Urolithiasis/Nephrolithiasis: What’s It All About? T I N · PDF fileUROLOGIC NURSING /...

UROLOGIC NURSING / December 2005 / Volume 25 Number 6 427

Urolithiasis/Nephrolithiasis:What’s It All About?Joan ColellaEileen Kochis

Bernadette GalliRavi Munver

T he term nephrolithiasis(kidney calculi or stones)refers to the entire clini-cal picture of the forma-

tion and passage of crystal agglom-erates called calculi or stones inthe urinary tract (Wolf, 2004).Urolithiasis (urinary calculi orstones) refers to calcifications thatform in the urinary system, pri-marily in the kidney (nephrolithi-asis) or ureter (ureterolithiasis),and may also form in or migrateinto the lower urinary system(bladder or urethra) (Bernier,2005). Urinary tract stone diseasehas been documented historicallyas far back as the Egyptian mum-mies (Wolf, 2004).

PrevalenceAs much as 10% of the U.S.

population will develop a kid-ney stone in their lifetime.Upper urinary tract stones (kid-ney, upper ureter) are more com-mon in the United States than in

Urolithiasis (urinary tract calculi or stones) and nephrolithiasis (kid-ney calculi or stones) are well-documented common occurrences inthe general population of the United States. The etiology of this disor-der is mutifactorial and is strongly related to dietary lifestyle habits orpractices. Proper management of calculi that occur along the urinarytract includes investigation into causative factors in an effort to pre-vent recurrences. Urinary calculi or stones are the most commoncause of acute ureteral obstruction. Approximately 1 in 1,000 adults inthe United States are hospitalized annually for treatment of urinarytract stones, resulting in medical costs of approximately $2 billion peryear (Ramello, Vitale, & Marangella, 2000; Tanagho & McAninch, 2004).

Joan Colella, MSN, MPA, RN, APRN-BC, NP-C, is an Advanced PracticeNurse, The Prostate Institute of TheCancer Center at HackensackUniversity Medical Center, Hackensack,NJ.

Eileen Kochis, RN, is a Staff Nurse,the Department of Urology, The CancerCenter at Hackensack UniversityMedical Center, Hackensack, NJ.

Bernadette Galli, MSN, RN, APRN-BC, NP-C, is an Advanced PracticeNurse, the Department of Urology, TheCancer Center at HackensackUniversity Medical Center, Hackensack,NJ.

the rest of the world. Researchersattribute the incidence ofnephrolithiasis in the UnitedStates to a dietary preference offoods high in animal protein(Billica, 2004).

Age and GenderThe literature reflects the

incidence of kidney (renal) stoneformation to be greater amongwhite males than black malesand three times greater in malesthan females. Although kidneystone disease is one-fourth toone-third more prevalent in adultwhite males, black males demon-strate a higher incidence ofstones associated with urinarytract infections caused by urea-splitting bacteria (Munver &Preminger, 2001).

Kidney stones are mostprevalent between the ages of 20to 40, and a substantial numberof patients report onset of the dis-ease prior to the age of 20(Munver & Preminger, 2001; Pak,1979, 1987). The lifetime risk forkidney stone formation in theadult white male approaches20% and approximately 5% to10% for women. The recurrencerate for kidney stones is approxi-mately 15% in year 1 and as highas 50% within 5 years of the ini-tial stone (Munver & Preminger,2001; Spirnak & Resnick, 1987).

PATHOPHYSIOLOGY OFNEPHROLITHIASIS

Any factor that reduces uri-nary flow or causes obstruction,which results in urinary stasis or

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Ravi Munver, MD, is Chief, Minimally Invasive Urologic Surgery, the Department ofUrology, The Cancer Center at Hackensack University Medical Center, Hackensack,NJ; an Assistant Professor of Surgery/Urology, UMDNJ-New Jersey Medical School,Newark, NJ; and an Adjunct Assistant Professor of Urology, Weill Medical College ofCornell University, New York, NY.

Note: CE Objectives and Evaluation Form appear on page 449.

428 UROLOGIC NURSING / December 2005 / Volume 25 Number 6

reduces urine volume throughdehydration and inadequatefluid intake, increases the risk ofdeveloping kidney stones. Lowurinary flow is the most commonabnormality, and most importantfactor to correct with kidneystones. It is important for healthpractitioners to concentrate oninterventions for correcting lowurinary volume in an effort toprevent recurrent stone disease(Munver & Preminger, 2001; Pak,Sakhaee, Crowther, & Brinkley,1980).

Contributing Factors Of Nephrolithiasis

Sex. Males tend to have athree times higher incidence ofkidney stones than females.Women typically excrete more cit-rate and less calcium than men,which may partially explain thehigher incidence of stone diseasein men (National Institutes ofHealth [NIH], 1998-2005).

Ethnic background. Stonesare rare in Native Americans,Africans, American Blacks, andIsraelis (Menon & Resnick, 2002).

Family history. Patients witha family history of stone forma-tion may produce excess amountsof a mucoprotein in the kidney orbladder allowing crystallites to bedeposited and trapped formingcalculi or stones. Twenty-five per-cent of stone-formers have a fami-ly history of urolithiasis. Familialetiologies include absorptivehypercalciuria, cystinuria, renaltubular acidosis, and primary hyper-oxaluria (Munver & Preminger,2001).

Medical history. Past medicalhistory may provide vital infor-mation about the underlying eti-ology of a stone’s formation (seeTable 1). A positive medical his-tory of skeletal fracture(s) andpeptic ulcer disease suggests adiagnosis of primary hyper-parathyroidism. Intestinal dis-

ease, which may include chronicdiarrheal states, ileal disease, orprior intestinal resection, may bea predisposition to enteric hyper-oxaluria or hypocitraturia. Thismay result in calcium oxalatenephrolithiasis because of dehy-dration and chemical imbalances(see Figure 1). Irritable bowel dis-ease or intestinal surgery mayprevent the normal absorption offat from the intestines and alterthe manner in which theintestines process calcium oroxalate. This may also lead tocalculi or stone formation.Patients with gout may formeither uric acid stones (see Figure2) or calcium oxalate stones.Patients with a history of urinarytract infections (UTIs) may beprone to infection nephrolithia-sis caused by urea-splitting bac-teria (Munver & Preminger,2001). Cystinuria is a homozy-gous recessive disease leading tostone formation. Renal tubular

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Figure 1.Calcium Oxalate Stone

Photo courtesy of Louis C. Herring& Co.

Figure 2.Uric Acid Stone


Table 1.Factors Contributing to Stone Development

Source: Tanagho & McAninch, 2004

� Congenital kidney defects (medullary sponge disease)

� Excess parathyroid hormone

� Medications (ephedrine, guaifenesin, indinavir, allopurinol)

� Gout

� Hypertension

� Colitis, inflammation of colon, and chronic diarrheal states

� Irritable bowel disease or intestinal surgery

� Renal tubular acidosis

� Crohn’s disease results in dehydration and low citrate.

� Arthritis (skeletal disease)

� Urinary tract infections

� Past medical history of kidney stones

� Obesity and high body mass index

� Prolonged inactivity

� Anatomic factors – Ureteropelvic junction (UPJ) obstruction

� Horseshoe or ectopic kidney

� Autosomal dominant polycystic kidney disease

� Vesicoureteral reflux

� Calyceal diverticula


acidosis is a familial disorderthat causes kidney stones in mostpatients who have this disorder.

Dietary habits. Fluid restric-tion or dehydration may causekidney stone formation. Dietaryintake that is high in sodium,oxalate, fat, protein, sugar, unre-fined carbohydrates, and ascor-bic acid (vitamin C) has beenlinked to stone formation. Lowintake of citrus fruits can resultin hypocitraturia, which mayincrease an individual’s risk fordeveloping stones.

Environmental factors. Fluidintake consisting of drinkingwater high in minerals may con-tribute to kidney stone develop-ment. Another contributing fac-tor may be related to geographi-cal variables such as tropical cli-mates (NIH, 1998-2005). Stone for-mation is greater in mountainous,high-desert areas that are found inthe United States, British Isles,Scandinavia, Mediterranean, Nor-thern India, Pakistan, NorthernAustralia, Central Europe, MalayanPeninsula, and China (Menon &Resnick, 2002). Affluent societieshave a higher rate of small uppertract stones whereas large stru-vite (infection) stones occur morecommonly in developing coun-tries (see Figure 3). Bladderstones are more common inunderserved countries and arelikely related to dietary habitsand malnutrition (Menon &Resnick, 2002).

Medications. Medications

such as ephedrine, guaifenesin,thiazide, indinavir, and allopuri-nol may be contributory factors inthe development of calculi (seeDrug-Induced Nephrolithiasis).

Occupations. Occupations inwhich fluid intake is limited orrestricted or those associatedwith fluid loss may be at greaterrisk for stone development as aresult of decreased urinary vol-ume.

CLINICAL PRESENTATION Symptoms may vary and

depend on the location and sizeof the kidney stones or calculiwithin the urinary collecting sys-tem. In general, symptoms mayinclude acute renal or ureteralcolic, hematuria (microscopic orgross blood in the urine), urinarytract infection, or vague abdomi-nal or flank pain. A thorough his-tory and physical examination,along with selected laboratoryand radiologic studies, are essen-tial to making the correct diagno-sis. Small nonobstructing stonesor “silent stones” located in thecalyces of the kidney are some-times found incidentally on x-rays or may be present withasymptomatic hematuria. Suchstones often pass without caus-ing pain or discomfort.

Kidney Stone Symptoms Stones in the kidneys can

become lodged at the junction ofthe kidney and ureter (uretero-pelvic junction), resulting in acuteureteral obstruction with severeintermittent colicky flank pain.Pain can be localized at the cos-tovertebral angle. Hematuria maybe present intermittently or per-sistently and it may be microscop-ic or gross.

Ureteral Stone SymptomsStones that can pass into the

ureter may produce ureteralcolic, which is an acute, sharp,spasm-like pain located in theflank. Hematuria may be present.Stones moving down the ureterto the pelvic brim and iliac ves-

sels will produce spasms withintermittent, sharp, colicky painradiating to the lateral flank andaround the umbilical region.

As a stone passes through thedistal ureter, near the bladder, thepain remains sharp but with a wax-ing and waning quality. Relief isoffered when the spasm subsides orthe pain may intensify and radiateto the groin, testicles, or labia.Nausea, vomiting, diaphoresis,tachycardia, and tachypnea may bepresent and patients are typicallyuncomfortable.

Bladder Stone SymptomsOnce a stone enters the blad-

der, dysuria, urgency, and frequen-cy may be the only symptomsexperienced. Immediate relief ofsymptoms occurs once the stonepasses out of the bladder.

Kidney Stone Complications Occasionally, stones can

injure the kidneys by causinginfection, resulting in fever,chills, and loss of appetite or uri-nary obstruction. If a UTI accom-panies the urinary obstruction,pyelonephritis or urosepsis canoccur. If stones are bilateral, theycan cause renal scarring anddamage, resulting in acute orchronic renal failure.

CALCIUM NEPHROLITHIASIS

HypercalciuriaEighty to eighty-five percent

of calculi or stones diagnosed inthe United States are idiopathic(spontaneous and without recog-nizable cause) or primary. Thesestones are comprised of calciumand are due to excess calciumexcretion in the urine, usuallyexceeding 200 mg/24-hour col-lection (see Table 2).

Absorptive hypercalciuria.The primary abnormality inabsorptive hypercalciuria isincreased absorption of calcium.Absorptive hypercalciuria Type Iis more severe and characterizedby a high urine calcium level,

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Figure 3.Struvite Stone



with high or low dietary calciumintake. There is a normal serumlevel of calcium and phosphorusand normal or low serum level ofparathyroid hormone.

Absorptive hypercalciuriaType II is a mild to moderateform of hypercalciuria and lesssevere than Type I. Type II hyper-calciuria only occurs with highcalcium intake. There is normalurinary calcium excretion whilefasting or on a restricted calciumdiet (Munver & Preminger, 2001).

Renal hypercalciuria. Renalhypercalciuria or “renal leakmechanism” is thought to becaused by impairment in renaltubular reabsorption of calcium(Munver & Preminger, 2001; Pak,1979). The loss of calcium in theurine leads to stimulation of theparathyroid function, causing ele-vated 1,25-vitamin D and increasedintestinal absorption to maintainserum levels of calcium.

Primary hyperparathyroidism.Excess parathyroid hormone(PTH) results in increased boneresorption of calcium from boneand accounts for less than 5% ofstones. Parathyroid hyperplasiaor adenomas secrete excessparathyroid hormone causingincreased intestinal absorption ofcalcium, increased 1,25-vitaminD3, and increased bone deminer-alization and calcium releasefrom bone. Laboratory tests

reveal elevated parathyroid hor-mone and serum calcium levels.

Less frequent causes of hyper-calciuria include chronic immobi-lization, metastatic cancer to bone,multiple myeloma, and vitamin Dintoxication. Calcium stones havebeen described as appearing spic-ulated, dotted, mulberry, or jack-stone in appearance.

HyperoxaluriaHyperoxaluria is defined by

urinary oxalate excretion in excessof 45 mg/day (Munver &Preminger, 2001). The cause ofthese calcium stones can be relat-ed to primary or secondary factors.

Primary hyperoxaluria. Type Ihyperoxaluria is a rare autosomalrecessive disorder that begins inchildhood in which a defect of thehepatic enzyme alanine-glyoxy-late aminotransfease (AGT) caus-es increased urinary excretion ofoxalic, glycolic, and glyoxylicacids (Danpure, 1994; Menon &Mahle, 1982; Munver &Preminger, 2001). This conditionis characterized by nephrocalci-nosis, oxalate deposition in tis-sues, and renal failure resulting indeath before age 20, if untreated.Diagnosis is made through percu-taneous liver biopsy and evalua-tion of the amount and distribu-tion of AGT in liver specimens.

Type II hyperoxaluria is avery rare deficiency of the hepat-

ic enzymes (D-glycerate dehy-drogenase and late reductase)resulting in increased urinaryoxalate and glycerate excretion.This results in the developmentof nephrocalcinosis, tubulointer-stitial nephropathy, and chronicrenal failure.

Secondary hyperoxaluria(dietary). Approximately 80% ofurinary oxalate is synthesizedwithin the liver and a small per-centage (20%) from dietaryintake. Overindulgence of dietsrich in oxalates can contribute tohyperoxaluria through intestinalabsorption of oxalate. Thisincludes foods such as rhubarb,green leafy vegetables, spinach,cocoa, beer, coffee or tea, orexcess ascorbic acid (vitamin C)intake.

Enteric hyperoxaluria. Theprimary site of oxalate absorptionis the distal colon. Intestinal mal-absorption can cause excessoxalate absorption due to variousdiseases such as chronic diar-rhea/short bowel inflammatorydisease, gastric or small bowelresection surgery. Additional sec-ondary causes can be the result oflow urinary output from intesti-nal fluid loss, low urinary citratedue to hypokalemia and metabol-ic acidosis, and low magnesiumlevels due to impaired intestinalmagnesium absorption.

HyperuricosuriaHyperuricosuria (excessive

urinary uric acid) accounts for10% of calcium stones. There is agenetic predisposition, commonin men, for stone developmentdue to high uric acid levels andexcess uric acid excretion, whichresults in hyperuricosuria. Ex-cessive uric acid excretion can befound in primary gout, and sec-ondary conditions of purine over-production including myeloprolif-erative disorders such as acuteleukemia, glycogen storage disease,and malignancy. Hyperuricosuriais often caused by excess intake ofpurine in meat, fish, and poultry.This purine diet causes a low uri-

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Table 2.Causes of Calcium Stones

Source: Tanagho & McAninch, 2004

� Supersaturation from any cause

� Dehydration

� Increased intestinal absorption

� Increased calcium excretion

� Excess oral vitamin D (intoxication)

� Alkaline urine pH

� Diet high in calcium or oxalate

� Chronic bowel disease (intestinal disease)

� Poor GI citrate absorption

� Sarcoidosis


nary pH. The features of hyperuri-cosuric calcium oxalate nephro-lithiasis include elevated urinaryuric acid (>600 mg/day), a nor-mal serum calcium level, normalurinary calcium and oxalate lev-els, normal fasting and calciumload response, and urinary pHtypically <5.5.

HypocitraturiaHypocitraturic calcium ne-

phrolithiasis may exist as an iso-lated abnormality (10%) or morecommonly in combination withother metabolic disorders (50%)(Menon & Mahle, 1982; Pak,1987; Pak, 1994). Acid-base sta-tus, acidosis in particular, is themost important factor affectingthe renal handling of citrate, withincreased acid levels resulting indiminished endogenous citrateproduction. Low urinary citratecauses the urinary environmentto become supersaturated withcalcium salts, promoting nucle-ation, growth, and aggregation,resulting in stone formation.

Distal renal tubular acidosis.A more common cause of hypo-citraturia is distal renal tubularacidosis (RTA). Acidosis impairsurinary citrate excretion byenhancing renal tubular reab-sorption of citrate as well as byreducing its synthesis (Pak,1982). Distal RTA can be com-plete or incomplete. In bothforms, hypercalciuria and pro-found hypocitraturia may beassociated. In combination withalkaline urine, the patient is atrisk for developing calciumoxalate or calcium phosphatestones (Munver & Preminger,2001; Preminger, Sakhaee,Skurla, & Pak, 1985).

Chronic diarrheal syndrome.Chronic diarrheal syndromecauses a loss of alkali in the formof bicarbonate through the gas-trointestinal tract resulting inmetabolic acidosis with subse-quent impairment in citrate syn-thesis (Munver & Preminger,2001; Rudman et al., 1980). Thedecreased citrate production

causes a lower urinary concen-tration of citrate. Patients withchronic diarrheal syndrome mayhave additional risk factors forstone formation such as low urinevolumes and hyperoxaluria.

Thiazide-induced hypocitra-turia. Thiazide diuretics can pro-duce hypokalemia (low potassi-um) leading to intracellular aci-dosis. This acidotic state inhibitsthe synthesis of citrate, resultingin hypocitraturia. The essentialmechanism is the inhibition ofcitrate production, which is aconsequence of chronic acidosis(Nicar, Peterson, & Pak, 1984).

Idiopathic hypocitraturia.Mechanisms that account forhypocitraturia in this conditioninclude a high animal proteindiet (with an elevated acid-ashcontent), strenuous physicalexercise (causing lactic acidosis),high sodium intake, and intesti-nal malabsorption of citrate.

HypomagnesuriaMagnesium, an inhibitor of

calcium nephrolithiasis, increasesthe solubility product of calciumoxalate and calcium phosphate.Hypomagnesuria is defined as uri-nary magnesium excretion <50mg/day. Many patients withnephrolithiasis will report a limit-ed intake of magnesium-richfoods such as nuts and chocolate,suggesting the dietary basis of thiscondition.

Gouty DiathesisGouty diathesis (predisposi-

tion to uric acid or calciumstones) may appear in a latent oran early phase of classic gout, orit may manifest fully with goutyarthritis and hyperuricemia.Patients develop renal stonescomposed purely of uric acid,uric acid in combination withcalcium oxalate or calcium phos-phate, or stones that reveal onlycalcium oxalate or calcium phos-phate. Some patients may formuric acid or calcium stones(Khatchadourian, Preminger,Whitson, Adams-Huet, & Pak,

1995). The invariant feature ofthis condition is persistentlyacidic urine (pH <5.5) and nospecific cause has been detectedfor the low urinary pH.

NON-CALCIUMNEPHROLITHIASIS

Uric Acid StonesUric acid stones may form in

the presence of gouty diathesis orin secondary causes of purineoverproduction. Secondary caus-es of these stones can includechronic diarrheal states such asileostomy, ulcerative colitis, andCrohn’s disease. These chronicdiarrheal states predispose uricacid precipitation, acidic urinarypH due to bicarbonate loss instool or urinary ammoniumexcretion defects, and reducedurinary volume (see Table 3).

Cystine StonesCystine stones are due to a

rare, congenital condition result-ing in large amounts of cystine(an amino acid) in the urine.Cystinuria causes cystine stones,requiring lifelong therapy (Uro-logy Channel, 1998). This disor-der typically presents duringchildhood and adolescence(Bernier, 2005). The diagnosisshould be suspected for patientswith an early onset of neph-rolithiasis, a significant familyhistory, or recurrent stone dis-ease. A positive sodium- nitro-prusside urine test or the pres-ence of flat, hexagonal crystals inurinary sediment provides a pre-sumptive diagnosis of cystinestone disease.

Struvite Stones (InfectionStones)

These stones are caused byUTIs, which affect the chemicalbalance of the urine, raising thepH. Urea-splitting bacteria (forexample, Proteus, Klebsiella, andPseudomonas) release chemicalsinto the urinary tract, neutraliz-ing acid in the urine, enablingthe bacteria to grow quickly and

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form struvite stones. Struvitestones are difficult to treatbecause the stone surrounds anucleus of bacteria, which is pro-tected from antibiotic therapy(Bernier, 2005). These stones arethree times more common inwomen than men due to anincreased incidence of UTIs inwomen. Struvite stones are mostcommonly found in patientswith chronic infections as well aspatients with anatomic or func-tional abnormalities of their uri-nary tract allowing stasis of urineand chronic bacteriuria. Theseabnormalities include neuro-genic bladder, diverticuli, andstrictures (Lingeman, Siegel, &Steele, 1995).

Struvite stones are jagged(staghorns) in appearance andmay be quite large at the time ofinitial presentation.

OTHER CAUSES OFNEPHROLITHIASIS

Low Urine VolumeLow urine output is defined

as <1 liter/day. The typical etiolo-gies of nephrolithiasis are lowfluid intake and reduced urinevolume. Other possible causes oflow urine volume include chron-ic diarrheal syndromes that resultin large fluid loses from the gas-trointestinal tract and fluid lossfrom perspiration, or evaporationfrom lungs or exposed tissue.Stone formation may be initiated

by a low urine output, providinga concentrated environment forsubstances such as calcium,oxalate, uric acid, and cystine tobegin crystallization.

No Pathological DisturbanceIn approximately 35% of the

stone-forming population, noidentifiable risk factors for stoneformation can be found (Levy,Adams-Huet, & Pak, 1995). Thisgroup includes individuals withnormal serum calcium and PTH,normal fasting and calcium loadresponse, normal urine volumes,normal pH, calcium, oxalate, uricacid, citrate, and magnesium lev-els in the presence of calciumnephrolithiasis.

Drug-Induced NephrolithiasisEphedrine calculi. Ephedrine

and its metabolites (norephedrine,pseudoephedrine, and norpseu-doephedrine) are sympathomimet-ic agents that have been used forthe treatment of enuresis, myasthe-nia gravis, narcolepsy, and rhinor-rhea (Powell, Hsu, Turk, & Hruska,1998). In addition to numerousside effects, ephedrine and itsderivatives have been associatedwith the production of urinarystones (Blau, 1998). The diagno-sis of these calculi is similar tothat of other radiolucent calculi.Twenty-four hour urine metabol-ic analyses can aid in identifyingephedrine or its respectivemetabolites.

Guaifenesin calculi. Guaifenesinis a widely used expectorant that hasbeen recently associated withnephrolithiasis. Guaifenesin calculiare radiolucent and present inpatients who ingest this medica-tion in excess. Twenty-four hoururine metabolic analysis can aidin the identification of guaifen-esin or b-2-methoxyphenoxy-lac-tic acid.

Indinavir calculi. Indinavirsulfate (Crixivan®) is currentlyone of the most frequently usedprotease inhibitors used againsthuman immunodeficiency virus,the virus that causes AIDS. Theincidence of calculi in patientstaking indinavir ranges from 3%to 20% (Schwartz, Schenkman,Armenakas, & Stoller, 1999).Indinavir calculi are radiolucentwhen they are pure, and areradiopaque when they containcalcium.

Xanthine calculi. These stonesoccur due to a rare hereditary con-dition with xanthine oxidase defi-ciency (see Figure 4). The deficien-cy in this enzyme results indecreased levels of serum and uri-nary uric acid. Acidic urine caus-es crystal precipitation, resultingin stone formation (Bernier,2005). These stones are also seenin patients treated with iatrogenicinhibition of xanthine oxidasewith xanthine oxidase inhibitorsfor hyperuricosuria such as allop-urinol.

DIAGNOSIS OF KIDNEYSTONES

Urolithiasis can mimic otheretiologies of visceral pain. It isimperative to consider causes ofsurgical abdomens such asappendicitis, cholecystitis, pepticulcer, pancreatitis, ectopic preg-nancy, and dissecting aneurysmin patients who present withabdominal pain. Initial assess-ment includes a thorough historyand physical examination, basicserum and urine chemistries, anda radiologic imaging study. First-time stone formers may benefitfrom a more detailed laboratory

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Table 3.Contributing Factors to Stone Development

Sources: Bernier, 2005; Moe et al., 2002

� Starvation causing chronic oliguric states

� Primary gout – genetic (25% of population)

� Secondary gout (50% of population)

� Medications causing rapid cell destruction in the treatment of neo-plastic disease

� Acute leukemia

� Hemolytic anemia/myeloproliferative disorders

� Excess exercise


evaluation to identify causal fac-tors for stone formation. Multipleor recurrent stone-formers (meta-bolically active stone formers)require a more comprehensive lab-oratory evaluation (NIH, 1998-2005).

METABOLIC EVALUATIONThe primary objective of a

diagnostic evaluation of nephro-lithiasis should be to efficiently andeconomically identify the particu-lar physiological defect present inthe patient to enable the selectionof specific and rational therapy.The evaluation should be able toidentify the metabolic disordersresponsible for recurrent stone dis-ease, including cystinuria, distalrenal tubular acidosis, enterichyperoxaluria, gouty diathesis, andprimary hyperparathyroidism.

A detailed history and physi-cal examination are imperativefor both first-time stone-formersand recurrent stone-formers. Pastmedical history emphasis shouldinclude information about previ-ous UTIs, diet and fluid intake,medications including vitaminintake, bowel disease, gout, renaldisease, bone or parathyroid dis-ease, and bowel surgery.

First-time stone-formers mayundergo an abbreviated diagnosticevaluation such as stone analysis,urinalysis, culture and sensitivity,and a comprehensive metabolicpanel, which includes serum cal-cium, uric acid, and phosphorus.Recurrent stone-formers and first-

time stone-formers are at risk forrecurrence. Both will benefit froman extensive diagnostic evaluationsuch as stone analysis, urinalysis,culture and sensitivity, compre-hensive metabolic panel, whichincludes serum calcium, uric acid,and phosphorus, parathyroid hor-mone level, and 24-hour urine col-lections (random and after beingon a special diet). Patients at riskinclude children, middle-agedwhite males with a family historyof stones, and patients with intesti-nal disease (chronic diarrheal ormalabsorptive states), gout,nephrocalcinosis, osteoporosis,pathologic skeletal fractures, orurinary tract infection. Stonescomposed of cystine, struvite, oruric acid should undergo a com-plete metabolic workup (Pre-minger, Peterson, Peters, & Pak,1985).

Urine AssessmentUrinalysis with urine culture

and sensitivity are mandatorytests. Reports may reveal micro-scopic or gross hematuria andpyuria with or without infection.Increase or decrease in urine pHand the presence of crystals maygive clues to whether the stone isalkaline or acidic. A cyanidenitroprusside test will screen forsuspected cystinuria.

Two 24-hour urine collec-tions should be performed evalu-ating calcium, sodium, phospho-rus, magnesium, oxalate, uricacid, citrate, sulfate, creatinine,pH, and total volume. The first24-hour urine should be a ran-dom specimen. The second 24-hour urine should be obtainedafter the patient has been on asodium, oxalate, and calcium-restricted diet.

Serum AssessmentComplete blood count (CBC)

may reveal an elevated whiteblood count (WBC) suggestingurinary systemic infection, ordepressed red blood cell countsuggesting a chronic disease stateor severe ongoing hematuria.

Serum electrolytes, BUN, creati-nine, calcium, uric acid, andphosphorus assess current renalfunction, dehydration, and themetabolic risk of future stone for-mation. An elevation in PTHlevel will confirm a diagnosis ofhyperparathyroidism.

Radiologic Assessment Intravenous pyelography (IVP).

Intravenous pyelography (urogra-phy) has long been consideredthe primary diagnostic study ofchoice for identifying urinarytract calculi. The IVP providesanatomical and functional infor-mation, identifies the precise sizeand location of a stone, the pres-ence and severity of the obstruc-tion, and renal or ureteral abnor-malities. For these reasons, theIVP has been among the mostimportant diagnostic tests thatmay enable successful manage-ment decisions.

Computed Tomography (CT)Scan

CT scan (with and withoutcontrast) is believed to be the bestradiographic examination foracute renal colic as it createsimages of the urinary tract andshows delayed penetration ofintravenous contrast through theobstructed kidney. The delayedpenetration of the contrast throughan obstructed kidney is the hall-mark of acute urinary obstruction.The CT findings indicative ofacute urinary obstruction sec-ondary to a stone would includerenal enlargement, hydronephro-sis, ureteral dilatation, perinephricstranding, and periureteral edema(Katz, Lane, & Sommer, 1996;Smith, Verga, Dalrymple, Mc-Carthy, Rosenfield, 1996). Otherconditions that can mimic ureteralcolic can be identified as well asanatomic abnormalities andobstruction. For many reasons, theCT scan is considered superior toan IVP in detecting both renal andureteral calculi, and is routinelyperformed on most patients inwhich a diagnosis of urolithiasis is

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Figure 4.Xanthine Stone



suspected (Smith, Verga, Dalry-mple, McCarthy, & Rosenfield,1996).

Radionuclide ImagingRenal scan is considered the

gold standard for assessing renalfunction, especially in the set-ting of recurrent or long-standingnephrolithiasis. It is noninva-sive, does not require any specialpreparation or bowel prepara-tion, exposes the patient to min-imal radiation, and is nearly freeof allergic complications.

Plain X-RaysPlain abdominal X-rays en-

tailing a flat plate radiograph ofkidney, ureter, and bladder(KUB) will identify renal stonesthat are radiopaque (Departmentof the Navy Bureau of Medicineand Surgery, 2004). AbdominalX-rays are helpful in document-ing the number, size, and loca-tion of stones in the urinary tractand the radiopacity may provideinformation on the type of stonespresent. Plain abdominal filmscan be useful in identifyingnephrocalcinosis, suggestive ofhyperparathyroidism, primaryhyperoxaluria, renal tubular aci-dosis, or sarcoidosis.

Renal Ultrasound Ultrasonography can be used

as a screening tool for hydro-nephrosis or stones within the kid-ney or renal pelvis. A renal ultra-sound can also determine theamount of renal parenchyma pre-sent in an obstructed kidney, inaddition to the presence ofstones. The ultrasound can beused in combination with plainabdominal radiograph to deter-mine hydronephrosis or ureteraldilation (Wolf, 2004). This maybe helpful in assessment duringpregnancy (see Table 4).

MEDICAL MANAGEMENTEffective kidney stone preven-

tion is dependent on the stone typeand identification of risk factors forstone formation (see Tables 5 & 6).

An individualized treatment planincorporating dietary changes, sup-plements, and medications can bedeveloped to help prevent the for-mation of new stones. Certain con-

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Table 4.Diagnostic Tests for Urinary Stones

Diagnostic Tests Rationale of Testing

Urinalysis Evaluate presence of blood or infection

Intravenous pyelogram (IVP) Evaluate urinary tract obstruction

Evaluate for stones

Evaluate anatomy of urinary stone

Chemistry

Creatinine Evaluate kidney function

BUN Evaluate presence of dehydration and

Electrolytes electrolyte imbalances

Calcium, PTH Diagnose hyperparathyroidism

CBC Evaluate presence of infection

Renal ultrasound Evaluate presence of stone

Evaluate urinary tract obstruction

Cystoscopy Evaluate for bladder stones

CT scan (non-contrast) Same as IVP

Abdominal X-rays Evaluate size, shape, and stone location

Table 5.Stone Management Guidelines

Sources: Tanagho & McAninch, 2004; Wolf, 2004

� Depends on size and location of the stone

� Presence or absence of associated infection

� Presence of one or two kidneys

� Degree of symptoms

� Majority will pass spontaneously with no residual damage

� Stones <4 mm pass spontaneously in approximately 90% of patients

� Stones 4-6 mm pass in approximately 50% of patients

� Stones >6 mm pass without intervention in 20% of patients

� Stones >8 mm will pass in only 20% of patients and usually requiresurgical intervention

� If obstruction and infection present, emergent decompression ofupper urinary collecting system (kidneys and upper ureter) required


servative recommendations shouldbe made for all patients regardlessof the underlying etiology of theirstone disease. Patients should beinstructed to increase their fluidintake in order to maintain a urineoutput of at least 2,000 ml/day.Patients should also limit theirdietary oxalate and sodium intake,thereby decreasing the urinary

excretion of oxalate and calcium. Arestriction of animal proteins isencouraged for patients with“purine gluttony” and hyperurico-suria.

Hypercalciuria (General) Besides treating underlying

disease, management of hypercal-ciuria includes:

• Low calcium diet (about 400mg calcium).

• Distilled water, if high calci-um content in water supply.

• Limit vitamin C (<0.5g/day).• High sodium intake.• Thiazide diuretics.• Cellulose phosphate.• Orthophosphate.

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Table 6.Selected Medical Management of Urinary Stones

Calcium Oxalate

Calcium Phosphate

Uric Acid Stones

Cystine Stones

Struvite Stones

Drug

Thiazides

Potassium citrate

Sodium citrate

Orthophosphate

Cellulose sodiumphosphate

Calcium carbonate/citrate

Cholestyramine

Potassium citrate

Sodium citrate

Citric acid

Potassium citrate

Sodium bicarbonate

Allopurinol

Penicillamine

Captopril

Tiopronin

Sodium bicarbonate

Acetohydroxamicacid

Dosage

25 mg qd

20-60mEq in 3-4 divided doses daily

2-3 g after meals and HS

1-2.5gm/day in divided doses

5 gms TID

1 gm 4-5x/day

2-4 g/packet/day

20-60 mEq in 3-4divided doses daily

2-3 m unit doses

After each meal and HS

60 mEq in 3-4 divided doses daily

325 mg-2 gm qid or 48 mEq

300 mg/day

300 mg TID

25 mg qd

800-1,000 mg/dayin divided doses

325 mg-2 gm qid or 48 mEq

250 mg 3-4x/day

Side Effects

Hypokalemia, frequent urination, sexual dysfunction

Abdominal discomfort, N/V/D

GI upset and hyperkalemia

Gas, diarrhea

Dyspepsia, loose bowel movements

Constipation, gas, increase calcium leak, nausea

Constipation, abdominal pain, gas, GI upset


GI upset and hyperkalemia


CHF, cirrhosis, possible increase calcium-typestones

Rash, diarrhea, increase liver enzymes, nausea

Rash, kidney damage, N/V/D, tinnitus, loss oftaste

Proteinuria, rash, hypotension, cough dizziness

Jaundice, kidney damage, decreased RBCs inbone marrow

CHF, cirrhosis, possibly increase in calcium-type stones

Headache, depression, N/V/D, DVT, hemolyticanemia, sweating

N/V/D = nausea, vomiting, diarrhea; DVT= deep vein thrombosis


Absorptive Hypercalciuria –Type I

Thiazides are commonly usedfor the management of absorptivehypercalciuria Type I as thesemedications stimulate calciumreabsorption in the distal nephron,preventing formation of kidneystones by reducing the amount ofcalcium in the urine. Thiazidesforce a mandatory increase in uri-nary volume but can cause elec-trolyte disorders. Side effectsinclude decreased level of potassi-um, frequent urination, sexual dys-function, and increased triglyc-erides.

Less-common medicationsused for treatment includeorthophosphate, sodium cellulosephosphate, and urease inhibitors.Orthophosphate and sodium cel-lulose phosphate reduce theabsorption of calcium from theintestines thereby reducing calci-um in the urine. The ureaseinhibitors dissolve crystals andstruvite kidney stones and pre-vent formation of new crystals.Side effects can include a badtaste in the mouth, diarrhea, anddyspepsia.

Neither sodium cellulosephosphate nor thiazide correctsthe basic, underlying physiologi-cal defect in absorptive hypercal-ciuria. Sodium cellulose phos-phate should be used in patientswith severe absorptive hypercal-ciuria Type I (urinary calcium>350 mg/day) or in those resistantto or intolerant of thiazide thera-py. In patients with absorptivehypercalciuria Type I, who maybe at risk for bone disease (forexample, growing children andpost-menopausal women), orwho presently have bone loss,thiazide may be the medication offirst choice. Sodium cellulosephosphate may be substituted forshort-term therapy when thiazideaction is decreased.

Potassium supplementation(Urocit-K®, Polycitra-K® crystalorsyrup) should be added whenusing thiazide therapy to preventhypokalemia and decrease uri-

nary citrate excretion. A typicaltreatment program might includechlorthalidone 25 mg/day. Pot-assium citrate 15 to 20 mEqtwice/day should be providedwith both of these diuretics. Sideeffects include abdominal dis-comfort, nausea, and vomiting.

Absorptive Hypercalciuria –Type II

In absorptive hypercalciuriaType II, specific drug therapymay not be necessary since thephysiologic defect is not as severeas in absorptive hypercalciuriaType I. Many patients show dis-dain for drinking fluids andexcreting concentrated urine. Alow intake of calcium (400-600mg/day) and a high intake of fluids(sufficient to achieve a minimumurine output of >2 liters/day)would be acceptable treatment.Normal urine calcium excretionwould be restored by dietary cal-cium restriction alone, and theincrease in urine volume wouldhelp reduce urinary saturation ofcalcium oxalate.

Renal HypercalciuriaThiazides are indicated for

the treatment of renal hypercalci-uria. This diuretic can correct therenal leak of calcium by augment-ing calcium reabsorption in thedistal tubule and by causingextracellular volume depletionand stimulating proximal tubularreabsorption of calcium.

HyperoxaluriaOral administration of large

amounts of calcium (0.25 g to 1.0g four times/day) or magnesiumhas been recommended for con-trolling enteric hyperoxaluria. Ahigh fluid intake is recommendedto assure adequate urine volumein patients with enteric hyperox-aluria. Calcium citrate may theo-retically have a role in the man-agement of enteric hyperoxaluria.This treatment may lower urinaryoxalate by binding oxalate in theintestinal tract. Calcium citratemay also raise the urinary citrate

level and pH. Side effects are con-stipation, gas, and increased cal-cium leak. Cholestyramine is alsoanother method used to treat calci-um oxalate stones. Cholestyraminebinds to bile in the intestineswhich limits the amount ofoxalate absorbed from theintestines, therefore less oxalate isexcreted in the urine. Side effectsinclude constipation, abdominalpain, gas, and heartburn.

HyperuricosuriaAllopurinol (300 mg/day) is

the drug of choice in patientswith hyperuricosuric calciumoxalate nephrolithiasis (with orwithout hyperuricemia) becauseof its ability to reduce uric acidsynthesis and lower urinary uricacid by inhibition of the enzymexanthine oxidase. The usual doseis 300 mg/day; however, thedosage should be reduced inpatients with renal insufficiency.Side effects are rash, diarrhea,and increased liver enzymes.

Potassium citrate representsan alternative to allopurinol inthe treatment of this condition.Use of potassium citrate inhyperuricosuric calcium oxalatenephrolithiasis is warrantedsince citrate has an inhibitoryactivity with respect to calciumoxalate (and calcium phosphate)crystallization, aggregation, andagglomeration. Potassium citrate(30 to 60 mEq/day in divideddoses) may reduce the urinarysaturation of calcium oxalate.

HypocitraturiaFor patients with hypocitra-

turic calcium oxalate nephrolithi-asis, treatment with potassiumcitrate can restore normal urinarycitrate, thus lowering urinary sat-uration of calcium and inhibitingcrystallization of calcium salts.

Distal Renal TubularAcidosis

Potassium citrate therapy isable to correct metabolic acidosisand hypokalemia found inpatients with distal RTA. It will

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also restore normal urinary citratelevels, although large doses (up to120 mEq/day) may be requiredfor severe acidosis. Since urinarypH is generally elevated inpatients with RTA, the overallrise in urinary pH is small. Citrateis a significant urinary calciumstone inhibitor that retards crys-tallization of calcium oxalate andcalcium phosphate. Potassiumcitrate binds to calcium in theurine, preventing formation ofcrystals and raising the urinarycitrate level and pH. It will effec-tively alkalinize the urine, whichmakes it useful in the treatment,dissolution, and prevention ofuric acid stones. Urinary pHshould be monitored periodicallyduring citrate therapy because ofexcessive alkalinization. Sideeffects are mucous loose stoolsand minor GI complaints. Sodiumcitrate and citric acids are otheralkalizing agents used to preventkidney stones by inhibiting stoneformation through alkalization.

Chronic Diarrheal StatesPatients with chronic diar-

rhea frequently have hypocitra-turia due to bicarbonate loss fromthe intestinal tract. Potassium cit-rate therapy can significantlyreduce the stone formation rate inthese patients. The dose of potas-sium citrate is dependent on theseverity of hypocitraturia inthese patients. The dosage rangesfrom 60 to 120 mEq/day in threeto four divided doses.

Gouty DiathesisThe major objective in the

management of gouty diathesis isto increase the urinary pH above5.5, preferably to a level betweenpH 6.0 and 6.5. Potassium citrateis the drug of choice in managingpatients with gouty diathesis.Potassium citrate is an adequatealkalinizing agent, capable ofmaintaining urinary pH atapproximately 6.5 at a dose of 30to 60 mEq per day in two divideddoses.

CystinuriaThe objective for treatment of

cystinuria is to reduce the urinaryconcentration of cystine to a levelbelow its solubility limit (200-250mg/liter). The initial treatmentprogram includes a high fluidintake and oral administration ofsoluble alkali (potassium citrate)at a dose sufficient to maintain theurinary pH at 6.5 to 7.0. When thisconservative program is ineffec-tive, d-penicillamine or alpha-mercaptopropionylglycine (1,000to 2,000 mg/day in divided doses)has been used. Potassium citrateis absorbed to prevent uric acidstones as it binds to calcium inurine, preventing formation ofcrystals. Sodium bicarbonatemakes the urine less acidic, whichmakes uric acid or cystine kidneystone formation less likely.Possible side effects includeincreased formation of calcium-type stones, fluid retention, andsodium in blood. Urinary pHshould be monitored periodicallyduring citrate therapy becauseexcessive alkalinization mayoccur, which can increase the riskof calcium phosphate precipita-tion and stones. Side effects aremucous loose stools and minor GIcomplaints. Sodium citrate andcitric acid are other alkalizingagents used to prevent kidneystones by inhibiting stone forma-tion through alkalization.

Struvite (Infection) LithiasisAcetohydroxamic acid (AHA)

is a urease inhibitor that retardsstone formation by reducing theurinary saturation of struvite.When administered at a dose of250 mg three times/day, it mayprevent recurrence of new stonesand inhibit the growth of stonesin patients with chronic urea-splitting infections. In addition,in a limited number of patients,use of AHA has resulted in disso-lution of existing struvite calculi.Side effects that have developedare deep venous thrombosis,headache, hemolytic anemia,and depression.

Drug-InducedNephrolithiasis

Ephedrine calculi. There areno limited studies that addressthe management of these calculi.As with other calculi, a urineoutput of at least two liters/day isrecommended.

Guaifenesin calculi. As withephedrine calculi, there are nolimited studies regarding phar-macologic management of thesecalculi.

Indinavir calculi. Initial mea-sures in the management of thesecalculi should focus on hydra-tion and analgesia as well as drugdiscontinuation and substitutionwith another protease inhibitor.

Xanthine calculi. The med-ical management of xanthine cal-culi is limited because the solu-bility of these calculi is essential-ly invariable within physiologicpH ranges. Currently the recom-mendation includes a fluidintake of at least three liters/day.If significant quantities of otherpurines are present in the urine,then urinary alkalization withpotassium citrate in the range of6.0 to 6.5 is indicated to preventhypoxanthine or uric acid cal-culi.

NURSING MANAGEMENTThe nurse conducts a com-

prehensive nursing assessmentto include all contributing factorssuch as dietary history and fluidintake, family history, environ-mental factors, medical history(diabetes, hypertension, hyper-parathyroidism, inflammatorybowel disease, bowel resection,Crohn’s disease, UTIs), social his-tory, review of systems, and sur-gical history. Next, the nursecounsels the patient on pertinentfindings elicited during the com-prehensive nursing assessmentand provides followup counsel-ing to support dietary and life-style changes and monitor out-comes and compliance. In ourinstitution, a Kidney StoneDisease in Adults teaching pam-phlet is given to patients at the

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time that teaching is initiated(see Figure 5). Specific dietarymodification education includesencouraging reduced animal pro-tein intake for elevated urinarysulfate. See Table 7 for more rec-ommendations for patients withstones. Additional dietary rec-ommendations may be found inKrieg (2005), in this issue ofUrologic Nursing.

Nursing InterventionsThe nurse should:

• Perform pain assessments toinclude Visual Analog, nu-merical, or Wong-Baker scalesas appropriate for patientpopulation to assess level ofpain and effectiveness of out-come with pain interventions.

• Provide pharmacological edu-cation. Narcotics are usuallyused liberally, such as par-enteral (IM/IV) narcotics(ketorolac, [Toradol®], mepere-dine [Demerol®], morphine,and oral narcotics/analgesiccombinations (Department ofthe Navy Bureau of Medicineand Surgery, 2004). Use of nar-cotic medication needs to beexplained as well as sideeffects, such as nausea, vomit-ing, constipation, and cautionwith driving or operatingmachinery.

• Review bowel patterns andsuggest interventions to pre-vent constipation due to painmedication.

• Assess contributing factors of dehydration such as nau-sea, vomiting, and diarrheaand administer antiemetics,such as metoclopramine (Re-glan®), prochlorperazine (Com-pazine®), granisetron (Kytril®),or ondansetron (Zofran®).Administer antidiarrheal agentssuch as loperamide (Imo-dium®), diphenoxylate, atro-pine (Lomotil®), or paregoricand assess effectiveness of out-comes. If severe nausea andvomiting occur, patients mustbe aware that prevention ofdehydration and electrolyte

imbalance, may require IVhydration, prescription ofanti-emetics, and solutionssuch as such as Gatorade® orPedialyte® to replace elec-trolytes lost via the GI tract.

• Assess for vital signs check-ing for orthostatic hypoten-sion (lowering of blood pres-sure and increase in pulsewith positional changes) andmonitoring patient weights.

• Encourage increases in dailyfluid intake, especially water,and monitor outcomes ofinterventions through patientvoiding history and 24-hoururine reports. The most impor-tant lifestyle change to preventstones is drinking more fluids,especially water up to 2quarts/day.

• Educate the patient on com-pleting a voiding diary totrack daily urine output.

• Educate the patient on theimportance of completinglaboratory tests ordered,especially 24-hour urines.This can become an imposi-tion on the patient’s qualityof life, especially if he isactive and working.

• Educate the patient on col-lecting urine specimens andstraining urine.

• Educate the patient on diag-nostic testing, including re-quired dietary or bowel prep-aration to reduce anxiety.

• Educate the patient on the

importance of weight loss,maintaining weight loss, anddaily exercise.

• Provide counseling on healthpromotion and maintenance,stressing the importance offollowup care to evaluatecauses of stone formation inan effort to prevent futurerecurrences.

Preventative HealthMaintenance/LifestyleChanges

Effective kidney stone pre-vention depends upon the stonetype and identifying risk factorsfor stone formation. An individu-alized treatment plan incorporat-ing dietary changes, supple-ments, and medications can bedeveloped to help prevent theformation of new stones. If kid-ney stones develop despiteincreasing fluid intake and mak-ing changes to diet, medicationscan be prescribed to help dis-solve the stones or to prevent for-mation of new stones.

As a health care provider, itis imperative that causes of stoneformation be investigated to pre-vent future occurrences that maylead to permanent kidney dam-age. Patient education and coun-seling are vital to effective care,and can be provided by the uro-logic nurse to promote lifestylechanges in this patient popula-tion. Weight management is acritical factor in managing stone

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Table 7.Recommended Dietary Lifestyle Changes

Source: NIH, 2003

1. Increase water intake to ensure urine output of 2,000 ml.

2. Maintain adequate (1,000 mg) calcium intake from dietary sources.

3. Avoid calcium in pill form.

4. Avoid foods with added vitamin D (and vitamin C if recommended).

5. Avoid certain antacids with a calcium base.

6. Limit coffee, tea, and cola to 1-2 cups/day.

7. Eat less meat, fish, and poultry (decreased protein).

8. Limit dietary sodium and oxalate intake.


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Figure 5.Kidney Stone Disease in Adults

Hackensack University Medical CenterDepartment of Urology

Kidney Stone Disease in Adults

Overview

Kidney stones are one of the most painful disorders to afflict humans. This ancient healthproblem has tormented people throughout history. Scientists have even found evidence ofkidney stones in an Egyptian mummy estimated to be more than 7,000 years old.

Kidney stones are also one of the most common disorders of the urinary tract. It is estimatedthat 10 percent of all people in the United States will have a kidney stone at some point in time.Men tend to be affected more frequently than women.

Most kidney stones pass out of the body without any treatment by a doctor. Cases that causelasting symptoms or other complications may be treated by various techniques, most of whichdo not involve major surgery. Research advances also have led to a better understanding ofthe many factors that cause stones to form.

Introduction to the Urinary Tract

The urinary tract, or system,consists of the kidneys,ureters, bladder, and urethra. Among other importantfunctions, the kidneys removeextra water and waste fromthe blood, converting it tourine.

Narrow tubes called ureterscarry urine from the kidneysto the bladder, atriangle-shaped chamber inthe lower abdomen. Like aballoon, the bladder's elasticwalls stretch and expand tostore urine. They flattentogether when urine isemptied through the urethrato outside the body.

Copyright © iMedConsent Dialog Medical, LLC. All rights reserved. Used with permission by Hackensack UniversityMedical Center.


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Figure 5. (continued)Kidney Stone Disease in Adults

Kidney Stone Development

A kidney stone developsfrom crystals that separatefrom urine and build up onthe inner surfaces of thekidney. Normally, urinecontains chemicals thatkeep the crystals fromforming. These chemicalsdo not work for everyone,however, and some peopleform stones. If the crystalsremain tiny, they will travelthrough the urinary tractand pass out of the body inthe urine without evenbeing noticed.

Kidney stones may containvarious combinations ofchemicals. The mostcommon type of stone contains calcium in combination with either oxalate or phosphate. Thesechemicals are part of a person's normal diet and make up important parts of the body, such asbones and muscles.

A less common type of stone is caused by infection in the urinary tract. This type of stone iscalled a struvite, or infection stone. Much less common are the uric acid stone and the rarecystine stone.

Urolithiasis is the medical term used to describe stones occurring in the urinary tract. Otherfrequently used terms are urinary tract stone disease and nephrolithiasis. Doctors also useterms that describe the location of the stone in the urinary tract. For example, ureterolithiasisis a stone found in the ureter. To keep things simple, the term "kidney stones" is usedthroughout this entire document.

Gallstones and kidney stones are not related. They form in different areas of the body. If aperson has a gallstone, he or she is not necessarily more likely to develop kidney stones.

Cause

Doctors do not always know what causes a stone to form. While certain foods may promotestone formation in people who are more prone to them, scientists do not believe that eating anyspecific food causes stones to form in people who are not susceptible.

A person with a family history of kidney stones may be more likely to develop stones. Urinarytract infections, kidney disorders such as cystic kidney diseases, and metabolic disorders, suchas hyperparathyroidism, also are linked to stone formation.



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In addition, more than 70 percent of patients with a hereditary disease called renal tubularacidosis develop kidney stones.

Cystinuria and hyperoxaluria are two other rare, inherited metabolic disorders that oftencause kidney stones. In cystinuria, the kidneys produce too much of the amino acid cystine.Cystine does not dissolve in urine and can build up to form stones. With hyperoxaluria, thebody produces too much of the salt oxalate. When there is more oxalate than can be dissolvedin the urine, the crystals settle out and form stones.

Absorptive hypercalciuria occurs when the body absorbs too much calcium from food andempties the extra calcium into the urine. This high level of calcium in the urine causes crystalsof calcium oxalate or calcium phosphate to form in the urinary tract.

Other causes of kidney stones are hyperuricosuria, a disorder of uric acid metabolism, gout,excess intake of vitamin D, and blockage of the urinary tact. Certain diuretics, or water pills, orcalcium-based antacids may increase the risk of forming kidney stones by increasing theamount of calcium in the urine.

Calcium oxalate stones may also form in people who have a chronic inflammation of the bowelor who have had ostomy, or intestinal bypass, surgery. As mentioned above, struvite stonescan form in people who have had a urinary tract infection.

At-Risk Groups

For some unknown reason, the number of people in the United States with kidney stones hasbeen increasing over the past 20 years. White people are more prone to kidney stones thanare African Americans. Although stones occur more frequently in men, the number of womenwho get kidney stones has been increasing over the past 10 years, causing the ratio to change.Kidney stones strike most people between the ages of 20 and 40. Once a person gets morethan one stone, he or she is more likely to develop others.

Symptoms

Usually, the first symptom of a kidney stone is extreme pain. The pain begins suddenly when astone moves in the urinary tract, causing irritation or blockage. Typically, a person feels asharp, cramping pain in the back and side in the area of the kidney, in the lower abdomen, orgroin. Additional symptoms of kidney stones include:

� Nausea and vomiting.� Blood in the urine.� Frequent need to urinate.� Burning during urination.

If fever and chills accompany any of these symptoms, an infection may be present and yourdoctor should be contacted immediately.



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Diagnosis

Sometimes "silent" stones -- those that do not cause symptoms -- are found on x-rays takenduring a general health exam. These stones would likely pass unnoticed.

More often, kidney stones are found on an X-ray, CT scan, or sonogram taken on someonewho complains of blood in the urine or sudden pain. These diagnostic images give the doctorvaluable information about the stone's size and location. Blood and urine tests help detect anyabnormal substance that might make stones form.

The doctor may decide toscan the urinary systemusing a special x-ray testcalled an intravenouspyelogram, or IVP, or CTscan.

Together, the results fromthese tests help determinethe proper treatment. IVPx-rays will miss somestones. CT scan will oftencall things stones that arenot.

Occasionally, a patient willneed both an IVP and CTscan or a repeat of the firsttest to confirm the presenceof stones.

Treatment

Fortunately, most stones can pass through the urinary system with plenty of water - two to threequarts a day - to help move them along. In most cases, a person can stay home during thisprocess, taking pain medicine as needed. The doctor usually asks the patient to save thepassed stone or stones for testing.

Some type of surgery may be needed to remove a kidney stone if the stone does not pass aftera reasonable period of time and causes constant pain, is too large to pass on its own, blocksthe urine flow, or causes ongoing urinary tract infection.

Surgery may also be required if damage is done to the kidney tissue, or if the stone causesconstant bleeding or has grown larger (as shown on follow up X-ray studies).

Until recently, surgery to remove a stone was very painful and required a recovery time of fourto six weeks. Today, treatment for these stones is greatly improved. Many options exist that donot require major surgery.



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Extracorporealshockwave lithotripsy(ESWL) is the mostfrequently used surgicalprocedure for thetreatment of kidneystones. ESWL usesshock waves that arecreated outside of thebody to travel through theskin and body tissues untilthe waves hit the densestones. The stonesbecome sand-like and areeasily passed through theurinary tract in the urine.

There are several types ofESWL devices. Onedevice positions thepatient in the water bath while the shock waves are transmitted. Other devices have a softcushion or membrane on which the patient lies. Most devices use either x-rays or ultrasound tohelp the surgeon pinpoint the stone during treatment. For most types of ESWL procedures,some type of anesthesia is needed.

In some cases, ESWL may be done on an outpatient basis. Recovery time is short, and mostpeople can resume normal activities in a few days.

Complications may occur with ESWL. Most patients have blood in the urine for a few days aftertreatment. Bruising and minor discomfort on the back or abdomen due to the shock waves arealso common. To reduce the chances of complications, doctors usually tell patients to avoidtaking aspirin and other drugs that affect blood clotting for several weeks before treatment.

In addition, the shattered stone fragments may cause discomfort as they pass through theurinary tract in the urine. In some cases, the doctor will insert a small tube called a stentthrough the bladder into the ureter to help the fragments pass. Sometimes the stone is notcompletely shattered with one treatment and additional treatments may be required.

Sometimes a procedure called percutaneous nephrolithotomy is recommended to remove astone. This treatment is often used when the stone is quite large or in a location that does notallow effective use of EWSL.

In this procedure, the surgeon makes a tiny incision, or opening, in the back and creates atunnel directly into the kidney. Using an instrument called a nephroscope, the stone is locatedand removed. For large stones, some type of energy probe may be needed to break the stoneinto small pieces. Generally, patients stay in the hospital for several days and may have asmall tube called a nephrostomy tube left in the kidney during the healing process.

One advantage of percutaneous nephrolithotomy over ESWL is that the surgeon removes thestone fragments instead of relying on their natural passage from the kidney.



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Although some ureteral stones can be treated with ESWL, ureteroscopy may be needed formiddle and lower ureter stones. No incision is made in this procedure. Instead, the surgeonpasses a small instrument called a ureteroscope through the urethra and bladder into theureter. The surgeon then locates the stone and either removes it with a cage-like device orshatters it with a special instrument that produces a form of shock wave (EHL) or with a laserdevice. A small stent may be left in the ureter for a few days after treatment to help the lining ofthe ureter heal.

Prevention

People who have had more than one kidney stone are likely to form another. Therefore,prevention is very important. To prevent stones from forming, their cause must be determined.The urologist will order laboratory tests, including urine and blood tests. A complete medicalhistory will be taken, along with information about the patient's work and eating habits. If astone has been removed, or if the patient has passed a stone and saved it, the lab can analyzethe stone to find out its chemical make-up.

A patient may be asked to collect urine for 24 hours after a stone has passed or been removed.The sample is used to measure urine volume and levels of acidity, calcium, sodium, uric acid,oxalate, citrate, and creatinine, a byproduct of how the body uses protein. The doctor will usethis information to determine the cause of the stone. A second 24-hour urine collection may beneeded to see if the prescribed treatment is working.

Lifestyle Changes

The most important lifestyle change to prevent stones is to drink more liquids -- water is best.Someone who has had stones before should try to drink enough liquids throughout the day toproduce at least two quarts of urine in every 24-hour period.

Patients with too much calcium or oxalate in the urine may need to eat fewer foods containingcalcium and oxalate. Not everyone will benefit from a low-calcium diet, however. Somepatients who have high levels of oxalate in their urine may benefit from extra calcium in theirdiet. Patients may be told to avoid food with added vitamin D and certain types of antacids thathave a calcium base.

Patients who have a very high level of acid in their urine may need to eat less meat, fish, andpoultry. These foods increase the amount of acid in the urine.

To prevent cystine stones, patients should drink enough water each day to reduce the amountof cystine that escapes into the urine. This is difficult because more than a gallon of water maybe needed every 24 hours, a third of which must be drunk during the night.

Medication

The doctor may prescribe certain medications to prevent calcium and uric acid stones. Thesedrugs control the amount of acid or alkali in the urine, key factors in crystal formation. The drugAllopurinol may also be useful in some cases of hypercalciuria and hyperuricosuria.



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Another way a doctor may try to control hypercalciuria, and thus prevent calcium stones, is byprescribing certain diuretics, such as Hydrochlorothiazide. These drugs decrease the amountof calcium released by the kidneys into the urine.

Some patients with absorptive hypercalciuria may be given the drug Sodium cellulosephosphate. This drug keeps calcium from leaking into the urine.

If cystine stones cannot be controlled by drinking more fluids, the doctor may prescribe the drugThiola. This medication helps reduce the amount of cystine in the urine.

For struvite stones that have been totally removed, the first line of prevention is to keep theurine free of bacteria that can cause infection. The patient's urine will be tested on a regularbasis to be sure that bacteria are not present.

If struvite stones cannot be removed the doctor may prescribe a new drug calledAetohydroxamic acid (AHA). AHA is used along with long-term antibiotic drugs to prevent theinfection that leads to stone growth.

Surgery

To prevent calcium stones that form in hyperparathyroid patients, a surgeon may remove all ofthe parathyroid glands (located in the neck). This is usually the treatment forhyperparathyroidism as well. In most cases, only one of the glands is enlarged. Removing thegland ends the patient's problem with kidney stones.

Research on Kidney Stones

The Division of Kidney, Urologic, and Hematologic Diseases of the National Institutes ofDiabetes and Digestive and Kidney Diseases (NIDDK) funds research on the causes,treatments, and prevention of kidney stones. The NIDDK is part of the federal government'sNational Institutes of Health.

New drugs and the growing field of lithotripsy have greatly improved the treatment of kidneystones. Still, NIDDK researchers and grantees seek to answer questions such as:

� Why do some people continue to have painful stones?� How can doctors predict who is as risk for getting stones?� What are the long-term effects of stones?



formation and prevention offuture occurrences as evidencedby a study at Brigham andWomen’s Hospital, Boston(Guttman, 2005). Researchersevaluated the correlation of obesi-ty and weight gain and the risk ofdeveloping kidney stones. Thefindings indicated obesity was acontributing factor in stone devel-opment since, as we age, themajority of weight gain is from fattissue not bone or muscle. Therisk of developing stonesincreased by 71% to 109%among younger and older womenin the highest weight, BMI, andwaist circumference and 33% to48% in men. These findings sup-port the need for health careproviders to emphasize theimportance of exercise andweight management in a preven-tion program. Dietary recommen-dations for stone formers are dis-cussed in detail by Krieg (2005).

ConclusionWith appropriate diagnosis

and treatment of specific disor-ders resulting in nephrolithiasis,a remission rate greater than 80%can be obtained (see Table 8). Inpatients with mild to moderateseverity of stone disease, virtual-ly total control of stone diseasecan be achieved with a remissionrate greater than 95% (Preminger,Harvey, & Pak, 1985). The needfor surgical stone removal may bereduced dramatically or elimi-nated with an effective prophy-lactic program. Selective phar-macologic therapy also has theadvantage of overcoming nonre-nal complications and avertingcertain side effects that may occurwith nonselective medical thera-py. It is clear that selective medicaltherapy alone cannot provide totalcontrol of stone disease. A satis-factory response requires contin-ued dedicated compliance by

patients to the recommended pro-gram and a commitment of thephysician to provide long-termfollowup and care with the inten-tion of improving quality of life byeliminating the symptoms causedby urinary tract stones.

ReferencesBernier, F. (2005). Management of clients

with urinary disorders. In J. Black &J. Hawks (Eds.), Medical- surgicalnursing: Clinical management forpositive outcomes (7th ed.) (pp. 857-911). St. Louis: Elsevier.

Billica, W. (2004). Urolithiasis. RetrievedJune 14, 2004, from http://www:5ncc.com/Assets/Summary/TP0970.html

Blau, J.J. (1998). Ephedrine nephrolithiasisassociated with chronic ephedrineabuse. Journal of Urology, 160, 825.

Danpure, C.J. (1994). Molecular and cellbiology of primary hyperoxaluriatype I. Clinical and InvestigativeMedicine – Medecine Clinicque EtExperimentale, 72, 725-727.

Department of the Navy Bureau ofMedicine and Surgery. (2004).Virtual naval hospital: General med-ical officer manual: Clinical section.

•

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For more information, contact:

National Kidney and Urologic Diseases Information Clearinghouse (NKUDIC)3 Information WayBethesda, MD 20892-3580kidney.niddk.nih.gov(301) 654-4415

National Kidney Foundation30 East 33rd StreetNew York, NY 10016www.kidney.org(800) 622-9010

Copyright © 2004 by iMedConsent Dialog Medical, LLC. All rights reserved.



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Table 8. Quick Reference

Type of Stone Cause Clinical Findings

Absorptive HypercalciuriaType I

Type II

Increased absorption of calcium,unknown

(high or low dietary calcium intake)

Excess calcium intakeExcess vitamin D intake

High urine calcium levelNormal serum calciumNormal serum phosphorusNormal of low serum parathyroid

hormone

Normal urine calcium

Renal HypercalcuriaDecreased renal absorption

Increased bone absorption

Impaired renal tubular re-absorptionof calcium →→ decreased urine calcium → increased intestinal calciumabsorption → PTH stimulation

Excess parathyroid hormone,increased ↑ bone resorption ofcalcium

Elevated 1, 25-vitamin D3

Increased 1, 25-vitamin D3Increased bone demineralizationIncreased parathyroid hormone and

↑ serum calcium

HyperoxaluriaPrimary Type I

Type II

Autosomal recessive disorderDefect in hepatic enzyme alanine-

glyoxylate Aminotransferase (AGT)

RareDeficiency of hepatic enzymes

D-glycerate dehydrogenase and glyoxylate reductase

Increased urine levels of oxalic, glycolic, and glyoxylic acid

Oxalate tissue depositsRenal failure

Increased urine level of oxalate andglycerate excretion

NephrocalcinosisTubular interstitial neuropathyChronic renal failure

Secondary DietaryHyperoxaluria

Excess dietary intake oxalate foodsExcess intake ascorbic acid

(vitamin C)

Increased urine oxalate

Enteric Hyperoxaluria Intestinal malabsorption (distalcolon)

Excess oxalate absorptionChronic diarrheal statesBowel surgery

Decreased urine citrateHypokalemiaMetabolic acidosisDecreased urine volumeDecreased potassiumDecreased magnesium

Hyperuricosuria Increased uric acid levelsExcess uric acid excretion Excess purine dietGenetic predispositionPurine overproduction

Acute leukemiaMalignancyGlycogen storage disease

Normal serum calcium Normal urinary calciumNormal urinary oxalateNormal fasting and calcium load

responseAcidic urineIncrease urine uric acid

Hypocitraturia Disruption of acid base balanceIncreased acid levelsDecreased endogenous citrate

production

Decreased urine citrate


Retrieved June 14, 2004, fromhttp://www.vnh.org/gmo/ClinicalSection/106Urolithiasis.html

Guttman, C. (2005). Healthy weightreduces risk of kidney stones.Urology Times, 1, 20.

Katz, D.S., Lane, M.J., & Sommer, F.G.(1996). Unenhanced helical CT ofureteral stones: Incidence of associ-ated urinary tract findings.American Journal of Roentgenology,166, 1319-1322.

Khatchadourian, J., Preminger, G.M.,Whitson, P.A., Adams-Huet, B., &Pak, C.Y. (1995). Clinical and bio-chemical presentation of goutydiathesis: Comparison of uric acidversus pure calcium stone forma-tion. Journal of Urology, 154, 1665-1669.

Krieg, C. (2005). The role of diet in theprevention of common kidneystones. Urologic Nursing, 25(6), 451-456.

Levy, F.L., Adams-Huet, B., & Pak, C.Y.(1995). Ambulatory evaluation ofnephrolithiasis: An update of a 1980protocol. American Journal ofMedicine, 98, 50-59.

Lingeman, J.E., Siegel, Y.I., & Steele, B.(1995). Metabolic evaluation of infect-ed renal lithiasis: Clinical relevance.Journal of Endourology, 9, 51-54.

Menon, M., & Mahle, C.J. (1982). Oxalatemetabolism and renal calculi.Journal of Urology, 127(1), 148-151.

Menon, M., & Resnick, M.I. (2002).Urinary lithiasis: Etiology, diagno-sis, and medical management. InE.S. Campbell (Ed.), Campbell’surology (8th ed.) (pp. 3229-3305).Philadelphia: W.B. Saunders.

Moe, O.W., Abate, N., & Sakhaee, K.(2002). Pathophysiology of uric acidnephrolithiasis. Endocrinology andMetabiology Clinics of NorthAmerica, 31(4), 895-914.

Munver, R., & Preminger, G. (2001).Urinary tract stones in comprehen-sive urology. St. Louis: Mosby.

National Institutes of Health. (1998-2005). NIH consensus statements: 67prevention and treatment of kidneystones. Retrieved February 9, 2005,from http://www.urologychannel.com/kidneystones/index.shtml

National Institute of Health Publications.(2003, April). National Kidney andUrologic Diseases Clearinghouse(No. 03-2495). Retrieved June 14,2005, from http://kidney.niddk.nih.gov/kudiseases/pubs/stone-sadults/index.htm

Nicar, M.J., Peterson, R., & Pak, C.Y. (1984).Use of potassium citrate as potassiumsupplement during thiazide therapyof calcium nephrolithiasis. Journal ofUrology, 131, 430-433.

Pak, C.Y. (1994). Citrate and renal calculi:An update. Mineral & ElectrolyteMetabolism, 20, 371-377.

Pak, C.Y. (1987). Citrate and renal calculi.

Mineral & Electrolyte Metabolism,13, 257-266.

Pak, C.Y. (1982). Medical management ofnephrolithiasis. Journal of Urology,128, 1157-1164.

Pak, C.Y. (1979). Physiological basis forabsorptive and renal hypercalciurias.American Journal of Physiology, 237,F415-F423.

Pak, C.Y., Sakhaee, K., Crowther, C., &Brinkley L. (1980). Evidence justifyinga high fluid intake in treatment ofnephrolithiasis. Annals of InternalMedicine, 93, 36-39.

Powell, T., Hsu, F.F., Turk, J., & Hruska, K.(1998). Ma-huang strikes again:Ephedrine nephrolithiasis. AmericanJournal of Kidney Diseases, 32, 153-159.

Preminger, G.M., Harvey, J.A., & Pak, C.Y.(1985). Comparative efficacy of “spe-cific” potassium citrate therapy ver-sus conservative management innephrolithiasis of mild to moderateseverity. Journal of Urology, 134,658-661.

Preminger, G.M., Peterson, R., Peters, P.C.,& Pak, C.Y. (1985). The current role ofmedical treatment of nephrolithiasis:The impact of improved techniques ofstone removal. Journal of Urology,134, 6-10.

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Table 8. (continued)Quick Reference

Type of Stone Cause Clinical Findings

Hypomagnesuria Low magnesium prevents inhibitionof solubility product of calciumoxalate and calcium phosphate

Low urine magnesium excretion<50 mg/day

Uric Acid Purine overproductionUric acid precipitation

Acidic urineLow urine volume

Cystine RareCongenital conditionLarge amounts of cystine in urine

Positive sodium-nitroprussideFlat, hexagonal crystals in urine

sediment

Struvite UTIs-urea-splitting bacteria (Proteus,Klebsiella, Pseudomonas)

Neurogenic bladderDiverticuliStricturesDrugs

SulfurSalicylatesTriamterene ephedrine

Bacteria in urine and culture andsensitivity

Increased WBCs in urinalysis

Xanthine RareHereditary deficiency in xanthine

oxidase

Decreased level serum uric acidDecreased level urine uric acidAcidic urine

continued on page 475


Preminger, G.M., Sakhaee, K., Skurla, C., & Pak, C.Y. (1985).Prevention of recurrent calcium stone formation with potassi-um citrate therapy in patients with distal renal tubular acido-sis. Journal of Urology, 134, 20-23.

Ramello, A., Vitale, C., & Marangella, M. (2000). Epidemiology ofnephrolithiasis. Journal of Nephrology, 13(Suppl. 3), S45-50.

Rudman, D., Dedonis, J.L., Fountain, M.T., Chandler, J.B., Gerron,G.G., Fleming, G.A., et al. (1980). Hypocitraturia in patientswith gastrointestinal malabsorption. New England Journal ofMedicine, 303(12), 657-661.

Schwartz, B.F., Schenkman, N., Armenakas, N.A., & Stoller, M.L.(1999). Imaging characteristics of indinavir calculi. Journal ofUrology, 161(4), 1085-1087.

Smith, R.C., Rosenfield, A.T., Choe, K.A., Essenmacher, K.R.,Verga, M., Glickman, M.G., et al. (1995). Acute flank pain:Comparison of non-contrast-enhanced CT and intravenousurography. Radiology, 194, 789-794.

Smith, R.C., Verga, M., Dalrymple, N., McCarthy, S., & Rosenfield,A.T. (1996). Acute ureteral obstruction: Value of secondarysigns of helical unenhanced CT. American Journal ofRoentgenology, 168, 1109-1113.

Spirnak, J.P., & Resnick, M.I. (1987). Retrograde percutaneousstone removal using modified Lawson technique. Urology,30(6), 551-553.

Tanagho, E.A., & McAninch, J.W. (2004). Smith’s general urology(16th ed). Norwalk, CT: Appleton & Lange.

Urology Channel. (1998). Kidney stones. Retrieved February 9,2005, from http://www.urologychannel.com/kidneystones/index.shtml

Wolf, J.S. (2004). Nephrolithiasis. Retrieved November 15, 2005,from http://www.emedicine.com/MED/topic1600.htm

Additional ReadingsBusby, J., & Low, R.K. (2004). Ureteroscopic treatment of renal cal-

culi. Urologic Clinics of North America, 31, 1-10.Jeong, H., Kwak, C., & Lee, S.E. (2004). Ureteric stenting after

ureteroscopy for ureteric stones: A prospective randomizedstudy assessing symptoms and complications. BJUInternational, 93(7), 1032-1035.

Merck Manual of Diagnosis and Therapy. Genitourinary disor-ders (stones/nephrolithiasis/urolithiasis). Retrieved June 14,2004, from http://www.merck.com/mrkshared/mmanual/section17/chapter 221/221a.jsp

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