Severe renal failure and nephrocalcinosis in anorexia nervosa

To the Editor: The recent article by Roberts et al1 requires further comment. In anorexia nervosa, hypercalcaemia is extremely unusual because patients are likely to be under- or malnourished, with consequent hypocalcaemia and hypovitaminosis D, rather than the opposite, as implied by the authors. In one of their references,2 hypercalcaemia is only briefly included, and the mechanism is not discussed or substantiated. Another of their references3 does not include hypercalcaemia at all as a metabolic disturbance. In addition, hypercalcaemia in itself is not a diagnosis, and indicates a significant underlying pathophysiological disturbance whose differential diagnoses need to be carefully dissected.

Where there are problems with the interpretation of calcium homoeostasis, such as renal impairment and hypoalbuminaemia, ionised calcium should be measured because it is the physiologically active agent. In the first patient described by Roberts et al, although the investigations are incomplete, primary hyperparathyroidism (PHPT) needs to be carefully considered, as the parathyroid hormone (PTH) level is not normal in the setting of hypercalcaemia. The normal physiological response would dictate that the PTH level should be low to suppressed. Nephrocalcinosis and renal impairment then fit snugly into the diagnosis of PHPT.4 Phosphate level, expected to be low in this condition, might have been masked by exogenous phosphate supplement.

For Patient 2, stool electrolyte analysis could further support the presence of laxative misuse and aid in the interpretation of urinary results. Faecal fluid in this situation should be high in sodium, potassium and calcium concentrations. The low urinary sodium and calcium levels are therefore appropriate, and indicate relatively intact tubular function. The diagnosis of hypercalcaemia is thus difficult without a PTH measurement and in the presence of gastrointestinal confounders, even if all investigations were available. Nevertheless, familial benign hypocalciuric hypercalcaemia (FBHH) is a strong probability given the low urinary calcium excretion, especially before iatrogenic manipulation of calcium and phosphate homoeostasis. Nephrocalcinosis can theoretically occur in FBHH.5 It is important that the diagnosis is made in both cases, so that a familial study can be carried out if indicated given the patients’ age. One may also wonder if the intermittent hypercalcaemia contributed to or aggravated the psychiatric disturbance in both patients.