Unexpected Nephrocalcinosis in a Chronic Heavy Cola Drinker

A 46-year-old HIV-infected, but never treated, woman was admitted because of headache, fever, pancytopaenia, asthaenia and poor nutritional status (albumin 2.9 g/dL). Cerebral toxoplasmosis was diagnosed according to the characteristic lesions on cerebral magnetic resonance imaging (MRI) examination (Fig. 1). Treatment with pyrimethamine, folinic acid and sulfadiazine (4 g/day) was prescribed in addition to intravenous fluid administration. The patient gradually improved during the following 4 weeks, but because of mild hyponatraemia (130 mEq/L) intravenous fluids were withdrawn. Renal function decreased promptly thereafter (serum creatinine 3 mg/dL) without any other clinical sign. Ultrasound scan showed bilateral nephrocalcinosis of the medullary area and a bladder stone. There was no previous history of nephrolithiasis, urinary infections or vesicoureteral reflux. Renal findings were initially linked to fluid restriction and medications (sulfadiazine was switched to clindamycin). Fresh urine microscope examination revealed plenty of typical calcium phosphate crystals instead of the expected sulfadiazine crystals (Fig. 1). Urine pH (6.0) was slightly acid. Intravenous fluid administration was enough for restoring renal function to normal values. Metabolic studies including oxalate, uric acid, serum calcium, phosphate, parathormone, etc. were within normal values except for a low citrate urine excretion. Plain X-ray examinations failed to prove other extra skeletal calcifications. The patient denied other drugs or illicit toxic abuse with the exception of a heavy habit of cola beverage intake (2 L/day over a minimum of 20 years) that continued despite hospitalization and fluid restriction. The diagnosis of AIDS was confirmed by CD4 count and the toxoplasma opportunistic infection. Antiretroviral therapy was then started and the patient was discharged. One month later, renal function was completely normal. Nephrolithiasis and acute kidney injury (AKI) due to obstructive uropathy or intratubular obstruction is a common side-effect of certain drugs, especially sulfadiazine, which is the treatment of choice for toxoplasma encephalitis in AIDS. Acidic urine pH, high dose and prolonged drug intake, dehydration and hypoalbuminaemia, that may increase serum free-drug levels, are responsible for sulfadiazine crystallization. All of these clinical features (in addition to the acidic urine pH) were present in the patient reported, but urine examination showed unexpected dicalcium phosphate crystals (brushite) and not sulphadiazine crystals. Although brushite crystallization typically requires a urinary pH over 6.0, crystals can be found at lower pH levels in the presence of very high calcium or phosphate urine concentrations. Moreover, ultrasound scan also revealed features of nehrocalcinosis that arguably required time for development. Hyperphosphataemia and hyperphosphaturia, independently of hypercalciuria, can cause nephrocalcinosis and AKI through the deposition of calcium-phosphate crystals. This phenomenon, which has been described when using sodium phosphate cleansing bowel preparations, as well as in other clinical settings, led us to the hypothesis that phosphaturia after high cola intake underlies the development of phosphate nephropathy in the patient described. Moreover, osmotic diuresis resulting from the high concentration of