Hypercalcemia as a Cause of Kidney Failure: Case Report

Abstract

BACKGROUND:Hypercalcemia is a common manifestation in clinical practice and occurs as a result of primary hyperparathyroidism, malignancy, milk-alkali syndrome, hyper or hypothyroidism, sarcoidosis and other known and unknown causes. Patients with milk-alkali syndrome typically are presented with renal failure, hypercalcemia, and metabolic alkalosis caused by the ingestion of calcium and absorbable alkali. This syndrome is caused by high intake of milk and sodium bicarbonate.CASE PRESENTATION:We present a 28-year old male admitted to hospital with a one-month history of nausea, vomiting, epigastric pain, increased blood pressure and worsening of renal function with hypercalcemia. His serum PTH level was almost undetectable; he had mild alkalosis, renal failure with eGFR of 42 ml/min, anemia, hypertension and abnormal ECG with shortened QT interval and ST elevation in V1-V4. He had a positive medical history for calcium-containing antacids intake and after ruling out primary hyperparathyroidism, malignancy, multiple myelomas, sarcoidosis, and thyroid dysfunction, it seemed plausible to diagnose him as having the milk-alkali syndrome.CONCLUSION:Although milk-alkali syndrome currently may be more probably a result of calcium and vitamin D intake in postmenopausal women, or in elderly men with reduced kidney function taking calcium-containing medications, one should not exclude the possibility of its appearance in younger patients taking calcium-containing medications and consider it a serious condition taking into account its possibility of inducing renal insufficiency.

Calcium-Alkali Syndrome: Historical Review, Pathophysiology and Post-Modern Update

“…Increased bicarbonate reabsorption leads to metabolic alkalosis [ 24 ]. Alkalosis in turn increases the hypercalcemia by enhancing calcium reabsorption in the distal nephron [ 24 ].…”

“…Increased bicarbonate reabsorption leads to metabolic alkalosis [ 24 ]. Alkalosis in turn increases the hypercalcemia by enhancing calcium reabsorption in the distal nephron [ 24 ]. Other effects of hypercalcemia include the activation of calcium-sensing receptors in the parathyroid gland that reduces PTH through negative feedback.…”

“…The presentations and pathophysiology of MAS continue to evolve. The demographics now comprise mostly pregnant and post-menopausal women, bulimic patients, solid organ transplant recipients, and those on dialysis [24]. Due to the changing etiopathology, many authors have suggested changing the name to calcium-alkali syndrome as proposed by Sulkin and Krentz in 2000 [24][25][26].…”

“…The demographics now comprise mostly pregnant and post-menopausal women, bulimic patients, solid organ transplant recipients, and those on dialysis [24]. Due to the changing etiopathology, many authors have suggested changing the name to calcium-alkali syndrome as proposed by Sulkin and Krentz in 2000 [24][25][26]. One group proposed further classification into calcium-alkali-thiazide syndrome given the frequency of this association [27].…”