Primary Hyperparathyroidism and Coexisting Nephrogenic Diabetes Insipidus: Rapid Postoperative Correction

Title: Primary Hyperparathyroidism and Coexisting Nephrogenic Diabetes Insipidus: Rapid Postoperative Correction
Authors: Ellis, George; Spirtos, George; Polsky, Fred
Publisher: Southern Medical Journal
Date Published: August 01, 1991
Reference Number: 318
Shortly after diagnosis of primary hyperparathyroidism, a patient had serum hyperosmolality, polyuria, isosthenuria, profound potassium depletion, and elevated plasma antidiuretic hormone levels, all consistent with nephrogenic diabetes insipidus. After parathyroidectomy, serum calcium and serum osmolality levels fell concurrently. Profound potassium deficits did not recur. We propose that (1) hypercalcemia produced a concentrating defect and polyuria; (2) renal tubular acidosis and polyuria combined to produce severe potassium depletion; (3) hypokalemia potentiated the nephrogenic diabetes insipidus caused by hypercalcemia; and (4) postoperative disappearance of the diabetes insipidus confirmed its reversible, purely metabolic causes.

This translation by the NDI Foundation is to assist the lay reader. To provide a clear, accessible interpretation of the original article, we eliminated or simplified some technical detail and complicated scientific language. We concentrated our translation on those aspects of the article dealing directly with NDI. The NDI Foundation thanks the researchers for their work toward understanding and more effectively treating this disorder.
© Copyright NDI Foundation 2007 (JC)

Ellis, et al., report on a 62-year-old male admitted to their hospital because of jaundice due to an alcoholic binge. The authors discovered that the patient was also suffering from primary hyperparathyroidism. This disorder is caused by excessive amounts of parathyroid hormone. Its symptoms include calcium deposits in the kidney tubules (the tiny tubes that form part of the nephron), bone decalcification, an excess of calcium in the blood leading to muscle weakness, anorexia, nausea, vomiting, drowsiness or dullness.

After release from the hospital, the patient did not return for follow-up. He returned to the hospital two months later complaining of muscle weakness, increasing thirst and urine output, and bouts of alcohol abuse. The authors noted the patient's polyuria (chronic, excessive urination), polydipsia (chronic, excessive thirst), serum hyperosmolality, extreme potassium depletion, and elevated blood levels of the antidiuretic hormone, arginine vasopressin (AVP). They concluded that their patient also had nephrogenic diabetes insipidus (NDI).

The authors proposed the patient's NDI was caused by the elevated levels of blood calcium brought on by the patient's primary hyperparathyroidism. Polyuria, in combination with the tubular acidosis of the patient's kidneys, produced a severe potassium depletion, and this exacerbated the patient's NDI.

To correct the patient's hyperparathyroidism, the authors performed surgery on him, removing three and one-half of his parathyroid glands. After the surgery, the patient's NDI disappeared, confirming it was caused by the metabolic conditions created by his primary hyperparathyroidism.