Nephrocalcinosis Treatment & Management: Approach Considerations, Pharmacologic and Other Nonsurgical Therapies, Surgical Intervention

Sections

Treatment

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.

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^[53](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.^[54]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.^[55]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.^[56]

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

Percutaneous nephrolithotomy
Laser and shock wave lithotripsy
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.

Consultations

The following consultations may be warranted:

Nephrology - For reduced renal 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 long-term pediatric registry of pediatric nephrolithiasis and nephrocalcinosis registries. Pediatric cohort may be less confounded by co-morbidities of adult ones and demonstrate better the effect of examined processes.

Medication

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Media Gallery

Diagram of nephron.
Nephrocalcinosis.
Nephrocalcinosis.
Nephrocalcinosis.
Nonenhanced coronal CT scans through kidneys, showing cortical and medullary nephrocalcinosis (left kidney). Both kidneys appear scarred. Note thinning of renal cortex at upper pole of left kidney. Patient gave long history of chronic pyelonephritis, which is unusual cause of nephrocalcinosis.
Axial CT scans from patient with long history of renal tubular acidosis. Images show bilateral medullary nephrocalcinosis (early arterial phase).
Ultrasonogram of right kidney in woman with nephrocalcinosis. Image shows hyperechoic foci in pyramids.
Excretory urogram obtained at 15 minutes in man with renal papillary necrosis (most likely, patient with diabetes mellitus and repeated urinary tract infections). Image shows bilateral hydronephrosis and hydroureter due to obstruction by sloughed papillae at lower end of ureter.
Plain kidney-ureter-bladder (KUB) radiograph in man with renal papillary necrosis (most likely, patient with diabetes mellitus and repeated urinary tract infections). Image shows bilateral renal calcification. Large, sloughed, and calcified renal papilla is present in region of left vesicoureteric junction. Note 2 pelvic phleboliths opposite ischial spine on right.

of 9

Author

Tibor Fulop, MD, PhD, FACP, FASN Professor of Medicine, Department of Medicine, Division of Nephrology, Medical University of South Carolina College of Medicine; Attending Physician; Medical Services, Ralph H Johnson VA Medical Center

Tibor Fulop, MD, PhD, FACP, FASN is a member of the following medical societies: American Academy of Urgent Care Medicine, American College of Physicians, American Society of Diagnostic and Interventional Nephrology, American Society of Hypertension, American Society of Nephrology, International Society for Apheresis, International Society for Hemodialysis, Magyar Orvosi Kamara (Hungarian Chamber of Medicine), Southern Society for Clinical Investigation

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Fresenius Medical Care, Hungary; Dialysis Clinic Inc., USA.

Coauthor(s)

Sohail Abdul Salim, MD, FASN, FACP Consultant Physician, Central Nephrology; Affiliate Faculty, Department of Internal Medicine, Division of Nephrology, University of Mississippi Medical Center

Sohail Abdul Salim, MD, FASN, FACP is a member of the following medical societies: American College of Physicians, American Society of Nephrology, Mississippi State Medical Association, Renal Physicians Association

Disclosure: Nothing to disclose.

Chief Editor

Vecihi Batuman, MD, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology, Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Additional Contributors

Mahendra Agraharkar, MD, MBBS, FACP, FASN Clinical Associate Professor of Medicine, Baylor College of Medicine; President and CEO, Space City Associates of Nephrology

Mahendra Agraharkar, MD, MBBS, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Nephrology, National Kidney Foundation

Disclosure: Nothing to disclose.

Rajiv Gupta, MD Assistant Professor, Department of Medicine, Texas A&M Health Science Center College of Medicine; Consulting Staff, Veterans Affairs Medical Center

Rajiv Gupta, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.

Acknowledgements

Eleanor Lederer, MD Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa

Disclosure: Dept of Veterans Affairs Grant/research funds Research

James W Lohr, MD Professor, Department of Internal Medicine, Division of Nephrology, Fellowship Program Director, University of Buffalo State University of New York School of Medicine and Biomedical Sciences

James W Lohr, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, and Central Society for Clinical Research

Disclosure: Alexion Salary Employment

Rupert Patel, MD Physician, Division of Nephrology, Houston, Texas

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Acknowledgments

The primary author would like to thank Dr Gurvinder Suri, Renal Fellow in the Nephrology Division at the University of Mississippi Medical Center, for his valuable peer review.

Nephrocalcinosis Treatment & Management

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Hypercalcemia and hypercalcemic nephropathy

Macroscopic nephrocalcinosis

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Nephrocalcinosis Treatment & Management

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Long-Term Monitoring

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