The Correlation Between Inflammatory Bowel Disease and Kidney Stones

BY THRESIA 030.0 .!3" E#$%ISH III

&AC'%TY (& )EDICI#E TRISAKTI '#I*ERSITY +AKARTA !0,,

-RE&ACE First I would like to thank Jesus Christ for the blessing, because only by His permit I could finish this paper on time. In this opportunity, I would like to thank to my mother and father with their support for me, and for my older sister to give me inspiration to finish this paper. And special thanks for my supervisor dr. Atut Cicih ayasari, !p."# for her guidance.

I made this paper to complete my duty in $nglish III and I hope this paper is useful for all of us. %ut as a writer, I know that this paper might be not entirely perfect and have many mistakes so I need critics from people who read my paper.

Jakarta, June &'((

)hresia '*'.'+.&*,

ABSTRACT

-idney stones are increased in patients with inflammatory bowel disease .I%/0, particularly those who have had resection of part of their gastrointestinal tract. )hese stones are usually calcium o1alate, but there is a marked increase in the tendency to form uric acid stones, as well, particularly in patients with colon resection. )hese patients all share a tendency to chronic volume contraction due to loss of water and salt in diarrheal stool, which leads to decreased urine volumes. )hey also have decreased absorption, and therefore diminished urinary e1cretion, of citrate and magnesium, which normally act as inhibitors of calcium o1alate crystalli2ation. 3atients with colon resection and ileostomy form uric acid stones, as loss of bicarbonate in the ileostomy effluent leads to formation of an acid urine. )his, coupled with low urine volume, decreases the solubility of uric acid, causing crystalli2ation and stone formation.. $nteric hypero1aluria .$H0 leads to supersaturation of urine with respect to calcium o1alate, in con4unction with low volume, hypocitraturia and hypomagnesuria. )hen another possible role in kidney stone formation may caused by infre5uency of coloni2ation with Oxalobacter formigenes in I%/.

KEY.(RDS I%/, $H, kidney stones, calcium o1alate, resection, Oxalobacter formigenes

TAB%E (& C(#TE#T Chapter I Chapter II II.( II.& II.* 6 Introduction 6 Inflammatory %owel /isease 6 /efinition 6 Causes 6 !ymptoms 77777777777 7777777777. 8 9

77777777777. 9 77777777777.. 9 77777777777.. : 77777777777.. + 77777777777.. , 77777777777. (& 77777777777. (& 77777777777. (& 77777777777. (* 77777777777 (; (9 &' &(

II.; 6 3hysical $1amination II. 8 Chapter III 6 3athophysiology 6 -idney stones

III.( 6 /efinition III.& 6 Causes III.* 6 !ymptoms and sign III.8 6 /iagnosis Chapter I< Chapter < =eferences

6 )he Correlation between kidney stones and I%/ 77777 6 Conclusion 77777777777 77777777777

CHA-TER I I#TR(D'CTI(# Chron disease and ulcerative colitis are chronic relapsing inflammatory disorders of unknown origin, collectively known as idiopathic inflammatory bowel disease .I%/0, which share many common features.(0. )he correlation between I%/ and kidney stones, first described in (,9+ by #el2ayd et al , has been confirmed in numerous studies. )he incidence of kidney stones is increased appreciably in I%/, with an overall incidence of 8>(8? / as compared with a (>8? incidence in the general population, +'? of stones in patients with I%/ are composed of calcium o1alate, and the remainder are uric acid .&0. In one study from !weden, a &+? incidence of calcium o1alate stones was found if @I'' cm of small intestine was resected.&0. Among those patients who have not had bowel surgery, the prevalence of stones has ranged from (.8 to 8?, which is not different from the usual values for Anited !tates stone prevalence rates .* to 8?0.*0. However, given bowel surgery, rates are about two> to threefold higher within each study, giving a stone prevalence of *.: to (9? for all surgeries combined .*). 3atients with I%/ who undergo total colectomy with permanent ileostomies are at a high risk of developing uric acid stones. )his risk is further increased if additional small>bowel resection was performed.

CHA-TER II

Inflammatory Bowel Disease

II., Defination )he term inflammatory bowel disease .I%/0 covers a group of disorders in which the intestines become inflamed .red and swollen0, probably as a result of an immune reaction of the body against its own intestinal tissue. , )wo ma4or types of I%/ are described6 ulcerative colitis .AC0 and CrohnBs disease.C/0. As the name suggests, ulcerative colitis is limited to the colon .large intestine0. Although CrohnBs disease can involve any part of the gastrointestinal tract from the mouth to the anus, it most commonly affects the small intestineandCor the colon. %oth ulcerative colitis and CrohnBs disease usually run a wa1ing and waning course in the intensity and severity of illness. Dhen there is severe inflammation, the disease is considered to be in an active stage, and the person e1periences a flare>up of the condition. Dhen the degree of inflammation is less .or absent0, the person usually is without symptoms, and the disease is considered to be inremission., II.! Ca0ses =esearchers do not yet know what causes inflammatory bowel disease. )herefore, I%/ is called an idiopathic disease .disease with an unknown cause0.,,(' An unknown factorCagent .or a combination of factors0 triggers the bodyEs immune system to produce an inflammatory reaction in the intestinal tract that continues without control. As a result of the inflammatory reaction, the intestinal wall is damaged leading to bloodydiarrhea and abdominal pain. #enetic, infectious, immunologic, and psychological factors have all been implicated in influencing the development of I%/.

)here is a genetic predisposition .or perhaps susceptibility0 to the development of I%/. However, the triggering factor for activation of the bodyEs immune system has yet to be identified. Factors that can turn on the bodyEs immune system include an infectious agent .as yet unidentified0, an immune response to an antigen .eg, protein from cow milk0, or anautoimmune process. As the intestines are always e1posed to things that can cause immune reactions, more recent thinking is that there is a failure of the body to turn off normal immune responses. II.3 Sym1tom "/,0 )he manifestations of inflammatory bowel disease .I%/0 generally depend on the area of the intestinal tract involved. !ome patients with I%/ also have irritable bowel syndrome .I%!0, which can produce occasional cramping, irregular bowel habits, and passage of mucus without blood or pus. !ystemic symptoms are common in I%/ and include fever, sweats, malaise, and arthralgias. A low>grade fever may be the first warning sign of a flare. 3atients are commonly fatigued, which is often related to the pain, inflammation, and anemia that accompany disease activity. =ecurrences may occur with emotional stress, infections or other acute illnesses, pregnancy, dietary indiscretions, use of cathartics or antibiotics, or withdrawal of anti> inflammatory or steroid medications. Children may present with growth retardation and delayed or failed se1ual maturation. In ('>&'? of cases, patients present with e1traintestinal manifestations, including arthritis, uveitis, or liver disease .see Complications0. #rossly bloody stools, occasionally with tenesmus, although typical of ulcerative colitis, are less common in Crohn disease. !tools may be formed, but loose stools predominate if the colon or the terminal ileum is involved e1tensively. "ne half of patients with Crohn disease present with perianal disease .eg, fistulas, abscesses0. "ccasionally, acute right lower 5uadrant pain and fever, mimicking appendicitis or intestinal obstruction, may be noted. Fot uncommonly, patients have been diagnosed with irritable bowel syndrome before being diagnosed with I%/. <arious intestinal and e1traintestinal manifestations of I%/ also may be observed in con4unction with either ulcerative colitis or Crohn disease .see Complications0.

Deight loss is observed more commonly in Crohn disease than in ulcerative colitis because of the malabsorption associated with small bowel disease. 3atients may reduce their food intake in an effort to control their symptoms. Commonly, the diagnosis is established only after several years of recurrent abdominal pain, fever, and diarrhea.

II.4 -hysi2al E3amination"/,0

Fever, tachycardia, dehydration, and to1icity may occur in patients with I%/. 3allor may be noted, reflecting anemia. )he magnitude of these factors is directly related to the severity of the attack. $valuate for signs of locali2ed peritonitis, although abdominal tenderness is common. 3atients with to1ic megacolon appear septic. )hese individuals have high feverG lethargyG chillsG tachycardiaG and increasing abdominal pain, tenderness, and distention. .!ee the )able below.0 3atients with Crohn disease may develop a mass in the right lower 5uadrant. Complications .eg, perianal fissures or fistulas, abscesses, rectal prolapse0 may be observed in up to ,'? of patients with this disease, and common presenting signs include occult blood loss and low>grade fever, weight loss, and anemia. #rowth retardation is seen in children and may be the only presenting sign in young patients. )he rectal e1amination often reveals bloody stool on gross or Hemoccult e1amination. )he physical e1amination should include a search for e1traintestinal manifestations, such as iritis, episcleritis, arthritis, and dermatologic involvement. .see Complications.0

)able. /istinguishing Features of Crohn /isease <ersus Alcerative Colitis &eat0res !kip areas Cobblestone mucosa Crohn Disease 'l2erati4e Colitis Common Common Fever =are "ccasional Fever Fever Fever "ccasional "ccasional

)ransmural involvement Common =ectal sparing 3erianal involvement Fistulas !trictures #ranulomas Common Common Common Common Common

II.5 -atho1hysiolo6y

)he pathophysiology of I%/ is under active investigation. )he common end pathway is inflammation of the mucosal lining of the intestinal tract, causing ulceration, edema, bleeding, and fluid and electrolyte loss.,,(' any inflammatory mediators have been identified in I%/, and considerable evidence suggests that these mediators play an important role in the pathologic and clinical characteristic of these disorders. Cytokines, released by macrophages in response to various antigenic stimuli, bind to different receptors and produce autocrine, paracrine, and endocrine effects. Cytokines differentiate lymphocytes into different types of ) cells. Helper ) cells, type ( .)h>(0, are associated principally with Crohn disease, whereas )h>& cells are associated principally with ulcerative colitis. )he immune response disrupts the intestinal mucosa and leads to a chronic inflammatory process. !everal animal models are used to study I%/. A local irritant .eg, acetic acid, trinitroben2ene sulfonic acid0 can be inserted via an enema into the colon of rats or rabbits to
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induce a chemical colitis. An interleukin>(' .IH>('0 knockout mouse has been genetically engineered to have some characteristics similar to those of a human with I%/. )he cotton>top marmoset, a !outh American primate, develops a Colitis very similar to ulcerative colitis when the animal is sub4ected to stress. 'l2erati4e 2olitis In ulcerative colitis, inflammation begins in the rectum and e1tends pro1imally in an uninterrupted fashion to the pro1imal colon, eventually involving the entire length of the large intestine. )he rectum is always involved in ulcerative colitis, and no Iskip areasI .ie, normal areas of the bowel interspersed with diseased areas0 are present, unlike Crohn disease. )he disease remains confined to the rectum in appro1imately &8? of cases, and in the remainder of cases, ulcerative colitis spreads pro1imally and contiguously. 3ancolitis occurs in ('? of patients. )he small intestine is never involved, e1cept when the distal terminal ileum is inflamed in a superficial manner, referred to as backwash ileitis. $ven with less than total colonic involvement, the disease is strikingly and uniformly continuous. As ulcerative colitis becomes chronic, the colon becomes a rigid foreshortened tube that lacks its usual haustral markings, leading to the lead pipe appearance observed on barium enema. Crohn disease Crohn disease can affect any portion of the #I tract from the mouth to the anus and causes * patterns of involvement6 inflammatory disease, strictures, and fistulas. )his disease consists of segmental involvement by a nonspecific granulomatous inflammatory process. )he most important pathologic feature of Crohn disease is that it is transmural, involving all layers of the bowel, not 4ust the mucosa and the submucosa, which is characteristic of ulcerative colitis. Furthermore, Crohn disease is discontinuous, with skip areas interspersed between one or more involved areas. !ee the image below.

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Inflammatory bowel disease. Inflammation in the terminal ileum noted during colonoscopy. Areas of inflammation, friability, and ulceration in the terminal ileum are consistent with mild>to>moderate Crohn disease. Hate in the disease, the mucosa develops a cobblestone appearance, which results from deep, longitudinal ulcerations interlaced with intervening normal mucosa. )he * ma4or patterns of involvement in Crohn disease are disease in the ileum and cecum .;'? of patients0G disease confined to the small intestine .*'? of patients0G and disease confined to the colon .&8? of patients0. =ectal sparing is a typical but not constant feature of Crohn disease. However, anorectal complications .eg, fistulas, abscesses0 are common. stomach, and duodenum. )he incidence of gallstones and kidney stones is increased in Crohn disease because of malabsorption of fat and bile salts. #allstones are formed because of increased cholesterol concentration in the bile, caused by a reduced bile salt pool. 3atients who have Crohn disease with ileal disease or resection are also likely to form calcium o1alate kidney stones. Dith the fat malabsorption, unabsorbed long>chain fatty acids bind calcium in the lumen. "1alate in the lumen is normally bound to calcium. Calcium o1alate is poorly soluble and poorly absorbedG however, if calcium is bound to malabsorbed fatty acids, o1alate combines with sodium to form sodium o1alate, which is soluble and is absorbed in the colon .enteric hypero1aluria0. )he development of calcium o1alate stones in Crohn disease re5uires an intact colon to absorb o1alate. 3atients with ileostomies generally do not develop calcium o1alate stones uch less commonly, Crohn disease involves the more pro1imal parts of the #I tract, including the mouth, tongue, esophagus,

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CHA-TER III KID#EY ST(#ES III. 3 DE&I#ITI(# )he kidney acts as a filter for blood, removing waste products from the body and making urine. It also helps regulate electrolyte levels that are important for body function. Arine drains from the kidney through a narrow tube called the ureter into the bladder. Dhen the bladder fills and there is an urge to urinate, the bladder empties to the outside through the urethra, a much wider tube than the ureter. In some people, chemicals crystalli2e in the urine and form the beginning, or nidus, of a kidney stone. )hese stones are very tiny when they form, smaller than a grain of sand, but gradually can grow over time to (C(' of an inch or larger. Arolithiasis is the term that refers to the presence of stones in the urinary tract, while nephrolithiasis refers to kidney stones and ureterolithiasis refers to stones lodged in the ureter. )he si2e of the stone doesnBt matter as much as where it is located and whether it obstructs or prevents urine from draining. Dhen the stone sits in the kidney, it rarely causes problems, but when it falls into the ureter, it acts like a dam. As the kidney continues to function and make urine, pressure builds up behind the stone and causes the kidney to swell. )his pressure is what causes the pain of a kidney stone, but it also helps push the stone along the course of the ureter. Dhen the stone enters the bladder, the obstruction in the ureter is relieved and the symptoms of a kidney stone are resolved.

III.! Ca0ses )here is no consensus as to why kidney stones form. Heredity !ome people are more susceptible to forming kidney stones, and heredity may play a role. )he ma4ority of kidney stones are made of calcium, andhypercalciuria .high levels of calcium in the urine0 is a risk factor. )he predisposition to high levels of
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calcium in the urine may be passed on from generation to generation. !ome rare hereditary diseases alsopredispose some people to form kidney stones. $1amples include people with renal tubular acidosis and people with problems metaboli2ing a variety of chemicals including cystine .an amino acid0, o1alate, .a type of salt0, and uric acid .as in gout0.

$eo6ra1hi2al lo2ation6 )here may be a geographic predisposition, and where a person lives may predispose them to form kidney stones. )here are regional Istone belts,I with people living in the southern Anited !tates having an increased risk of stone formation. )he hot climate in this region combined with poor fluid intake may cause people to be relatively dehydrated, with their urine becoming more concentrated and allowing chemicals to come in closer contact to form the nidus, or beginning, of a stone.

Diet6 /iet may or may not be an issue. If a person is susceptible to forming stones, then foods high in calcium may increase the riskG however, if a person isnBt susceptible to forming stones, diet probably will not change that risk.

)edi2ations6 3eople taking diuretics .or Iwater pillsI0 and those who consume e1cess calcium>containing antacids can increase the amount of calcium in their urine and potentially increase their risk of forming stones. )aking e1cess amounts of vitamins A and / are also associated with higher levels of calcium in the urine. 3atients with HI< who take the medicationindinavir .Cri1ivan0 may form indinavir stones. "ther commonly prescribed medications associated with stone formation include dilantin and antibioticslike ceftria1one .=ocephin0 and ciproflo1acin .Cipro0.

Anderlying illnesses6 !ome chronic illnesses are associated with kidney stone formation, including cystic fibrosis, renal tubular acidosis, andinflammatory bowel disease.

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III. 3 Symptoms and Signs

Dhen a tubular structure is blocked in the body, waves of pain occur as the body tries to unblock the obstruction. )hese waves of pain are called colic. )his is opposed to non>colicky type pain, like that associated with appendicitisor pancreatitis, in which movement causes increased pain and the patient tries to hold very still. =enal colic .renal is the medical term for things related to the kidney0 has a classic presentation when a kidney stone is being passed. )he pain is intense and comes on suddenly. It may wa1 and wane, but there is usually a significant underlying ache between the acute spasms of pain. It is usually located in the flank or the side of the mid back and may radiate to the groin. ales may complain of pain in the testicle or scrotum. )he patient cannot find a comfortable position and often writhes or paces with pain. !weating, nausea, and vomiting are common. %lood may or may not be visible in the urine because the stone has irritated the kidney or ureter. %lood in the urine .hematuria0, however, does not always mean a person has a kidney stone. )here may be other reasons for the blood, including kidney and bladder infections, trauma, or tumors. Arinalysis with amicroscope may detect blood even if it is not appreciated by the naked eye. !ometimes, if the stone causes complete obstruction, no blood may be found in the urine because it cannot get past the stone. III.7 Dia6nosis !ymptom control is very important, and medication for pain and nausea may be provided before the confirmation of the diagnosis occurs. A urinalysis may detect blood in the urine. It is also done to look for evidence of infection, a complication of kidney stone disease.
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%lood tests are usually not indicated, unless the health>care provider has concerns about the diagnosis or is worried about kidney stone complications. Computeri2ed tomography .C)0 scanning of the abdomen without oral or intravenous contrast dye is the most commonly used diagnostic test. )he scan will demonstrate the anatomy of the kidneys, ureter, and bladder and can detect a stone, its location, its si2e, and whether it is causing dilation of the ureter and inflammation of the kidney. )he C) can also evaluate many other organs in the abdomen, including the appendi1, gallbladder, liver, pancreas, aorta, and bowel. However, since no contrast material is used, there are some limitations to the detail that can be observed in the images of the scan. Altrasound is another way of looking for kidney stones and obstruction and may be useful when the radiation risk of a C) scan is unwanted .for e1ample, if a woman is pregnant0. Altrasound re5uires a specially trained person to interpret the images and may not always be available. In those patients who already have the diagnosis of a kidney stone, plain abdominal J> rays may be used to track its movement down the ureter toward the bladder. As well, in patients with known kidney stone disease, no imaging may be necessary if the diagnosis seems certain, so that the amount of J>ray radiation that can accumulate over a lifetime is minimi2ed.

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CHA-TER I* THE C(RRE%ATI(# BET.EE# KID#EY ST(#ES A#D IBD

any mechanisms have been proposed to account for the increased incidence of kidney stones. $nteric hypero1aluria .$H0 is the most plausible mechanism for calcium o1alate stone formation.&,;0. Increased absorption of dietary o1alate in this condition leads to increased urinary o1alate e1cretion, which readily e1ceeds the solubility product for calcium o1alate. )he increased urinary o1alate concentration in the presence of nucleation factors, such as calcium and uric acid crystals, leads to formation of o1alate stones, mainly in the form of calcium o1alate. In patients with resection or disease of the terminal ileum, malabsorption of fat and bile acids may occur. Calcium ions will bind preferentially to the unabsorbed fatty acids, leaving the unbound dietary o1alate to be absorbed in the large bowel and subse5uently e1creted in the urine. In addition, the unabsorbed bile salts will increase the permeability of the colonic mucosa to o1alate. Anatomic preservation of the colon is an important factor in the pathogenesis of calcium o1alate stones, because the colon is the main site of dietary o1alate absorption, and studies on colectomi2ed patients fail to show hypero1aluria. Hypero1aluria also occurs in ulcerative colitis .AC0, because the inflamed colon is more permeable to o1alate. %ut not all patients with I%/ with calcium o1alate stones demonstrate hypero1aluria. How levels of urinary citrate and magnesium have been proposed as an important lithogenic factor in patients with C/ and AC. Formally, citrate forms soluble comple1es with calcium, thereby decreasing its availability as a nidus for stone formation. agnesium inhibits renal tubular reabsorption of citrate by chelating it in the tubular urine. )hus, low levels of urinary magnesium and citrate in I%/ may result in increased calcium stone formation. <olume depletion from gastrointestinal fluid losses may also contribute to higher concentrations of o1alate and stone formation.;0. 3atients who have undergone e1tensive resection of the colon, especially with ileostomy, are known to be chronically dehydrated as a result of decreased water and electrolyte absorption. )hese losses are partially corrected by the compensatory mechanism of the terminal ileum and kidney. Arinary output and Fa e1cretion are decreased to prevent e1cessive loss of body water and sodium. As a result of decreased Fa e1cretion, tritable urinary acid e1cretion increases and
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urinary pH decreases. Arid acid calculi may occur in these patients since urid acid is less soluble in acidic urine. )he authors investigated the incidences of urinary calculi and urinary chemistry in patients with I%/ who underwent total colectomy or proctocolectomy.80. )he other references said that infre5uency of coloni2ation with Oxalobacter formigenes in I%/ have a possible role in kidney stone formation. Oxalobacter formigenes, a recently identified bacterium, coloni2es gastrointestinal tracts of vertebrates, including man. Oxalobacter formigenes cataboli2es o1alate in the intestine and therefore, reduces its concentration in plasma and urine. Oxalobacter formigenes has been suggested to play a role in hypero1aluria and kidney stones. /ata on Oxalobacter formigenes in I%/, a condition with a higher risk of kidney stones, is scant. Accordingly, the authors hypothesi2ed that absence of Oxalobacter formigenes could cause hypero1aluria and kidney stones in patients with I%/. "ther factors that could contribute to development of stones in these patients include low levels of anti>lithogenic agents like magnesium and citrate. !tudies on lithogenic and antilithogenic solutes in the urine of patients with I%/ are few. )hey aimed to study Oxalobacter formigenes in patients with I%/ and relationship between coloni2ation with Oxalobaceter formigenes and urinary o1alate e1cretion.90. Treatment aintaining ade5uate hydration is important in all patients with I%/ to reduce the incidence of kidney stones. In patients with known hypero1aluria, prevention of calcium o1alate stones may be achieved by reducing dietary intake of o1alate and fat, and by treatment with cholestyramine .;g three or four times a day0, which binds bile salts and o1alate in the gut. 3otassium citrate .&' m$5 orally three times a day0 is helpful in reducing the incidence of calcium stones, especially in patients with hypocitraturia. )he use of additional calcium supplements to bind o1alate in the gut before absorption is controversial, because accurate repeated urinary o1alate levels are needed to monitor this therapy. )he prophylactic use of sodium bicarbonate .; g per day0 in patients who have undergone colectomy has been advised by some authors to prevent uric acid stones from developing.&, :0. Dietary Considerations for Red02in6 Kidney Stones -idney stones are painful and common complications in I%/, particularly in patients who have had intestinal surgery. I%/ patients are at risk for the most common types of stones>>
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those composed of either calcium o1alate or uric acid crystals. )he following are some considerations in reducing the risk for stones. )he most important dietary recommendations for reducing the risk for kidney stones are increasing fluid and restricting sodium intake. Himiting protein is recommended for reducing kidney stones. "f note, however, people with I%/ with fre5uent diarrhea are protein deficient. !ufficient protein, particularly in children with I%/, is very important and should be weighed against any risk for stones. 3atients should increase intake of potassium>rich foods. 3atients should try to correct any dietary habits that cause acidic or alkaline imbalances in the urine that promote stone formation. any kidney stones are formed from calcium>o1alate stones. 3atients should avoid or limit intake o1alate>rich foods, such as beets, beet tops, black tea, chenopodium, chocolate, cocoa, dried figs, ground pepper, lamb 5uarters, lime peel, nuts, parsley, poppy seeds, purslane, rhubarb, sorrel, spinach, and !wiss chard. A high calcium diet does not appear to increase the risk for kidney stones as long as it also contains plenty of fluids and dietary potassium and phosphate. Importantly calcium is associated with protection against colon cancer and osteoporosis>>two conditions that are associated with I%/. 3atients who have stones associated with short>bowel syndrome should restrict their intake of fat as well o1alates. In such cases, calcium may bind to unabsorbed fat instead of to o1alates, which increase o1alate levels.+0

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C(#C%'SI(# -idney stones are more common in patients with inflammatory bowel disease .I%/0 than in the general population. )he main lithogenetic risk factors were evaluated in patients affected by CrohnBs disease and ulcerative colitis. $nteric hypero1aluria .$H0 is the most plausible mechanism for calcium o1alate stone formation. How levels of urinary magnesium and citrate in I%/ may result in increased calcium stone formation. <olume depletion from gastrointestinal fluid losses may also contribute to higher concentrations of o1alate and stone formation. Another references said that infre5uency of coloni2ation with Oxalobacter formigenes in I%/ have a possible role in kidney stone formation. =ecurrent stones are preventable with dietary modifications and medical therapy, but appropriate evaluation of both recurrent and first>time stone formers is key.

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RE&ERE#CES (. -umar, Abbas, Fausto, itchell. Inflammatory %owel /isease. =obbins %asic 3athology. + th

$dition. !aunders $lsevierG &'':.p. 9((. &. $l>!erag H, Kwas F, %onheim F, Cirillo F, Appel #. )he renal and urologic complications of inflammatory bowel disease. Crohns and Colitis Foundation of America &''96*6&(:>&;. Available at 6 http6CCwww*.interscience.wiley.comCcgi>binCfullte1tC((*8&&9&*C3/F!)A=). Accesed June &;, &'(( *. 3arks J H, Dorcester $ International !5/!0,,. ;. Dorcester $ . !tones from bowel disease. $ndocrinology And Accesed on June &;, &'((. 8. Fukushima ), Lama2aki L, !ugita A, )suchiya !. 3rophyla1is of uric acid stone in patients with inflammatory bowel disease following e1tensive colonic resection. Journal of #astroenterology (,,(6&96;*'>*;. Available at 6 htt1899www.s1rin6erlin:.2om92ontent9 3<!=5,<,m!3,56 39. Accesed June &;, &'((. 9. . -umar =, #hoshal A, !ingh #, ittal = /. Infre5uency of coloni2ation with Oxalobacter etabolism Clinics "f Forth !ociety , "BConnor =, Coe F H. Arine stone risk factors in nephrolithiasis of Fephrology &''*69*6&88>98. Available A22esed on at 6

patients with and without bowel disease. -idney International. "fficial Journal of )he htt1899www.nat0re.2om9 :i9;o0rnal94<39n,9f0ll977"37!0a.html. +0ne

America &''&6*(6,:,>,,. Available at 6 http6CCwww.ncbi.nlm.nih.govC pubmedC(&;:;9;(.

formigenes in inflammatory bowel disease6 3ossible role in renal stone formation. /epartments of Arology and #astroenterology, !an4ay #andhi 3ost #raduate Institute of edical !ciences, Hucknow, India. Journal of #astroenterology and Hepatology &'';6(,6(;'*M,. Available at 6 htt1899sear2h.e>s2ohost.2om9lo6in.as13? dire2t@tr0eAd>@mnhAA#@,5<,03,5Asite@ehostBli4e. Accesed June &;, &'((.

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:. %handari A, *&.

enon Available

. =educing the risk of kidney stone recurrence. Fellow, <attikuti ich. 3atient Care &''; Apr6 *+6 &9> at 6 htt1899sear2h.e>s2ohost.2om9lo6in.as13?

Arology Institute, Henry Ford Health !ystem, /etroit,

dire2t@tr0eAd>@2 hAA#@!00",!! 5< NsiteOehost>live . Accesed June &;, &'((. +. CrohnBs /isease6 Inflammatory %owel /isease. About.com 6 Health )opics A>K. Available at 6 htt1899adam.a>o0t.2om9re1orts9000,03C<.htm. Accesed June &; , &'((. ,. Rowe A .illiam. Inflammatory Bowel Disease. )eds2a1eD !0,,. A4aila>le from htt1899emedi2ine.meds2a1e.2om9arti2le9,="03=Bo4er4iew. A22esed +0ne !3, &'((. ('. Fauci, %raunwald, -asper, Hauser, Hongo, Jameson, dkk. HarrisonEs 3rinciples of Internal edicine. (:thed. Anited !tates of America 6 c #raw>Hill Companies, IncG &''+.p. (+,,.

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