A 47-year-old obese woman of Caucasian ethnicity (weight: 115 kg, height: 1.67 m, body-mass index: 41 kg/m2) presented in an emergency room for syncope and tachypnea with Kussmaul breathing pattern. The patient had a type-2 diabetes treated with oral antidiabetics, arterial hypertension, and chronic kidney disease (Kidney Disease: Improving Global Outcomes stage G3a). She fasted repeatedly for 7 days in a row to attempt weight loss. Following a fasting period one year earlier, exsiccosis leading to unconsciousness prompted an emergency-room visit without hospitalization. At the time of this visit, serum creatinine was 112 µmol/L (estimated glomerular filtration rate: 49.1 ml/min/1.73 m2).
At the current presentation, the patient felt unwell shortly after starting the fasting period and vomitted repeatedly. She, however, continued to take her medications including sitagliptin 50 mg BID, metformin 1 g BID, candesartan 16 mg BID, hydrochlorothiazide 12.5 mg QD and metoprolol 47.5 mg BID. A drug overdose was denied. In addition, the patient reported that diuresis declined as she was unable to drink sufficiently prior to hospitalization. On physical examination, the patient showed signs of exsiccosis, and moist rales over both lungs. The respiratory rate was 24 per minute, temperature was 36.7 °C. Laboratory results proved a severe acute kidney injury complicated by severe lactic acidosis being consistent with MALA (Table 1). In addition, a chest X-ray showed signs of pulmonary congestion, an evolving alveolar pulmonary edema and suspected pulmonary infiltrates in the right lung. Ultrasound of the kidneys revealed no abnormalities, especially no acute renal obstruction. There were no signs of venous congestion as the inferior caval vein was not dilated. For the treatment of MALA,, 100 ml sodium bicarbonate solution (8.4%) was applied 3 times without resolving the lactic acidosis, supplemental nasal oxygen (3 L/min) was provided, and the patient was transferred to the nephrology department for placment of a temporary dialysis catheter within 2.5 h of admission. Then, a high-efficiency hemodialysis using a single-use, high-flux polyethersulfone dialyzer (Revaclear 300, Baxter, IL, USA) with an effective surface of 1.4 m2 was initiated and maintained for 1 h. Plasma potassium was 5.5 mmol/L prior to hemodialysis, dialysate potassium concentration was 2 mmol/L. The counter-current flow rates of hemodialysate and blood were 500 mL/min and 250 mL/min, respectively. As for anticoagulation therapy, a bolus of 2000 units of unfractionated heparin was given intravenously. Blood pressure was 82/48 mmHg prior to hemodialysis, 71/41 mmHg afterwards. In order to avoid a rapid alleviation of uremia, the intermittent hemodialysis was paused after 1 h of treatment, and the patient was transferred to an intermediate care unit. There, 8 h post admission, a CVVHDF using a single-use acrylonitrile-copolymer dialyzer (M150, Baxter, IL, USA) with an effective surface of 1.5 m2 was started and maintained for 46 h. Hemodialysate flow rate was 1.2 L/h or 20 mL/min; the respective effluent rate was 10.4 mL/kg/h. Potassium in the hemodialysate was 4 mmol/L. An ultrafiltration rate of 0 to 50 ml/hour was applied initially (1 L ultrafiltration on day 1). After 24 h, ultrafiltration was stopped because the patient complained of muscle cramps. Intravenous antibiotics including piperacillin (4 g/) and tazobactam (0.5 g) thrice daily were administered for treatment of suspected sepsis. The capillary-blood lactate and bicarbonate concentrations stabilized during the initial 24 h (Fig. 1). However, by day 3 in hospital, serum sodium still increased to a maximum of 149 mmol/L. Although the patient was allowed to drink ad libitum, intravenous rehydration had to be applied to compensate for the polyuria. In addition norepinephrine was infused (0.01 – 0.05 µg/kg body weight/h) from day 2 to day 4 for arterial hypotension. Respiratory rate peaked at 34/min during the first 4 days in hospital. As the oxygen saturation remained stable, supplemental oxygen was discontinued on day 5.
On day 2 in hospital, during ongoing renal-replacement therapy, the patient experienced an acute coronary syndrome with a rise of troponin T from 57.6 ng/L on day 1 to 632 ng/L on day 2 in hospital. Troponin T peaked off from day 4 on (172 ng/L on day 4, 158 ng/L on day 5). Creatinine kinase did not rise at any time. N-terminal pro-brain natriuretic peptide (NT pro-BNP) was determined on day 2 in hospital for the first time (1095 pmol/L), rose to 3043 pmol/L on day 3 and fell off by day 4 (2314 pmol/L) and day 5 (757 pmol/L). Electrocardiogram showed a ST-depression by 0.1 mV in leads II, III, aVF, transthoracic echocardiography, performed on the day of discharge, proved a normal left-ventricular function without regional hypokinesia. Laboratory testing for vasculitis was unrevealing. Therapeutic anticoagulation with unfractionated heparin was maintained for 6 days. Blood pressure remained stable, and, after stopping renal-replacement therapy, the acute kidney injury reversed. Blood and urine cultures taken prior to antibiotic therapy remained negative. Laboratory results (C-reactive protein, procalcitonin, leukocyte count) were not consistent with an infection or sepsis as a possible cause of lactic acidosis. As for medication, oral antidiabetics were stopped upon admission. Sitagliptin (25 mg/d) was reintroduced on day 3. The dose was increased to 50 mg/d at the time of discharge.
The patient fully recovered and left the hospital on the 11th day following admission. At discharge, patient weight was 108.3 kg, body-mass index 38.8 kg/m2. In a follow-up call with the patient 18 months later, the patient had no complaints and reported no rehospitalization since discharge. Sitagliptin (50 mg/d) was maintained as oral diabetes medication.