Chronic thiazide therapy causes persistent hypercalcemia which is due to:
Chronic thiazide administration leads to reduction in urinary calcium; the hypocalciuric effect appears to reflect the enhancement of proximal tubular resorption of sodium and calcium in response to sodium depletion. Some of this renal effect is due to augmentation of PTH action and is more pronounced in individuals with intact PTH secretion. Most serious adverse effects of thiazides are related to abnormalities of fluid and electrolyte balance. These adverse effects include, Extracellular volume depletion Hypotension Hypokalemia Hyponatremia Hypochloremia Metabolic alkalosis Hypomagnesemia Hypercalcemia Hyperuricemia Ref: Potts, J.T., Juppner H. (2012). Chapter 353. Disorders of the Parathyroid Gland and Calcium Homeostasis. In D.L. Longo, A.S. Fauci, D.L. Kasper, S.L. Hauser, J.L. Jameson, J. Loscalzo (Eds), Harrison's Principles of Internal Medicine, 18e.
Renal tubular acidosis
Fanconi's syndrome
Hypervitaminosis D
Hyperparathyroidism