- Hypercalcemic nephropathy
Your QuestionMy son has nephrocalcinosis. Could you please tell me about it? Is it genetic? How might it be treated?
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Nephrocalcinosis may be caused by a variety of things, including underlying disorders or conditions, medications or supplements, and infections. Causes may include:
- Primary hyperparathyroidism is the single most common cause of nephrocalcinosis in adults. While nephrocalcinosis is a relatively rare complication (5%), primary hyperparathryroidism is relatively common, especially in the elderly. Rarely, hyperparathyroidism can be associated with multiple endocrine neoplasia type 1 (MEN1).
- Distal renal tubular acidosis (RTA) is the second most common cause of medullary nephrocalcinosis.
- hypervitaminosis-D states resulting from excessive treatment of hypoparathyroidism, self-administration of vitamins, and the presence of a granulomatous disease, such as sarcoidosis.
- Any other cause of hypercalcemia (increased calcium in the blood), particularly when associated with hypercalciuria (increased calcium in the urine). Causes include milk-alkali syndrome (due to excess ingestion of antacids), hyperparathyroidism, and malignant disease. Idiopathic hypercalciuria, a common metabolic disease, is also a known cause.
- Nephrocalcinosis and renal failure are increasingly being recognized as common complications of phosphate supplementation, particularly in the elderly. Phosphate supplements may contribute to renal calcifications in children with hypophosphatemic rickets.
- Medullary sponge kidney
- Rapidly progressive osteoporosis due to immobilization, menopause, aging, or steroids.
- Primary (familial) hyperoxaluria, or secondary hyperoxaluria due to increased intake of oxalates, increased absorption due to intestinal disease, or ingestion of ethylene glycol.
- Chronic disorders such as Bartter syndrome, primary hyperaldosteronism, Liddle syndrome, and 11-beta hydroxylase deficiency are associated with reduced urine citrate and tubular damage, leading to calcium deposits.
- Autosomal dominant hypophosphatemic rickets and X-linked hypophosphatemic conditions, possibly due to phosphate supplementation for the condition.
- Premature, sick infants have been observed to develop diffuse nephrocalcinosis, typically when exposed to diuretic therapy or prolonged O 2 therapy.
- Other causes may include the use of certain medications such as acetazolamide; tuberculosis of the kidney; and infections related to AIDS
- Multiple endocrine neoplasia type 1 (MEN1)
- Familial distal renal tubular acidosis
- Chronic granulomatous disease
- Primary hyperoxaluria
- Bartter syndrome
- primary hyperaldosteronism
- Liddle syndrome
- 11-beta hydroxylase deficiency, a form of congenital adrenal hyperplasia (CAH)
- Autosomal dominant hypophosphatemic rickets and X-linked hypophosphatemic conditions
Treatment of hypercalcemia (increased calcium levels in the blood) and hypercalcemic nephropathy typically includes adequate hydration by isotonic sodium chloride (normal saline) solution to reverse hypercalcemia and protect the kidneys. Treatment of macroscopic nephrocalcinosis (calcium deposition that is visible without magnification) may include thiazide diuretics and dietary salt restriction; potassium and magnesium supplementation; and citrate supplementation in idiopathic hypercalciuria (of unknown cause) and in distal renal tubular acidosis. Lessening of nephrocalcinosis may occur over time, but in many cases, such as when it results from primary hyperoxaluria or distal renal tubular acidosis, nephrocalcinosis is largely irreversible. Therefore, early detection and treatment are important.
Individuals interested in learning about treatment options for themselves should speak with their health care provider or a nephrologist.
- Louis S. Liou, David Zieve. Nephrocalcinosis. PubMed Health. August 30, 2009; http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001522. Accessed 2/24/2011.
- Tibor Fulop, Mahendra Agraharkar, Rupert Patel, Rajiv Gupta. Nephrocalcinosis. eMedicine. April 21, 2009; http://emedicine.medscape.com/article/243911-overview. Accessed 2/24/2011.