Uro Flash
Uro Flash 2016 › Uro Flash Vol-2, No-7, 2016

Epidemiological Aspects and Medical Management of Urolithiasis in Special Populations

Introduction

Urolithiasis, defined as the formation of stones or calculi in the urinary collecting system, represents the third most common urological disease after urinary infection and prostatic pathology. Calcium stones (calcium oxalate or phosphate) are believed to be the most common stone type. Other stone compositions include uric acid, struvite (magnesium ammonium phosphate), and other miscellaneous components such as cystine.1,2

Researchers suggest urolithiasis to be a fairly common disease in India. Estimates from the 2011 Indian census3   reveal a total population of 1.21 billion people, out of which 12%, i.e., 145.2 million people have urolithiasis (figure 1).4

It has been observed that the occurrence rate of the disease is remarkably high at the age of 20-40 years, with a significant predilection for males due to increased testosterone-induced hepatic oxalate production in them. In addition, hot climatic conditions tend to concentrate the urine, providing a suitable milieu for initiation and precipitation of crystal formation. Besides, high intake of animal protein, salt, and sugar causes excessive excretion of urinary calcium, uric acid, and oxalate accentuating the formation of calculi. The other extrinsic factors like low fluid intake, sedentary occupation, and stress can also intervene as risk factors for urolithiasis (figure 2).5

Important considerations in special populations

Epidemiological data reveals urolithiasis to be a common entity among specific subpopulations such as children, elderly individuals, and women.6,7    Among women, those who are pregnant or have attained menopause are particularly at a higher risk of developing the disease.8,9  

Children

The rising incidence and prevalence of urolithiasis among children has made it an increasingly important public health issue in the current pediatric urology practice. Researchers have suggested a fivefold increase in the prevalence of pediatric urolithiasis in the past decade. This has been validated by some authors who have shown the number of annual pediatric referrals for urolithiasis to rise by nearly 5 times in the recent years.10   A 25-year populationbased study11 that examined 207 children under the age of 18 years with computerized tomographic (CT) imaging reported 41% to be incident stone formers (figure 3). Furthermore, analysis of data obtained from the Pediatric Health Information System (PHIS) database revealed that the diagnosis of renal calculi increased from 18.4 to 57 per 1,00,000 patients between 1999 and 2008.12  

Intriguingly, among the pediatric patients, girls are more susceptible to urolith formation than boys. A study showed the greatest increase in incidence of pediatric renal stone disease between 1996 and 2007 among adolescent girls.13

The etiology of urolithiasis in children is quite variable, as a number of factors – including those of metabolic, genetic, anatomic, dietary and environmental origin− cover a significant risk for the formation of urinary tract calculi. In broad terms, however, the etiology can be divided into three major categories: (i) metabolic abnormalities that promote excessive urinary excretion of solutes which are susceptible to crystallization or reduced excretion of inhibitors of crystallization, (ii) anatomic defects that cause disturbances in voiding or urinary stasis, and (iii) idiopathic.14   A large proportion of pediatric urolithiasis cases have unknown etiology. An identifiable underlying cause such as metabolic or neurological disorder, or congenital urinary system structural anomaly is present in only 9-24% cases.13 Among these, stone diseases of metabolic origin appear to be the most prevalent.15   An array of metabolic disorders is known to promote the concentration of calcium, oxalate, phosphorous, and cystine in the urine, making metabolic evaluation essential. Among children with greater body fat content, higher rates of hyperoxaluria, hyperuricosuria, hypercalciuria and hypocitraturia, and renal tubular acidosis have been identified, strongly indicating that obesity may predispose to stone formation. Multiple other factors have also been cited in association with renal calculi in both children and adolescents, including intake of sweetened beverages, various hormones, animal protein consumption, and climate change (figure 4).14   

Pediatric stone composition is distinct from that of adults.13   Calcium oxalate is the most common stone worldwide, and accounts for 60-90% of pediatric urolithiasis. Sturvite, cystine, calcium phosphate, uric acid, and mixed or miscellaneous stones constitute the less prevalent stone types in this subpopulation (figure 5).10   The spectrum of clinical presentation of stone disease in children is somewhat similar to adults, but may be largely confined to hematuria, generalized abdominal pain, or symptoms of urinary tract infection.16   General manifestations such as nausea, vomiting, anorexia and malaise may be present. This clinical presentation is also observed in adolescents, with abdominal pain being the most common complaint among school students. Lack of specificity related to localized pain is characteristically seen in lithiasic infants, toddlers and preschool children.

Although less frequent than adult stone disease, urolithiasis in the pediatric age group is also responsible for significant morbidity, particularly since stones have a propensity to recur, and, thus, should not be underestimated.17  

Elderly

Stone disease is believed to occur more often in elderly persons than in children.18   The incidence of urolithiasis in older adults is rising in parallel with an increase in their life expectancy.7   Hypocitraturia and hypernatriuria are the most prevalent metabolic diseases among elderly men with urolithiasis.19  

Researchers suggest that older patients with urolithiasis have higher morbidity rates than younger patients as they usually have larger and more complex stones, and are also more likely to have comorbidities.20,21      Patients older than 65 years are believed to develop uric acid stones at twice the rate of their younger counterparts.22   The National Health and Nutrition Examination Survey (NHANES II) validated this by demonstrating increase in rates of stone disease in males up to age 65 years and in women up to 70 years of age.7   Daudon and colleagues20   further showed that octogenarian men, and those beyond 90 years of age constituted 40% of the patients with urinary bladder calculi (figure 6). Based on these evidences, investigators have propounded that the geriatric stone population is not merely an extension of younger stone forming patients presenting at an older age; rather, these patients commonly experience the first symptomatic stone episode in their advanced stages of life.24  

Pathophysiological studies indicate that elderly patients are prone to developing stones due to the inexorable age-induced metabolic changes.25   The fact that ageing is associated with a cluster of metabolic conditions (hypertension, obesity, dyslipidemia, diabetes type 2) is well-known.26   In addition, it is also known that metabolic derangements are a major contributor to urolithiasis. With regard to this, some of the best lines of evidence suggest that presence of metabolic syndrome may impact stone risk factors that promote the formation of calcium oxalate, calcium phosphate, or mixed stones (uric acid/calcium oxalate or calcium oxalate/calcium phosphate). Investigators have attested to this by demonstrating the odds of self-reported stone disease to be nearly twice more likely in individuals with metabolic syndrome than their healthy counterparts. There is an evidently higher prevalence of type 2 diabetes, glucose intolerance, and hypertriglyceridemia in pure uric acid stone formers. Likewise, patients with type 2 diabetes have a notably greater prevalence of uric acid stones. The probability of stone formation is also much higher in hypertensive patients than their normotensive counterparts.27  

As previously discussed, besides the elderly patients, certain subsets among the female population are also at a high risk of urolithiasis development.8

Women

Pregnancy

An increase in stone events has been quite dramatic for adult women and incidence is now comparable between both sexes, while earlier it was far more common in men.28   Urolithiasis does not spare the pregnant population and presents a potentially serious issue for the mother, the fetus, and the treating physicians.29,30     Acute urolithiasis has been demonstrated to be the leading cause of nonobstetric hospital admission during pregnancy.28   The incidence and risk factors for pregnant females are usually the same as in nonpregnant, sexually active, childbearing women.30

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Several anatomical and metabolic changes occur in the pregnant female to alter the urinary environment (figure 7). Increased progesterone and mechanical compression lead to urinary stasis. Elevated glomerular filtration rate, calcium supplementation, and increased circulating vitamin D levels collaborate in raising the urinary pH and causing hypercalciuria.28   Other metabolic effects in pregnancy such as hyperuricuria, changes in inhibitors of lithiasis formation, relative dehydration, and the presence of infection all have an impact on stone formation.30   Together, these changes provide a suitable milieu for calcium phosphate stone formation. It has been demonstrated that nearly threefourths of pregnant women with kidney stones have calcium phosphate stones as opposed to the general population where calcium oxalate is the most prevalent stone type.28

Clinical presentation for stone disease during pregnancy is seen after 5 months of gestation with 90% of the cases encountered during the second and third trimesters.8,31     Renal colic, dull aching pain, tenderness, fever, hematuria, and irritative voiding are the common complaints. Renal colic is reportedly the most frequent nonobstetric cause for abdominal pain and hospitalization among the pregnant population. Renal colic has been associated with a variety of complications, including preterm labor and delivery, recurrent abortions, preeclampsia, gestational diabetes, and cesarean deliveries.30,32      Pregnant women hospitalized for nephrolithiasis have a nearly two-times higher risk of pre-term delivery than their healthy counterparts.33   In addition, a higher incidence of preterm premature rupture of membranes has been reported in pregnancies complicated by urinary stones.34   Overall, these complications may be severe and underscore the importance of prompt and appropriate diagnosis.32

Ultrasonography is widely considered the front-line diagnostic test in pregnant women with nephrolithiasis. However, its poor specificity, and inefficiency to distinguish ureteral obstruction secondary to calculi from physiologic hydronephrosis may oftentimes present diagnostic perplexities. In such cases, magnetic resonance imaging (MRI) should be considered. Lowdose CT is deemed the last-line test for the detection of uroliths in pregnancy.32,35

Post-menopause

In addition to pregnancy, menopause is also an important predisposing factor for development of urinary stone disease in women. Nephrolithiasis is believed to affect 5-7% of postmenopausal women. Scores of research papers in literature suggest that menopause is associated with an increase in urinary calcium excretion, which may amplify the risk for calcium-containing stone formation. In women matched for serum total and ionized calcium levels, urinary calcium excretion was 50% greater in post-menopausal women than those yet to attain menopause. Hence, it is evident that the onset of menopause may increase urinary calcium excretion and the risk for kidney stone formation. Factors that signal an increased risk for the occurrence of urolithiasis in postmenopausal women include a history of hypertension, a low dietary intake of magnesium, and low use of calcium supplements.

It has been suggested that in addition to the morbidity caused by symptomatic stone episodes, the condition may also result in long-term complications such as renal insufficiency among post-menopausal women.36,38

Approach to management

The objectives of stone management encompass complete stone clearance, prevention of stone recurrence, preservation of renal function, control of urinary tract infections, correction of anatomical abnormalities, and correction of the underlying metabolic disorders.39   Several therapeutic paths are open for patients with urolithiasis, ranging from noninvasive medical therapy to major surgical interventions depending on the indication. Generally, the choice of therapy is made considering stone size, location, and composition, and patient factors, such as age and urinary tract anatomy.40

Symptomatic therapy

As previously discussed, renal colic is a common complaint among urolithiasis patients which drives them to seek medical care. The effect of NSAIDs on relieving pain in acute renal colic is believed to be similar to opiates. However, the side effects associated with the use of NSAIDs, which include nausea, vomiting, feeling of heat/pressure in the chest, fatigue, and lethargy, give credence to choosing alternative therapeutic agents, particularly if long-term management is required. In this context, drotaverine, which is an inhibitor of phosphodiesterase 4 (PDE4) in smooth muscles can be used. Drotaverine exerts antispasmodic effect and induces ureteral muscle relaxation without anti-cholinergic adverse effects.41   A study conducted on 632 patients suffering from urologic colic demonstrated the efficacy of drotaverine treatment to be 90%. Furthermore, it has been suggested that in patients with large kidney stones located in the pyelon, the administration of IV drotaverine at the onset of symptoms (given 3-4 times if necessary) results in rapid relief of pain.42   These evidences highlight the benefits of drotaverine administration in patients with colicky pain due to urinary stone disease.

Pharmacotherapy is also used for dissolution of stones via alkalinization of urine; struvite stones which form only in the setting of infection are however an exception to urinary alkalinization. Researchers suggest that use of alkalinizing agents, like oral potassium citrate, which raise the urinary pH and/ or provide increased citrate in the urine can be effective in patients with stone disease.43,44      Oral potassium citrate is mainly used for supplementation because of its documented superior efficacy over sodium-containing salts (sodium bicarbonate or sodium citrate). The use of sodium salts has largely fallen out of favor. Some authors have reported the net effect of high sodium intake to be an increased propensity of crystallization of calcium salts in the urine, and shown reduced sodium consumption to decrease stone episodes by nearly 50%.45   Potassium citrate on the other hand, targets multiple metabolic abnormalities in stone formers including normocalcemic hypercalciuria, hypocitraturia, hyperuricosuria, cysteinuria, thereby preventing stone recurrence in general.46   Administration of potassium citrate in patients with idiopathic hypercalciuria results in a decrease in urine calcium and an increase in urine citrate, hence proving beneficial.47,48      Evidences of beneficial effects of potassium citrate are highlighted in box 1.49

Some authors48   suggest that oral potassium citrate may also serve as an effective preventive supplement against kidney stones in children on ketogenic diet, and therefore believe that its universal supplementation may help reduce the number of incident stone formers in the pediatric population.49   Other advantages with potassium citrate include high palatability, pleasant taste, and tolerability. The pleasant taste is a particularly important attribute as it enables long-term adherence of patients to the drug. The good palatability and pleasant taste of potassium citrate favorably contribute to its utility in stone patients. It is also recommended for use as per AUA guidelines (box 2).50

Medical expulsive therapy

Medical expulsive therapy (MET), which entails the use of various pharmacotherapeutic agents to enable spontaneous stone passage and alleviate symptoms, has been widely employed in adults with distal ureteral calculi. While there are several drug options for MET, optimal choice of therapy is fundamental to maximize clinical effectiveness. In this context, alpha blockers appear to be a good choice as they cause smooth muscle relaxation, inhibition of peristalsis, and relieve spasm.51   Accordingly, they not only facilitate the passage of ureteral calculi, but also significantly combat lower urinary tract symptoms correcting obstruction and improving the urine flow.52,53     Tamsulosin has been demonstrated to provide excellent expulsive effectiveness in adult patients with distal ureteral calculi requiring MET.54   It is recommended for use in stone patients as per EAU guidelines (box 3).

Kaneko et al55   evaluated the efficacy of tamsulosin versus no medication in patients with ureteral stones. The results showed the stone expulsion rate to be significantly higher in tamsulosin group than in the comparator group (77% versus 50%, respectively). Similar overwhelming results have also been obtained in pediatric stone formers, with a stone-free rate of 87.8% on treatment with tamsulosin versus 64.2% with placebo.56   Another study suggested tamsulosin to increase spontaneous expulsion of distal ureteral stones while decreasing time to expulsion, pain episodes, and need for analgesics in children with urolithiasis. In addition, no adverse effects were observed in these patients.57   It has also been suggested that MET with tamsulosin is not associated with adverse maternal or fetal outcomes and may therefore be considered as a reasonable adjunctive option for urolithiasis during pregnancy.58   Even among the elderly patients, tamsulosin enhances spontaneous stone passage by approximately 50% for small distal stones without any significant safety concerns.59  

References

  1. Chung C, Stern PJ, Dufton J. Urolithiasis presenting as right flank pain: a case report. The Journal of the Canadian Chiropractic Association. 2013;57(1):69-75.
  2. Shekarriz B, Stoller MI. Metabolic evaluation of stone disease. Brazilian Journal of Urology. 2001 Jan-Feb;27(1):10-18.
  3. Institute of Medicine (US). Facing the Reality of Drug- Resistant Tuberculosis in India: Challenges and Potential Solutions: Summary of a Joint Workshop by the Institute of Medicine, the Indian National Science Academy, and the Indian Council of Medical Research. Washington (DC): National Academies Press (US); 2012. 1, Introduction. Available from: http://www.ncbi.nlm.nih.gov/books/ NBK100396/
  4. Gupta SK, Baghel MS, Bhuyan C, Ravishankar B, Ashok BK, Patil PD. Evaluation of anti-urolithiatic activity of Pashanabhedadi Ghrita against experimentally induced renal calculi in rats. Ayu. 2012;33(3):429-434.
  5. Sodimbaku V, Pujari L. Urolithiasis–an updated review over genetics, pathophysiology and its Clinical management. Int J Pharm Pharm Sci. 2014;6(11):23-31.
  6. Trinchieri A. Epidemiology of urolithiasis: an update. Clinical Cases in Mineral and Bone Metabolism. 2008;5(2):101-106.
  7. Krambeck AE, Lieske JC, Li X, Bergstralh EJ, Melton LJ, Rule AD. Effect of Age on the Clinical Presentation of Incident Symptomatic Urolithiasis in the General Population. The Journal of urology. 2013;189(1):158-164.
  8. Cormier CM, Canzoneri BJ, Lewis DF, Briery C, Knoepp L, Mailhes JB. Urolithiasis in pregnancy: Current diagnosis, treatment, and pregnancy complications. Obstet Gynecol Surv. 2006 Nov;61(11):733-41.
  9. Hall WD, Pettinger M, Oberman A, Watts NB, Johnson KC, Paskett ED, Limacher MC, Hays J. Risk factors for kidney stones in older women in the southern United States. Am J Med Sci. 2001 Jul;322(1):12-8.
  10. Sharma AP, Filler G. Epidemiology of pediatric urolithiasis. Indian Journal of Urology : IJU : Journal of the Urological Society of India. 2010;26(4):516-522.
  11. Dwyer ME, Krambeck AE, Bergstralh EJ, Milliner DS, Lieske JC, Rule AD. Temporal trends in incidence of kidney stones among children: A 25-year population based study. J Urol. 2012;188:247-52.
  12. Routh JC, Graham DA, Nelson CP. Epidemiological trends in pediatric urolithiasis at United States freestanding pediatric hospitals. J Urol. 2010 Sep;184(3):1100-4.
  13. Roudakova K, Monga M. The evolving epidemiology of stone disease. Indian Journal of Urology : IJU : Journal of the Urological Society of India. 2014;30(1):44-48.
  14. Chen JN, Dieguez LM, Trachtman H. The Changing Epidemiology of Urolithiasis in Pediatric Patients. J Nephrol Therapeutic. 2014;S11:S11-006.
  15. Bastug F, Düsünsel R. Pediatric urolithiasis: causative factors, diagnosis and medical management. Nat Rev Urol. 2012 Feb 7;9(3):138-46.
  16. Worcester EM, Coe FL. Nephrolithiasis. Primary care. 2008;35(2):369-vii.
  17. Penido MGMG, Tavares M de S. Pediatric primary urolithiasis: Symptoms, medical management and prevention strategies. World Journal of Nephrology. 2015;4(4):444-454.
  18. Portis AJ, Sundaram CP. Diagnosis and initial management of kidney stones. Am Fam Physician. 2001 Apr 1;63(7):1329-38.
  19. Freitas Junior CH, Mazzucchi E, Danilovic A, Brito AH, Srougi M. Metabolic assessment of elderly men with urolithiasis. Clinics (Sao Paulo). 2012;67(5):457-61.
  20. McCarthy JP, Skinner TA, Norman RW. Urolithiasis in the elderly. Can J Urol. 2011 Jun;18(3):5717-20.
  21. Arampatzis S, Lindner G, Irmak F, Funk GC, Zimmermann H, Exadaktylos AK. Geriatric urolithiasis in the emergency department: risk factors for hospitalisation and emergency management patterns of acute urolithiasis. BMC Nephrol. 2012 Sep 24;13:117.
  22. Ngo TC, Assimos DG. Uric Acid Nephrolithiasis: Recent Progress and Future Directions. Reviews in Urology. 2007;9(1):17-27.
  23. Prstojevic JK, Junuzovic D, Hasanbegovic M, Lepara Z, Selimovic M. Characteristics of Calculi in the Urinary Tract.ts NB, Johnson KC, Paskett ED, Limacher MC, Hays J. Risk factors for kidney stones in older women in the southern United States. Am J Med Sci. 2001 Jul;322(1):12-8.
  24. Gentle DL, Stoller ML, Bruce JE, Leslie SW. Geriatric urolithiasis. J Urol. 1997 Dec;158(6):2221-4.
  25. Dursun M, Ozbek E, Otunctemur A, Sahin S, Cakir SS. Clinical presentation of urolithiasis in older and younger population. Arch Ital Urol Androl. 2014 Dec 30;86(4):249-52.
  26. Oxenkrug GF. Metabolic syndrome, age-associated neuroendocrine disorders, and dysregulation of tryptophankynurenine metabolism. Ann N Y Acad Sci. 2010 Jun;1199:1-14.
  27. Gorbachinsky I, Akpinar H, Assimos DG. Metabolic Syndrome and Urologic Diseases. Reviews in Urology. 2010;12(4):e157- e180.
  28. Semins MJ, Matlaga BR. Management of urolithiasis in pregnancy. International Journal of Women’s Health. 2013;5:599-604.
  29. Semins MJ, Matlaga BR. Kidney stones and pregnancy. Adv Chronic Kidney Dis. 2013 May;20(3):260-264.
  30. Swanson SK, Heilman RL, Eversman WG. Urinary tract stones in pregnancy. Surg Clin North Am. 1995 Feb;75(1):123-42.
  31. Abdel-Kader MS, Tamam A-A, Elderwy AA. Management of symptomatic ureteral calculi during pregnancy: Experience of 23 cases. Urology Annals. 2013;5(4):241-244.
  32. Masselli G, Derme M, Bernieri MG, et al. Stone disease in pregnancy: imaging-guided therapy. Insights into Imaging. 2014;5(6):691-696.
  33. Swartz MA, Lydon-Rochelle MT, Simon D, Wright JL, Porter MP. Admission for nephrolithiasis in pregnancy and risk of adverse birth outcomes. Obstet Gynecol. 2007 May;109(5):1099-104.
  34. Lewis DF, Robichaux AG 3rd, Jaekle RK, Marcum NG, Stedman CM. Urolithiasis in pregnancy. Diagnosis, management and pregnancy outcome. J Reprod Med. 2003 Jan;48(1):28-32.
  35. Masselli G, Derme M, Laghi F, Polettini E, Brunelli R, Framarino ML, Gualdi G. Imaging of stone disease in pregnancy. Abdom Imaging. 2013 Dec;38(6):1409-14.
  36. Maalouf NM, Sato AH, Welch BJ, et al. Postmenopausal Hormone Use and the Risk of Nephrolithiasis: Results From the Women’s Health Initiative Hormone Therapy Trials. Archives of Internal Medicine. 2010;170(18):1678-1685.
  37. Mattix Kramer HJ, Grodstein F, Stampfer MJ, Curhan GC. Menopause and postmenopausal hormone use and risk of incident kidney stones. J Am Soc Nephrol. 2003 May;14(5):1272-7.
  38. Hall WD, Pettinger M, Oberman A, Watts NB, Johnson KC, Paskett ED, Limacher MC, Hays J. Risk factors for kidney stones in older women in the southern United States. Am J Med Sci. 2001 Jul;322(1):12-8.
  39. Lojanapiwat B, Tanthanuch M, Pripathanont C, Ratchanon S, Srinualnad S, Taweemonkongsap T, Kanyok S, Lammongkolkul S. Alkaline citrate reduces stone recurrence and regrowth after shockwave lithotripsy and ercutaneous nephrolithotomy. Int Braz J Urol. 2011 Sep-Oct;37(5):611-6.
  40. Hwang K, Mason MD, Peters CA. Clinical practice: Surgical approaches to urolithiasis in children. European journal of pediatrics. 2011;170(6):681-688.
  41. Golzari SE, Soleimanpour H, Rahmani F, Mehr NZ, Safari S, Heshmat Y, Bakhtavar HE. Therapeutic approaches for renal colic in the emergency department: a review article. Anesth Pain Med. 2014; 3(3): e16222.
  42. Blasko G. Pharmacology, Mechanism of Action and Clinical Significance of a Convenient Antispasmodic Agent: Drotaverine. JAMA India-The Physicians’ Update. 4(12) (REPRINT): 59-66.
  43. Fathallah-Shaykh S, Neiberger R, Langman CB, et al. Pediatric Urolithiasis. Available at: http://emedicine.medscape.com/ article/983884-medication#2. Accessed on: 25.11.15.
  44. Sakhaee K, Nicar M, Hill K, Pak CY. Contrasting effects of potassium citrate and sodium citrate therapies on urinary chemistries and crystallization of stoneforming salts. Kidney Int. 1983 Sep;24(3):348-52.
  45. Xu H, Zisman AL, Coe FL, Worcester EM. Kidney stones: an update on current pharmacological management and future directions. Expert Opin Pharmacother. 2013;14(4):435–447.
  46. Singh SK, Agarwal MM, Sharma S. Medical therapy for calculus disease. BJU Int. 2011 Feb;107(3):356-68.
  47. Alon US. Medical treatment of pediatric urolithiasis. Pediatric Nephrology (Berlin, Germany). 2009;24(11):2129-2135.
  48. McNally MA, Pyzik PL, Rubenstein JE, Hamdy RF, Kossoff EH. Empiric use of potassium citrate reduces kidneystone incidence with the ketogenic diet. Pediatrics. 2009 Aug;124(2):e300-4.
  49. Robert M. Kliegman, Bonita Stanton, Joseph St. Geme, Nina Felice Schor, Richard E. Behrman. In: XXIV Urologic Disorders in Infants and Children. Elsevier Health Sciences, 22-Apr-2015. pp 2554-2605.
  50. Pearle MS, Goldfarb DS, Assimos DG, Curhan G, Denu- Ciocca CJ, Matlaga BR, Monga M, Penniston KL, Preminger GM, Turk TM, White JR; American Urological Assocation. Medical management of kidney stones: AUA guideline. J Urol. 2014 Aug;192(2):316-24.
  51. Arrabal-Martin M, Valle-Diaz de la Guardia F, Arrabal- Polo MA, Palao-Yago F, Mijan-Ortiz JL, Zuluaga-Gomez A. Treatment of ureteral lithiasis with tamsulosin: literature review and meta-analysis. Urol Int. 2010;84(3):254-9.
  52. Porpiglia F, Ghignone G, Fiori C, Fontana D, Scarpa RM. Nifedipine versus tamsulosin for the management of lower ureteral stones. J Urol. 2004 Aug;172(2):568-71.
  53. Cervenàkov I, Fillo J, Mardiak J, Kopecný M, Smirala J, Lepies P. Speedy elimination of ureterolithiasis in lower part of ureters with the alpha 1-blocker–Tamsulosin. Int Urol Nephrol. 2002;34(1):25-9.
  54. Griwan MS, Singh SK, Paul H, Pawar DS, Verma M. The efficacy of tamsulosin in lower ureteral calculi. Urology Annals. 2010;2(2):63-66.
  55. Kaneko T, Matsushima H, Morimoto H. Efficacy of low dose tamsulosin in medical expulsive therapy for ureteral stones in Japanese male patients: A randomized controlled study. Int Urol. 2010;17:462–5.
  56. Aldaqadossi HA, Shaker H, Saifelnasr M, Gaber M. Efficacy and safety of tamsulosin as a medical expulsive therapy for stones in children. Arab Journal of Urology. 2015;13(2):107-111.
  57. Tasian GE, Cost NG, Granberg CF, Pulido JE, Rivera M, Schwen Z, Schulte M, Fox JA. Tamsulosin and spontaneous passage of ureteral stones in children: a multi-institutional cohort study. J Urol. 2014 Aug;192(2):506-11.
  58. Bailey G, Vaughan L, Rose C, Krambeck A4. Perinatal Outcomes with Tamsulosin Therapy for Symptomatic Urolithiasis. J Urol. 2015 Jul 2. pii: S0022-5347(15)04312-8.
  59. Welk BK, Teichman JM. Pharmacological management of renal colic in the older patient. Drugs Aging. 2007;24(11):891-900.