the correlation between inflammatory bowel disease and kidney stones.doc

8/12/2019 The Correlation Between Inflammatory Bowel Disease and Kidney Stones.doc

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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,,

1


2/21

-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

'*'.'+.&*

2


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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

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TAB%E (& C(#TE#T

Chapter I 6 Introduction 77777777777 8

Chapter II 6 Inflammatory %owel /isease 7777777777. 9

II.( 6 /efinition 77777777777. 9

II.& 6 Causes 77777777777.. 9

II.* 6 !ymptoms 77777777777.. :

II.; 6 3hysical $1amination 77777777777.. +

II. 8 6 3athophysiology 77777777777..

Chapter III 6 -idney stones 77777777777. (&

III.( 6 /efinition 77777777777. (&

III.& 6 Causes 77777777777. (&

III.* 6 !ymptoms and sign 77777777777. (*

III.8 6 /iagnosis 77777777777 (;

Chapter I< 6 )he Correlation between kidney stones and I%/ 77777 (9

Chapter < 6 Conclusion 77777777777 &'

=eferences 77777777777 &(

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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 nited !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.

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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 colitisC0 andCrohnBs diseaseC/0.

As the name suggests, ulcerative colitis is limited to the colonlarge intestine0. Although CrohnBs

disease can involve any part of thegastrointestinal tract from the mouth to the anus, it mostcommonly affects the small intestineandor 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.! Cases

=esearchers do not yet know what causes inflammatory bowel disease. )herefore, I%/ is

called an idiopathicdisease disease with an unknown cause0.,('

An unknown factoragent or a combination of factors0 triggers the bodyEs immune

systemto 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

bloodydiarrheaand abdominal pain.

#enetic, infectious, immunologic, and psychological factors have all been implicated in

influencing the development of I%/.

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)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. ot

uncommonly, patients have been diagnosed with irritable bowel syndrome before being

diagnosed with I%/.


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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 Eamination"/,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

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)able. /istinguishing Features of Crohn /isease (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>(' I>('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 skip areas 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.

ate 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. uch less commonly, Crohn

disease involves the more pro1imal parts of the #I tract, including the mouth, tongue, esophagus,

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

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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. rine 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 ((' of an inch or larger. rolithiasis 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 kidneystone, 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.! Cases

)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, andhypercalciuriahigh

levels of calcium in the urine0 is arisk 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 alsopredisposesome people to form kidney stones. $1amples

include people with renal tubular acidosis and people with problems metaboli2ing a

variety of chemicals including cystinean amino acid0, o1alate, a type of salt0,

and uric acidas 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 stone

belts, with people living in the southern nited !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 water pills0 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


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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>colickytype pain, like that associated withappendicitisorpancreatitis, 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 vomitingare common.

%lood may or may not be visible in the urine because the stone has irritated the kidney or

ureter. %lood in the urinehematuria0, however, does not always mean a person has a kidney

stone. )here may be other reasons for the blood, including kidney andbladder

infections,trauma, or tumors. rinalysiswith amicroscopemay 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.

ltrasound is another way of looking for kidney stones and obstruction and may be

useful when the radiation risk of a C) scanis unwanted for e1ample, if a woman is pregnant0.

ltrasound 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>

raysmay 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 >ray radiation that can accumulate over a lifetime is minimi2ed.

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CHA-TER I*

THE C(RRE%ATI(# BETEE# 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

C0, because the inflamed colon is more permeable to o1alate. %ut not all patients with I%/with calcium o1alate stones demonstrate hypero1aluria. ow levels of urinary citrate and

magnesium have been proposed as an important lithogenic factor in patients with C/ and C.

ormally, 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.


17/21

urinary pH decreases. rid 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 proctocolectomy80.

)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 e1cretion90.

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 Red2in6 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>>

17


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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. imiting

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

18


19/21

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. ow levels of urinary magnesium and citrate in

I%/ may result in increased calcium stone formation. time

stone formers is key.

19


20/21

RE&ERE#CES

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

$dition. !aunders $lsevierG &'':.p. 9((.

&. $l>!erag H, KwasF, %onheim , Cirillo , Appel #. )he renal and urologic complications of

inflammatory bowel disease. Crohns and Colitis Foundation of America &''96*6&(:>&;.

Available at 6 http6www*.interscience.wiley.comcgi>binfullte1t((*8&&9&*3/F!)A=).

Accesed June &;, &'((

*. 3arks J H, Dorcester $ , "BConnor =, Coe F . rine stone risk factors in nephrolithiasis

patients with and without bowel disease. -idney International. "fficial Journal of )he

International !ociety of ephrology &''*69*6&88>98. Available at 6

htt1899www.natre.2om9 :i9;ornal94. Available at 6 http6www.ncbi.nlm.nih.gov pubmed(&;:;9;(.

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

s2ohost.2om9lo6in.as1?

dire2t@tred>@mnhA#@,5


21/21

:. %handari A, enon . =educing the risk of kidney stone recurrence. Fellow,

*&. Available at 6 htt1899sear2h.e>s2ohost.2om9lo6in.as1?

dire2t@tred>@2hA#@!00",!!5live . Accesed June &;, &'((.

+. CrohnBs /isease6 Inflammatory %owel /isease. About.com 6 Health )opics A>K. Available at 6

htt1899adam.a>ot.2om9re1orts9000,03

the correlation between inflammatory bowel disease and kidney stones.doc

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