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Nephrolithiasis – Most Debilitating Renal Disorder
Abstract
Both metabolic and environmental risk factors are involved in the pathogenetic mechanisms of kidney stone formation. Major advances have been made in the concept of the pathogenesis, diagnosis, and treatment of kidney stone disease over the last decade. It remains a major health burden worldwide. It is considered a systemic disorder associated with chronic kidney disease, bone loss and fractures, increased risk of coronary artery disease, hypertension, type 2 diabetes mellitus, and the metabolic syndrome. Many therapeutic interventions which can effectively target the stones are available but these are associated with untoward effects. In the pursuit of finding better alternatives, large number of plants was screened for their antiurolithiatic activity. They were found to possess potent activity with minimal/no side effects. Development of new therapeutic agents is possible by understanding the link between nephrolithiasis and these systemic disorders.
References
Sakhaee K. Nephrolithiasis as a systemic disorder. CurrOpinNephrolHypertens.2008; 17: 304-309p.
Sakhaee K, Maalouf NM, Kumar R, Pasch A, Moe OW. Nephrolithiasis-associated bone disease: pathogenesis and treatment options. Kidney Int. 2011; 79: 393-403p.
Rodman JS. Struvite stones. Nephron 1999; 81(1):50p.
Harrison. Principles of internal medicine. McGraw-Hill, New Delhi, volume 2001; 2(15): 1615p.
KokDJandKhanSR.“Calcium oxalate Nephrolithiasis, a free or fixed particle disease” Kidney Int.1994; 46 (3): 847-854p.
Curhan GC et al. Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk of kidney stones in women. Ann Intern Med. 1997; 126:497p.
Segura JW et al. Ureteral Stones Clinical Guidelines Panel summery report on the management of ureteral calculi. J Urol. 1997; 158:1915p.
Bruno M, Marangella M. Cystinuria: recent advances in pathophysiology and genetics. Contribnephrol. 1997; 122:173p.
AggarwalS, TandonCD, ForouzandehM, SinglaSK, KiranR, and JethiRK.“Role of biomolecules from human renal stone matrix on COM crystal growth.” Molecular and cellular biochemistry. 2000; 210 (1-2): 109-119p.
Romero V, Akpinar H, Assimos DG. Kideny stones: a global picture of prevalence, incidence, and associated risk factors. Rev Urol. 2010; 12: e86- e96p.
Williams HE. Nephrolithiasis. N Engl J Med. 1974; 33: 290p.
Borghi L et al. Urinaryvolume, water and recurrences in idiopathic calcium nephrolithiasis: A 5 year randomized prospective study. J Urol. 1996; 155:839p.
Coe FL, Parks JH. New insights into the pathophysiology of and treatment of nephrolithiasis: new research venues. J Bone Miner Res. 1997; 12:522p.
VermevlenC, WandlonES.“Mechanism of genesis and growth of calculi” The American Journal of Medicine. 1956; 45(5): 684-691p.
Mandel NS, Mandel GS. Urinary tract stone disease in the United States veteran population. II. Geographical analysis of variations in composition. J Urol. 1989; 142: 1516-1521p.
Christos Paliouras, EiriniTsampikaki, PolichronisAlivanis, GeorgiosAperis. Pathophysiology of nephrolirhiasis. Nephrology Reviews. 2012; 4(14): 58-65p.
Mandel N. Mechanism of stone formation. SeminNephrol.1996; 16: 364-74p.
Morse RM and ResnickMI. ”A new approach to the study of urinary macromolecules as a participant in calcium oxalate crystallization” The journal of Urology. 1988; 139 (4): 869-873p.
RoyallRL, HarnetRL, HibberdCM, EdyeaneKA, Marshall VR. “Effects of chondroitin sulphate, human serum albumin and Tamm-Horsfallmucoprotein on calcium oxalate crysstallization in undiluted human urine”. Urological Research. 1991; 19(3): 181-188p.
Khan SR, ShevockPN, Hackett RL. “Presence of lipids in urinary stones: results of preliminary studies” Calsified Tissue International. 1988; 42(2): 91-96p.
Coe FL, Evan AP, Worcester EM, Lingeman JE. Three pathways for human kidney stone formation. Urol Res. 2010; 38: 147-60p.
Thomas Knoll. Epidemilogy, pathogenesis, and pathophysiology of urolithiasis. European Urology Supplements. 2010; 9: 802-806p.
Evan AP, Lingeman JE, Coe FL, Shao Y, Parks JH, Bledsoe SB, Phillips CL, Bonsib S, Worcester EM, Sommer AJ, Kim SC, Tinmouth WW, Grynpas M. Crystal-associated nephropathy in patients with brushite.Nephrolirhiasis. 2005; 67: 576-591p.
KhashayarSakhaee, NaimMaalouf M, Bridget Sinnott. Kidney stones: Pathogenesis, diagnosis, and management. J ClinEndocrinolMetab. 2012; 97(6): 1847-1860p.
Asplin JR, Parks JH, Coe FL. Dependence of upper limit of metastability on supersaturation in nephrolirhiasis. Kidney Int. 1997; 52: 1602-8p.
Evan AP. Pathophysiology and etiology of stone formation in the kidney and the urinary tract. PediatrNephrol. 2010; 25: 831-41p.
CarvahloM, NakagawaY. “Urinary supersaturation and recurrence in nephrolithiasis”. International Brazilian Journal of Urology. 1999; 25: 475-479p.
LieskeJC, DeanelloS, TobackFG.“Cell-crystal interactions and kidney stone formation”. Nephron. 1999; 81(1): 8-17p.
Kramer G et al. Role of bacteria in the development of kidney stones. CurrOpinUrol. 2000; 10:35p.
Orson Moe W. Kidney stones: Pathophysiology and medical management. The Lancet. 2006; 367(9507): 333-344p.
Consensus Conference. Prevention and treatment of kidney stones. JAMA. 1988; 260:977p.
Charlotte Dawson H, Charles Tomson RV.Clinical Medicine. 2012; 12(5): 467-71p.
Pearle MS, Roehrborn CG, Pak CY. Meta-analysis of randomized trial for medical prevention of calcium oxalate nephrolirhiasis. J Endourol. 1999; 13: 679-85p.
Yendt ER, Cohanim M. Prevention of calcium stones with thiazides. Kidney Int. 1978; 13: 397p.
Heilberg IP. Update on dietary recommendation and medical treatment of renal stone disease. Nephrol Dial Transplant. 2000; 15:117p.
Borghi L, Meschi T, Amato F et al. Urinary volume, water and recurrences in idiopathic calcium nephrolirhiasis: a 5-year randomized prospective study. J Urol.1996; 155: 839-43p.
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