INTRODUCTION:
Kidney and urinary tract stone disease also described as urolithiasis or nephrolithiasis, has manifest oneself as a grievous health problems throughout the world1. It is appraise that 15 percent of the population bear kidney stone disease at some stage in their life and the ubiquity and manifestation of the urolithiasis is alleged to be raising worldwide2,3. Kidney stone can result from dehydration, high intake of oxalate, sodium, animal protein, or due to imbalance in urine, or family history (genetic) or from some medication, urinary tract infection and metabolic disorder can increase the risk.
A modern study found that 5.8% of Chinese adults have urolithiasis disease, with a ubiquity of 6.5% in males and 5.1% in females. This means that approximately 1 in 17 adults are presently impacted4.
The worldwide ubiquity of urolithiasis has risen over the ten-year periods. Urolithiasis is frequently a recurrent and lifelong disease with a rate of relapse 50% within 5 to 10 years and 75% in the span of 20 years5. Some studies unveiled that an raising in urolithiasis manifestation is foreseen, due a range of environmental conditions, such as shifts in lifestyle and dietary patterns, along with global climate change6,7. However, the exact trigger of the raising ubiquity and revival of urolithiasis have stay unresolved. Due to its Elevated ubiquity in employed age individuals, urolithiasis disease Dramatically affects the people and communities, and has become a masses health concern, especially in population segment living in arid and warm climate8,9. There are predominantly 5 types of urolithiasis based on their ore structure: calcium oxalate (CaOx; 65.9%), carbonapatite (15.6%), urate (12.4%), struvite (magnesium ammonium phosphate; 2.7%), and brushite (1.7%)10,11.
Urolithiasis are widely assorted into calcareous (calcium-containing) stones and non-calcareous stones. The most prevalent types of kidney stones in humans are calcium oxalate (CaOx) and calcium phosphate (CaP), either separately or together, which are calcareous and radio-opaque stones12. urolithiasis or nephrolithiasis fluctuate greatly in size, extending from μm to several cm in diameter, and habitually go unnoticed for extended periods. They are frequently detected occasionally through radiography or ultrasound imaging, or sometimes due to painful symptoms13.
Research on papillary specimen collection in patients with urolithiasis has shown that, depending on the stone and urine composition, the processes resulting in stone formation differ considerably14.
Major types of kidney stone:
Urolithiasis can be found in various part of renal, ureteral, vesical or bladder
Kidney stones are classified into two types,
1. Staghorn: (filling numerous major and minor cavities)
2. Non-Staghorn: Non-staghorn urolithiasis are described as Cup-shaped or pelvic area in location, while ureteral stones are defined as adjacent, middle or peripheral. Tiny urolithiasis, i.e., less than five mm in diameter have a augmented likelihood of expulsion, while this likelihood decrease the size of the stones increases with those of 5 mm to 7 mm having only 50% chance, and Stones larger than 7 mm are unable to pass naturally and constantly required medical treatment15. Due to the variance in their pathogenesis and formation urolithiasis have been classified into various types.
a. CA Stones: Ca in fusion with oxalate, phosphate and also with uric acid makes up the majority of urolithiasis16. Oxalate, a naturally occurring substance, is present in various food sources, including certain fruits, vegetables, nuts, and chocolate, which have high oxalate levels. It is also metabolically produced by the liver. In a healthy adult, the normal oxalate level is approximately 20-40 mg per day17. Several dietary factors, such as high doses of vitamin D, an oxalate-rich diet, various metabolic disorders, and intestinal bypass surgery, can result in increased concentrations of oxalate and calcium in the urine. Calcium oxalate and calcium phosphate stones, which are white, grey, or black in colour, exhibit a radio-opaque appearance. These stones are typically about 1 cm in diameter and appear as dense, sharply defined structures in radiographs18. Medical conditions like renal tubular acidosis and hyperparathyroidism are associated with the formation of calcium phosphate stones19.
b. Struvite Stones: Making up about 10-15% of kidney stones, struvite stones, also known as triple phosphate stones, form in the presence of bacterial infections. These crystalline stones consist of magnesium ammonium phosphate. The bacterial enzyme urease, which converts bacteria into ammonia and carbon dioxide, creating alkaline urine, promotes their development. Struvite stones are typically large, smooth, and laminated, and they are commonly found in individuals with certain metabolic conditions such as gout, idiopathic hypercalciuria, and hyperparathyroidism20.
c. Uric Acid Stones: Comprising about 5-10% of kidney stones, uric acid stones are yellow-orange, round, and smooth. In radiographs, they appear nearly transparent unless mixed with calcium crystals or struvite. Typically, these stones are square, diamond, or rod-shaped pleomorphic crystals that are polarizable21. Individuals with conditions like gout syndrome, obesity, or diets high in proteins and purines, especially those consuming meat and fish, are prone to developing uric acid stones22.
d. Protease-Related Stones: Often seen in HIV-positive patients, these stones form as a result of using the protease inhibitor drug indinavir sulfate. This medication can cause stone formation in 4-12% of patients undergoing treatment23.
e. Cystine Stones: These rare stones result from hereditary disorders causing the kidneys to secrete excessive amino acids, a condition known as cystinuria. They have a moderate radio-opaque and rounded appearance, with shiny crystallites and a greenish-yellow colour24.
f. Silica Stones: These stones, also known as drug-induced stones, can form due to the use of certain medicines and herbal products, including zonisamide, sulfa medications, indinavir, guaifenesin, laxatives (when abused), acetazolamide, ciprofloxacin, triamterene, ephedrine, loop diuretics, topiramate, and products containing silica25.
Figure 1: Types of kidney stones
Mechanism of kidney stones formation:
1. Physicochemical mechanism of kidney stones formation:
Urinary supersaturation and crystallization play important roles in the production of intrarenal crystals, which are primarily caused by inherited or acquired disorders that impair kidney function. Urine pH and excess substances such as calcium oxalate (CaOx), calcium phosphate (CaP), uric acid, urates, struvite, cysteine, purines (2,8-dihydroxyadenine and xanthine), and certain drugs (such as atazanavir, sulfamethoxazole, amoxicillin, ceftriaxone) can impact these processes26. Furthermore, crystal formation and growth are influenced by a variety of molecules that function as receptors, promoters, and inhibitors.
Promoters of stone formation include several receptors and receptor-like features that are crucial in crystal-cell interaction, a key process for crystal retention in the kidney.27 Recent studies have screened protein alterations in a CaOx monohydrate (COM) crystal-cell interaction model, identifying 1,141 differentially expressed proteins (DEPs) in COM-treated HK-2 cells. Certain proteins and glycosaminoglycans, such as CD44, nucleolin, hyaluronan (HA), heat shock protein 90 (HSP90)28. Annexin II, and osteopontin (OPN), have been recognized as modulators of stone formation. These findings have been extensively reviewed in previous research.29 Various structures and molecular components serve as receptors in crystal attachments, including the phosphatidylserine in the lipid bilayer and the acidic side chains of proteins. The primary promoters of crystal formation are calcium, oxalate, urate, and phosphate ions, which facilitate the crystallization or aggregation of stone constituents via several mechanisms.
Research by Ketha et al. indicated that first-time nephrolithiasis patients exhibited higher serum calcium and 1,25(OH)2D levels compared to healthy individuals, suggesting that stone formation is linked to altered calcium and vitamin D regulation. Elevated serum calcium concentrations, regulated by the calcium-sensing receptor (CaSR), play a significant role in lithogenesis through various pathways.30 Similarly, urate and phosphate ions promote heterogeneous nucleation and enhance crystal attachment to epithelial cells. Urine pH is another crucial factor in stone formation. Low urine pH can lead to CaOx crystallization and precipitation, while high-alkaline urine can also encourage CaOx crystal precipitation and nucleation. Additionally, lysozyme and lactoferrin have been recently identified as proteins that promote COM growth by accelerating the layer advancement rate on crystal surfaces.31
Figure 2: Physicochemical mechanisms of kidney stone formation. The reduced inhibitors (left panel) and increased promoters (right panel) are suggested to play critical roles in kidney stone formation.
2. Randall's plaque and calcium oxalate stone (CaC2O4) formation
Randall's plaques (RPs), first introduced by Alexander Randall in 1937, are regions of subepithelial mineralized tissue located at the papillary tip, around the openings of the ducts of Bellini, containing calcium phosphate (CaP). Scanning electron microscopy (SEM) has revealed that RPs consist of a mix of tubules with calcified walls and tubules blocked by CaP plugs32. RPs are composed of CaP crystals intertwined with an organic matrix rich in various proteins and lipids, including membrane-bound vesicles or exosomes, collagen fibres, and other components of the extracellular matrix. A growing body of research suggests that RPs are the origin of renal stones. Winfree et al.33 clarified that kidney stones form as an overgrowth on RPs, which possess a unique organic composition, including fibrillar collagen, distinguishable from the stone overgrowth by specific autofluorescence signatures. Notably, a study using a murine model of RP indicated that vitamin D supplementation and calcium intake could significantly accelerate RP formation.34 However, the exact mechanisms behind RP formation remain unclear.
3. Role of sex hormones in calcium oxalate nephrolithiasis:
Statistical analyses indicate that men have a higher incidence of calcium oxalate (CaOx) nephrolithiasis compared to women, with a ratio of 2-3:1, although the exact mechanism is still unclear. Previous studies have shown that androgens increase, while estrogens decrease, urinary oxalate excretion, plasma oxalate concentration, and kidney CaOx crystal deposition. Enhanced androgen signalling may explain the link between sex and kidney stone formation. Androgen receptor (AR) signalling can directly upregulate hepatic glycolate oxidase35 and the kidney epithelial nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit p22-PHOX at the transcriptional level, leading to increased oxalate biosynthesis and subsequent kidney stone formation. Peng et al. reported that testosterone promotes nephrolithiasis development by inducing apoptosis and necrosis of renal tubular epithelial cells through the HIF-1α/BNIP3 pathway. Chang tong et al36. found that testosterone can enhance kidney stone disease by increasing COM crystal-cell adhesion through elevated surface α-enolase. Zhu et al37. demonstrated that AR inhibits macrophage recruitment and suppresses the phagocytic ability of macrophages for COM crystals by decreasing colony-stimulating factor 1 (CSF-1) signals via miR-185-5p upregulation. These findings suggest that androgen receptor signalling may play a crucial role in the development of nephrolithiasis. (fig. 3)
On paper, the androgen receptor (AR) appears to be a good target for the development of novel kidney stone prevention medications. It has been demonstrated that testosterone's impact on COM crystallization is neutralized by the 5α-reductase inhibitor finasteride38. Furthermore, it has been documented that dimethyl curcumin (ASC-J9), a novel AR degradation enhancer, inhibits oxalate crystal formation by regulating oxalate production and lessens ROS-induced damage to kidney tubular epithelial cells in a rat model39. On the other hand, estrogen might prevent kidney stones from forming. A study conducted in vitro revealed that estrogen changed the cellular proteome of renal tubular cells in Madin-Darby canine kidney (MDCK). This resulted in a decrease in the expression of CaOx crystal receptor surfaces (annexin A1 and α-enolase), a reduction in intracellular ATP, and an increase in tissue healing and cell proliferation in the renal tubular cells40. data indicates that by directly binding to estrogen response elements (EREs) on the promoter of NADPH oxidase subunit 2 (NOX2), estrogen receptor β (ERβ) can transcriptionally suppress NADPH oxidase subunit 2 (NOX2)41, protecting against renal CaOx crystal deposition.
All of these discoveries could help to explain why males experience a higher incidence of nephrolithiasis than females. It may be possible to develop therapy that targets AR. for renal stone disease caused by CaOx crystals. But only celllines or animal models were used in these in vitro and in vivo investigations. Clinical research and more validation are needed. It has been shown that finasteride and ASC-J9 decrease certain AR-mediated disorders, such as liver cancer, spinal and bulbar muscular atrophy neuron disease, and prostate cancer42. Before finasteride and ASC-J9 are clinically used to prevent kidney stones, more research is needed to fully understand the potential adverse effects, which include sexual dysfunction43.
Figure 3: Role of sex hormones in calcium oxalate nephrolithiasis.
Prevention:
Improvements in lifestyle, supplementation with citrate, and medication are strategies to prevent the recurrence of kidney stones, with lifestyle changes being the cornerstone44. Citrate supplements and medications are intended for individuals with recurrent kidney stones, while preventive measures are recommended after a first kidney stone for patients with a low risk of recurrence. For those at high risk of recurrent kidney stones, preventive care should be tailored based on the results of a metabolic evaluation45.
Lifestyle modification:
Increasing fluid intake to 2.5 to 3 liters per day is the most important lifestyle modification to prevent recurrent kidney stones. This will ensure a urine output of 2 to 2.5 liters per day and achieve a urine specific gravity below a specified threshold46. Drinking fluids should be a regular part of your day, and they should include neutral-pH beverages. To ensure the diuresis goal is met, urine production may need to be tracked for a full day. Reducing the consumption of carbonated beverages might also lessen the chance of a recurrence of stones, especially colas and other drinks high in phosphoric acid47. Kidney stones can be prevented from recurring with a well-balanced diet. In addition to limiting sodium intake to 4–5 grams per day and animal protein to 0.8–1.0 grams per kilogram of body weight per day, a diet high in fiber and vegetables should also aim for a typical calcium intake of 1.0 – 1.2 grams per day. Obese or overweight people should strive for a normal body weight by food adjustments and increased exercise48. Although there is little evidence to support lifestyle changes for reducing kidney stone recurrence, they are essential for preventing other comorbidities.
Medication For Prevention of Urolithiasis:
|
Types of Stone |
Types of Medication |
Purpose |
|
Calcium stones |
Thiazide diuretics |
Which helps to reduce calcium level in the urine |
|
Potassium citrate |
Hepls to make the urine less acidic and prevent calcium stone. |
|
|
Allopurinol |
Used if the stones are related to high uric acid level |
|
|
Phosphate supplements |
Occasionally prescribed to bind calcium in the intestines |
|
|
Magnesium supplement |
Sometime recommended to help prevent stone formation |
|
|
Struvite stones |
Antibiotic |
To treat and prevent the underlying urinary tract infections(UTIs) that cause struvite stones |
|
Acetohydroxamice acid(AHA) |
This urease inhibitor helps prevent the formation of struvite stones by inhibiting the bacteria’s ability to produce ammonia ,which contributes to stone formation. |
|
|
Uric acid stones |
Allopurinol |
Reduce uric acid level in the blood and urine,helping to prevent the formation of uric acid stones. |
|
Potassium citrate |
Alkalinizes the urine, making it less acidic,which helps dissolve uric acid stones and prevent their formation. |
|
|
Sodium bicarbonate |
Another option to alkalinize the urine, though less commonly used than potassium citrate. |
|
|
Cystine stones |
Potassium citrate |
Alkalinize urine, making cystine more soluble and reducing stone formation. |
|
Tiopronil(thiola) |
Binds to cystine in the urine, forming a more soluble compound and reducing stone formation. |
|
|
Penicillamine |
Another medication that binds to cystine to form a more soluble compound, though it has more potential side effects compared to tiopronin. |
|
|
captopril |
An ACE inhibitor that can reduce cystine stone formation, although it is less commonly used for this purpose. |
CONCLUSION:
Kidney stones arise from a confluence of environmental, nutritional, and hereditary factors. The four primary forms of kidney stones—struvite, uric acid, cystine, and calcium oxalate—develop via various pathways. The most common kind of stones, calcium stones, are caused by the supersaturation of urine with calcium and either phosphate or oxalate. Urinary tract infections are associated with struvite stones, very acidic urine is associated with uric acid stones, and an overabundance of cystine in the urine is caused by a hereditary disease. Medication, dietary adjustments, and lifestyle changes are all part of kidney stone prevention. In order to dilute urine and lower the concentration of chemicals that can cause stones, it is imperative to increase fluid consumption. Some forms of stones can be avoided by following certain dietary recommendations, such as reducing intake of purines, oxalate, and sodium. Drugs such as potassium citrate, thiazide diuretics, tiopronin, and allopurinol treat the underlying metabolic problems that cause stones to develop. The key to treating and preventing kidney stones from recurring is early diagnosis and individualized treatment programs. Healthcare professionals' routine examinations and monitoring can greatly lower the chance of recurrence and improve patient outcomes.
REFERENCES:
1. Allison MJ, Sidhu H, et al. Materials and methods for treating or preventing oxalate-related disease. United States patent 2004.
2. Romero V, Akpinar H and Assimos DG: Kidney stones: A global picture of prevalence, incidence, and associated risk factors. Rev Urol . 2010; 12: e86‑e96.
3. Morgan MS and Pearle MS: Medical management of renal stones. BMJ 352: i52, 2016.
4. Zeng G, Mai Z, Xia S, Wang Z, Zhang K, Wang L, Long Y, Ma J, Li Y, Wan SP, et al: Prevalence of kidney stones in China: An ultrasonography based cross‑sectional study. BJU Int. 2017; 120: 109‑116.
5. Eisner BH and Goldfarb DS: A nomogram for the prediction of kidney stone recurrence. J Am Soc Nephrol. 2014; 25: 2685‑2687.
6. Ziemba JB and Matlaga BR: Epidemiology and economics of nephrolithiasis. Investig Clin Urol, 2017; 58: 299‑306.
7. Brikowski TH, Lotan Y and Pearle MS: Climate‑related increase in the prevalence of urolithiasis in the United States. Proc Natl Acad Sci USA. 2008; 105: 9841‑9846.
8. Abeywickarama B, Ralapanawa U and Chandrajith R: Geoenvironmental factors related to high incidence of human urinary calculi (kidney stones) in Central Highlands of Sri Lanka. Environ Geochem Health. 2016; 38: 1203‑1214.
9. Wang Z, Zhang JW, Zhang Y, Zhang SP, Hu QY and Liang H: Analyses of long non‑coding RNA and mRNA profiling using RNA sequencing in calcium oxalate monohydrate‑stimulated renal tubular epithelial cells. Urolithiasis. 2019; 47: 225‑234.
10. Parmar MS: Kidney stones. BMJ. 2004; 328: 1420‑1424.
11. Ye Z, Zeng G, Yang H, Li J, Tang K, Wang G, Wang S, Yu Y, Wang Y, Zhang T, et al: The status and characteristics of urinary stone composition in China. BJU Int. 2020; 125: 801‑809.
12. Aggarwal K.P., Narula S., Kakkar M. and Tandon C.: Nephrolithiasis: Molecular mechanism of renal stone formation and the critical role played by modulators. Biomed Res Int. 2013: 292953, 2013.
13. Fisang C, Anding R, Müller SC, et al. Urolithiasis-anInterdisciplinary Diagnostic, Therapeutic and Secondary Preventive Challenge. Dtsch Arztebl Int. 2015; 112: 83-91.
14. Evan AP. Physiopathology and etiology of stone formation in the kidney and the urinary tract. Pediatr Nephrol. 2010; 25: 831-41.
15. Gupta S, Shamsher SK. Kidney stones: Mechanism of formation, pathogenesis and possible treatments. J Biomol Biochem. 2018; 2(1): 1-5.
16. Barbasa C, Garciaa A, Saavedraa L, et al. Urinary analysis of nephrolithiasis markers. J Chromatogr B. 2002; 781: 433-55.
17. Han H, Segal AM, Seifter JL, et al. Nutritional Management of Kidney Stones (Nephrolithiasis). Clin Nutr Res. 2015; 4: 137-52.
18. Tiwari A, Soni V, Londhe V, et al. An overview on potent Indigenous herbs for urinary tract infirmity: urolithiasis. Asian J Pharm Clin Res. 2012; 5: 7-12.
19. Mirian AB, Ita PH, Schor N, et al. Phyllanthus niruri as a promising alternative treatment for nephrolithiasis. International Braz J Urol. 2010; 36: 657-64.
20. Aray P, Pandey S, Verma V, et al. Kidney stone formation and use of medicinal plants as anti-urolithiatic agents. UJPSR. 2017; 2: 43-48.
21. Evan AP, Lingeman JE, Coe FL, et al. Crystal-associated nephropathy in patients with brushite nephrolithiasis. Kidney Int. 2005; 67: 576-91.
22. Hamid M, Mohammad MN, Ghanea L, et al. Evaluation of theRaphanus sativus effect on urinary pH. J of Res in Med Sc. 2007; 12: 58.
23. Aggarwal A, Tandon S, Singla SK, et al. Diminution of oxalate induced renal tubular epithelial cell injury and inhibition of calciumoxalate crystallization in vivo by aqueous extract of Tribulu terrestris. International Braz J Urol. 2010; 36: 480-9.
24. Combest W, Newton M, Combest A, et al. Effects of herbal supplements on the kidney. Urol Nurs. 2005; 25: 381-6.
25. Umashankar D, Chandra R, Chawla AS, et al. High-pressure liquid chromatographic determination of bergenin and (+)-afzelechin from different parts of Paashaanbhed (Bergenia ligulata yeo). Phytochem Anal. 1999; 10: 44-7.
26. Daudon M, Frochot V, Bazin D and Jungers P: Drug‑induced kidney stones and crystalline nephropathy: Pathophysiology, prevention and treatment. Drugs. 2018; 78: 163‑201.
27. Thongboonkerd V: Proteomics of crystal‑cell interactions: A model for kidney stone research. Cells. 2019; 8: 1076.
28. Fong‑Ngern K, Sueksakit K and Thongboonkerd V: Surface heat shock protein 90 serves as a potential receptor for calcium oxalate crystal on apical membrane of renal tubular epithelial cells. J Biol Inorg Chem. 2016; 21: 463‑474.
29. Wiener SV, Ho SP and Stoller ML: Beginnings of nephrolithiasis: Insights into the past, present and future of Randall's plaque formation research. Curr Opin Nephrol Hypertens. 2018; 27: 236‑242.
30. Vezzoli G, Macrina L, Magni G and Arcidiacono T: Calcium‑sensing receptor: Evidence and hypothesis for its role in nephrolithiasis. Urolithiasis. 2019; 47: 23‑33.
31. Farmanesh S, Chung J, Sosa RD, Kwak JH, Karande P and Rimer JD: Natural promoters of calcium oxalate monohydrate crystallization. J Am Chem Soc. 2014; 136: 12648‑12657.
32. Daudon M, Bazin D and Letavernier E: Randall's plaque as the origin of calcium oxalate kidney stones. Urolithiasis. 2015; 43(Suppl 1): S5‑S11.
33. Winfree S, Weiler C, Bledsoe SB, Gardner T, Sommer AJ, Evan AP, Lingeman JE, Krambeck AE, Worcester EM, El‑Achkar TM and Williams JC Jr: Multimodal imaging reveals a unique autofluorescence signature of Randall's plaque. Urolithiasis. 2021 49: 123‑135.
34. Bouderlique E, Tang E, Perez J, Coudert A, Bazin D, Verpont MC, Duranton C, Rubera I, Haymann JP, Leftheriotis G, et al: Vitamin D and calcium supplementation accelerates Randall's plaque formation in a murine model. Am J Pathol. 2019; 189: 2171‑2180.
35. Yoshihara H, Yamaguchi S and Yachiku S: Effect of sex hormones on oxalate‑synthesizing enzymes in male and female rat livers. J Urol. 1999; 161: 668‑673.
36. Changtong C, Peerapen P, Khamchun S, Fong‑Ngern K, Chutipongtanate S and Thongboonkerd V: In vitro evidence of the promoting effect of testosterone in kidney stone disease: A proteomics approach and functional validation. J Proteomics. 2016; 144: 11‑22.
37. Zhu W, Zhao Z, Chou F, Zuo L, Liu T, Yeh S, Bushinsky D, Zeng G and Chang C: Loss of the androgen receptor suppresses intrarenal calcium oxalate crystals deposition via altering macrophage recruitment/M2 polarization with change of the miR‑185‑5p/CSF‑1 signals. Cell Death Dis. 2019; 10: 275.
38. Sueksakit K and Thongboonkerd V: Protective effects of finasteride against testosterone‑induced calcium oxalate crystallization and crystal‑cell adhesion. J Biol Inorg Chem. 2019 24: 973‑983.
39. Zhu W, Zhao Z, Chou F, Zuo L, Liu T, Yeh S, Bushinsky D, Zeng G and Chang C: Loss of the androgen receptor suppresses intrarenal calcium oxalate crystals deposition via altering macrophage recruitment/M2 polarization with change of the miR‑185‑5p/CSF‑1 signals. Cell Death Dis. 2019; 10: 275.
40. Peerapen P and Thongboonkerd V: Protective cellular mechanism of estrogen against kidney stone formation: A proteomics approach and functional validation. Proteomics. 2019; 19: e1900095.
41. Zhu W, Zhao Z, Chou FJ, Zuo L, Liu T, Bushinsky D, Chang C, Zeng G and Yeh S: The protective roles of estrogen receptor β in renal calcium oxalate crystal formation via reducing the liver oxalate biosynthesis and renal oxidative stress‑mediated cell injury. Oxid Med Cell Longev. 2019: 5305014, 2019.
42. Tian H, Chou FJ, Tian J, Zhang Y, You B, Huang CP, Yeh S, Niu Y and Chang C: ASC‑J9® suppresses prostate cancer cell proliferation and invasion via altering the ATF3‑PTK2 signaling. J Exp Clin Cancer Res. 2021; 40: 3.
43. Andy G, John M, Mirna S, Rachita D, Michael K, Maja K, Aseem S and Zeljana B: Controversies in the treatment of androgenetic alopecia: The history of finasteride. Dermatol Ther. 2019; 32: e12647.
44. Pearle MS, Goldfarb DS, Assimos DG, et al. Medical management of kidney stones: AUA guideline. J Urol. 2014; 192(2): 316-324.
45. Skolarikos A, Straub M, Knoll T, et al. Metabolic evaluation and recurrence prevention for urinary stone patients: EAU guidelines. Eur Urol. 2015; 67(4): 750-763.
46. Qaseem A, Dallas P, Forciea MA, Starkey M, Denberg TD. Dietary and pharmacologic management to prevent recurrent nephrolithiasis in adults: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2014; 161(9): 659-667.
47. Fink HA, Wilt TJ, Eidman KE, et al. Medical management to prevent recurrent nephrolithiasis in adults: a systematic review for an American College of Physicians clinical guideline [published correction appears in Ann Intern Med. 2013; 159(3): 230-232]. Ann Intern Med. 2013; 158(7): 535-543.
48. Frassetto L, Kohlstadt I. Treatment and prevention of kidney stones: an update. Am Fam Phsician. 2011; 84(11): 1234-1242.
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Received on 13.08.2024 Revised on 03.09.2024 Accepted on 19.09.2024 Published on 17.12.2024 Available online on December 23, 2024 Asian Journal of Pharmaceutical Research. 2024; 14(4):381-386. DOI: 10.52711/2231-5691.2024.00060 ©Asian Pharma Press All Right Reserved
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