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In recent years, the identification of a calcium-sensing receptor (CaR) has provided new insight into disorders of calcium metabolism [1]. As well as being located in numerous extra-renal tissues such as the parathyroid glands, gastrointestinal tract and bone [1], these CaRs are found on the basolateral aspect of the epithelial cells of the thick ascending limb of the loop of Henle [2]. Here they respond to a rise in serum calcium by reducing the diffusion of potassium back into the tubular lumen (Figure 1). This results in a reduced electrical gradient between the lumen and the blood which reduces the passive paracellular flow of calcium (magnesium and sodium) back into the bloodstream and consequently calcium excretion in the urine is increased. The CaR is, therefore, pivotal in maintaining blood calcium levels within the pre-determined range. In certain conditions, however, the predetermined target range for calcium is set higher than normal, such that higher calcium levels are required in the peritubular space to downregulate the reabsorption of calcium in the renal tubule and in the parathyroid gland to suppress parathyroid hormone (PTH) secretion. In adults, the clinical picture in these conditions is usually one of asymptomatic mild hypercalcaemia and hyperparathyroidism, with patients being identified when blood is taken for other purposes. We present a case where a basic understanding of calcium handling in the kidney as well as an awareness of function of the CaR helped simplify a case which was otherwise becoming increasingly complex.

Disturbed calcium metabolism in a patient with bipolar disorder and impaired renal function