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 ^[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
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 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.

Medication

Tasic V, Gucev Z. Nephrolithiasis and Nephrocalcinosis in Children - Metabolic and Genetic Factors. Pediatr Endocrinol Rev. 2015 Sep. 13 (1):468-76. [Medline].
Sands JM, Naruse M, Baum M, et al. Apical extracellular calcium/polyvalent cation-sensing receptor regulates vasopressin-elicited water permeability in rat kidney inner medullary collecting duct. J Clin Invest. 1997 Mar 15. 99(6):1399-405. [Medline]. [Full Text].
Epstein FH. Calcium and the kidney. Am J Med. 1968 Nov. 45(5):700-14. [Medline].
Jonsson KB, Zahradnik R, Larsson T, et al. Fibroblast growth factor 23 in oncogenic osteomalacia and X-linked hypophosphatemia. N Engl J Med. 2003 Apr 24. 348(17):1656-63. [Medline]. [Full Text].
Schiavi SC, Kumar R. The phosphatonin pathway: new insights in phosphate homeostasis. Kidney Int. 2004 Jan. 65(1):1-14. [Medline].
Evan AP, Lingeman J, Coe F, et al. Renal histopathology of stone-forming patients with distal renal tubular acidosis. Kidney Int. 2007 Apr. 71(8):795-801. [Medline].
Oguzkurt L, Karabulut N, Haliloglu M, et al. Medullary nephrocalcinosis associated with vesicoureteral reflux. Br J Radiol. 1997 Aug. 70(836):850-1. [Medline]. [Full Text].
Gambaro G, Feltrin GP, Lupo A, et al. Medullary sponge kidney (Lenarduzzi-Cacchi-Ricci disease): a Padua Medical School discovery in the 1930s. Kidney Int. 2006 Feb. 69(4):663-70. [Medline].
Ketteler M, Chen K, Gosmanova EO, Signorovitch J, Mu F, Young JA, et al. Risk of Nephrolithiasis and Nephrocalcinosis in Patients with Chronic Hypoparathyroidism: A Retrospective Cohort Study. Adv Ther. 2021 Apr. 38 (4):1946-1957. [Medline]. [Full Text].
Karet FE. Inherited distal renal tubular acidosis. J Am Soc Nephrol. 2002 Aug. 13(8):2178-84. [Medline]. [Full Text].
Trepiccione F, Prosperi F, de la Motte LR, Hübner CA, Chambrey R, Eladari D, et al. New Findings on the Pathogenesis of Distal Renal Tubular Acidosis. Kidney Dis (Basel). 2017 Dec. 3 (3):98-105. [Medline].
Scarpelli DG, Tremblay G, Pearce AG. A comparative cytochemical and cytologic study of vitamin D induced nephrocalcinosis. Am J Pathol. 1960 Mar. 36:331-53. [Medline]. [Full Text].
Gobel U, Kettritz R, Schneider W, et al. The protean face of renal sarcoidosis. J Am Soc Nephrol. 2001 Mar. 12(3):616-23. [Medline]. [Full Text].
Finsterer J, Scorza FA. Renal manifestations of primary mitochondrial disorders. Biomed Rep. 2017 May. 6 (5):487-494. [Medline].
Frick KK, Bushinsky DA. Molecular mechanisms of primary hypercalciuria. J Am Soc Nephrol. 2003 Apr. 14(4):1082-95. [Medline]. [Full Text].
Gigante M, Santangelo L, Diella S, Caridi G, Argentiero L, D''Alessandro MM, et al. Mutational Spectrum of CYP24A1 Gene in a Cohort of Italian Patients with Idiopathic Infantile Hypercalcemia. Nephron. 2016. 133 (3):193-204. [Medline].
Markowitz GS, Stokes MB, Radhakrishnan J, et al. Acute phosphate nephropathy following oral sodium phosphate bowel purgative: an underrecognized cause of chronic renal failure. J Am Soc Nephrol. 2005 Nov. 16(11):3389-96. [Medline]. [Full Text].
Markowitz GS, Nasr SH, Klein P, et al. Renal failure due to acute nephrocalcinosis following oral sodium phosphate bowel cleansing. Hum Pathol. 2004 Jun. 35(6):675-84. [Medline].
Hurst FP, Bohen EM, Osgard EM, et al. Association of oral sodium phosphate purgative use with acute kidney injury. J Am Soc Nephrol. 2007 Dec. 18(12):3192-8. [Medline]. [Full Text].
Ori Y, Herman M, Tobar A, et al. Acute phosphate nephropathy-an emerging threat. Am J Med Sci. 2008 Oct. 336(4):309-14. [Medline].
Balaban DH. Guidelines for the safe and effective use of sodium phosphate solution for bowel cleansing prior to colonoscopy. Gastroenterol Nurs. 2008 Sep-Oct. 31(5):327-34; quiz 334-5. [Medline].
Barnett SM, Jackson AH, Rosen BA, Garb JL, Braden GL. Nephrolithiasis and Nephrocalcinosis From Topiramate Therapy in Children With Epilepsy. Kidney Int Rep. May 2018. 3 (3):684-690. [Full Text].
Mihatsch MJ, Khanlari B, Brunner FP. Obituary to analgesic nephropathy--an autopsy study. Nephrol Dial Transplant. 2006 Nov. 21 (11):3139-45. [Medline].
Leumann E, Hoppe B. The primary hyperoxalurias. J Am Soc Nephrol. 2001 Sep. 12(9):1986-93. [Medline]. [Full Text].
Hoppe B, Langman CB. A United States survey on diagnosis, treatment, and outcome of primary hyperoxaluria. Pediatr Nephrol. 2003 Oct. 18(10):986-91. [Medline].
Dickson FJ, Sayer JA. Nephrocalcinosis: A Review of Monogenic Causes and Insights They Provide into This Heterogeneous Condition. Int J Mol Sci. 2020 Jan 6. 21 (1):[Medline]. [Full Text].
Park E, Kang HG, Choi YH, Lee KB, Moon KC, Jeong HJ, et al. Focal segmental glomerulosclerosis and medullary nephrocalcinosis in children with ADCK4 mutations. Pediatr Nephrol. 2017 Sep. 32 (9):1547-1554. [Medline].
Alon U, Lovell HB, Donaldson DL. Nephrocalcinosis, hyperparathyroidism, and renal failure in familial hypophosphatemic rickets. Clin Pediatr (Phila). 1992 Mar. 31(3):180-3. [Medline].
Hoopes RR Jr, Shrimpton AE, Knohl SJ, et al. Dent Disease with mutations in OCRL1. Am J Hum Genet. 2005 Feb. 76(2):260-7. [Medline]. [Full Text].
Benigno V, Canonica CS, Bettinelli A, et al. Hypomagnesaemia-hypercalciuria-nephrocalcinosis: a report of nine cases and a review. Nephrol Dial Transplant. 2000 May. 15(5):605-10. [Medline]. [Full Text].
Weber S, Schneider L, Peters M, et al. Novel paracellin-1 mutations in 25 families with familial hypomagnesemia with hypercalciuria and nephrocalcinosis. J Am Soc Nephrol. 2001 Sep. 12(9):1872-81. [Medline]. [Full Text].
Knoers NV. Inherited forms of renal hypomagnesemia: an update. Pediatr Nephrol. 2008 Sep 26. [Medline].
Claverie-Martin F. Familial hypomagnesaemia with hypercalciuria and nephrocalcinosis: clinical and molecular characteristics. Clin Kidney J. 2015 Dec. 8 (6):656-664. [Medline].
Claverie-Martin F. Familial hypomagnesaemia with hypercalciuria and nephrocalcinosis: clinical and molecular characteristics. Clin Kidney J. 2015 Dec. 8 (6):656-64. [Medline].
Yamaguti PM, Neves FA, Hotton D, Bardet C, de La Dure-Molla M, Castro LC, et al. Amelogenesis imperfecta in familial hypomagnesaemia and hypercalciuria with nephrocalcinosis caused by CLDN19 gene mutations. J Med Genet. 2017 Jan. 54 (1):26-37. [Medline].
Sikora P, Zaniew M, Haisch L, Pulcer B, Szczepańska M, Moczulska A, et al. Retrospective cohort study of familial hypomagnesaemia with hypercalciuria and nephrocalcinosis due to CLDN16 mutations. Nephrol Dial Transplant. 2015 Apr. 30 (4):636-44. [Medline].
Schell-Feith EA, Moerdijk A, van Zwieten PH, et al. Does citrate prevent nephrocalcinosis in preterm neonates?. Pediatr Nephrol. 2006 Dec. 21(12):1830-6. [Medline].
Schell-Feith EA, Kist-van Holthe JE, van der Heijden AJ. Nephrocalcinosis in preterm neonates. Pediatr Nephrol. 2010 Feb. 25(2):221-30. [Medline].
Huynh M, Clark R, Li J, Filler G, Dave S. A case control analysis investigating risk factors and outcomes for nephrocalcinosis and renal calculi in neonates. J Pediatr Urol. 2017 Aug. 13 (4):356.e1-356.e5. [Medline].
Andrioli V, Highmore K, Leonard MP, Guerra LA, Tang K, Vethamuthu J, et al. Infant nephrolithiasis and nephrocalcinosis: Natural history and predictors of surgical intervention. J Pediatr Urol. 2017 Aug. 13 (4):355.e1-355.e6. [Medline].
Evenepoel P, Daenen K, Bammens B, Claes K, Meijers B, Naesens M, et al. Microscopic nephrocalcinosis in chronic kidney disease patients. Nephrol Dial Transplant. 2015 May. 30 (5):843-8. [Medline].
Cozzolino M, Staniforth ME, Liapis H, et al. Sevelamer hydrochloride attenuates kidney and cardiovascular calcifications in long-term experimental uremia. Kidney Int. 2003 Nov. 64(5):1653-61. [Medline].
Vergine G, Fabbri E, Pedini A, Tedeschi S, Borsa N. Bartter Syndrome Type 1 Presenting as Nephrogenic Diabetes Insipidus. Case Rep Pediatr. 2018. 2018:9175271. [Medline].
Wongsaengsak S, Vidmar AP, Addala A, Kamil ES, Sequeira P, Fass B, et al. A novel SLC12A1 gene mutation associated with hyperparathyroidism, hypercalcemia, nephrogenic diabetes insipidus, and nephrocalcinosis in four patients. Bone. 2017 Apr. 97:121-125. [Medline].
Anglani F, Terrin L, Brugnara M, Battista M, Cantaluppi V, Ceol M, et al. Hypercalciuria and nephrolithiasis: Expanding the renal phenotype of Donnai-Barrow syndrome. Clin Genet. 2018 Mar 13. [Medline].
Daga A, Majmundar AJ, Braun DA, Gee HY, Lawson JA, Shril S, et al. Whole exome sequencing frequently detects a monogenic cause in early onset nephrolithiasis and nephrocalcinosis. Kidney Int. 2018 Jan. 93 (1):204-213. [Medline].
Braun DA, Lawson JA, Gee HY, Halbritter J, Shril S, Tan W, et al. Prevalence of Monogenic Causes in Pediatric Patients with Nephrolithiasis or Nephrocalcinosis. Clin J Am Soc Nephrol. 2016 Apr 7. 11 (4):664-72. [Medline].
Evans R, Zdebik A, Ciurtin C, Walsh SB. Renal involvement in primary Sjögren’s syndrome. Rheumatology. 2015 Jun 10. 54(9):1541-8.
Tang X, Bergstralh EJ, Mehta RA, Vrtiska TJ, Milliner DS, Lieske JC. Nephrocalcinosis is a risk factor for kidney failure in primary hyperoxaluria. Kidney Int. 2015 Mar. 87 (3):623-31. [Medline].
Gambaro G, Goldfarb DS, Baccaro R, Hirsch J, Topilow N, D'Alonzo S, et al. Chronic pain in medullary sponge kidney: a rare and never described clinical presentation. J Nephrol. 2018 Feb 21. [Medline].
Sanderson PH. Functional aspects of renal calcification in rats. Clin Sci (Lond). 1959 Feb. 18(1):67-79. [Medline].
Al-Modhefer AK, Atherton JC, Garland HO, et al. Kidney function in rats with corticomedullary nephrocalcinosis: effects of alterations in dietary calcium and magnesium. J Physiol. 1986 Nov. 380:405-14. [Medline]. [Full Text].
Koruyucu M, Seymen F, Gencay G, Gencay K, Tuna EB, Shin TJ, et al. Nephrocalcinosis in Amelogenesis Imperfecta Caused by the FAM20A Mutation. Nephron. 2018 Feb 13. [Medline].
Keskin M, Savaş-Erdeve Ş, Sağsak E, Çetinkaya S, Aycan Z. Risk factors affecting the development of nephrocalcinosis, the most common complication of hypophosphatemic rickets. J Pediatr Endocrinol Metab. 2015 Nov 1. 28 (11-12):1333-7. [Medline].
Chesher D, Oddy M, Darbar U, Sayal P, Casey A, Ryan A, et al. Outcome of adult patients with X-linked hypophosphatemia caused by PHEX gene mutations. J Inherit Metab Dis. 2018 Sep. 41 (5):865-876. [Medline].
Chandrashekar KB, Fulop T, Juncos LA. Medical management and prevention of nephrolithiasis. Am J Med. 2012 Apr. 125 (4):344-7. [Medline].
Hoppe B, Kemper MJ. Diagnostic examination of the child with urolithiasis or nephrocalcinosis. Pediatr Nephrol. 2008 Dec 23. [Medline].
Hoppe B, Kemper MJ. Diagnostic examination of the child with urolithiasis or nephrocalcinosis. Pediatr Nephrol. 2010 Mar. 25(3):403-13. [Medline]. [Full Text].
Cheidde L, Ajzen SA, Tamer Langen CH, et al. A critical appraisal of the radiological evaluation of nephrocalcinosis. Nephron Clin Pract. 2007. 106(3):c119-24. [Medline].
Curry NS, Gordon L, Gobien RP, et al. Renal medullary "rings": possible CT manifestation of hypercalcemia. Urol Radiol. 1984. 6(1):48-50. [Medline].
Barre PE, Gascon-Barre M, Meakins JL, et al. Hydroxychloroquine treatment of hypercalcemia in a patient with sarcoidosis undergoing hemodialysis. Am J Med. 1987 Jun. 82(6):1259-62. [Medline].
Jamerson K, Weber MA, Bakris GL, et al. Benazepril plus amlodipine or hydrochlorothiazide for hypertension in high-risk patients. N Engl J Med. 2008 Dec 4. 359(23):2417-28. [Medline].
Sakhaee K, Nicar M, Hill K, et al. Contrasting effects of potassium citrate and sodium citrate therapies on urinary chemistries and crystallization of stone-forming salts. Kidney Int. 1983 Sep. 24(3):348-52. [Medline].
Bhagat SK, Chacko NK, Kekre NS, et al. Is there a role for tamsulosin in shock wave lithotripsy for renal and ureteral calculi?. J Urol. 2007 Jun. 177(6):2185-8. [Medline].
Fogo AB, Lusco MA, Najafian B, Alpers CE. AJKD Atlas of Renal Pathology: Nephrocalcinosis and Acute Phosphate Nephropathy. Am J Kidney Dis. 2017 Mar. 69 (3):e17-e18. [Medline].
Soliman NA, Nabhan MM, Abdelrahman SM, Abdelaziz H, Helmy R, Ghanim K, et al. Clinical spectrum of primary hyperoxaluria type 1: Experience of a tertiary center. Nephrol Ther. 2017 May. 13 (3):176-182. [Medline].
Çeltik A, Şen S, Yılmaz M, Demirci MS, Aşçı G, Tamer AF, et al. The effect of hypercalcemia on allograft calcification after kidney transplantation. Int Urol Nephrol. 2016 Nov. 48 (11):1919-1925. [Medline].
Davidson Peiris E, Wusirika R. A Case Report of Compound Heterozygous CYP24A1 Mutations Leading to Nephrolithiasis Successfully Treated with Ketoconazole. Case Rep Nephrol Dial. 2017 Sep-Dec. 7 (3):167-171. [Medline].
Misgar RA, Hassan Z, Wani AI, Bashir MI. Amelogenesis Imperfecta with Distal Renal Tubular Acidosis: A Novel Syndrome?. Indian J Nephrol. 2017 May-Jun. 27 (3):225-227. [Medline].
Bhojani N, Paonessa JE, Hameed TA, Worcester EM, Evan AP, Coe FL, et al. Nephrocalcinosis in Calcium Stone Formers Who Do Not have Systemic Disease. J Urology. 2015 Nov 1. 194(5):1308-12.
Schoelwer MJ, Viswanathan V, Wilson A, Nailescu C, Imel EA. Infants With Congenital Adrenal Hyperplasia Are at Risk for Hypercalcemia, Hypercalciuria, and Nephrocalcinosis. J Endocr Soc. 2017 Sep 1. 1 (9):1160-1167. [Medline].
Anders HJ, Suarez-Alvarez B, Grigorescu M, Foresto-Neto O, Steiger S, Desai J, et al. The macrophage phenotype and inflammasome component NLRP3 contributes to nephrocalcinosis-related chronic kidney disease independent from IL-1-mediated tissue injury. Kidney Int. 2018 Mar. 93 (3):656-669. [Medline].
Alhazmi HH. Renal oxalate stones in children with Zellweger spectrum disorders. Saudi J Anaesth. 2018 Apr-Jun. 12 (2):332-334. [Medline].
Liu S, Gao B, Wang G, Wang W, Lian X, Wu S, et al. Recurrent primary hyperoxaluria type 2 leads to early post-transplant renal function loss: A case report. Exp Ther Med. 2018 Apr. 15 (4):3169-3172. [Medline].
Al-Bderat JT, Mardinie RI, Salaita GM, Al-Bderat AT, Farrah MK. Nephrocalcinosis among children at king hussein medical center: Causes and outcome. Saudi J Kidney Dis Transpl. 2017 Sep-Oct. 28 (5):1064-1068. [Medline].

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.

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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 Hypertension, American Society of Nephrology, International Society for Apheresis, International Society for Hemodialysis, Magyar Orvosi Kamara (Hungarian Chamber of Medicine)

Disclosure: Nothing to disclose.

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, Interim Chair, Deming Department of Medicine, Tulane University School of Medicine

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.