Sir, A 64-year-old Austrian female patient presented to a Hungarian hospital with dyspnoea, sensory aphasia and disorientation. Apart from a pulmonary embolism years earlier, she had no apparent medical history. The laboratory findings were as follows: Na 142.2 mmol/l, K 4.8 mmol/l, Ca 2.38 mmol/l, GOT 23U/l, GPT 22U/l, ALP 130U/l, GGT 20U/l, Hb 10.2 g/dl, Hkt 49%, thrombocytes 217000/l, creatinine 317 mmol/l, LDH 644U/l, pH 7.10, pCO2 9.8 mmHg, pO2 146.4 mmHg, O2 Sat 98.1%. No information on chloride levels and serum osmolality to differentiate the metabolic acidosis were provided. A computed tomography of the brain showed no pathologies, neither did an ultrasound of the abdomen. She was treated for her acute renal failure with intravenous fluid administration combined with forced diuresis and transferred to our hospital in Vienna, Austria, as soon as the neurological symptoms allowed transportation. In our hospital, a computed tomography, an EEG, a renal ultrasound and urine analysis, as well as the acid–base status, were normal. The patient’s history gave no hint of intoxication; the patient denied intake of non-steroidal anti-inflammatory drugs or any other nephrotoxic substances. A renal biopsy was performed when renal function did not improve after several days of adequate intravenous fluid administration. The biopsy showed a severe acute dystrophy of the tubuli with loss of brush borders, shedding of tubular epithelial cells and intraluminal discrete amounts of birefringent crystalline deposits (Figure 1). The histological findings were highly suspicious for oxalosis. Primary oxalosis was ruled out by the age of the patient. Of the causes of secondary oxalosis, the only plausible cause for the acute tubular necrosis caused by calcium oxalate crystals was ingestion of ethylene glycol [1, 2]. Intensive questioning of the patient revealed accidental intake of anti-freeze solution by brewing coffee with liquid falsely thought to be water from a container in the kitchen in her summer cottage in Hungary. The patient recovered from her neurological symptoms and her renal impairment without specific therapy. Her most recent creatinine was 1.1 mg/dl. In most cases, the common causes of acute renal failure—pre-renal disease, acute tubular necrosis and urinary tract obstruction—can be diagnosed without renal biopsy. Prior to renal biopsy, laboratory findings, urine sediment analysis and ultrasound examination are used as non-invasive techniques to establish a diagnosis. In our case, the typical acid–base disorder [3] was no longer present at presentation at our hospital and the patient was completely oblivious to the poisoning. Biopsy is indicated in settings like our case, in which the cause of renal failure is still uncertain after all non-invasive diagnostic measurements [4], and can reveal the most unexpected diagnoses.