UNJ Dec 2005-427.ps 11/29/05 3:43 PM Page 427 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- (kidney calculi or stones) ney calculi or stones) are well-documented common occurrences in refers to the entire clini- the general population of the United States. 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 calcifications that the United States are hospitalized annually for treatment of urinary T form in the urinary system, 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 ureter (ureterolithiasis), O and may also form in or migrate N into the lower urinary system (bladder or urethra) (Bernier, 2005). Urinary tract stone disease the rest of the world. Researchers Kidney stones are most has been documented historically attribute the incidence 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 protein 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 urea- Any factor that reduces uri- splitting bacteria (Munver & nary flow or causes obstruction, Eileen Kochis, RN, is a Staff Nurse, Preminger, 2001). which results in urinary stasis or the Department of Urology, 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. UROLOGIC NURSING / December 2005 / Volume 25 Number 6 427 UNJ Dec 2005-428.ps 11/29/05 3:43 PM Page 428 C Table 1. Figure 1. O Factors Contributing to Stone Development Calcium Oxalate Stone N H Congenital kidney defects (medullary sponge disease) T H Excess parathyroid hormone I H Medications (ephedrine, guaifenesin, indinavir, allopurinol) N H Gout U H Hypertension I H Colitis, inflammation of colon, and chronic diarrheal states N H Irritable bowel disease or intestinal surgery G H Renal tubular acidosis Photo courtesy of Louis C. Herring H Crohn’s disease results in dehydration and low citrate. & Co. E H Arthritis (skeletal disease) Figure 2. D H Urinary tract infections Uric Acid Stone U H Past medical history of kidney stones C H Obesity and high body mass index A H Prolonged inactivity T H Anatomic factors – Ureteropelvic junction (UPJ) obstruction I H Horseshoe or ectopic kidney O H Autosomal dominant polycystic kidney disease H N Vesicoureteral reflux H Calyceal diverticula Photo courtesy of Louis C. Herring Source: Tanagho & McAninch, 2004 & Co. reduces urine 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). hypercalciuria, cystinuria, 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 428 UROLOGIC NURSING / December 2005 / Volume 25 Number 6 UNJ Dec 2005-429.ps 11/29/05 3:43 PM Page 429 Figure 3. such as ephedrine, guaifenesin, sels will produce spasms with C Struvite Stone thiazide, 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. Nausea, 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 Bladder Stone 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, dysuria, urgency, and frequen- C Dietary habits. Fluid restric- include acute renal or ureteral cy may be the only symptoms tion or dehydration may cause colic, hematuria (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 sodium, tract infection, or vague abdomi- passes out of the bladder. oxalate, fat, protein, sugar, unre- nal or flank pain. A thorough his- I fined carbohydrates, and ascor- tory and physical examination, Kidney Stone Complications O bic acid (vitamin C) 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- pyelonephritis or urosepsis can intake consisting of drinking rays or may be present with occur.