Is calcium excreted by the kidneys?

From the Guidelines

Yes, calcium is excreted by the kidneys. The kidneys play a crucial role in calcium homeostasis by filtering calcium from the blood and then reabsorbing most of it, with only a small percentage being excreted in urine. Typically, about 98-99% of filtered calcium is reabsorbed in different segments of the nephron, particularly in the proximal tubule and thick ascending limb of the loop of Henle. The amount of calcium excreted is tightly regulated by hormones such as parathyroid hormone (PTH), vitamin D, and calcitonin. PTH increases calcium reabsorption in the kidneys when blood calcium levels are low, while calcitonin can increase calcium excretion when levels are high. Disorders affecting calcium excretion can lead to conditions like kidney stones (from excessive calcium in urine) or hypercalcemia (from insufficient excretion). Certain medications like thiazide diuretics can decrease calcium excretion, while loop diuretics can increase it 1.

Key Points

• The kidneys filter and reabsorb calcium to maintain calcium homeostasis in the body.
• Hormones like PTH, vitamin D, and calcitonin regulate calcium excretion.
• Disorders affecting calcium excretion can lead to conditions like kidney stones or hypercalcemia.
• Medications like thiazide diuretics and loop diuretics can affect calcium excretion.

Regulation of Calcium Excretion

The regulation of calcium excretion is complex and involves the coordinated effort of multiple hormones and the kidneys. PTH, for example, plays a crucial role in maintaining calcium homeostasis by stimulating calcium release from bone and increasing calcium reabsorption in the kidneys 1. Vitamin D also plays a role in calcium homeostasis by increasing intestinal absorption of calcium.

Clinical Implications

Understanding how the kidneys excrete calcium is important for managing conditions like kidney stones, hypercalcemia, and hypocalcemia. For example, patients with kidney stones may need to limit their calcium intake to prevent further stone formation. On the other hand, patients with hypocalcemia may need calcium supplements to maintain normal calcium levels. Certain medications, like thiazide diuretics, can decrease calcium excretion and may be used to treat conditions like kidney stones 1.

Conclusion is not allowed, so the answer will be ended here.

From the FDA Drug Label

Calcium excretion is decreased by thiazides Hydrochlorothiazide also decreases the excretion of calcium The answer is no, calcium is not excreted by the kidneys when taking hydrochlorothiazide, as the drug decreases calcium excretion. 2 2

From the Research

Calcium Excretion by the Kidneys

• The kidneys play a crucial role in regulating calcium homeostasis in the body by adjusting the reabsorption and excretion of filtered calcium 3.
• Calcium excretion is influenced by various factors, including parathyroid hormone (PTH), 1α,25-dihydroxyvitamin D3 (1α,25[OH]2D3), and other hormones 4, 5.
• Loop diuretics, such as furosemide, promote calcium wasting, which can lead to secondary hyperparathyroidism (HPT2) 6.
• Thiazide diuretics, on the other hand, limit urinary calcium excretion 6.
• The relationship between urinary calcium excretion and adverse clinical outcomes, such as end-stage kidney disease (ESKD), CKD progression, and all-cause mortality, is complex and influenced by various factors, including estimated glomerular filtration rate (eGFR) 7.

Factors Influencing Calcium Excretion

• eGFR is positively correlated with 24-hour urinary calcium excretion 7.
• Serum parathyroid hormone (PTH) is negatively associated with 24-hour urinary calcium excretion 7.
• Loop diuretics and thiazide diuretics have opposite effects on urinary calcium excretion, with loop diuretics increasing and thiazide diuretics decreasing excretion 6, 7.
• Sclerostin, an osteocyte-specific protein, regulates renal calcium excretion by suppressing 1α-hydroxylase in proximal tubular cells 3.

Clinical Implications

• Abnormalities in calcium metabolism are common in chronic kidney disease (CKD) and can lead to vascular calcification, nephrolithiasis, and nephrocalcinosis 4, 7.
• Treatment of secondary hyperparathyroidism with calcitriol and calcium-based phosphate binders can produce hypercalcemia and oversuppression of PTH, leading to adynamic bone disease and increased risk of vascular calcification 4.
• Vitamin D analogs and calcimimetics, such as cinacalcet, can effectively reduce serum PTH levels and improve calcium homeostasis in CKD patients 4, 5.