Advertisement

Pathophysiology of Kidney Stone Formation

  • Elaine M. WorcesterEmail author
Chapter
Part of the Nutrition and Health book series (NH)

Abstract

Kidney stone formation is common, and most stone formers have no known systemic disease as the cause of their stone formation but may have one or more metabolic abnormalities that result from a combination of genetic predisposition and environmental factors. Calcium stones are by far the most common, accounting for 80% of all stones; uric acid stones are found in about 10% of stone formers, struvite in about 5%, and other types of stones are considered rare. Stones form because urine becomes supersaturated with the stone material, allowing crystals to form in the kidney. All stone formers have at least modest crystal deposits in papillary tissue, which often serve as anchor sites for stone formation and growth. Idiopathic calcium oxalate stones are the most commonly seen in practice and affect people of all ages, increasingly including children. Many idiopathic stone formers have one or more metabolic abnormalities that provoke supersaturation, including hypercalciuria, hyperoxaluria, or hypocitraturia. The physiologic processes that lead to abnormal excretion of these solutes are currently under investigation.

Keywords

Calcium oxalate Calcium phosphate Supersaturation Citrate Idiopathic hypercalciuria Hyperoxaluria Randall’s plaque 

Notes

Acknowledgments

The author gratefully acknowledges the contributions of Dr. Fredric Coe and Andrew Evan to the work presented here, as well as support from NIH NIDDK P01 56788.

References

  1. 1.
    Scales CD Jr, Smith AC, Hanley JM, Saigal CS. Prevalence of kidney stones in the United States. Eur Urol. 2012;62(1):160–5.PubMedPubMedCentralCrossRefGoogle Scholar
  2. 2.
    Sas DJ. An update on the changing epidemiology and metabolic risk factors in pediatric kidney stone disease. Clin J Am Soc Nephrol. 2011;6(8):2062–8.PubMedCrossRefPubMedCentralGoogle Scholar
  3. 3.
    Costa-Bauza A, Ramis M, Montesinos V, Grases F, Conte A, Piza P, et al. Type of renal calculi: variation with age and sex. World J Urol. 2007;25:415–21.PubMedCrossRefPubMedCentralGoogle Scholar
  4. 4.
    Lieske JC, Rule AD, Krambeck AE, Williams JC, Bergstralh EJ, Mehta RA, et al. Stone composition as a function of age and sex. Clin J Am Soc Nephrol. 2014;9(12):2141–6.PubMedPubMedCentralCrossRefGoogle Scholar
  5. 5.
    Daudon M, Frochot V, Bazin D, Jungers P. Drug-induced kidney stones and crystalline nephropathy: pathophysiology, prevention and treatment. Drugs. 2018;78(2):163–201.PubMedCrossRefPubMedCentralGoogle Scholar
  6. 6.
    Qiu SR, Orme CA. Dynamics of biomineral formation at the near-molecular level. Chem Rev. 2008;108(11):4784–822.PubMedCrossRefPubMedCentralGoogle Scholar
  7. 7.
    Coe FL, Evan AP, Worcester E. Pathogenesis and treatment of nephrolithiasis. In: Alpern RJ, Caplan MJ, Moe OW, editors. Seldin and giebisch the kidney. 5thed. ed. Amsterdam: Academic Press; 2013. p. 2311–49.CrossRefGoogle Scholar
  8. 8.
    Werness PG, Brown CM, Smith LH, Finlayson B. Equil 2: a basic computer program for the calculation of urinary saturation. J Urol. 1985;134:1242–4.PubMedCrossRefPubMedCentralGoogle Scholar
  9. 9.
    Lemann J Jr, Pleuss JA, Worcester EM, Hornick L, Schrab D, Hoffmann RG. Urinary oxalate excretion increases with body size and decreases with increasing dietary calcium intake among healthy adults. Kidney Int. 1996;49(1):200–8.PubMedCrossRefPubMedCentralGoogle Scholar
  10. 10.
    Bergsland KJ, Coe FL, Gillen DL, Worcester EM. A test of the hypothesis that the collecting duct calcium-sensing receptor limits rise of urine calcium molarity in hypercalciuric calcium kidney stone formers. Am J Physiol Renal Physiol. 2009;297(4):F1017–23.PubMedPubMedCentralCrossRefGoogle Scholar
  11. 11.
    De Yoreo JJ, Qiu SR, Hoyer JR. Molecular modulation of calcium oxalate crystallization. Am J Physiol Renal Physiol. 2006;291(6):F1123–31.PubMedCrossRefPubMedCentralGoogle Scholar
  12. 12.
    Aggarwal KP, Narula S, Kakkar M, Tandon C. Nephrolithiasis: molecular mechanism of renal stone formation and the critical role played by modulators. Biomed Res Int. 2013;2013:292953.PubMedPubMedCentralCrossRefGoogle Scholar
  13. 13.
    Asplin JR, Parks JH, Chen MS, Lieske JC, Toback FG, Pillay SN, et al. Reduced crystallization inhibition by urine from men with nephrolithiasis. Kidney Int. 1999;56(4):1505–16.PubMedCrossRefPubMedCentralGoogle Scholar
  14. 14.
    Asplin JR, Parks JH, Nakagawa Y, Coe FL. Reduced crystallization inhibition by urine from women with nephrolithiasis. Kidney Int. 2002;2002:1821–9.CrossRefGoogle Scholar
  15. 15.
    Aggarwal KP, Tandon S, Naik PK, Singh SK, Tandon C. Peeping into human renal calcium oxalate stone matrix: characterization of novel proteins involved in the intricate mechanism of urolithiasis. PLoS One. 2013;8(7):e69916.PubMedPubMedCentralCrossRefGoogle Scholar
  16. 16.
    Rimer JD, An Z, Zhu Z, Lee MH, Goldfarb DS, Wesson JA, et al. Crystal growth inhibitors for the prevention of L-cystine kidney stones through molecular design. Science. 2010;330(6002):337–41.PubMedPubMedCentralCrossRefGoogle Scholar
  17. 17.
    Coe FL, Evan AP, Worcester EM, Lingeman JE. Three pathways for human kidney stone formation. Urol Res. 2010;38(3):147–60.PubMedPubMedCentralCrossRefGoogle Scholar
  18. 18.
    Miller NL, Gillen DL, Williams JC Jr, Evan AP, Bledsoe SB, Coe FL, et al. A formal test of the hypothesis that idiopathic calcium oxalate stones grow on Randall’s plaque. BJU Int. 2009;103(7):966–71.PubMedCrossRefPubMedCentralGoogle Scholar
  19. 19.
    Evan AP, Lingeman JE, Coe FL, Parks JH, Bledsoe SB, Shao Y, et al. Randall’s plaque of patients with nephrolithiasis begins in basement membranes of thin loops of Henle. J Clin Invest. 2003;111(5):607–16.PubMedPubMedCentralCrossRefGoogle Scholar
  20. 20.
    Kuo RL, Lingeman JE, Evan AP, Paterson RF, Parks JH, Bledsoe SB, et al. Urine calcium and volume predict coverage of renal papilla by Randall’s plaque. Kidney Int. 2003;64(6):2150–4.PubMedCrossRefPubMedCentralGoogle Scholar
  21. 21.
    Evan AP, Lingeman JE, Coe FL, Worcester EM. Role of interstitial apatite plaque in the pathogenesis of the common calcium oxalate stone. Semin Nephrol. 2008;28(2):111–9.PubMedPubMedCentralCrossRefGoogle Scholar
  22. 22.
    Evan AP, Coe FL, Lingeman JE, Shao Y, Sommer AJ, Bledsoe SB, et al. Mechanism of formation of human calcium oxalate renal stones on Randall’s plaque. Anat Rec (Hoboken). 2007;290(10):1315–23.CrossRefGoogle Scholar
  23. 23.
    Evan AP, Lingeman JE, Worcester EM, Sommer AJ, Phillips CL, Williams JC, et al. Contrasting histopathology and crystal deposits in kidneys of idiopathic stone formers who produce hydroxy apatite, brushite, or calcium oxalate stones. Anat Rec (Hoboken). 2014;297(4):731–48.CrossRefGoogle Scholar
  24. 24.
    Evan AP, Coe FL, Lingeman JE, Shao Y, Matlaga BR, Kim SC, et al. Renal crystal deposits and histopathology in patients with cystine stones. Kidney Int. 2006;69(12):2227–35.PubMedCrossRefPubMedCentralGoogle Scholar
  25. 25.
    Evan AE, Lingeman JE, Coe FL, Miller NL, Bledsoe SB, Sommer AJ, et al. Histopathology and surgical anatomy of patients with primary hyperparathyroidism and calcium phosphate stones. Kidney Int. 2008;74(2):223–9.PubMedCrossRefPubMedCentralGoogle Scholar
  26. 26.
    Evan AP, Lingeman J, Coe F, Shao Y, Miller N, Matlaga B, et al. Renal histopathology of stone-forming patients with distal renal tubular acidosis. Kidney Int. 2007;71(8):795–801.PubMedCrossRefPubMedCentralGoogle Scholar
  27. 27.
    O’Connor RC, Worcester EM, Evan AP, Meehan S, Kuznetsov D, Laven B, et al. Nephrolithiasis and nephrocalcinosis in rats with small bowel resection. Urol Res. 2005;33(2):105–15.PubMedCrossRefPubMedCentralGoogle Scholar
  28. 28.
    Evan AP, Lingeman JE, Coe FL, Bledsoe SB, Sommer AJ, Williams JC Jr, et al. Intra-tubular deposits, urine and stone composition are divergent in patients with ileostomy. Kidney Int. 2009;76(10):1081–8.PubMedPubMedCentralCrossRefGoogle Scholar
  29. 29.
    Worcester EM, Evan AP, Coe FL, Lingeman JE, Krambeck A, Sommers A, et al. A test of the hypothesis that oxalate secretion produces proximal tubule crystallization in primary hyperoxaluria type I. Am J Physiol Renal Physiol. 2013;305(11):F1574–84.PubMedPubMedCentralCrossRefGoogle Scholar
  30. 30.
    Coe FL, Evan AP, Lingeman JE, Worcester EM. Plaque and deposits in nine human stone diseases. Urol Res. 2010;38(4):239–47.PubMedPubMedCentralCrossRefGoogle Scholar
  31. 31.
    Evan AP, Worcester EM, Williams JC Jr, Sommer AJ, Lingeman JE, Phillips CL, et al. Biopsy proven medullary sponge kidney: clinical findings, histopathology, and role of osteogenesis in stone and plaque formation. Anat Rec (Hoboken). 2015;298(5):865–77.CrossRefGoogle Scholar
  32. 32.
    Thorleifsson G, Holm H, Edvardsson V, Walters GB, Styrkarsdottir U, Gudbjartsson DF, et al. Sequence variants in the CLDN14 gene associate with kidney stones and bone mineral density. Nat Genet. 2009;41(8):926–30.PubMedCrossRefGoogle Scholar
  33. 33.
    Coe FL, Parks JH, Moore ES. Familial idiopathic hypercalciuria. N Engl J Med. 1979;300(7):337–40.PubMedCrossRefGoogle Scholar
  34. 34.
    Bergsland KJ, Coe FL, White MD, Erhard MJ, DeFoor WR, Mahan JD, et al. Urine risk factors in children with calcium kidney stones and their siblings. Kidney Int. 2012;81(11):1140–8.PubMedPubMedCentralCrossRefGoogle Scholar
  35. 35.
    Worcester EM, Coe FL. New insights into the pathogenesis of idiopathic hypercalciuria. Semin Nephrol. 2008;28(2):120–32.PubMedPubMedCentralCrossRefGoogle Scholar
  36. 36.
    Coe FL, Worcester EM. Idiopathic hypercalciuria. In: Coe FL, Worcester EM, Lingeman J, Evan AP, editors. Kidney stones:medical and surgical management. 2nded. ed. New Delhi: Jaypee Brothers Medical Publishers; 2018. p. 276–302.Google Scholar
  37. 37.
    Coe FL, Favus MJ, Crockett T, Strauss AL, Parks JH, Porat A, et al. Effects of low-calcium diet on urine calcium excretion, parathyroid function and serum 1,25(OH)2D3 levels in patients with idiopathic hypercalciuria and in normal subjects. Am J Med. 1982;72(1):25–32.PubMedCrossRefPubMedCentralGoogle Scholar
  38. 38.
    Sakhaee K, Maalouf NM, Kumar R, Pasch A, Moe OW. Nephrolithiasis-associated bone disease: pathogenesis and treatment options. Kidney Int. 2011;79(4):393–403.PubMedCrossRefGoogle Scholar
  39. 39.
    Worcester EM, Gillen DL, Evan AP, Parks JH, Wright K, Trumbore L, et al. Evidence that postprandial reduction of renal calcium reabsorption mediates hypercalciuria of patients with calcium nephrolithiasis. Am J Physiol Renal Physiol. 2007;292(1):F66–75.PubMedCrossRefPubMedCentralGoogle Scholar
  40. 40.
    Worcester EM, Coe FL, Evan AP, Bergsland KJ, Parks JH, Willis LR, et al. Evidence for increased postprandial distal nephron calcium delivery in hypercalciuric stone-forming patients. Am J Physiol Renal Physiol. 2008;295(5):F1286–94.PubMedPubMedCentralCrossRefGoogle Scholar
  41. 41.
    Ko B, Bergsland K, Gillen DL, Evan AP, Clark DL, Baylock J, et al. Sex differences in proximal and distal nephron function contribute to the mechanism of idiopathic hypercalcuria in calcium stone formers. Am J Physiol Regul Integr Comp Physiol. 2015;309(1):R85–92.PubMedPubMedCentralCrossRefGoogle Scholar
  42. 42.
    Worcester EM, Bergsland KJ, Gillen DL, Coe FL. Evidence for increased renal tubule and parathyroid gland sensitivity to serum calcium in human idiopathic hypercalciuria. Am J Physiol Renal Physiol. 2013;305(6):F853–60.PubMedPubMedCentralCrossRefGoogle Scholar
  43. 43.
    Bergsland KJ, Worcester EM, Coe FL. Role of proximal tubule in the hypocalciuric response to thiazide of patients with idiopathic hypercalciuria. Am J Physiol Renal Physiol. 2013;305(4):F592–9.PubMedPubMedCentralCrossRefGoogle Scholar
  44. 44.
    Coe FL, Parks JH, Bushinsky DA, Langman CB, Favus MJ. Chlorthalidone promotes mineral retention in patients with idiopathic hypercalciuria. Kidney Int. 1988;33(6):1140–6.PubMedCrossRefPubMedCentralGoogle Scholar
  45. 45.
    Lemann J Jr, Piering WF, Lennon EJ. Possible role of carbohydrate-induced calciuria in calcium oxalate kidney-stone formation. N Engl J Med. 1969;280:232–7.PubMedCrossRefPubMedCentralGoogle Scholar
  46. 46.
    Yoon V, Adams-Huet B, Sakhaee K, Maalouf NM. Hyperinsulinemia and urinary calcium excretion in calcium stone formers with idiopathic hypercalciuria. J Clin Endocrinol Metab. 2013;98(6):2589–94.PubMedPubMedCentralCrossRefGoogle Scholar
  47. 47.
    Bergeron MJ, Clemencon B, Hediger MA, Markovich D. SLC13 family of Na(+)-coupled di- and tri-carboxylate/sulfate transporters. Mol Aspects Med. 2013;34(2–3):299–312.PubMedCrossRefPubMedCentralGoogle Scholar
  48. 48.
    Curhan GC, Taylor EN. 24-h uric acid excretion and the risk of kidney stones. Kidney Int. 2008;73(4):489–96.PubMedCrossRefPubMedCentralGoogle Scholar
  49. 49.
    Dawson-Hughes B, Harris SS, Palermo NJ, Gilhooly CH, Shea MK, Fielding RA, et al. Potassium bicarbonate supplementation lowers bone turnover and calcium excretion in older men and women: arandomized dose-finding trial. J Bone Miner Res. 2015;30(11):2103–11.PubMedPubMedCentralCrossRefGoogle Scholar
  50. 50.
    Song Y, Hernandez N, Shoag J, Goldfarb DS, Eisner BH. Potassium citrate decreases urine calcium excretion in patients with hypocitraturic calcium oxalate nephrolithiasis. Urolithiasis. 2016;44(2):145–8.PubMedCrossRefPubMedCentralGoogle Scholar
  51. 51.
    Moseley KF, Weaver CM, Appel L, Sebastian A, Sellmeyer DE. Potassium citrate supplementation results in sustained improvement in calcium balance in older men and women. J Bone Miner Res. 2013;28(3):497–504.PubMedPubMedCentralCrossRefGoogle Scholar
  52. 52.
    Shea MK, Dawson-Hughes B. Association of urinary citrate with acid-base status, bone resorption, and calcium excretion in older men and women. J Clin Endocrinol Metab. 2018;103(2):452–9.PubMedCrossRefPubMedCentralGoogle Scholar
  53. 53.
    Holmes RP, Goodman HO, Assimos DG. Contribution of dietary oxalate to urinary oxalate excretion. Kidney Int. 2001;59:270–6.PubMedCrossRefPubMedCentralGoogle Scholar
  54. 54.
    von Unruh GE, Voss S, Sauerbruch T, Hesse A. Dependence of oxalate absorption on the daily calcium intake. J Am Soc Nephrol. 2004;15:1567–73.CrossRefGoogle Scholar
  55. 55.
    Bergsland KJ, Zisman AL, Asplin JR, Worcester EM, Coe FL. Evidence for net renal tubule oxalate secretion in patients with calcium kidney stones. Am J Physiol Renal Physiol. 2011;300(2):F311–8.PubMedCrossRefPubMedCentralGoogle Scholar
  56. 56.
    Alper SL, Sharma AK. The SLC26 gene family of anion transporters and channels. Mol Aspects Med. 2013;34(2–3):494–515.PubMedPubMedCentralCrossRefGoogle Scholar
  57. 57.
    Moreland AM, Santa Ana CA, Asplin JR, Kuhn JA, Holmes RP, Cole JA, et al. Steatorrhea and hyperoxaluria in severely obese patients before and after Roux-en-Y gastric bypass. Gastroenterology. 2017;152(5):1055–67.PubMedCrossRefPubMedCentralGoogle Scholar
  58. 58.
    Amin R, Asplin J, Jung D, Bashir M, Alshaikh A, Ratakonda S, et al. Reduced active transcellular intestinal oxalate secretion contributes to the pathogenesis of obesity-associated hyperoxaluria. Kidney Int. 2018;93(5):1098–107.PubMedPubMedCentralCrossRefGoogle Scholar
  59. 59.
    Holmes RP, Knight J, Assimos DG. Lowering urinary oxalate excretion to decrease calcium oxalate stone disease. Urolithiasis. 2016;44(1):27–32.PubMedCrossRefPubMedCentralGoogle Scholar
  60. 60.
    Ferraro PM, Curhan GC, Gambaro G, Taylor EN. Total, dietary, and supplemental vitamin C intake and risk of incident kidney stones. Am J Kidney Dis. 2016;67(3):400–7.PubMedCrossRefPubMedCentralGoogle Scholar
  61. 61.
    Moe OW, Xu LHR. Hyperuricosuric calcium urolithiasis. J Nephrol. 2018;31(2):189–96.PubMedCrossRefPubMedCentralGoogle Scholar
  62. 62.
    Ettinger B, Tang A, Citron JT, Livermore B, Williams T. Randomized trial of allopurinol in the prevention of calcium oxalate calculi. N Engl J Med. 1986;315:1386–9.PubMedCrossRefPubMedCentralGoogle Scholar
  63. 63.
    Pak CYC, Sakhaee K, Crowther C, Brinkley L. Evidence justifying a high fluid intake in treatment of nephrolithiaisis. Ann Intern Med. 1980;93:36–9.PubMedCrossRefPubMedCentralGoogle Scholar
  64. 64.
    Ferraro PM, Taylor EN, Gambaro G, Curhan GC. Dietary and lifestyle risk factors associated with incident kidney stones in men and women. J Urol. 2017;198(4):858–63.PubMedPubMedCentralCrossRefGoogle Scholar
  65. 65.
    Borghi L, Meschi T, Amato F, Briganti A, Novarini A, Giannini A. Urinary volume, water and recurrences of idiopathic calcium nephrolithiasis: a 5-year randomized prospective study. J Urol. 1996;155:839–43.PubMedCrossRefPubMedCentralGoogle Scholar
  66. 66.
    Parks JH, Worcester EM, Coe FL, Evan AP, Lingeman JE. Clinical implications of abundant calcium phosphate in routinely analyzed kidney stones. Kidney Int. 2004;66(2):777–85.PubMedCrossRefPubMedCentralGoogle Scholar
  67. 67.
    Gault MH, Chafe LL, Morgan JM, Parfrey PS, Harnett JD, Walsh EA, et al. Comparison of patients with idiopathic calcium phosphate and calcium oxalate stones. Medicine. 1991;70:345–58.PubMedCrossRefPubMedCentralGoogle Scholar
  68. 68.
    Zhang J, Fuster DG, Cameron MA, Quinones H, Griffith C, Xie XS, et al. Incomplete distal renal tubular acidosis from a heterozygous mutation of the V-ATPase B1 subunit. Am J Physiol Renal Physiol. 2014;307(9):F1063–71.PubMedPubMedCentralCrossRefGoogle Scholar
  69. 69.
    Parks JH, Coe FL, Evan AP, Worcester EM. Urine pH in renal calcium stone formers who do and do not increase stone phosphate content with time. Nephrol Dial Transplant. 2009;24(1):130–6.PubMedCrossRefPubMedCentralGoogle Scholar
  70. 70.
    Worcester EM, Bergsland KJ, Gillen DL, Coe FL. Mechanism for higher urine pH in normal women compared with men. Am J Physiol Renal Physiol. 2018;314(4):F623–9.PubMedCrossRefPubMedCentralGoogle Scholar
  71. 71.
    Parks JH, Coe FL, Evan AP, Worcester EM. Clinical and laboratory characteristics of calcium stone-formers with and without primary hyperparathyroidism. BJU Int. 2009;103(5):670–8.PubMedCrossRefPubMedCentralGoogle Scholar
  72. 72.
    Cipriani C, Biamonte F, Costa AG, Zhang C, Biondi P, Diacinti D, et al. Prevalence of kidney stones and vertebral fractures in primary hyperparathyroidism using imaging technology. J Clin Endocrinol Metab. 2015;100(4):1309–15.PubMedPubMedCentralCrossRefGoogle Scholar
  73. 73.
    Bilezikian JP, Bandeira L, Khan A, Cusano NE. Hyperparathyroidism. Lancet. 2018;391(10116):168–78.PubMedCrossRefPubMedCentralGoogle Scholar
  74. 74.
    Shinall MC Jr, Dahir KM, Broome JT. Differentiating familial hypocalciuric hypercalcemia from primary hyperparathyroidism. Endocr Pract. 2013;19(4):697–702.PubMedCrossRefPubMedCentralGoogle Scholar
  75. 75.
    Parks JH, Worcester EM, O’Connor RC, Coe FL. Urine stone risk factors in nephrolithiasis patients with and without bowel disease. Kidney Int. 2003;63:255–65.PubMedCrossRefPubMedCentralGoogle Scholar
  76. 76.
    Worcester EM. Stones from bowel disease. Endocrinol Metab Clin North Am. 2002;31:979–99.PubMedCrossRefGoogle Scholar
  77. 77.
    Worcester EM. Stones due to bowel disease. In: Coe FL, Favus MJ, Pak CYC, Parks JH, Preminger GM, editors. Kidney stones: medical and surgical management. 1st ed. Philadelphia: Lippincott-Raven; 1996. p. 883–904.Google Scholar
  78. 78.
    Tarplin S, Ganesan V, Monga M. Stone formation and management after bariatric surgery. Nat Rev Urol. 2015;12(5):263–70.PubMedCrossRefPubMedCentralGoogle Scholar
  79. 79.
    Whittamore JM, Hatch M. The role of intestinal oxalate transport in hyperoxaluria and the formation of kidney stones in animals and man. Urolithiasis. 2017;45(1):89–108.PubMedCrossRefPubMedCentralGoogle Scholar
  80. 80.
    Kwan TK, Chadban SJ, McKenzie PR, Saunders JR. Acute oxalate nephropathy secondary to orlistat-induced enteric hyperoxaluria. Nephrology (Carlton). 2013;18(3):241–2.CrossRefGoogle Scholar
  81. 81.
    Milliner D, Matsumoto J. Primary hyperoxaluria. In: Coe FL, Worcester EM, Lingeman JE, Evan AP, editors. Kidney stones: medical and surgical management. 2nd ed. New Delhi: Jaypee Brothers Medical Publishers; 2018. p. 412–42.Google Scholar
  82. 82.
    Maalouf NM, Langston JP, Van Ness PC, Moe OW, Sakhaee K. Nephrolithiasis in topiramate users. Urol Res. 2011;39(4):303–7.PubMedCrossRefPubMedCentralGoogle Scholar
  83. 83.
    Sakhaee K. Epidemiology and clinical pathophysiology of uric acid kidney stones. J Nephrol. 2014;27(3):241–5.PubMedPubMedCentralCrossRefGoogle Scholar
  84. 84.
    Marchini GS, Sarkissian C, Tian D, Gebreselassie S, Monga M. Gout, stone composition and urinary stone risk: a matched case comparative study. J Urol. 2013;189(4):1334–9.PubMedCrossRefPubMedCentralGoogle Scholar
  85. 85.
    Cameron M, Maalouf NM, Poindexter J, Adams-Huet B, Sakhaee K, Moe OW. The diurnal variation in urine acidification differs between normal individuals and uric acid stone formers. Kidney Int. 2012;81(11):1123–30.PubMedPubMedCentralCrossRefGoogle Scholar
  86. 86.
    Maalouf NM, Cameron MA, Moe OW, Sakhaee K. Novel insights into the pathogenesis of uric acid nephrolithiasis. Curr Opin Nephrol Hypertens. 2004;13(2):181–9.PubMedCrossRefPubMedCentralGoogle Scholar
  87. 87.
    Sakhaee K. Uric acid stones: epidemiology, pathyphysiology and treatment. In: Coe FL, Worcester EM, Lingeman JE, Evan AP, editors. Kidney stones: medical and surgical management. 2nd ed. New Delhi: Jaypee Brothers Medical Publishers; 2018. p. 514–29.Google Scholar
  88. 88.
    Maalouf NM, Sakhaee K, Parks JH, Coe FL, Adams-Huet B, Pak CY. Association of urinary pH with body weight in nephrolithiasis. Kidney Int. 2004;65(4):1422–5.PubMedCrossRefPubMedCentralGoogle Scholar
  89. 89.
    Worcester EM, Coe FL, Evan AP, Parks JH. Reduced renal function and benefits of treatment in cystinuria vs other forms of nephrolithiasis. BJU Int. 2006;97(6):1285–90.PubMedCrossRefPubMedCentralGoogle Scholar

Copyright information

© Springer Nature Switzerland AG 2019

Authors and Affiliations

  1. 1.University of Chicago MedicineChicagoUSA

Personalised recommendations