The effect of endogenous parathyroid hormone, exogenous calcitonin, and dibutyryl cyclic AMP on urinary excretion of N-acetyl-beta-D-glucosaminidase.

Urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) transiently increases after PTH(1-34) infusion in idiopathic hypoparathyroidism (IHP) but this response is impaired in pseudohypoparathyroidism (PHP) type I. We investigated the effects of endogenous PTH, exogenous calcitonin (CT), and dibutyryl cAMP (DBcAMP) on urinary excretion of NAG. Urinary NAG excretion in 14 patients with primary hyperparathyroidism (1 degree HPT) was more than in normal subjects (P < 0.001) and decreased after parathyroidectomy (P < 0.01). Urinary NAG excretion increased after the infusion of 1.5 MRC/kg of eel CT in eight normal subjects (P < 0.001), two patients with IHP, and a patient with PHP type Ib but not in a patient with PHP type Ia. The increases of urinary NAG excretion by CT and by PTH(1-34) were positively correlated with the increases of urinary cAMP excretion (r = 0.752; P < 0.001 and r = 0.534; P < 0.002, respectively). Urinary NAG excretion increased after DB-cAMP infusion in five normal subjects (P < 0.01), two patients with IHP, and two with PHP type I. The increase of urinary NAG by 6.0 mg/kg of DBcAMP was more than by 2.5 mg/kg of DBcAMP in normal subjects (P < 0.01). The increase of urinary NAG by 2.5 mg/kg of DBcAMP in PHP type I was comparable with that by 6.0 mg/kg in normal subjects, suggesting a hyperresponsiveness to DBcAMP in PHP type I. Urinary excretion of NAG is a useful indicator of renal tubular responsiveness to PTH and CT. Cyclic AMP-dependent mechanism is probably involved in PTH and CT-induced increase in urinary excretion of NAG.