Nephrocalcinosis Treatment & Management

Updated: Aug 09, 2021
  • Author: Tibor Fulop, MD, PhD, FACP, FASN; Chief Editor: Vecihi Batuman, MD, FASN  more...
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Approach Considerations

Medical treatment is provided as appropriate for the type of nephrocalcinosis present (see below). Surgical management is indicated in some cases. Dietary interventions can be formulated as part of consultation with an appropriate specialist after the underlying metabolic abnormality has been identified. Management depends mostly on treating the underlying etiology of nephrocalcinosis.

Patients with a primary loin pain–hematuria syndrome experience a poorly understood combination of pain associated with hematuria. Some of these individuals have concurrent nephrocalcinosis that, incorrectly, may be blamed for the generation of pain. However, any associated hypercalciuria or hyperuricosuria should be addressed aggressively for symptomatic control of pain in loin pain–hematuria syndrome.


Pharmacologic and Other Nonsurgical Therapies

Hypercalcemia and hypercalcemic nephropathy

Adequate hydration with an isotonic sodium chloride solution is the single most effective measure for reversing hypercalcemia and protecting the kidneys. This may be combined with furosemide to enhance calcium excretion only if there is evidence of hypervolemia.

Other treatments include the following:

  • Calcium-sensing receptor stimulant cinacalcet (for correction of hyperparathyroidism)
  • Chemotherapeutic agents (for osteolytic malignancies)
  • Steroids (to decrease intestinal calcium absorption and vitamin-D activity)
  • Hydroxychloroquine [61] (for sarcoid granulomas)
  • Calcitonin or bisphosphonates (to inhibit bone resorption)

Calcium-channel blockers have no role in management.

Macroscopic nephrocalcinosis

Thiazide diuretics and dietary salt restriction will reduce renal calcium excretion. Hydrochlorothiazide, the most commonly employed thiazide diuretic, is appropriate to use if the serum calcium level is not high; it may correct coincidental high blood pressure. [62] The usual dose range is 12.5-25 mg/day, though in rare cases, it may be as high as 50 mg/day. However, if hydrochlorothiazide is used, the daily dose should be split into 2 divided doses to cover a full 24-hour period. Chlorthalidone can be used at lower doses but can cause hypokalemia and hypocitraturia.

Potassium and magnesium supplementation will increase the solubility of urinary calcium. Magnesium supplementation may be helpful in magnesium-losing nephropathy.

Citrate supplementation (preferably as potassium citrate) can be used in idiopathic hypercalciuria and in distal renal tubular acidosis (RTA) because it increases urinary citrate excretion, acting as a chelating agent for urinary calcium to decrease stone formation. [63] In type 1 hyperoxaluria, treatment with large doses of pyridoxine can lower oxalate production.

Lessening of nephrocalcinosis may occur over time, especially in idiopathic absorptive hypercalciuria and enteric hyperoxaluria after gastrointestinal bypass surgery. In most other cases, however (eg, when it results from primary hyperoxaluria, distal RTA, papillary necrosis, or magnesium-losing nephropathy), nephrocalcinosis is largely irreversible. Therefore, early detection and treatment are important.

Oral fluid intake to make a daily urine output of at least 2 liters is recommended. Dietary measures include restriction of animal protein to no more than 0.7 mg/kg daily and of sodium to no more than 2.3 g/day.


Surgical Intervention

With copious fluid intake by the patient and appropriate use of pain control, stones passing the mid-ureter and measuring less than 5-7 mm usually pass on their own. Anecdotal evidence suggests that peripheral vasodilators (eg, alpha-blockers and calcium-channel blocker antihypertensive agents) may facilitate stone passage. [64]

Surgery may be required for urinary stones causing obstruction; options include the following:

  • Percutaneous nephrolithotomy
  • Stent placement
  • Open surgery (rarely necessary)

Parathyroidectomy to remove enlarged adenomas is very helpful in primary hyperparathyroidism and results in a low recurrence rate. Attempting to remove calcium nodules from within the renal parenchyma itself has no obvious benefit and is likely to cause harm.



The following consultations may be warranted:

  • Nephrology - For reduced kidney function and associated metabolic abnormalities; electrolyte disorders, including metabolic acidosis, hypercalcemia and hypercalciuria; and recurrent nephrolithiasis
  • Endocrinology - For hypercalcemia, vitamin-D and phosphate disorders, and sarcoid in association with hypercalcemia
  • Rheumatology - For distal RTA associated with rheumatologic disease (eg, Sjögren syndrome or systemic lupus erythematosus)
  • Otorhinolaryngologic or endocrine surgery - For surgical parathyroidectomy (the personal skill and experience of the operating surgeon are important)

Long-Term Monitoring

Efforts are under way to develop a long-term registry of pediatric nephrolithiasis and nephrocalcinosis. A pediatric cohort may be less confounded by co-morbidities of adult ones and demonstrate better the effect of examined processes.