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C Urolithiasis/Nephrolithiasis: O N What’s It All About? T I Joan Colella Bernadette Galli N Eileen Kochis Ravi Munver U I N G he term nephrolithiasis Urolithiasis (urinary tract calculi or stones) and nephrolithiasis (kid- ( calculi or stones) ney calculi or stones) are well-documented common occurrences in refers to the entire clini- the general population of the . The etiology of this disor- E cal picture of the forma- der is mutifactorial and is strongly related to dietary lifestyle habits or D Ttion and passage of crystal agglom- practices. Proper management of calculi that occur along the urinary U erates called calculi or stones in tract includes investigation into causative factors in an effort to pre- the urinary tract (Wolf, 2004). vent recurrences. Urinary calculi or stones are the most common C Urolithiasis (urinary calculi or cause of acute ureteral obstruction. Approximately 1 in 1,000 adults in A stones) refers to that the United States are hospitalized annually for treatment of urinary T form in the , pri- tract stones, resulting in medical costs of approximately $2 billion per marily in the kidney (nephrolithi- I year (Ramello, Vitale, & Marangella, 2000; Tanagho & McAninch, 2004). asis) or (ureterolithiasis), O and may also form in or migrate N into the lower urinary system (bladder or ) (Bernier, 2005). Urinary tract stone the rest of the world. Researchers Kidney stones are most has been documented historically attribute the of prevalent between the ages of 20 as far back as the Egyptian mum- nephrolithiasis in the United to 40, and a substantial number mies (Wolf, 2004). States to a dietary preference of of patients report onset of the dis- foods high in animal ease prior to the age of 20 Prevalence (Billica, 2004). (Munver & Preminger, 2001; Pak, 1979, 1987). The lifetime risk for As much as 10% of the U.S. Age and Gender population will develop a kid- kidney stone formation in the ney stone in their lifetime. The literature reflects the adult white male approaches Upper urinary tract stones (kid- incidence of kidney (renal) stone 20% and approximately 5% to ney, upper ureter) are more com- formation to be greater among 10% for women. The recurrence mon in the United States than in white males than black males rate for kidney stones is approxi- and three times greater in males mately 15% in year 1 and as high than females. Although kidney as 50% within 5 years of the ini- stone disease is one-fourth to tial stone (Munver & Preminger, Joan Colella, MSN, MPA, RN, APRN- one-third more prevalent in adult 2001; Spirnak & Resnick, 1987). BC, NP-C, is an Advanced Practice white males, black males demon- Nurse, The Prostate Institute of The PATHOPHYSIOLOGY OF Cancer Center at Hackensack strate a higher incidence of University Medical Center, Hackensack, stones associated with urinary NEPHROLITHIASIS NJ. tract infections caused by - Any factor that reduces uri- splitting (Munver & nary flow or causes obstruction, Eileen Kochis, RN, is a Staff Nurse, Preminger, 2001). which results in urinary stasis or the Department of , The Cancer Center at Hackensack University Medical Center, Hackensack, NJ. Ravi Munver, MD, is Chief, Minimally Invasive Urologic Surgery, the Department of Bernadette Galli, MSN, RN, APRN- Urology, The Cancer Center at Hackensack University Medical Center, Hackensack, BC, NP-C, is an Advanced Practice NJ; an Assistant Professor of Surgery/Urology, UMDNJ-New Jersey Medical School, Nurse, the Department of Urology, The Newark, NJ; and an Adjunct Assistant Professor of Urology, Weill Medical College of Cancer Center at Hackensack Cornell University, New York, NY. University Medical Center, Hackensack, NJ. Note: CE Objectives and Evaluation Form appear on page 449.

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C Table 1. Figure 1. O Factors Contributing to Stone Development Stone N H Congenital kidney defects (medullary sponge disease) T H Excess I H Medications (ephedrine, , , ) N H U H I H Colitis, inflammation of colon, and chronic diarrheal states N H Irritable bowel disease or intestinal surgery G H Photo courtesy of Louis C. Herring H Crohn’s disease results in and low citrate. & Co. E H (skeletal disease) Figure 2. D H Urinary tract infections Stone U H Past medical history of kidney stones C H and high A H Prolonged inactivity T H Anatomic factors – Ureteropelvic junction (UPJ) obstruction I H Horseshoe or ectopic kidney O H Autosomal dominant polycystic H N H Calyceal diverticula Photo courtesy of Louis C. Herring Source: Tanagho & McAninch, 2004 & Co.

reduces volume through Ethnic background. Stones ease, which may include chronic dehydration and inadequate are rare in Native Americans, diarrheal states, ileal disease, or fluid intake, increases the risk of Africans, American Blacks, and prior intestinal resection, may be developing kidney stones. Low Israelis (Menon & Resnick, 2002). a predisposition to enteric hyper- urinary flow is the most common Family history. Patients with oxaluria or hypocitraturia. This abnormality, and most important a family history of stone forma- may result in calcium oxalate factor to correct with kidney tion may produce excess amounts nephrolithiasis because of dehy- stones. It is important for health of a mucoprotein in the kidney or dration and chemical imbalances practitioners to concentrate on bladder allowing crystallites to be (see Figure 1). Irritable bowel dis- interventions for correcting low deposited and trapped forming ease or intestinal surgery may urinary volume in an effort to calculi or stones. Twenty-five per- prevent the normal absorption of prevent recurrent stone disease cent of stone-formers have a fami- fat from the intestines and alter (Munver & Preminger, 2001; Pak, ly history of urolithiasis. Familial the manner in which the Sakhaee, Crowther, & Brinkley, etiologies include absorptive intestines process calcium or 1980). , , renal oxalate. This may also lead to tubular acidosis, and primary hyper- calculi or stone formation. Contributing Factors oxaluria (Munver & Preminger, Patients with gout may form Of Nephrolithiasis 2001). either uric acid stones (see Figure Sex. Males tend to have a Medical history. Past medical 2) or calcium oxalate stones. three times higher incidence of history may provide vital infor- Patients with a history of urinary kidney stones than females. mation about the underlying eti- tract infections (UTIs) may be Women typically excrete more cit- ology of a stone’s formation (see prone to infection nephrolithia- rate and less calcium than men, Table 1). A positive medical his- sis caused by urea-splitting bac- which may partially explain the tory of skeletal fracture(s) and teria (Munver & Preminger, higher incidence of stone disease peptic ulcer disease suggests a 2001). Cystinuria is a homozy- in men (National Institutes of diagnosis of primary hyper- gous recessive disease leading to Health [NIH], 1998-2005). parathyroidism. Intestinal dis- stone formation. Renal tubular

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Figure 3. such as ephedrine, guaifenesin, sels will produce spasms with C Stone , indinavir, and allopuri- intermittent, sharp, colicky pain O nol may be contributory factors in radiating to the lateral flank and the development of calculi (see around the umbilical region. N Drug-Induced Nephrolithiasis). As a stone passes through the T Occupations. Occupations in distal ureter, near the bladder, the I which fluid intake is limited or pain remains sharp but with a wax- restricted or those associated ing and waning quality. Relief is N with fluid loss may be at greater offered when the spasm subsides or U risk for stone development as a the pain may intensify and radiate I result of decreased urinary vol- to the groin, testicles, or labia. ume. , vomiting, diaphoresis, N Photo courtesy of Louis C. Herring tachycardia, and tachypnea may be G & Co. CLINICAL PRESENTATION present and patients are typically Symptoms may vary and uncomfortable. depend on the location and size E acidosis is a familial disorder of the kidney stones or calculi Symptoms D that causes kidney stones in most within the urinary collecting sys- Once a stone enters the blad- U patients who have this disorder. tem. In general, symptoms may der, , urgency, and frequen- C Dietary habits. Fluid restric- include acute renal or ureteral cy may be the only symptoms tion or dehydration may cause , (microscopic or experienced. Immediate relief of A kidney stone formation. Dietary gross blood in the urine), urinary symptoms occurs once the stone T intake that is high in , tract infection, or vague abdomi- passes out of the bladder. oxalate, fat, protein, , unre- nal or flank pain. A thorough his- I fined carbohydrates, and ascor- tory and physical examination, Kidney Stone Complications O bic acid () has been along with selected laboratory Occasionally, stones can N linked to stone formation. Low and radiologic studies, are essen- injure the kidneys by causing intake of citrus fruits can result tial to making the correct diagno- infection, resulting in fever, in hypocitraturia, which may sis. Small nonobstructing stones chills, and loss of appetite or uri- increase an individual’s risk for or “silent stones” located in the nary obstruction. If a UTI accom- developing stones. calyces of the kidney are some- panies the urinary obstruction, Environmental factors. Fluid times found incidentally on x- or urosepsis can intake consisting of drinking rays or may be present with occur. If stones are bilateral, they water high in may con- asymptomatic hematuria. Such can cause renal scarring and tribute to kidney stone develop- stones often pass without caus- damage, resulting in acute or ment. Another contributing fac- ing pain or discomfort. chronic renal failure. tor may be related to geographi- cal variables such as tropical cli- Kidney Stone Symptoms CALCIUM mates (NIH, 1998-2005). Stone for- Stones in the kidneys can NEPHROLITHIASIS mation is greater in mountainous, become lodged at the junction of high-desert areas that are found in the kidney and ureter (uretero- Hypercalciuria the United States, British Isles, pelvic junction), resulting in acute Eighty to eighty-five percent Scandinavia, Mediterranean, Nor- ureteral obstruction with severe of calculi or stones diagnosed in thern India, Pakistan, Northern intermittent colicky flank pain. the United States are idiopathic Australia, Central Europe, Malayan Pain can be localized at the cos- (spontaneous and without recog- Peninsula, and China (Menon & tovertebral angle. Hematuria may nizable cause) or primary. These Resnick, 2002). Affluent societies be present intermittently or per- stones are comprised of calcium have a higher rate of small upper sistently and it may be microscop- and are due to excess calcium tract stones whereas large stru- ic or gross. excretion in the urine, usually vite (infection) stones occur more exceeding 200 mg/24-hour col- commonly in developing coun- Ureteral Stone Symptoms lection (see Table 2). tries (see Figure 3). Bladder Stones that can pass into the Absorptive hypercalciuria. stones are more common in ureter may produce ureteral The primary abnormality in underserved countries and are colic, which is an acute, sharp, absorptive hypercalciuria is likely related to dietary habits spasm-like pain located in the increased absorption of calcium. and malnutrition (Menon & flank. Hematuria may be present. Absorptive hypercalciuria Type I Resnick, 2002). Stones moving down the ureter is more severe and characterized Medications. Medications to the pelvic brim and iliac ves- by a high urine calcium level,

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C Table 2. ic enzymes (D-glycerate dehy- O Causes of Calcium Stones drogenase and late reductase) resulting in increased urinary N H from any cause oxalate and glycerate excretion. T H Dehydration This results in the development I H Increased intestinal absorption of , tubulointer- stitial nephropathy, and chronic H N Increased calcium excretion renal failure. U H Excess oral (intoxication) Secondary I H Alkaline urine pH (dietary). Approximately 80% of urinary oxalate is synthesized H Diet high in calcium or oxalate N within the and a small per- G H Chronic bowel disease (intestinal disease) centage (20%) from dietary H Poor GI citrate absorption intake. Overindulgence of diets E H Sarcoidosis rich in can contribute to hyperoxaluria through intestinal D Source: Tanagho & McAninch, 2004 absorption of oxalate. This U includes foods such as , C green leafy vegetables, spinach, with high or low dietary calcium reveal elevated parathyroid hor- cocoa, beer, coffee or tea, or A intake. There is a normal mone and serum calcium levels. excess ascorbic acid (vitamin C) T level of calcium and phosphorus Less frequent causes of hyper- intake. I and normal or low serum level of calciuria include chronic immobi- Enteric hyperoxaluria. The parathyroid hormone. lization, metastatic cancer to bone, primary site of oxalate absorption O Absorptive hypercalciuria multiple myeloma, and vitamin D is the distal colon. Intestinal mal- N Type II is a mild to moderate intoxication. Calcium stones have absorption can cause excess form of hypercalciuria and less been described as appearing spic- oxalate absorption due to various severe than Type I. Type II hyper- ulated, dotted, mulberry, or jack- such as chronic diar- calciuria only occurs with high stone in appearance. rhea/short bowel inflammatory calcium intake. There is normal disease, gastric or small bowel urinary calcium excretion while Hyperoxaluria resection surgery. Additional sec- fasting or on a restricted calcium Hyperoxaluria is defined by ondary causes can be the result of diet (Munver & Preminger, 2001). urinary oxalate excretion in excess low urinary output from intesti- Renal hypercalciuria. Renal of 45 mg/day (Munver & nal fluid loss, low urinary citrate hypercalciuria or “renal leak Preminger, 2001). The cause of due to hypokalemia and metabol- mechanism” is thought to be these calcium stones can be relat- ic acidosis, and low caused by impairment in renal ed to primary or secondary factors. levels due to impaired intestinal tubular reabsorption of calcium . Type I magnesium absorption. (Munver & Preminger, 2001; Pak, hyperoxaluria is a rare autosomal 1979). The loss of calcium in the recessive disorder that begins in urine leads to stimulation of the childhood in which a defect of the Hyperuricosuria (excessive parathyroid function, causing ele- hepatic enzyme alanine-glyoxy- urinary uric acid) accounts for vated 1,25-vitamin D and increased late aminotransfease (AGT) caus- 10% of calcium stones. There is a intestinal absorption to maintain es increased urinary excretion of genetic predisposition, common serum levels of calcium. oxalic, glycolic, and glyoxylic in men, for stone development Primary . acids (Danpure, 1994; Menon & due to high uric acid levels and Excess parathyroid hormone Mahle, 1982; Munver & excess uric acid excretion, which (PTH) results in increased bone Preminger, 2001). This condition results in hyperuricosuria. Ex- resorption of calcium from bone is characterized by nephrocalci- cessive uric acid excretion can be and accounts for less than 5% of nosis, oxalate deposition in tis- found in primary gout, and sec- stones. Parathyroid hyperplasia sues, and renal failure resulting in ondary conditions of over- or adenomas secrete excess death before age 20, if untreated. production including myeloprolif- parathyroid hormone causing Diagnosis is made through percu- erative disorders such as acute increased intestinal absorption of taneous liver biopsy and evalua- leukemia, glycogen storage disease, calcium, increased 1,25-vitamin tion of the amount and distribu- and malignancy. Hyperuricosuria D3, and increased bone deminer- tion of AGT in liver specimens. is often caused by excess intake of alization and calcium release Type II hyperoxaluria is a purine in meat, fish, and poultry. from bone. Laboratory tests very rare deficiency of the hepat- This purine diet causes a low uri-

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nary pH. The features of hyperuri- causes a lower urinary concen- 1995). The invariant feature of C cosuric calcium oxalate nephro- tration of citrate. Patients with this condition is persistently O lithiasis include elevated urinary chronic diarrheal syndrome may acidic urine (pH <5.5) and no uric acid (>600 mg/day), a nor- have additional risk factors for specific cause has been detected N mal serum calcium level, normal stone formation such as low urine for the low urinary pH. T urinary calcium and oxalate lev- volumes and hyperoxaluria. I els, normal fasting and calcium Thiazide-induced hypocitra- NON-CALCIUM load response, and urinary pH turia. Thiazide can pro- NEPHROLITHIASIS N typically <5.5. duce hypokalemia (low potassi- U um) leading to intracellular aci- Uric Acid Stones I Hypocitraturia dosis. This acidotic state inhibits Uric acid stones may form in Hypocitraturic calcium ne- the synthesis of citrate, resulting the presence of gouty diathesis or N phrolithiasis may exist as an iso- in hypocitraturia. The essential in secondary causes of purine G lated abnormality (10%) or more mechanism is the inhibition of overproduction. Secondary caus- commonly in combination with citrate production, which is a es of these stones can include E other metabolic disorders (50%) consequence of chronic acidosis chronic diarrheal states such as (Menon & Mahle, 1982; Pak, (Nicar, Peterson, & Pak, 1984). , , and D 1987; Pak, 1994). Acid-base sta- Idiopathic hypocitraturia. Crohn’s disease. These chronic U tus, acidosis in particular, is the Mechanisms that account for diarrheal states predispose uric C most important factor affecting hypocitraturia in this condition acid precipitation, acidic urinary the renal handling of citrate, with include a high animal protein pH due to bicarbonate loss in A increased acid levels resulting in diet (with an elevated acid-ash stool or urinary ammonium T diminished endogenous citrate content), strenuous physical excretion defects, and reduced I production. Low urinary citrate exercise (causing lactic acidosis), urinary volume (see Table 3). causes the urinary environment high sodium intake, and intesti- O to become supersaturated with nal malabsorption of citrate. Stones N calcium salts, promoting nucle- Cystine stones are due to a ation, growth, and aggregation, Hypomagnesuria rare, congenital condition result- resulting in stone formation. Magnesium, an inhibitor of ing in large amounts of cystine Distal renal tubular acidosis. calcium nephrolithiasis, increases (an ) in the urine. A more common cause of hypo- the product of calcium Cystinuria causes cystine stones, citraturia is distal renal tubular oxalate and calcium . requiring lifelong therapy (Uro- acidosis (RTA). Acidosis impairs Hypomagnesuria is defined as uri- logy Channel, 1998). This disor- urinary citrate excretion by nary magnesium excretion <50 der typically presents during enhancing renal tubular reab- mg/day. Many patients with childhood and adolescence sorption of citrate as well as by nephrolithiasis will report a limit- (Bernier, 2005). The diagnosis reducing its synthesis (Pak, ed intake of magnesium-rich should be suspected for patients 1982). Distal RTA can be com- foods such as nuts and , with an early onset of neph- plete or incomplete. In both suggesting the dietary basis of this rolithiasis, a significant family forms, hypercalciuria and pro- condition. history, or recurrent stone dis- found hypocitraturia may be ease. A positive sodium- nitro- associated. In combination with Gouty Diathesis prusside urine test or the pres- alkaline urine, the patient is at Gouty diathesis (predisposi- ence of flat, hexagonal crystals in risk for developing calcium tion to uric acid or calcium urinary sediment provides a pre- oxalate or stones) may appear in a latent or sumptive diagnosis of cystine stones (Munver & Preminger, an early phase of classic gout, or stone disease. 2001; Preminger, Sakhaee, it may manifest fully with gouty Skurla, & Pak, 1985). arthritis and . Struvite Stones (Infection Chronic diarrheal syndrome. Patients develop renal stones Stones) Chronic diarrheal syndrome composed purely of uric acid, These stones are caused by causes a loss of alkali in the form uric acid in combination with UTIs, which affect the chemical of bicarbonate through the gas- calcium oxalate or calcium phos- balance of the urine, raising the trointestinal tract resulting in phate, or stones that reveal only pH. Urea-splitting bacteria (for metabolic acidosis with subse- calcium oxalate or calcium phos- example, , , and quent impairment in citrate syn- phate. Some patients may form Pseudomonas) release chemicals thesis (Munver & Preminger, uric acid or calcium stones into the urinary tract, neutraliz- 2001; Rudman et al., 1980). The (Khatchadourian, Preminger, ing acid in the urine, enabling decreased citrate production Whitson, Adams-Huet, & Pak, the bacteria to grow quickly and

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C Table 3. Guaifenesin calculi. Guaifenesin O Contributing Factors to Stone Development is a widely used expectorant that has been recently associated with H N Starvation causing chronic oliguric states nephrolithiasis. Guaifenesin calculi T H Primary gout – genetic (25% of population) are radiolucent and present in I H Secondary gout (50% of population) patients who ingest this medica- tion in excess. Twenty-four hour N H Medications causing rapid cell destruction in the treatment of neo- plastic disease urine metabolic analysis can aid U in the identification of guaifen- H I Acute leukemia esin or b-2-methoxyphenoxy-lac- H Hemolytic anemia/myeloproliferative disorders tic acid. N Indinavir calculi. Indinavir H Excess exercise G sulfate (Crixivan®) is currently Sources: Bernier, 2005; Moe et al., 2002 one of the most frequently used E protease inhibitors used against human immunodeficiency virus, D the virus that causes AIDS. The U form struvite stones. Struvite by a low urine output, providing incidence of calculi in patients C stones are difficult to treat a concentrated environment for taking indinavir ranges from 3% because the stone surrounds a substances such as calcium, to 20% (Schwartz, Schenkman, A nucleus of bacteria, which is pro- oxalate, uric acid, and cystine to Armenakas, & Stoller, 1999). T tected from antibiotic therapy begin crystallization. Indinavir calculi are radiolucent I (Bernier, 2005). These stones are when they are pure, and are three times more common in No Pathological Disturbance radiopaque when they contain O women than men due to an In approximately 35% of the calcium. N increased incidence of UTIs in stone-forming population, no calculi. These stones women. Struvite stones are most identifiable risk factors for stone occur due to a rare hereditary con- commonly found in patients formation can be found (Levy, dition with xanthine oxidase defi- with chronic infections as well as Adams-Huet, & Pak, 1995). This ciency (see Figure 4). The deficien- patients with anatomic or func- group includes individuals with cy in this enzyme results in tional abnormalities of their uri- normal serum calcium and PTH, decreased levels of serum and uri- nary tract allowing stasis of urine normal fasting and calcium load nary uric acid. Acidic urine caus- and chronic bacteriuria. These response, normal urine volumes, es crystal precipitation, resulting abnormalities include neuro- normal pH, calcium, oxalate, uric in stone formation (Bernier, genic bladder, diverticuli, and acid, citrate, and magnesium lev- 2005). These stones are also seen strictures (Lingeman, Siegel, & els in the presence of calcium in patients treated with iatrogenic Steele, 1995). nephrolithiasis. inhibition of xanthine oxidase Struvite stones are jagged with xanthine oxidase inhibitors (staghorns) in appearance and Drug-Induced Nephrolithiasis for hyperuricosuria such as allop- may be quite large at the time of Ephedrine calculi. Ephedrine urinol. initial presentation. and its metabolites (norephedrine, pseudoephedrine, and norpseu- DIAGNOSIS OF KIDNEY OTHER CAUSES OF doephedrine) are sympathomimet- STONES NEPHROLITHIASIS ic agents that have been used for Urolithiasis can mimic other the treatment of enuresis, myasthe- etiologies of visceral pain. It is Low Urine Volume nia gravis, narcolepsy, and rhinor- imperative to consider causes of Low urine output is defined rhea (Powell, Hsu, Turk, & Hruska, surgical abdomens such as as <1 liter/day. The typical etiolo- 1998). In addition to numerous , cholecystitis, peptic gies of nephrolithiasis are low side effects, ephedrine and its ulcer, pancreatitis, ectopic preg- fluid intake and reduced urine derivatives have been associated nancy, and dissecting aneurysm volume. Other possible causes of with the production of urinary in patients who present with low urine volume include chron- stones (Blau, 1998). The diagno- . Initial assess- ic diarrheal syndromes that result sis of these calculi is similar to ment includes a thorough history in large fluid loses from the gas- that of other radiolucent calculi. and physical examination, basic trointestinal tract and fluid loss Twenty-four hour urine metabol- serum and urine chemistries, and from perspiration, or evaporation ic analyses can aid in identifying a radiologic imaging study. First- from lungs or exposed tissue. ephedrine or its respective time stone formers may benefit Stone formation may be initiated metabolites. from a more detailed laboratory

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Figure 4. time stone-formers are at risk for Serum , BUN, creati- C Xanthine Stone recurrence. Both will benefit from nine, calcium, uric acid, and O an extensive diagnostic evaluation phosphorus assess current renal such as stone analysis, urinalysis, function, dehydration, and the N culture and sensitivity, compre- metabolic risk of future stone for- T hensive metabolic panel, which mation. An elevation in PTH I includes serum calcium, uric acid, level will confirm a diagnosis of and phosphorus, parathyroid hor- hyperparathyroidism. N mone level, and 24-hour urine col- U lections (random and after being Radiologic Assessment I on a special diet). Patients at risk Intravenous pyelography (IVP). include children, middle-aged Intravenous pyelography (urogra- N Photo courtesy of Louis C. Herring white males with a family history phy) has long been considered G & Co. of stones, and patients with intesti- the primary diagnostic study of nal disease (chronic diarrheal or choice for identifying urinary E malabsorptive states), gout, tract calculi. The IVP provides evaluation to identify causal fac- nephrocalcinosis, , anatomical and functional infor- D tors for stone formation. Multiple pathologic skeletal fractures, or mation, identifies the precise size U or recurrent stone-formers (meta- . Stones and location of a stone, the pres- C bolically active stone formers) composed of cystine, struvite, or ence and severity of the obstruc- require a more comprehensive lab- uric acid should undergo a com- tion, and renal or ureteral abnor- A oratory evaluation (NIH, 1998- plete metabolic workup (Pre- malities. For these reasons, the T 2005). minger, Peterson, Peters, & Pak, IVP has been among the most I 1985). important diagnostic tests that METABOLIC EVALUATION may enable successful manage- O The primary objective of a Urine Assessment ment decisions. N diagnostic evaluation of nephro- Urinalysis with urine culture lithiasis should be to efficiently and and sensitivity are mandatory Computed Tomography (CT) economically identify the particu- tests. Reports may reveal micro- Scan lar physiological defect present in scopic or gross hematuria and CT scan (with and without the patient to enable the selection pyuria with or without infection. contrast) is believed to be the best of specific and rational therapy. Increase or decrease in urine pH radiographic examination for The evaluation should be able to and the presence of crystals may acute as it creates identify the metabolic disorders give clues to whether the stone is images of the urinary tract and responsible for recurrent stone dis- alkaline or acidic. A cyanide shows delayed penetration of ease, including cystinuria, distal nitroprusside test will screen for intravenous contrast through the renal tubular acidosis, enteric suspected cystinuria. obstructed kidney. The delayed hyperoxaluria, gouty diathesis, and Two 24-hour urine collec- penetration of the contrast through primary hyperparathyroidism. tions should be performed evalu- an obstructed kidney is the hall- A detailed history and physi- ating calcium, sodium, phospho- mark of acute urinary obstruction. cal examination are imperative rus, magnesium, oxalate, uric The CT findings indicative of for both first-time stone-formers acid, citrate, sulfate, creatinine, acute urinary obstruction sec- and recurrent stone-formers. Past pH, and total volume. The first ondary to a stone would include medical history emphasis should 24-hour urine should be a ran- renal enlargement, hydronephro- include information about previ- dom specimen. The second 24- sis, ureteral dilatation, perinephric ous UTIs, diet and fluid intake, hour urine should be obtained stranding, and periureteral medications including vitamin after the patient has been on a (Katz, Lane, & Sommer, 1996; intake, bowel disease, gout, renal sodium, oxalate, and calcium- Smith, Verga, Dalrymple, Mc- disease, bone or parathyroid dis- restricted diet. Carthy, Rosenfield, 1996). Other ease, and bowel surgery. conditions that can mimic ureteral First-time stone-formers may Serum Assessment colic can be identified as well as undergo an abbreviated diagnostic (CBC) anatomic abnormalities and evaluation such as stone analysis, may reveal an elevated white obstruction. For many reasons, the urinalysis, culture and sensitivity, blood count (WBC) suggesting CT scan is considered superior to and a comprehensive metabolic urinary systemic infection, or an IVP in detecting both renal and panel, which includes serum cal- depressed count ureteral calculi, and is routinely cium, uric acid, and phosphorus. suggesting a chronic disease state performed on most patients in Recurrent stone-formers and first- or severe ongoing hematuria. which a diagnosis of urolithiasis is

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C suspected (Smith, Verga, Dalry- Table 4. O mple, McCarthy, & Rosenfield, Diagnostic Tests for Urinary Stones 1996). N Diagnostic Tests Rationale of Testing Radionuclide Imaging T Urinalysis Evaluate presence of blood or infection I Renal scan is considered the gold standard for assessing renal Intravenous (IVP) Evaluate urinary tract obstruction N function, especially in the set- U ting of recurrent or long-standing Evaluate for stones I nephrolithiasis. It is noninva- Evaluate anatomy of urinary stone sive, does not require any special N preparation or bowel prepara- Chemistry G tion, exposes the patient to min- Creatinine Evaluate kidney function imal radiation, and is nearly free E of allergic complications. BUN Evaluate presence of dehydration and D Plain X-Rays Electrolytes imbalances U Plain abdominal X-rays en- Calcium, PTH Diagnose hyperparathyroidism C tailing a flat plate radiograph of kidney, ureter, and bladder CBC Evaluate presence of infection A (KUB) will identify renal stones T that are radiopaque (Department Renal Evaluate presence of stone I of the Navy Bureau of Medicine Evaluate urinary tract obstruction and Surgery, 2004). Abdominal O X-rays are helpful in document- Evaluate for bladder stones N ing the number, size, and loca- CT scan (non-contrast) Same as IVP tion of stones in the urinary tract and the radiopacity may provide Abdominal X-rays Evaluate size, shape, and stone location information on the type of stones present. Plain abdominal films can be useful in identifying nephrocalcinosis, suggestive of hyperparathyroidism, primary Table 5. hyperoxaluria, renal tubular aci- Stone Management Guidelines dosis, or sarcoidosis. H Depends on size and location of the stone Renal Ultrasound H Presence or absence of associated infection Ultrasonography can be used H Presence of one or two kidneys as a screening tool for hydro- H Degree of symptoms nephrosis or stones within the kid- H ney or renal . A renal ultra- Majority will pass spontaneously with no residual damage sound can also determine the H Stones <4 mm pass spontaneously in approximately 90% of patients amount of renal parenchyma pre- H Stones 4-6 mm pass in approximately 50% of patients sent in an obstructed kidney, in H Stones >6 mm pass without intervention in 20% of patients addition to the presence of stones. The ultrasound can be H Stones >8 mm will pass in only 20% of patients and usually require used in combination with plain surgical intervention abdominal radiograph to deter- H If obstruction and infection present, emergent decompression of mine or ureteral upper urinary collecting system (kidneys and upper ureter) required dilation (Wolf, 2004). This may be helpful in assessment during Sources: Tanagho & McAninch, 2004; Wolf, 2004 pregnancy (see Table 4).

MEDICAL MANAGEMENT An individualized treatment plan Effective kidney stone preven- incorporating dietary changes, sup- tion is dependent on the stone type plements, and medications can be and identification of risk factors for developed to help prevent the for- stone formation (see Tables 5 & 6). mation of new stones. Certain con-

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Table 6. C Selected Medical Management of Urinary Stones O Drug Dosage Side Effects N T Calcium Oxalate 25 mg qd Hypokalemia, , sexual dysfunction I citrate 20-60mEq in 3-4 Abdominal discomfort, N/V/D N divided doses daily U Sodium citrate 2-3 g after meals GI upset and hyperkalemia I and HS N Orthophosphate 1-2.5gm/day in Gas, diarrhea G divided doses Cellulose sodium 5 gms TID Dyspepsia, loose bowel movements E phosphate D Calcium carbonate/ 1 gm 4-5x/day Constipation, gas, increase calcium leak, U citrate nausea C Cholestyramine 2-4 g/packet/day Constipation, abdominal pain, gas, GI upset A Calcium Phosphate 20-60 mEq in 3-4 Abdominal discomfort, N/V/D T divided doses daily I Sodium citrate 2-3 m unit doses GI upset and hyperkalemia O After each meal N and HS Uric Acid Stones Potassium citrate 60 mEq in 3-4 Abdominal discomfort, N/V/D divided doses daily 325 mg-2 gm qid CHF, cirrhosis, possible increase calcium-type or 48 mEq stones Allopurinol 300 mg/day Rash, diarrhea, increase liver enzymes, nausea Cystine Stones 300 mg TID Rash, kidney damage, N/V/D, tinnitus, loss of taste Captopril 25 mg qd Proteinuria, rash, hypotension, cough dizziness Tiopronin 800-1,000 mg/day Jaundice, kidney damage, decreased RBCs in in divided doses bone marrow Sodium bicarbonate 325 mg-2 gm qid CHF, cirrhosis, possibly increase in calcium- or 48 mEq type stones Struvite Stones Acetohydroxamic 250 mg 3-4x/day Headache, depression, N/V/D, DVT, hemolytic acid anemia, sweating N/V/D = nausea, vomiting, diarrhea; DVT= deep vein thrombosis

servative recommendations should excretion of oxalate and calcium. A • Low calcium diet (about 400 be made for all patients regardless restriction of animal is mg calcium). of the underlying etiology of their encouraged for patients with • , if high calci- stone disease. Patients should be “purine gluttony” and hyperurico- um content in water supply. instructed to increase their fluid suria. • Limit vitamin C (<0.5g/day). intake in order to maintain a urine • High sodium intake. output of at least 2,000 ml/day. Hypercalciuria (General) • Thiazide diuretics. Patients should also limit their Besides treating underlying • Cellulose phosphate. dietary oxalate and sodium intake, disease, management of hypercal- • Orthophosphate. thereby decreasing the urinary ciuria includes:

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C Absorptive Hypercalciuria – nary citrate excretion. A typical level and pH. Side effects are con- O Type I treatment program might include stipation, gas, and increased cal- Thiazides are commonly used chlorthalidone 25 mg/day. Pot- cium leak. Cholestyramine is also N for the management of absorptive assium citrate 15 to 20 mEq another method used to treat calci- T hypercalciuria Type I as these twice/day should be provided um oxalate stones. Cholestyramine I medications stimulate calcium with both of these diuretics. Side binds to bile in the intestines reabsorption in the distal nephron, effects include abdominal dis- which limits the amount of N preventing formation of kidney comfort, nausea, and vomiting. oxalate absorbed from the U stones by reducing the amount of intestines, therefore less oxalate is I calcium in the urine. Thiazides Absorptive Hypercalciuria – excreted in the urine. Side effects Type II N force a mandatory increase in uri- include constipation, abdominal nary volume but can cause elec- In absorptive hypercalciuria pain, gas, and heartburn. G trolyte disorders. Side effects Type II, specific drug therapy include decreased level of potassi- may not be necessary since the Hyperuricosuria E um, frequent urination, sexual dys- physiologic defect is not as severe Allopurinol (300 mg/day) is function, and increased triglyc- as in absorptive hypercalciuria the drug of choice in patients D erides. Type I. Many patients show dis- with hyperuricosuric calcium U Less-common medications dain for drinking fluids and oxalate nephrolithiasis (with or C used for treatment include excreting concentrated urine. A without hyperuricemia) because orthophosphate, sodium cellulose low intake of calcium (400-600 of its ability to reduce uric acid A phosphate, and inhibitors. mg/day) and a high intake of fluids synthesis and lower urinary uric T Orthophosphate and sodium cel- (sufficient to achieve a minimum acid by inhibition of the enzyme I lulose phosphate reduce the urine output of >2 liters/day) xanthine oxidase. The usual dose absorption of calcium from the would be acceptable treatment. is 300 mg/day; however, the O intestines thereby reducing calci- Normal urine calcium excretion dosage should be reduced in N um in the urine. The urease would be restored by dietary cal- patients with renal insufficiency. inhibitors dissolve crystals and cium restriction alone, and the Side effects are rash, diarrhea, struvite kidney stones and pre- increase in urine volume would and increased liver enzymes. vent formation of new crystals. help reduce urinary saturation of Potassium citrate represents Side effects can include a bad calcium oxalate. an alternative to allopurinol in taste in the mouth, diarrhea, and the treatment of this condition. dyspepsia. Renal Hypercalciuria Use of potassium citrate in Neither sodium cellulose Thiazides are indicated for hyperuricosuric calcium oxalate phosphate nor thiazide corrects the treatment of renal hypercalci- nephrolithiasis is warranted the basic, underlying physiologi- uria. This can correct the since citrate has an inhibitory cal defect in absorptive hypercal- renal leak of calcium by augment- activity with respect to calcium ciuria. Sodium cellulose phos- ing calcium reabsorption in the oxalate (and calcium phosphate) phate should be used in patients distal tubule and by causing crystallization, aggregation, and with severe absorptive hypercal- extracellular volume depletion agglomeration. Potassium citrate ciuria Type I (urinary calcium and stimulating proximal tubular (30 to 60 mEq/day in divided >350 mg/day) or in those resistant reabsorption of calcium. doses) may reduce the urinary to or intolerant of thiazide thera- saturation of calcium oxalate. py. In patients with absorptive Hyperoxaluria hypercalciuria Type I, who may Oral administration of large Hypocitraturia be at risk for bone disease (for amounts of calcium (0.25 g to 1.0 For patients with hypocitra- example, growing children and g four times/day) or magnesium turic calcium oxalate nephrolithi- post-menopausal women), or has been recommended for con- asis, treatment with potassium who presently have bone loss, trolling enteric hyperoxaluria. A citrate can restore normal urinary thiazide may be the medication of high fluid intake is recommended citrate, thus lowering urinary sat- first choice. Sodium cellulose to assure adequate urine volume uration of calcium and inhibiting phosphate may be substituted for in patients with enteric hyperox- crystallization of calcium salts. short-term therapy when thiazide aluria. Calcium citrate may theo- action is decreased. retically have a role in the man- Distal Renal Tubular Potassium supplementation agement of enteric hyperoxaluria. Acidosis (Urocit-K®, Polycitra-K® crystalor This treatment may lower urinary Potassium citrate therapy is syrup) should be added when oxalate by binding oxalate in the able to correct metabolic acidosis using thiazide therapy to prevent intestinal tract. Calcium citrate and hypokalemia found in hypokalemia and decrease uri- may also raise the urinary citrate patients with distal RTA. It will

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also restore normal urinary citrate Cystinuria Drug-Induced C levels, although large doses (up to The objective for treatment of Nephrolithiasis O 120 mEq/day) may be required cystinuria is to reduce the urinary Ephedrine calculi. There are for severe acidosis. Since urinary concentration of cystine to a level no limited studies that address N pH is generally elevated in below its solubility limit (200-250 the management of these calculi. T patients with RTA, the overall mg/liter). The initial treatment As with other calculi, a urine I rise in urinary pH is small. Citrate program includes a high fluid output of at least two liters/day is is a significant urinary calcium intake and oral administration of recommended. N stone inhibitor that retards crys- soluble alkali (potassium citrate) Guaifenesin calculi. As with U tallization of calcium oxalate and at a dose sufficient to maintain the ephedrine calculi, there are no I calcium phosphate. Potassium urinary pH at 6.5 to 7.0. When this limited studies regarding phar- N citrate binds to calcium in the conservative program is ineffec- macologic management of these urine, preventing formation of tive, d-penicillamine or alpha- calculi. G crystals and raising the urinary mercaptopropionylglycine (1,000 Indinavir calculi. Initial mea- citrate level and pH. It will effec- to 2,000 mg/day in divided doses) sures in the management of these E tively alkalinize the urine, which has been used. Potassium citrate calculi should focus on hydra- makes it useful in the treatment, is absorbed to prevent uric acid tion and analgesia as well as drug D dissolution, and prevention of stones as it binds to calcium in discontinuation and substitution U uric acid stones. Urinary pH urine, preventing formation of with another protease inhibitor. C should be monitored periodically crystals. Sodium bicarbonate Xanthine calculi. The med- during citrate therapy because of makes the urine less acidic, which ical management of xanthine cal- A excessive alkalinization. Side makes uric acid or cystine kidney culi is limited because the solu- T effects are mucous loose stools stone formation less likely. bility of these calculi is essential- I and minor GI complaints. Sodium Possible side effects include ly invariable within physiologic citrate and citric acids are other increased formation of calcium- pH ranges. Currently the recom- O alkalizing agents used to prevent type stones, fluid retention, and mendation includes a fluid N kidney stones by inhibiting stone sodium in blood. Urinary pH intake of at least three liters/day. formation through alkalization. should be monitored periodically If significant quantities of other during citrate therapy because are present in the urine, Chronic Diarrheal States excessive alkalinization may then urinary alkalization with Patients with chronic diar- occur, which can increase the risk potassium citrate in the range of rhea frequently have hypocitra- of calcium phosphate precipita- 6.0 to 6.5 is indicated to prevent turia due to bicarbonate loss from tion and stones. Side effects are hypoxanthine or uric acid cal- the intestinal tract. Potassium cit- mucous loose stools and minor GI culi. rate therapy can significantly complaints. Sodium citrate and reduce the stone formation rate in citric acid are other alkalizing NURSING MANAGEMENT these patients. The dose of potas- agents used to prevent kidney The nurse conducts a com- sium citrate is dependent on the stones by inhibiting stone forma- prehensive nursing assessment severity of hypocitraturia in tion through alkalization. to include all contributing factors these patients. The dosage ranges such as dietary history and fluid from 60 to 120 mEq/day in three Struvite (Infection) Lithiasis intake, family history, environ- to four divided doses. Acetohydroxamic acid (AHA) mental factors, medical history is a urease inhibitor that retards (, hypertension, hyper- Gouty Diathesis stone formation by reducing the parathyroidism, inflammatory The major objective in the urinary saturation of struvite. bowel disease, bowel resection, management of gouty diathesis is When administered at a dose of Crohn’s disease, UTIs), social his- to increase the urinary pH above 250 mg three times/day, it may tory, review of systems, and sur- 5.5, preferably to a level between prevent recurrence of new stones gical history. Next, the nurse pH 6.0 and 6.5. Potassium citrate and inhibit the growth of stones counsels the patient on pertinent is the drug of choice in managing in patients with chronic urea- findings elicited during the com- patients with gouty diathesis. splitting infections. In addition, prehensive nursing assessment Potassium citrate is an adequate in a limited number of patients, and provides followup counsel- alkalinizing agent, capable of use of AHA has resulted in disso- ing to support dietary and life- maintaining urinary pH at lution of existing struvite calculi. style changes and monitor out- approximately 6.5 at a dose of 30 Side effects that have developed comes and compliance. In our to 60 mEq per day in two divided are deep venous thrombosis, institution, a Kidney Stone doses. headache, hemolytic anemia, Disease in Adults teaching pam- and depression. phlet is given to patients at the

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C time that teaching is initiated Table 7. O (see Figure 5). Specific dietary Recommended Dietary Lifestyle Changes modification education includes N encouraging reduced animal pro- 1. Increase water intake to ensure urine output of 2,000 ml. T tein intake for elevated urinary 2. Maintain adequate (1,000 mg) calcium intake from dietary sources. I sulfate. See Table 7 for more rec- 3. Avoid calcium in pill form. ommendations for patients with 4. Avoid foods with added vitamin D (and vitamin C if recommended). N stones. Additional dietary rec- U ommendations may be found in 5. Avoid certain antacids with a calcium base. I Krieg (2005), in this issue of 6. Limit coffee, tea, and to 1-2 cups/day. N Urologic Nursing. 7. Eat less meat, fish, and poultry (decreased protein). G Nursing Interventions 8. Limit dietary sodium and oxalate intake. The nurse should: Source: NIH, 2003 E • Perform pain assessments to include Visual Analog, nu- D merical, or Wong-Baker scales U as appropriate for patient imbalance, may require IV importance of weight loss, hydration, prescription of maintaining weight loss, and C population to assess level of pain and effectiveness of out- anti-emetics, and daily exercise. ® A come with pain interventions. such as such as Gatorade or • Provide counseling on health ® T • Provide pharmacological edu- Pedialyte to replace elec- promotion and maintenance, trolytes lost via the GI tract. I cation. Narcotics are usually stressing the importance of used liberally, such as par- • Assess for vital signs check- followup care to evaluate O enteral (IM/IV) narcotics ing for orthostatic hypoten- causes of stone formation in N (ketorolac, [Toradol®], mepere- sion (lowering of blood pres- an effort to prevent future dine [Demerol®], , sure and increase in pulse recurrences. and oral narcotics/ with positional changes) and combinations (Department of monitoring patient weights. Preventative Health the Navy Bureau of Medicine • Encourage increases in daily Maintenance/Lifestyle and Surgery, 2004). Use of nar- fluid intake, especially water, Changes cotic medication needs to be and monitor outcomes of Effective kidney stone pre- explained as well as side interventions through patient vention depends upon the stone effects, such as nausea, vomit- voiding history and 24-hour type and identifying risk factors ing, constipation, and caution urine reports. The most impor- for stone formation. An individu- with driving or operating tant lifestyle change to prevent alized treatment plan incorporat- machinery. stones is drinking more fluids, ing dietary changes, supple- • Review bowel patterns and especially water up to 2 ments, and medications can be suggest interventions to pre- quarts/day. developed to help prevent the vent constipation due to pain • Educate the patient on com- formation of new stones. If kid- medication. pleting a voiding diary to ney stones develop despite • Assess contributing factors track daily urine output. increasing fluid intake and mak- of dehydration such as nau- • Educate the patient on the ing changes to diet, medications sea, vomiting, and diarrhea importance of completing can be prescribed to help dis- and administer antiemetics, laboratory tests ordered, solve the stones or to prevent for- such as metoclopramine (Re- especially 24-hour . mation of new stones. glan®), prochlorperazine (Com- This can become an imposi- As a health care provider, it pazine®), granisetron (Kytril®), tion on the patient’s quality is imperative that causes of stone or ondansetron (Zofran®). of life, especially if he is formation be investigated to pre- Administer antidiarrheal agents active and working. vent future occurrences that may such as loperamide (Imo- • Educate the patient on col- lead to permanent kidney dam- dium®), diphenoxylate, atro- lecting urine specimens and age. Patient education and coun- pine (Lomotil®), or paregoric straining urine. seling are vital to effective care, and assess effectiveness of out- • Educate the patient on diag- and can be provided by the uro- comes. If severe nausea and nostic testing, including re- logic nurse to promote lifestyle vomiting occur, patients must quired dietary or bowel prep- changes in this patient popula- be aware that prevention of aration to reduce anxiety. tion. Weight management is a dehydration and electrolyte • Educate the patient on the critical factor in managing stone

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Figure 5. C in Adults O N Hackensack University Medical Center T Department of Urology I N U I N Kidney Stone Disease in Adults G

E Overview D Kidney stones are one of the most painful disorders to afflict humans. This ancient health U problem has tormented people throughout history. Scientists have even found evidence of C kidney stones in an Egyptian estimated to be more than 7,000 years old. A T Kidney stones are also one of the most common disorders of the urinary tract. It is estimated that 10 percent of all people in the United States will have a kidney stone at some point in time. I Men tend to be affected more frequently than women. O N Most kidney stones pass out of the body without any treatment by a doctor. Cases that cause lasting symptoms or other complications may be treated by various techniques, most of which do not involve major surgery. Research advances also have led to a better understanding of the many factors that cause stones to form.

Introduction to the Urinary Tract

The urinary tract, or system, consists of the kidneys, , bladder, and urethra. Among other important functions, the kidneys remove extra water and waste from the blood, converting it to urine.

Narrow tubes called ureters carry urine from the kidneys to the bladder, a triangle-shaped chamber in the lower abdomen. Like a balloon, the bladder's elastic walls stretch and expand to store urine. They flatten together when urine is emptied through the urethra to outside the body.

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C Figure 5. (continued) O Kidney Stone Disease in Adults N T Kidney Stone Development I N A kidney stone develops from crystals that separate U from urine and build up on I the inner surfaces of the N kidney. Normally, urine G contains chemicals that keep the crystals from forming. These chemicals E do not work for everyone, D however, and some people U form stones. If the crystals remain tiny, they will travel C through the urinary tract A and pass out of the body in T the urine without even I being noticed. O Kidney stones may contain N various combinations of chemicals. The most common type of stone contains calcium in combination with either oxalate or phosphate. These chemicals are part of a person's normal diet and make up important parts of the body, such as bones and muscles.

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

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

Gallstones and kidney stones are not related. They form in different areas of the body. If a person 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 promote stone formation in people who are more prone to them, scientists do not believe that eating any specific 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. Urinary tract infections, kidney disorders such as cystic kidney diseases, and metabolic disorders, such as hyperparathyroidism, also are linked to stone formation.

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Figure 5. (continued) C Kidney Stone Disease in Adults O N T In addition, more than 70 percent of patients with a hereditary disease called renal tubular I acidosis develop kidney stones. N Cystinuria and hyperoxaluria are two other rare, inherited metabolic disorders that often U cause kidney stones. In cystinuria, the kidneys produce too much of the amino acid cystine. I Cystine does not dissolve in urine and can build up to form stones. With hyperoxaluria, the N body produces too much of the salt oxalate. When there is more oxalate than can be dissolved G in the urine, the crystals settle out and form stones.

Absorptive hypercalciuria occurs when the body absorbs too much calcium from food and E empties the extra calcium into the urine. This high level of calcium in the urine causes crystals D of calcium oxalate or calcium phosphate to form in the urinary tract. U C Other causes of kidney stones are hyperuricosuria, a disorder of uric acid , gout, excess intake of vitamin D, and blockage of the urinary tact. Certain diuretics, or water pills, or A calcium-based antacids may increase the risk of forming kidney stones by increasing the T amount of calcium in the urine. I O Calcium oxalate stones may also form in people who have a chronic inflammation of the bowel or who have had ostomy, or intestinal bypass, surgery. As mentioned above, struvite stones N can 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 has been increasing over the past 20 years. White people are more prone to kidney stones than are African Americans. Although stones occur more frequently in men, the number of women who 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 more than 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 a stone moves in the urinary tract, causing irritation or blockage. Typically, a person feels a sharp, cramping pain in the back and side in the area of the kidney, in the lower abdomen, or groin. Additional symptoms of kidney stones include:

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

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

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C Figure 5. (continued) O Kidney Stone Disease in Adults N Diagnosis T I Sometimes "silent" stones -- those that do not cause symptoms -- are found on x-rays taken N during a general health exam. These stones would likely pass unnoticed. U I More often, kidney stones are found on an X-ray, CT scan, or sonogram taken on someone who complains of blood in the urine or sudden pain. These diagnostic images give the doctor N valuable information about the stone's size and location. Blood and urine tests help detect any G abnormal substance that might make stones form.

E The doctor may decide to D scan the urinary system using a special x-ray test U called an intravenous C pyelogram, or IVP, or CT A scan. T I Together, the results from these tests help determine O the proper treatment. IVP N x-rays will miss some stones. CT scan will often call things stones that are not.

Occasionally, a patient will need both an IVP and CT scan or a repeat of the first test to confirm the presence of stones.

Treatment

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

Some type of surgery may be needed to remove a kidney stone if the stone does not pass after a reasonable period of time and causes constant pain, is too large to pass on its own, blocks the 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 causes constant 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 four to six weeks. Today, treatment for these stones is greatly improved. Many options exist that do not require major surgery.

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Figure 5. (continued) C Kidney Stone Disease in Adults O Extracorporeal N shockwave T (ESWL) is the most I frequently used surgical N procedure for the treatment of kidney U stones. ESWL uses I shock waves that are N created outside of the G body to travel through the skin and body tissues until the waves hit the dense E stones. The stones D become sand-like and are U easily passed through the urinary tract in the urine. C A There are several types of T ESWL devices. One I device positions the patient in the water bath while the shock waves are transmitted. Other devices have a soft O cushion or membrane on which the patient lies. Most devices use either x-rays or ultrasound to N help the surgeon pinpoint the stone during treatment. For most types of ESWL procedures, some type of is needed.

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

Complications may occur with ESWL. Most patients have blood in the urine for a few days after treatment. Bruising and minor discomfort on the back or abdomen due to the shock waves are also common. To reduce the chances of complications, doctors usually tell patients to avoid taking 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 the urinary tract in the urine. In some cases, the doctor will insert a small tube called a through the bladder into the ureter to help the fragments pass. Sometimes the stone is not completely shattered with one treatment and additional treatments may be required.

Sometimes a procedure called percutaneous nephrolithotomy is recommended to remove a stone. This treatment is often used when the stone is quite large or in a location that does not allow effective use of EWSL.

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

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

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C Figure 5. (continued) O Kidney Stone Disease in Adults N T Although some ureteral stones can be treated with ESWL, may be needed for I middle and lower ureter stones. No incision is made in this procedure. Instead, the surgeon N passes a small instrument called a ureteroscope through the urethra and bladder into the ureter. The surgeon then locates the stone and either removes it with a cage-like device or U shatters it with a special instrument that produces a form of shock wave (EHL) or with a I device. A small stent may be left in the ureter for a few days after treatment to help the lining of N the ureter heal. G Prevention

E People who have had more than one kidney stone are likely to form another. Therefore, D prevention is very important. To prevent stones from forming, their cause must be determined. U The urologist will order laboratory tests, including urine and blood tests. A complete medical C history will be taken, along with information about the patient's work and eating habits. If a stone has been removed, or if the patient has passed a stone and saved it, the lab can analyze A the stone to find out its chemical make-up. T I A patient may be asked to collect urine for 24 hours after a stone has passed or been removed. O 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 use N this information to determine the cause of the stone. A second 24-hour urine collection may be needed 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 to produce 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 containing calcium and oxalate. Not everyone will benefit from a low-calcium diet, however. Some patients who have high levels of oxalate in their urine may benefit from extra calcium in their diet. Patients may be told to avoid food with added vitamin D and certain types of antacids that have a calcium base.

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

To prevent cystine stones, patients should drink enough water each day to reduce the amount of cystine that escapes into the urine. This is difficult because more than a gallon of water may be 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. These drugs control the amount of acid or alkali in the urine, key factors in crystal formation. The drug Allopurinol may also be useful in some cases of hypercalciuria and hyperuricosuria.

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Figure 5. (continued) C Kidney Stone Disease in Adults O N Another way a doctor may try to control hypercalciuria, and thus prevent calcium stones, is by T prescribing certain diuretics, such as . These drugs decrease the amount I of calcium released by the kidneys into the urine. N Some patients with absorptive hypercalciuria may be given the drug Sodium cellulose U phosphate. This drug keeps calcium from leaking into the urine. I N If cystine stones cannot be controlled by drinking more fluids, the doctor may prescribe the drug G Thiola. 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 the E urine free of bacteria that can cause infection. The patient's urine will be tested on a regular D basis to be sure that bacteria are not present. U C If struvite stones cannot be removed the doctor may prescribe a new drug called Aetohydroxamic acid (AHA). AHA is used along with long-term antibiotic drugs to prevent the A infection that leads to stone growth. T I Surgery O To prevent calcium stones that form in hyperparathyroid patients, a surgeon may remove all of N the parathyroid glands (located in the neck). This is usually the treatment for hyperparathyroidism as well. In most cases, only one of the glands is enlarged. Removing the gland ends the patient's problem with kidney stones.

Research on Kidney Stones

The Division of Kidney, Urologic, and Hematologic Diseases of the National Institutes of Diabetes 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's National Institutes of Health.

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

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

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C Figure 5. (continued) O Kidney Stone Disease in Adults N T For more information, contact: I N National Kidney and Urologic Diseases Information Clearinghouse (NKUDIC) 3 Information Way U Bethesda, MD 20892-3580 I kidney.niddk.nih.gov N (301) 654-4415 G National Kidney Foundation E 30 East 33rd Street New York, NY 10016 D www.kidney.org U (800) 622-9010 C A T I Copyright © 2004 by iMedConsent Dialog Medical, LLC. All rights reserved. O N Copyright © iMedConsent Dialog Medical, LLC. All rights reserved. Used with permission by Hackensack University Medical Center.

formation and prevention of Conclusion patients to the recommended pro- future occurrences as evidenced With appropriate diagnosis gram and a commitment of the by a study at Brigham and and treatment of specific disor- physician to provide long-term Women’s Hospital, Boston ders resulting in nephrolithiasis, followup and care with the inten- (Guttman, 2005). Researchers a remission rate greater than 80% tion of improving quality of life by evaluated the correlation of obesi- can be obtained (see Table 8). In eliminating the symptoms caused ty and weight gain and the risk of patients with mild to moderate by urinary tract stones. • developing kidney stones. The severity of stone disease, virtual- findings indicated obesity was a ly total control of stone disease References contributing factor in stone devel- Bernier, F. (2005). Management of clients can be achieved with a remission with urinary disorders. In J. Black & opment since, as we age, the rate greater than 95% (Preminger, J. Hawks (Eds.), Medical- surgical majority of weight gain is from fat Harvey, & Pak, 1985). The need nursing: Clinical management for tissue not bone or muscle. The for surgical stone removal may be positive outcomes (7th ed.) (pp. 857- risk of developing stones reduced dramatically or elimi- 911). St. Louis: Elsevier. increased by 71% to 109% Billica, W. (2004). Urolithiasis. Retrieved nated with an effective prophy- June 14, 2004, from http://www: among younger and older women lactic program. Selective phar- 5ncc.com/Assets/Summary/TP0970 in the highest weight, BMI, and macologic therapy also has the .html waist circumference and 33% to advantage of overcoming nonre- Blau, J.J. (1998). Ephedrine nephrolithiasis 48% in men. These findings sup- associated with chronic ephedrine nal complications and averting abuse. Journal of Urology, 160, 825. port the need for health care certain side effects that may occur Danpure, C.J. (1994). Molecular and cell providers to emphasize the with nonselective medical thera- biology of primary hyperoxaluria importance of exercise and py. It is clear that selective medical type I. Clinical and Investigative weight management in a preven- therapy alone cannot provide total Medicine – Medecine Clinicque Et tion program. Dietary recommen- Experimentale, 72, 725-727. control of stone disease. A satis- Department of the Navy Bureau of dations for stone formers are dis- factory response requires contin- Medicine and Surgery. (2004). cussed in detail by Krieg (2005). ued dedicated compliance by Virtual naval hospital: General med- ical officer manual: Clinical section.

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Table 8. Quick Reference

Type of Stone Cause Clinical Findings Absorptive Hypercalciuria C Type I Increased absorption of calcium, High urine calcium level unknown Normal serum calcium O (high or low dietary calcium intake) Normal serum phosphorus N Normal of low serum parathyroid hormone T I Type II Excess calcium intake Normal urine calcium Excess vitamin D intake N U Renal Hypercalcuria Decreased renal absorption Impaired renal tubular re-absorption Elevated 1, 25-vitamin D3 I of calcium →→ decreased N urine calcium → increased intestinal calcium G absorption → PTH stimulation

Increased bone absorption Excess parathyroid hormone, Increased 1, 25-vitamin D3 E increased ↑ bone resorption of Increased bone demineralization D calcium Increased parathyroid hormone and U ↑ serum calcium C Hyperoxaluria Primary Type I Autosomal recessive disorder Increased urine levels of oxalic, A Defect in hepatic enzyme alanine- glycolic, and T glyoxylate Oxalate tissue deposits Aminotransferase (AGT) Renal failure I O Type II Rare Increased urine level of oxalate and Deficiency of hepatic enzymes glycerate excretion N D-glycerate dehydrogenase and Nephrocalcinosis Tubular interstitial neuropathy Chronic renal failure Secondary Dietary Excess dietary intake oxalate foods Increased urine oxalate Hyperoxaluria Excess intake ascorbic acid (vitamin C) Enteric Hyperoxaluria Intestinal malabsorption (distal Decreased urine citrate colon) Hypokalemia Excess oxalate absorption Metabolic acidosis Chronic diarrheal states Decreased urine volume Bowel surgery Decreased potassium Decreased magnesium Hyperuricosuria Increased uric acid levels Normal serum calcium Excess uric acid excretion Normal urinary calcium Excess purine diet Normal urinary oxalate Genetic predisposition Normal fasting and calcium load Purine overproduction response Acute leukemia Acidic urine Malignancy Increase urine uric acid Glycogen storage disease Hypocitraturia Disruption of acid base balance Decreased urine citrate Increased acid levels Decreased endogenous citrate production

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C Table 8. (continued) O Quick Reference N Type of Stone Cause Clinical Findings T Hypomagnesuria Low magnesium prevents inhibition Low urine magnesium excretion I of solubility product of calcium <50 mg/day N oxalate and calcium phosphate U Uric Acid Purine overproduction Acidic urine I Uric acid precipitation Low urine volume N Cystine Rare Positive sodium-nitroprusside Congenital condition Flat, hexagonal crystals in urine G Large amounts of cystine in urine sediment Struvite UTIs-urea-splitting bacteria (Proteus, Bacteria in urine and culture and E Klebsiella, Pseudomonas) sensitivity D Neurogenic bladder Increased WBCs in urinalysis Diverticuli U Strictures C Drugs Sulfur A Salicylates T ephedrine I Xanthine Rare Decreased level serum uric acid O Hereditary deficiency in xanthine Decreased level urine uric acid oxidase Acidic urine N

Retrieved June 14, 2004, from Menon, M., & Resnick, M.I. (2002). & Electrolyte Metabolism, http://www.vnh.org/gmo/Clinical Urinary lithiasis: Etiology, diagno- 13, 257-266. Section/106Urolithiasis.html sis, and medical management. In Pak, C.Y. (1982). Medical management of Guttman, C. (2005). Healthy weight E.S. Campbell (Ed.), Campbell’s nephrolithiasis. Journal of Urology, reduces risk of kidney stones. urology (8th ed.) (pp. 3229-3305). 128, 1157-1164. Urology Times, 1, 20. Philadelphia: W.B. Saunders. Pak, C.Y. (1979). Physiological basis for Katz, D.S., Lane, M.J., & Sommer, F.G. Moe, O.W., Abate, N., & Sakhaee, K. absorptive and renal hypercalciurias. (1996). Unenhanced helical CT of (2002). Pathophysiology of uric acid American Journal of Physiology, 237, ureteral stones: Incidence of associ- nephrolithiasis. Endocrinology and F415-F423. ated urinary tract findings. Metabiology Clinics of North Pak, C.Y., Sakhaee, K., Crowther, C., & American Journal of Roentgenology, America, 31(4), 895-914. Brinkley L. (1980). Evidence justifying 166, 1319-1322. Munver, R., & Preminger, G. (2001). a high fluid intake in treatment of Khatchadourian, J., Preminger, G.M., Urinary tract stones in comprehen- nephrolithiasis. Annals of Internal Whitson, P.A., Adams-Huet, B., & sive urology. St. Louis: Mosby. Medicine, 93, 36-39. Pak, C.Y. (1995). Clinical and bio- National Institutes of Health. (1998- Powell, T., Hsu, F.F., Turk, J., & Hruska, K. chemical presentation of gouty 2005). NIH consensus statements: 67 (1998). Ma-huang strikes again: diathesis: Comparison of uric acid prevention and treatment of kidney Ephedrine nephrolithiasis. American versus pure calcium stone forma- stones. Retrieved February 9, 2005, Journal of Kidney Diseases, 32, 153- tion. Journal of Urology, 154, 1665- from http://www.urologychannel. 159. 1669. com/kidneystones/index.shtml Preminger, G.M., Harvey, J.A., & Pak, C.Y. Krieg, C. (2005). The role of diet in the National Institute of Health Publications. (1985). Comparative efficacy of “spe- prevention of common kidney (2003, April). National Kidney and cific” potassium citrate therapy ver- stones. Urologic Nursing, 25(6), 451- Urologic Diseases Clearinghouse sus conservative management in 456. (No. 03-2495). Retrieved June 14, nephrolithiasis of mild to moderate Levy, F.L., Adams-Huet, B., & Pak, C.Y. 2005, from http://kidney.niddk. severity. Journal of Urology, 134, (1995). Ambulatory evaluation of nih.gov/kudiseases/pubs/stone- 658-661. nephrolithiasis: An update of a 1980 sadults/index.htm Preminger, G.M., Peterson, R., Peters, P.C., protocol. American Journal of Nicar, M.J., Peterson, R., & Pak, C.Y. (1984). & Pak, C.Y. (1985). The current role of Medicine, 98, 50-59. Use of potassium citrate as potassium medical treatment of nephrolithiasis: Lingeman, J.E., Siegel, Y.I., & Steele, B. supplement during thiazide therapy The impact of improved techniques of (1995). Metabolic evaluation of infect- of calcium nephrolithiasis. Journal of stone removal. Journal of Urology, ed renal lithiasis: Clinical relevance. Urology, 131, 430-433. 134, 6-10. Journal of Endourology, 9, 51-54. Pak, C.Y. (1994). Citrate and renal calculi: Menon, M., & Mahle, C.J. (1982). Oxalate An update. Mineral & Electrolyte continued on page 475 metabolism and renal calculi. Metabolism, 20, 371-377. Journal of Urology, 127(1), 148-151. Pak, C.Y. (1987). Citrate and renal calculi.

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characterized by leakage of small amounts of References urine in response to increases in intra-abdominal Gray, M. (1992). Genitourinary disorders. St. Louis: Mosby Year Book. pressure and precipitated by a strong urge to void O’Dell, K.K., & Jacelon, C.S. (2005). Not the surgery for a young (Gray, 1992). person: Women’s experience with vaginal closure surgery 2. C – Answer A might be indicated, but only if for severe prolapse. Urologic Nursing, 25(5), 345-351. additional history, physical and preliminary Weber, A.E. (2004a). Prolapse with lower urinary tract symptoms. testing document the need for more complex In E.A. Weber, L. Brubaker, J. Schaffer, & M.R. Toglia (Eds.), Office urogynecology: Practical pathways in obstetrics and (and expensive) studies. Although Ms. Case gynecology (pp. 237-270). New York: McGraw-Hill Medical reports a history of falls, the fact that these Publishing Division. occurred en route to the bathroom and at night Weber, A.E. (2004b). Symptomatic prolapse. In E.A. Weber, L. may indicate the need for secondary interven- Brubaker, J. Schaffer, & M.R. Toglia (Eds.), Office urogyne- cology: Practical pathways in obstetrics and gynecology (pp. tion measures such as additional lighting, bed- 209-234). New York: McGraw-Hill Medical Publishing side commode use, and patient education about Division. fall prevention prior to assuming that the falls are due to neurologic changes. However, answer B would be appropriate as a “referral” to neurol- ogy should additional history and physical find- ings (positive neurologic assessment) support the decision. Answer D is premature prior to obtain- ing information regarding length of time the symptoms have been present (UA), and would result in unnecessary expense if the urinalysis results were negative (culture/sensitivity). 3. A – The simple cystometry can provide infor- Urolithiasis/Nephrolithiasis mation about bladder filling, emptying, sensa- continued from page 448 tion as well as evaluate for urinary retention and overflow. This test is minimally invasive and Preminger, G.M., Sakhaee, K., Skurla, C., & Pak, C.Y. (1985). can be performed in the office, thus the necessi- Prevention of recurrent calcium stone formation with potassi- um citrate therapy in patients with distal renal tubular acido- ty for the patient to return for additional testing sis. Journal of Urology, 134, 20-23. appointments is avoided. Answer B is incorrect Ramello, A., Vitale, C., & Marangella, M. (2000). Epidemiology of due to the history of ductal breast cancer which nephrolithiasis. Journal of , 13(Suppl. 3), S45-50. was hormone dependent (evident by history of Rudman, D., Dedonis, J.L., Fountain, M.T., Chandler, J.B., Gerron, G.G., Fleming, G.A., et al. (1980). Hypocitraturia in patients tamoxifen therapy). Answer C is not the correct with gastrointestinal malabsorption. New England Journal of answer because cystoproctography and MRI, Medicine, 303(12), 657-661. although used diagnostically for prolapse in Schwartz, B.F., Schenkman, N., Armenakas, N.A., & Stoller, M.L. women, would not be ordered prior to simple (1999). Imaging characteristics of indinavir calculi. Journal of cystometry and are “not routinely recommended Urology, 161(4), 1085-1087. Smith, R.C., Rosenfield, A.T., Choe, K.A., Essenmacher, K.R., for clinical care” (Weber, 2004a, p. 222; Weber, Verga, M., Glickman, M.G., et al. (1995). Acute flank pain: 2004b). Answer D is incorrect because the UA Comparison of non-contrast-enhanced CT and intravenous was negative for both RBCs and WBCs; the find- urography. , 194, 789-794. ing of on microscopic examination is Smith, R.C., Verga, M., Dalrymple, N., McCarthy, S., & Rosenfield, A.T. (1996). Acute ureteral obstruction: Value of secondary within normal limits and not indicative of UTI. signs of helical unenhanced CT. American Journal of 4. A – Answer A would not be correct due to avail- Roentgenology, 168, 1109-1113. ability of significantly less-drastic alternative Spirnak, J.P., & Resnick, M.I. (1987). Retrograde percutaneous surgical options and the co-morbid conditions stone removal using modified Lawson technique. Urology, of this patient to undergo any surgery, particu- 30(6), 551-553. Tanagho, E.A., & McAninch, J.W. (2004). Smith’s general urology larly a procedure this extensive. All other (16th ed). Norwalk, CT: Appleton & Lange. answer options would be appropriate interven- Urology Channel. (1998). Kidney stones. Retrieved February 9, tions given the patient’s symptoms, history, and 2005, from http://www.urologychannel.com/kidneystones/ co-morbid conditions. Although estrogen thera- index.shtml Wolf, J.S. (2004). Nephrolithiasis. Retrieved November 15, 2005, py is preferable in conjunction with pessary use, from http://www.emedicine.com/MED/topic1600.htm it is not essential. The pessary can be placed by the practitioner and the patient scheduled for Additional Readings followup to remove the pessary, assess for prob- Busby, J., & Low, R.K. (2004). Ureteroscopic treatment of renal cal- lems, and evaluate continued use of this thera- culi. Urologic Clinics of North America, 31, 1-10. Jeong, H., Kwak, C., & Lee, S.E. (2004). Ureteric stenting after py. In women with advanced vaginal prolapse ureteroscopy for ureteric stones: A prospective randomized (Stage 3-4), a previous history of symptoms of study assessing symptoms and complications. BJU , subsiding as the prolapse International, 93(7), 1032-1035. increased, is not uncommon. Ms. Case is not a Merck Manual of Diagnosis and Therapy. Genitourinary disor- good surgical risk, and this option should be ders (stones/nephrolithiasis/urolithiasis). Retrieved June 14, 2004, from http://www.merck.com/mrkshared/mmanual/ avoided if possible (O’Dell & Jacelon, 2005). • section17/chapter 221/221a.jsp

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