000003100000005/v0_201502091634/X2013251411052439/v0_201502091634/en/main.assets" "Apartado" => array:4 [ "identificador" => "35438" "tipo" => "SECCION" "en" => array:2 [ "titulo" => "Letters to the Editor - Brief papers about basic research or clinical experiences" "idiomaDefecto" => true ] "idiomaDefecto" => "en" ] "PDF" => "https://static.elsevier.es/multimedia/20132514/0000003100000005/v0_201502091634/X2013251411052439/v0_201502091634/en/P1-E524-S3361-A10899-EN.pdf?idApp=UINPBA000064&text.app=https://revistanefrologia.com/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/X2013251411052439?idApp=UINPBA000064" ]
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| 2015 October | 67 | 0 | 67 |
| 2015 September | 54 | 0 | 54 |
| 2015 August | 55 | 0 | 55 |
| 2015 July | 63 | 0 | 63 |
| 2015 June | 33 | 0 | 33 |
| 2015 May | 50 | 0 | 50 |
| 2015 April | 6 | 0 | 6 |
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