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) t ype I. We investigated the effects of endogenous PTH, exogenous calcit onin (CT), and dibutyryl cAMP (DBcAMP) on urinary excretion of NAG. Ur inary NAG excretion in 14 patients with primary hyperparathyroidism (1 degrees HPT) was more than in normal subjects (P < 0.001) and decreas ed 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 excret ion by CT and by PTH(1-34) were positively correlated with the increas es of urinary cAMP excretion (r = 0.752; P < 0.001 and r = 0.534; P < 0.002, respectively). Urinary NAG excretion increased after DBcAMP inf usion in five normal subjects (P < 0.01), two patients with IHP, and t wo 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). T he increase of urinary NAG by 2.5 mg/kg of DBcAMP in PHP type I was co mparable with that by 6.0 mg/kg in normal subjects, suggesting a hyper responsiveness 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 in crease in urinary excretion of NAG.