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Urology:

Edited by Alex J. Weinstein MD, FACS, Urologist.

Last updated on 26 Sept 2011

Published by C.G. Weber MD at Smashwords.

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❑ The Clinical Medicine Consult (includes all 35 of these modules as all are pulled from this one highly integrated text). Clinical Endocrinology, Neurology, Orthopedics, Nephrology, Dermatology, Gastroenterology, ENT, Psychiatry, Urology, Infectious Disease, Women’s Health, Hematology / Oncology, Geriatrics-Death & Dying, Rheumatology, Pulmonology, Allergy, Pediatrics, Pain Management, Ethics-Alternative Medicine-Evidence Based Medicine-Communication (Compendium), Cardiology, Ophthalmology, Travel Medicine, Procedures in Medicine, Wound Care & Skin Infections, Sports Medicine, Wilderness, Survival, Alternative and Complementary Medicine, Cancer Medicine, Hospice & Palliative Care. The goal is for these texts is to have >95% of clinical of the information you need at your fingertips.

• Note: Information is added as important new information is published. We perform an ongoing review of >320 journals, textbooks, online sources, and many other expert resources. The file size of The Clinical Medicine Consult 2012v4 was 58,940 kb, the last quarterly versions were sized at 50,147, 48,272, 43,583, 41,818, 35,336, 30,243, 28,800, 26,946, 24,114, 23,164, 21,901, 17,451, 16,918, 16,516, 15,858, 15,176, 14,580, 13,980, 12,950, 12,276, 11,715, 11,097, 10,752, 10,249, 9,769, 9,298, 8,977, 8,004, 6,805 and 5,364 kb....tons more information for you to use at your fingertips and even more with each new release.

Male Anatomy: Link: See Womens Health: Reproductive / Anatomy |

Male Genital Organs

Scrotum: an outpouching of the lower part of the anterior abdominal wall. It contains the testes, the epididymides, and the lower ends of the spermatic cords. The wall of the scrotum has the following layers:

1. Skin: The skin of the scrotum is thin, wrinkled, and pigmented and forms a single pouch. A slightly raised ridge in the midline indicates the line of fusion of the two lateral labioscrotal swellings. In the female, the swellings remain separate and form the labia majora.

2. Superficial fascia: This is continuous with the fatty and membranous layers of the anterior abdominal wall; the fat is, however, replaced by smooth muscle called the dartos muscle. This is innervated by sympathetic nerve fibers and is responsible for the wrinkling of the overlying skin. The membranous layer of the superficial fascia (often referred to as Colles' fascia) is continuous in front with the membranous layer of the anterior abdominal wall (Scarpa's fascia), and behind it is attached to the perineal body and the posterior edge of the perineal membrane.

3. Spermatic fasciae: These three layers lie beneath the superficial fascia and are derived from the three layers of the anterior abdominal wall on each side. The external spermatic fascia is derived from the aponeurosis of the external oblique muscle; the cremasteric fascia is derived from the internal oblique muscle; and, finally, the internal spermatic fascia is derived from the fascia transversalis. The cremaster muscle is supplied by the genital branch of the genitofemoral nerve. The cremaster muscle can be made to contract by stroking the skin on the medial aspect of the thigh. This is called the cremasteric reflex. The afferent fibers of this reflex arc travel in the femoral branch of the genitofemoral nerve (L1 and 2), and the efferent motor nerve fibers travel in the genital branch of the genitofemoral nerve. The function of the cremaster muscle is to raise the testis and the scrotum upward for warmth and for protection against injury. Normal spermatogenesis can occur only if the testes are at a temperature lower than that of the abdominal cavity.

Testis: a firm, mobile organ lying within the scrotum. The left testis usually lies at a lower level than the right. Each testis is surrounded by a tough fibrous capsule, the tunica albuginea. Extending from the inner surface of the capsule is a series of fibrous septa that divide the interior of the organ into lobules. Lying within each lobule are one to three coiled seminiferous tubules. The tubules open into a network of channels called the rete testis. Small efferent ductules connect the rete testis to the upper end of the epididymis.

Epididymis: a firm structure lying posterior to the testis, with the vas deferens lying on its medial side. It has an expanded upper end, the head, a body, and a pointed tail inferiorly. Laterally, a distinct groove lies between the testis and the epididymis, which is lined with the inner visceral layer of the tunica vaginalis and is called the sinus of the epididymis.

Vas Deferens: a thick-walled tube about 18 in. (45 cm) long that conveys mature sperm from the epididymis to the ejaculatory duct and the urethra. It arises from the lower end or tail of the epididymis and passes through the inguinal canal. It emerges from the deep inguinal ring and passes around the lateral margin of the inferior epigastric artery. It then passes downward and backward on the lateral wall of the pelvis and crosses the ureter in the region of the ischial spine. The vas deferens then runs medially and downward on the posterior surface of the bladder. The terminal part of the vas deferens is dilated to form the ampulla of the vas deferens. The inferior end of the ampulla narrows down and joins the duct of the seminal vesicle to form the ejaculatory duct.

Seminal Vesicles: two lobulated organs about 2 in. (5 cm) long lying on the posterior surface of the bladder. On the medial side of each vesicle lies the terminal part of the vas deferens. Posteriorly, the seminal vesicles are related to the rectum. Inferiorly, each seminal vesicle narrows and joins the vas deferens of the same side to form the ejaculatory duct. Each seminal vesicle consists of a much-coiled tube embedded in connective tissue.

Spermatic Cord: a collection of structures that pass through the inguinal canal to and from the testis). It begins at the deep inguinal ring lateral to the inferior epigastric artery and ends at the testis. The structures are as follows: Vas deferens. Testicular artery. Testicular veins (pampiniform plexus). Testicular lymph vessels. Autonomic nerves. Remains of the processus vaginalis. Genital branch of the genitofemoral nerve, which supplies the cremaster muscle.

Ejaculatory Ducts: The two ducts are each less than 1 in. (2.5 cm) long and are formed by the union of the vas deferens and the duct of the seminal vesicle. The ejaculatory ducts pierce the posterior surface of the prostate and open into the prostatic part of the urethra, close to the margins of the prostatic utricle; their function is to drain the seminal fluid into the prostatic urethra.

Prostate: a fibromuscular glandular organ that surrounds the prostatic urethra. It is about 1.25 in. (3 cm) long and lies between the neck of the bladder above and the urogenital diaphragm below. The prostate is surrounded by a fibrous capsule. The somewhat conical prostate has a base, which lies against the bladder neck above, and an apex, which lies against the urogenital diaphragm below. The two ejaculatory ducts pierce the upper part of the posterior surface of the prostate to open into the prostatic urethra at the lateral margins of the prostatic utricle.

Abx Prophylaxis prior to Urologic Surgery: need to cover Streptococci and G- bacilli. 30 minutes before surgery give Cefazolin 1 g IV q8h for 1-3 dose then (TMP-SMX or nitrofurantoin) PO for 10 days or until a catheter is removed.

Transrectal Prostate Biopsy: 30 minutes before surgery give Ciprofloxacin 500 PO 12 hrs prior and after biopsy.

Urinary Calculi (Stones / Urolithiasis / Nephrolithiasis):

A relatively common problem, has a 5-15% lifetime risk worldwide, M: F, 3:1, most between ages 20-50, has a 50% recurrence rate within 5 years. The first episode in men tends to occur at an average age of 30 yo, where as women have a bimodal age of onset, with episodes peaking at 35 and 55 years. Peak incidence is the early morning due to hyperconcentration and low urine output. 55% of those with stones have a FHx of stones. Kidney stones are solid deposits that form in the kidneys from substances excreted in urine. Children under 16 years of age constitute ~ 7% of all cases of renal stones with a 1:1 sex distribution. ~80% of pt’s with urolithiasis form calcium stones, most of which are composed primarily of calcium oxalate, and less often, calcium phosphate.

PP: The precise cause of urinary stone formation is unknown. It requires three elements: supersaturation, lack of inhibitors, and stasis. The process of stone formation depends on urinary volume; concentrations of calcium, phosphate, oxalate, sodium, and uric acid ions; concentrations of natural calculus inhibitors (e.g., citrate, magnesium, Tamm-Horsfall mucoproteins, bikunin); and urinary pH.⁴ High ion levels, low urinary volume, low pH, and low citrate levels favor calculus formation. When waste materials in urine do not dissolve completely, microscopic particles begin to form and over time grow into kidney stones. Supersaturation of urine --> crystallizes, and then aggregates. May have dec amount of urinary stone inhibitors (primarily citrate). Nanobacteria (small intracellular bacteria that from a Ca-phosphate shell) were present in the central nidus of 97% of kidney stones in ones study, but this was never replicated by others, thus likely was a contaminent (Kidney Int 1999;56:1893). A polymorphism of the Vit-D receptor gene (Fok-1) appears to be associated with some aspects of calcium urolithiasis (OR = 2.15) (BJU Int 2007;99:1534-1538)(higher first-void morning urinary calcium levels)...They were also significantly younger than the median age of 45 years at the onset of the first episode (OR = 3.23).

Risks: Hot weather and high humidity. Occupations associated with a sedentary lifestyle or with a hot, dry workplace. FHx of stones (seen in ~50%) (3-fold risk, J Am Soc Nephrol 1997;8:1568), prolonged immobilization, recurrent urinary infections, drugs (Indinavir, acetazolamide, triamterene, ephedrine, felbamate, topiramate and zonisamide, guaifenesin, calcium + Vit-D, or sulfadiazine). Bowel disease (chronic diarrheal states) promotes low urine volume, acidic urine (depletes available citrate) and hyperoxaluria. Diet high in protein, refined carbohydrates, and sodium. Excess dietary meat (including poultry) creates acidic urinary milieu, depletes available citrate; promotes hyperuricosuria. Excess dietary oxalate promotes hyperoxaluria. Excess dietary sodium promotes hypercalciuria. Low urine volume allows stone constituents to supersaturate. White > African American. Obesity may promote hypercalciuria; other results similar to excess dietary meat. Primary hyperparathyroidism creates persistent hypercalciuria. Prolonged immobilization leads to bone turnover, whick creates hypercalciuria. Renal tubular acidosis (type 1) give an alkaline urine promotes calcium phosphate supersaturation; loss of citrate. Idiopathic hypercalciuria (autosomal dominant). Cystinuria, Lesch-Nyan syndrome, hyperoxaluria types I and II (all autosomal recessive). Ehler-Danlos syndrome, Marfan syndrome and Wilson disease. Systemic illnesses that may increase the risk for kidney stone formation or otherwise affect the clinical course include primary hyperparathyroidism, renal tubular acidosis, cystinuria, gout, diabetes mellitus, inflammatory bowel disease, renal insufficiency, sarcoidosis, and medullary sponge kidney. Insulin resistance leads to ammonia mishandling; alters pH of urine. Gout promotes hyperuricosuria. Hypercalcemia (due to hyperparathyroidism, sarcoidosis, malignancy, Pagets disease or multiple myeloma). Chronically sleeping on the side at risk of calculi formation can be seen in pt’s with unilateral stone dz (J Urol 2001;165:1085), consider attaching a tennis ball to sleep ware to break this habit. HTN in 32.8% (Semin Nephrol 1995;5:519–525). Men who work in the steel industry and are exposed to high temperatures have an increased risk of developing urinary lithiasis (Urology 2005:65:858-861) (related to dehydration and hypocitraturia). The risk of developing kidney stones rises with the number of traits of metabolic syndrome a patient has (obesity, hyperglycemia, hypertriglyceridemia, low HDL-cholesterol levels, and hypertension) (Am J Kidney Dis 2008;51:741-747).....the prevalence rose from 3% with no traits to 9.8% with five traits. As temperatures across the U.S. increase because of global warming, the prevalence of kidney stones is expected to grow (PNAS 2008;July)....Assuming a mean temperature increase of 2.38 C, climate change is expected to create 1.61 to 2.25 million new cases of nephrolithiasis by 2050, an increase of 7% to 10.4% from 2000.....The "stone belt" would spread from the Southeast northward into the Midwest, covering much of the southern half of the country and all of California by 2050. Roux-en-Y gastric bypass surgery is associated with an increased postoperative risk for kidney stones according to the results of a study of insurance claims data (OR = 1.71)(J Urol. 2009;181:2573-2577).

Urine pH: Calcium oxalate stones are not pH-dependent. Most people excrete an acid urine which favors uric acid precipitation which may promote the formation of calcium stones. Calcium phosphate stones form in a relatively alkaline urine.

Child: Kidney stones are rare in children, but a study shows they increased four-fold among South Carolina children between 1996 and 2007 (J Pediatr 2010;April 15)....the number of cases per 100,000 children climbed from 7.9 to 18.5 over the 12 years of the study......The greatest increase occurred among white adolescents between the ages of 14 and 18.....several suspects: obesity, too much salt and too little milk in the diet, and changes in antibiotic use (It's hypothesized that over-use of antibiotics may kill normal gut bacteria that help protect against stone formation).

ICD-9 Codes:

592.0 Calculus of kidney - Nephrolithiasis NOS

592.1 Calculus of ureter

592.9 Urinary calculus, unspecified

594.1 Other calculus in bladder - bladder stone

594.9 Calculus of lower urinary tract, unspecified

788.0 Renal colic

S/s: Urinary stone sx's are varied and may include: Acute renal or ureteral colic—the cla ssic symptoms include colicky flank pain with radiation to the groin, ipsilateral testicle, or labia. Mild abdominal or flank discomfort. Nausea and vomiting. Hematuria (microscopic or gross). UTI. High-grade fevers or sepsis may ensue. Irritative LUTS—distal ureteric stones may present with frequency, urgency, and dysuria.

Presentation of stones in the urinary tract: Incidental finding on X-ray. Loin pain. Ureteric colic. Painful passage of small stones via urethra. Cystitis. Pyelonephritis. Haematuria. Impaired renal function.

Renal colic: a misnomer, aching flank pain that is usually constant, sometimes waxes and wanes. No position of comfort (unlike Appy, diverticulosis, salpingitis/ peritoneal inflammation (makes pt want to lay still). Pain starts as a colicky flank pain radiating to the groin / testicle or labia and can be accompanied by N/V and hematuria. Character of the pain changes as is passes down the ureter and may diminish even if stuck as transition from a hyperperistaltic to an aperistaltic ureter. At renal calyces is a deep, dull flank/back ache. At the renal pelvis it is a sharp pain radiating to the ipsilateral abd quadrant. At the upper-mid ureter it is sharp, bandlike radiating to the mid-low abd. At the distal ureter it is boring that radiates to the ipsilateral groin. Urgency and frequency can occur if stone is close to bladder. In the bladder it may produce a suprapubic pain with stranguria, urgency, frequency and/or dysuria. Pain resolves with passage of stone, may persist temporarily from ureteral edema.

Ddx: appendicitis, PID, pyelonephritis, diverticulitis, dissecting AAA, cholecystitis, ovarian pathology and ectopic pregnancy. Renal cell carcinoma. Acute intestinal obstruction.

Lab: U/A, BUN or Cr. +CBC, lytes, Ca, P. Gross or microscopic hematuria in 90-95%. Non-contrast helical CT is the imaging study of choice to evaluate patients with suspected stone disease, in the acute setting (emergency department). If known history of nephrolithiasis is present, a KUB, U/S, or both may provide initial low-cost confirmation of a recurrent stone that requires further radiographic evaluation. Link: W/u Recurrent |

X-ray / KUB: A plain abd x-ray will identify radiopaque stones such as calcium, struvite, and cystine stones, but will miss radiolucent uric acid stones, may miss small stones or stones overlying bony structures, and will not detect obstruction. Best study if PMHx of stones. 90% contain calcium and are radiopaque (yet only 30% seen in ER, up to 70% with IVP), if >2-3 mm should see on KUB. (r/o calcified mesenteric lymph node, phlebolith, fecalith, renal calcification, barium), misses 10% as uric acid, struvite calculi and cysteine are radiolucent or poorly visualized on plain film radiography. Has no role when helical CT is available. Helpful in documenting the number, size, and location of stones. Will identify calcium stones >1–2 mm in diameter. Will miss most uric acid and some cystine calculi. Will identify nephrocalcinosis—seen in hyperparathyroidism, primary hyperoxaluria, renal tubular acidosis, or sarcoidosis.

Spiral (helical) CT: without contrast (unenhanced) now considered best overall study to establish dx (96% sensitive), takes < 5 minutes, no risk of contrast reaction, detects all stone types, rules out other pathologic processes (r/o AAA if age >55yo). Takes 0.5mm cuts from top of bladder to top of kidneys (nl abd CT take 1cm cuts). To distinguish ureteral stones from phleboliths overlying the course of the ureter, look for the soft tissue "rim" = circumferential edema from a ureteral stone (Radiology 1997;202:709). Noncontrast helical CT consistently has outperformed IVP in studies of pt’s with suspected ureteral stones. Because helical CT has other advantages in this setting (no use of contrast material, visualization of other intra-abd causes of sx’s), it is becoming the imaging procedure of choice for these pt’s (Ann Emerg Med 2002;40:280-6). An unenhanced low-dose abd CT (LDCT) protocol should replace the initial abd plain film in pt's with a clinical suspicion of renal colic (Urology. 2006;67:64-68) (sensitivity of 95-100% with a 2.1-mSv radiation dose to women and 1.6 mSv to men) (the mean effective dose [all testing done] was 3.5 mSv in group 1 and 6.9 mSv in group 2). The accuracy and speed (26 versus 69 minutes) of diagnosis of helical CT vs IVP appear to outweigh its cost ($600 versus $400) (Am Fam Physician 2001;63:1329). If the obstruction is acute, proximal ureter and renal pelvis is dilated to the level of obstruction and perinephric "stranding" is seen. If chronic, renal atrophy may be noted.

IVP: Often the only test required for making management decisions in stone patients. Can be performed by a non-radiologist in an emergency. Provides precise information on the relationship of the calculus to the pelvicalyceal system and the ureter. Computed tomography: Helical CT more sensitive than KUB, IVU, or U/S. Will detect radiolucent calculi. Other conditions that mimic ureteral colic can be easily identified. May be useful in determining some composition. Poor detection of Indinavir stones. Delayed images required if high-grade obstruction (delayed “blush” if obstructed). IVP was previously the diagnostic procedure of choice, but is no longer because of potential contrast reactions, lower sensitivity, and higher radiation exposure and has now been replaced by non-contrasted helical CT as the test of choice.

Ultrasound: has a lower sens/spec, but it is the preferred imaging modality in pregnant women. Useful as a screening tool for hydronephrosis or stones within the kidney or renal pelvis. Provides information on renal parenchyma in an obstructed kidney. May detect radiolucent calculi. Useful to rule out other causes of abdominal pain. Middle and distal ureter are not clearly visible. Useful for follow-up evaluation in recurrent nephrolithiasis. The procedure of choice for patients who should avoid radiation, pregnant women and possibly women of child bearing age where gynecologic process or cholecystitis is a prominent consideration. U/S can detect radiolucent stones missed on KUB; however, it may miss small stones and ureteral stones (Ann Emerg Med 1989;18:556). Distal ureteral stones may be detected by transvaginal ultrasonography. May need an alternative study if ultrasound is negative and the clinical suspicion remains high. A retrospective study on 817 consecutive adults who underwent renal ultrasound for suspected urolithiasis at two academic EDs in Ontario, Canada, during 1 year found that patients with normal renal ultrasound results had a low rate of urologic intervention within 90 days (0.6%) than in those with scans that suggested ureterolithiasis (6.8%) or showed stones (6.2%) (CJEM 2010;12:201).......Whether imaging of any type is routinely necessary in patients with renal colic and previous imaging-documented ureterolithiasis has not been established. The key issue is the certainty of the clinical diagnosis of ureterolithiasis. If the diagnosis is uncertain — particularly in patients with no history of stones or who might have vascular disease — further imaging is important to exclude other serious diagnoses, such as abdominal aortic aneurysm, renal artery or vein occlusion, or other vascular emergencies.

Three places stones get caught: ureteropelvic junction (UPJ), midureteral (at iliac vessels), ureterovesical junction.

Stone Types seen in the USA:

Mixed Ca-oxalate and Ca-phosphate@37%.

Calcium oxalate@26%.

Calcium phosphate@7%.

Uric acid@5%.

Struvite@22%.

Cystine@2%.

(Kelly's Textbook of Medicine. New York, Lippincott Williams & Wilkins, 2006, pp 1243-1248).

Fetuin-A: a glycoprotein that inhibits the precipitation of hydroxyapatite from supersaturated solutions of calcium and phosphate in vitro; and is considered one of the more powerful inhibitors of hydroxyapatite formation. Fetuin-A concentrations are decreased in acute inflammation and end-stage renal disease. Patients with urolithiasis have lower levels of urine fetuin-A than do healthy controls, according to a case-control study (BJU Int 2008;101:1151-1154).

Tx: Links: Basic Tx & Stone Size Considerations | Medical Expulsive Therapy | Consult Indications, F/u & Surgical Options | PV |

No urgent intervention needed unless the upper urinary tract is obstructed and infected, the renal function is compromised, or there is intractable pain or vomiting. Most pt's can be managed conservatively / expectantly with analgesics...NSAIDs like Motrin 600-800mg TID, adequeat hydration, strain urine, local heat with an electric blanket at lateral abd & lower back. Takes an average of 8 days to pass, if not passed by then or fever or increased pain etc, need to monitor serum Cr. For acute pain IV Toradol better than morphine.

4 Scenarios of Acute Management: (Clev Clin J Med 2009;76;592-98)

• CT shows obstruction or hydronephrosis and the pt has signs of infections (WBC >15, chills, sweats): Admit. Start broad spectrum Abx. Drain kidney via percutaneous nephrolithotomy with ureteral stent.

• CT shows obstruction or hydronephrosis but the pt has no signs of infections: Send home. Rx oral pain med. Rx an alpha-blocker. F/u with urologist.

• CT shows no obstruction but pt has a solitary kidney or persistent pain or vomiting: Admit. IV fluid at maintenance rate. Control pain. Drain kidney if it is solitary.

• CT shows no obstruction andt pt has 2 kidneys and no persistent pain or vomiting: Send home. Rx oral pain med. Rx an alpha-blocker. F/u 1 week if not passed stone for check of serum Cr.

NSAIDs: Pt's treated with NSAIDs for renal colic report better pain relief and are less likely to need further analgesia than those treated with opioids (and less N/V) (BMJ 2004;328:1401-4), based on a pooled analysis of 10 trials. NSAIDs lower requirement for rescue analgesia and thus lower incidence of adverse effects such nausea and vomiting. Of note, in ED's, NSAIDs discourages opiate-seeking patients who may spuriously present with symptoms of renal colic. Caution is advised in patients with preexisting renal disease, consider Sulindac. A combination of IV morphine 5mg + Ketorolac 15 mg (both repeated in 20min) was superior to either drug alone for tx of acute renal colic (Ann Emerg Med 2006;48:173-81).

Other: Hydration (no benefit to stone passage), strain urine, NSAIDs, Abx if evidence of infection. Local heat with an electric blanket at lateral abd & lower back (42 C) decreases the pain, anxiety and nausea of renal colic (J Urol 2003;170:741-44).

Stone size: The likelihood of spontaneous stone passage is directly related to the size of the stone and the time needed for passage.

If stone <5 mm: 98% of proximal and distal stones pass spontaneously (J Urol 1997;158:1915–1921) (within 4 weeks, may take up to 40 days).

If 5-10mm: ~53% pass spontaneously. Observation and periodic intervention for pt’s with newly diagnosed stones <10 mm in diameter and controlled sx’s, with drugs offered when necessary to facilitate stone passage, is an appropriate tx option (AUA 2007 Annual Meeting: AUA/EAU Guidelines Update: Ureteral Stone Management. Presented May 21, 2007).

>10mm: ~20% pass and thus pt will likely need an intervention.

Time: Takes an average of 8 days to pass if <2mm, 12 days if 2-4mm and 22 days if >4mm (Time to stone passage. J Urol 1999;162:688-91). If no stone movement has occurred after a 4-6 weeks, intervention is warranted because the incidence of complications (renal deterioration, sepsis, ureteral stricture) is increased.

Medical Expulsive Therapy (MET): Indicated in most pt’s with ureteral stones measuring <1 cm who are candidates for observation, especially those with stones in the distal ureter. Medical tx costs just a fraction of the average cost of ureteroscopy ($2,645) or shock wave lithotripsy ($4,225). The estimated cost for medical tx ranges from $10 to $74 for a 28-day course of Cardura (doxazosin) to $104 to $141 for a 42-day course of Flomax. The likelihood of spontaneous urinary stone passage can be increased significantly by tx with calcium channel blockers or alpha-blockers, according to meta-analysis of 9 RCT’s with nearly 700 pt’s with urinary calculi (Lancet 2006; 368:1171-79) (chance of expulsion is 65% greater) (Risk Ratio: CCB or alpha blockers @ 1.65. Alpha blockers @ 1.54. CCB @ 1.51. CCB + steroids @ 1.90). There are large numbers of alpha-1 adrenoceptors in the distal ureter, these blockers inhibit basal ureteral tone and peristaltic frequency and decrease the intensity of ureteral contractions. A meta-analysis of 22 trials, tamsulosin (alpha-blockers) and nifedipine (calcium-channel blockers) increased the rate of spontaneous expulsion of moderate-sized (5mm) distal ureteral stones (Ann Emerg Med 2007;50:552)....recipients were more likely than controls to pass stones without need for additional intervention (risk ratio, 1.59)......four pt’s had to be treated to prevent one case of failure to pass a stone....editorialist notes that the potential benefits of these generally well-tolerated drugs probably outweigh the potential harms for most pt’s.

Tamsulosin (Flomax): 0.4 mg qd x 5-7 days. Instead of immediately performing cystoscopy or lithotripsy, new research suggests that pt’s with distal ureteral stones should be given a trial of MET (J Urol 2005;174:167-172)....210 pt's were randomized to receive home tx with tamsulosin, phloroglucinol, or nifedipine + oral corticosteroid + Abx prophylaxis. Injectable diclofenac was given on an as-needed basis. All were encouraged to drink 2 L of water daily. The expulsion rate for tamsulosin was 97.1%, whereas phloroglucinol and nifedipine had rates of 64.3% and 77.1%, respectively. Pt's treated with tamsulosin achieved stone passage in a shorter period of time and were less likely to be hospitalized and has less renal colic than pt's treated with the other agents. In another study, stone expulsion was noted in 80%, 85%, and 43%, in the nifedipine, tamsulosin, and control groups, respectively. With lower ureteral stones < 1cm in diameter, tx with nifedipine or tamsulosin increases the rate of ureteral stone expulsion and decreases the need for analgesic therapy (J Urol 2004;172:568-571). Stone expulsion in 80% on nifedipine (ave 9.3 days) and 85% with tamsulosin (ave 7.9 days) Vs 43% of controls (ave 12 days) after 4 weeks. The authors conclude that for lower ureteral stones nearest to the bladder the most effective tx is tamsulosin with cortisone, Nifedipine plus cortisone is useful for stones which are lower-ureteral but further away from the bladder (Nifedipine versus tamsulosin for the management of lower ureteral stones. J Urol 2004;172:568-71). Adjunctive tx with tamsulosin after ureteroscopic laser lithotripsy for large renal and ureteric calculi improves the stone-free rate as well as pt’s' quality of life (AUA annual meeting. Abstract 1707. May 26, 2006)(4.3% experienced ureteric colic episodes Vs 23.4% of controls and 94.6% were stone-free Vs 83.1%). Studies directly comparing nifedipine and tamsulosin have reported similar rates of stone passage, however, tamsulosin showed a somewhat faster stone passage and fewer hospitalizations and procedures (Lancet 2006;368:1171). Other alpha blockers appear to be similarly effective (The comparison and efficacy of 3 different alpha1-adrenergic blockers for distal ureteral stones. J Urol 2005;173:2010). 4 weeks of alpha blockers to facilitate spontaneous stone passage in patients with stones 10 mm in diameter. Re-image pt if spontaneous passage has not occurred. Tamsulosin 0.4 mg daily as first-line medical therapy is not associated with improved rates of ureteral stone expulsion or time to passage of the stone in patients with ureteral stones with a mean diameter of 3.1 mm (European Association of Urology 23rd Annual Congress: Abstract 313 . Presented March 27, 2008). Tamsulosin 0.4 mg taken for 10 days after unsuccessful treatment with tamsulosin and deflazacort for 10 days is associated with improved rates of ureteral stone expulsion of 80% (vs 49% for placebo), but not with shorter time to expulsion or less pain from renal colic, for stones with a mean diameter of 5.9 mm (European Association of Urology 23rd Annual Congress: Abstract 314. Presented March 27, 2008). A RCT treated 69 consecutive patients who each had a distal ureteral calculus measuring 8 mm (mean size, 4 mm) with either the selective 1a-blocker alfuzosin (Uroxatral) or placebo until passage of the stone (J Urol 2008;179:2244).....The rate of spontaneous stone passage was similar in the alfuzosin and placebo groups (74% and 77%), but stones passed significantly faster with alfuzosin than with placebo (mean time to stone passage, 5.2 vs. 8.5 days).....Alfuzosin modestly (but statistically significantly) lowered pain scores compared with placebo.

Calcium channel blockers (Nifedipine SR 30mg qd = Procardia XL or Adalat CC): x 7-28 days, and oral steroids can facilitate stone passage, both may inc the success rate & also dec the pain after ESWL (Urology 2002;59:835-38). Nifedipine 40mg qd + oral methylprednisolone 16 mg qd x 45 days lead to stone passage in 87% of pt’s Vs 65% who received methylprednisolone alone. Stone passage occurred at 11.2 +7.5 days in the pt’s treated with combo tx Vs 16.4 +11.0 days in pt’s treated with methylprednisolone alone (J Urol 1994;152:1095-98). A RCT with an oral corticosteroid and nifedipine compared with corticosteroid alone found an improved stone expulsion rate (79% Vs 35%), faster expulsion time (7 Vs 20 days) as well as a decreased requirement for analgesia (Urology 2000; 56:579–583).

Consult Urology: Immediate intervention is indicated in a pt with a high grade (anuria) obstructed solitary or transplanted kidney, bilateral obstruction or infected upper urinary tract with signs of sepsis. Urgent intervention needed if impending renal deterioration or intractable pain or vomiting. Patients with stones >10 mm in diameter, and patients with significant discomfort or who have not passed the stone after 4 to 6 weeks, should be referred to urology for potential intervention. Consider early referral if an upcoming away trip from home, persistent hydronephrosis, staghorn calculus or certain occupations (pilot or bus driver). Women who develop nephrolithiasis during pregnancy have nearly double the risk of preterm delivery as pregnant women who do not (Obstet Gynecol 2007;109:1099-1104).

F/u: If fail to pass stone in 5-7 days, fever, unrelenting pain, vomiting. Check radiograph of kidney and upper bladder (KUB), UA and serum Cr.

Urine strainer: can use a coffee filter or place a small square cut from a pair of nylon panty hose (rinse & re-use) over the urethra while voiding to catch the stone for analysis. Send passed or removed stone for analysis. (Acute renal colic from ureteral calculus. NEJM 2004;350:684-93)

Indications for removal of urinary tract stones: Obstruction of urinary flow. Infection. Persistent, recurrent or severe pain. Stones likely to cause future obstruction or infection. Small 'metabolic' stones likely to grow rapidly in size. In patients where colic could be disastrous, e.g. airline or military pilots. Patients with a solitary kidney .

For treating urolithiasis, shock wave lithotripsy, ureteroscopy, and percutaneous nephrolithotomy have replaced open surgery (BMJ. 2007;334:468-472).....Shock wave lithotripsy is effective in approximately 80% to 85% of simple renal calculi. For complex renal calculi, percutaneous nephrolithotomy is the tx of choice. Staghorn calculi should be treated, preferably with percutaneous nephrolithotomy in most pt’s. For pt’s who are pregnant, morbidly obese, or have coagulopathy, ureteroscopy is the preferred tx. Consider immediate referral for patients with larger calculi, (>1.5 cm) stone of harder composition (eg, cystine or calcium oxalate monohydrate) or for stones in complex renal or ureteral locations (lower pole calyx or mid-ureter), SWL is only successful in approximately 50% of cases and thus endoscopic stone fragmentation with a percutaneous or ureteroscopic approach is preferred.

1. Emergent Decompression: With either a nephrostomy tube (percutaneous nephrolitholapaxy = PCNL) or ureteral stent. Septic pt’s with obstruction should have nephrostomy tube placed (can be done with local anesthesia), drainage can be monitored as opposed to internal stent that might not be draining properly. When asymptomatic lower pole renal calculi require intervention, percutaneous nephrolithotomy provides a higher stone-free rate than shock wave lithotripsy, and with less scarring (J Urol 2010;183:1424-1428)....All 31 subjects in the nephrolithotomy group were stone free at 12 months. One patient (3.2%) had scarring at 3 months.....With lithotripsy, however, only 19 of 31 patients (61.3%) were stone free at 12 months, and five patients (16.1%) had renal scarring.

2. Extracorporeal Shock Wave Lithotripsy (ESWL): Usually under mild IV sedation although some machines require general or regional anesthesia Shock waves break up the stone into small fragments that pass out on own. Best choice for renal, proximal and mid ureteral stones <1-2 cm. 85% overall success rate. Occasionally a fragment can obstruct the ureter and require intervention. Repeat tx required 10-20%. Lower-pole stones have been consistently associated with decreased stone-free rates following SWL when compared with upper and middle-pole stones. Cystine, brushite and calcium oxalate monohydrate stones have demonstrated a high degree of resistance to fragmentation by SWL owing to their high density, whereas less dense stones (calcium oxalate dihydrate, hydroxyapatite and uric acid) are more susceptible to SWL (Prediction of shockwave failure in pt’s with urinary tract stones. Curr Opin Urol 2006;16:88-92). Can gait the shocks to the pt’s ECG (heart rate) such that arrhythmia potential is lowered… R-wave triggered mode, where ESWL can trigger the atrial output pulse and the subsequent inhibition of the following ventricular pulse if pt has a dual pacemakers to the VVI or VOO mode prior to ESWL to prevent this occurrence. The rate of clearance of renal stones after ESWL is lower in elderly pt’s than in younger pt’s (BJU Int 2007;100:392-395)(stone-free rate after ESWL: in the >60 year age group at 37.6% Vs in the 40-and-under at 54% and 41-60 at 43%)....suggest that "more endoscopic procedures should be offered to the elderly population." A slower rate of shock wave delivery can reduce renal injury during shock wave lithotripsy (BJU Int 2007;100:624-628)...Kidneys treated with 120 shock waves/minute showed focal to extensive subcapsular hematomas and parenchymal lesions that extended, in some cases, across the full thickness of the kidney....In contrast, kidneys treated with 30 shock waves/minute showed no surface bleeding, and parenchymal hemorrhage was limited to papillae in the region of the focal treatment area...and a majority have found a significant effect of rate of better stone breakage. Extracorporeal shock wave lithotripsy (ESWL) alters renal perfusion, particularly in elderly patients (BJU Int 2008;101:731-735).....causes considerable renal parenchymal damage, resulting in disturbances in renal perfusion on MRA. Contrary to an earlier report, shock wave lithotripsy does not increase the risk of diabetes according to 6-yr f/u data on 1947 patients treated with ESWL (Urology 2009;73:4-8). For SWL, potential benefits in treating renal stones outweigh the foreseeable risks (American Urological Association (AUA) White Paper. Published online November 25, 2009).....shock waves needed to break up stones may potentially cause tissue damage and acute injury, resulting in long-term adverse effects such as scar formation and long-term loss of functional renal tissue......Damage to renal veins may result in parenchymal bleeding and mild to severe subcapsular hematomas, with risk for hematomas doubling with each additional decade of patient age.....SWL has been associated with the development of diabetes mellitus and new-onset hypertension, some patients with renal calculi are already at greater risk for the development of diabetes mellitus and hypertension before being treated with SWL.

Pneumatic lithotripter: Can generate contact pressures of up to 2.9 MPa at the tip of the probe. The device is powered by a carbon dioxide cartridge that can deliver at least 80 shocks via a spring-loaded hammer that drives a projectile into contact with the probe. The "StoneBreaker" is a rapid and effective means of fragmenting urinary stones (BJU Internat 2007;100:629-631)...Hand-held portable, appears to offer much faster intracorporeal lithotripsy compared with other ballistic lithotripters.

Laser lithotripsy: During semirigid ureteroscopy with holmium laser lithotripsy, retrieving all stone fragments leads to better outcomes than allowing them to pass spontaneously (J Urol 2010;online ahead of print Feb 9)......"Not actively retrieving fragments during semirigid ureteroscopy and holmium laser lithotripsy is associated with a higher risk of unplanned medical visits than complete intraoperative extraction."

3. Ureteroscopy / ureterorenoscopy (URS) Stone Removal: Stone fragments are removed using suction, graspers, or basket extraction. Endoscopic (laser) lithotripsy can be successful in up to 95% for distal stones. Tx of choice for distal stones or proximal stones > 1-2cm. Indicated for ESWL failures. Ureteroscopy traditionally requires the placement of a stent in order to minimize the risk of flank pain secondary to ureteric edema and facilitate the passage of residual fragments. The presence of a ureteric stent, however, has been shown to reduce quality of life in up to 80% of pt’s and thus many authors have shown that it is not necessary on a routine basis (The management of ureteric colic. Curr Opin Urol 2006;16:71-76)….risk factors for complication included renal pelvic stone location, bilateral procedure, lithotripsy, history of urolithiasis, diabetes mellitus, recurrent/recent infection, operative time of 45 min or more plus lithotripsy and operative time of 45 min or more plus ureteral dilatation. Treatment of ureteric lithiasis with retrograde ureteroscopy and holmium:YAG laser lithotripsy appears generally more successful than ESWL (BJU Int 2009;104:1144-1147)......At 3 weeks an overall success rate of 96.4% vs 48% of the patients (NNT 2). Staged flexible ureteroscopy/holmium laser lithotripsy (URS) is a less costly alternative to percutaneous nephrostolithotomy (PNL) for renal stones 2 to 3 cm in diameter (J Urol 2009;182:1012-1017)......"Although PNL has a higher stone-free rate, it is more invasive, has a higher rate of second stage procedures, and typically requires at least one night of hospitalization, while URS has very good success rates and is much less expensive.".....The estimated cost of PNL was $19,845, significantly higher than the estimated cost of $6,675 for URS, according to their report. Transureteral lithotripsy is more effective than shockwave lithotripsy for distal ureteral stones in young children - as long as the operators are very experienced and the appropriate instruments are available (J Urol 2010;184:1106-1110).....The stone-free rate at discharge was 38% in the shockwave lithotripsy group and 66% in the transureteral group....At 2 weeks, stone-free rates in the two groups still differed significantly, at 56% with shockwave lithotripsy and 78% with transureteral lithotripsy (p=0.004).

4. Percutaneous Lithotripsy: Best for large/staghorn renal calculi, can be followed by ESWL for residual fragments. Conventional PCNL is recommended in this situation only when there is a significant stone burden or when external shock-wave lithotripsy fails. Minimally invasive percutaneous nephrolithotomy (mPCNL) is an effective and safe strategy for dealing with upper urinary tract calculi in transplanted kidneys (BJU International 2007;99:1467-1471)....should be the initial approach for most cases of upper urinary tract stones in transplanted kidneys, except for simple and small stones in the middle or lower calyx

Complications of Urolithiasis: renal failure, ureteral stricture, infection/ sepsis, urine extravasation, perinephric abscess, xanthogranulomatous pyelonephritis. Stone bulk, dilated pelvicalyceal systems, and previous UTI have strong associations with UTI after kidney stone surgery, while infected stones, pelvic urine, and cloudy urine are predictors of urosepsis after percutaneous nephrolithotomy (EAU 22nd Annual Congress: Abstract 876. Presented March 23, 2007). Patients who develop kidney stones may be at increased risk (60% more likely) of developing chronic kidney disease a cohort study on 4,066 residents of Olmsted County who had a first kidney stone from 1986 through 2003 (mean age 44, 59% males) (ASN Meeting 2008; Abstract F-FC202).......Some potential explanations for the relationship proposed by other researchers are that patients with kidney stones are predisposed to urinary tract infections or that lithotripsy could lead to kidney damage during the elimination of stones.

Retained Stones: likely no problems if in the renal pelvis. Consider annual KUB to monitor for size changes. Non-obstructing ureteral stones need annual monitoring of renal US.

Prevention of Ca stones:

Normalization of body weight (BMI) and cardiovascular risk factors, sufficient physical activity, balanced nutrition and sufficient circadian fluid intake would be the appropriate measures to avoid new calculus formation. Up to 85% of all stone pt’s could anticipate lower risk of stone recurrence with basic changes in lifestyle and dietary habits, ~15% of pt’s require additional specific pharmacological prevention (Curr Opin Urology. 2005;15:119–126).

Fluids: Increase fluid intake with the goal to produce at least 2 liters of urine per day to increase the urine flow rate and lower the urine solute concentration, both of which protect against stone formation to lower the 5 yr recurrence rate from 27% to 12% (J Urol 1996;155:839). A low urinary volume increases urinary supersaturation, thus fluid therapy is safe, cheap and effective: Increased water (8-10 cups a day) will dec recurrence by 55%. Try to maintain 2L urine output a day or try to maintain a clear-colored urine rather than yellow urine. Lemon juice/ lemonade increases citrate excretion, particularly in the hypocitraturic stone former. Lemon juice (4 ounces of concentrate per day in water or as lemonaid) resulted in increased urinary citrate levels in >92% of pt's (average increase of 142 to 346 mg/day (J Urol 1996; 156:907). Can add lemon juice or diluted potassium citrate to just plain water. The type of fluid consumed may be important; grapefruit juice may enhance the risk of stone formation (Ann Intern Med 1998;128:534), whereas pt’s who ingest one bottle of beer a day may reduce the risk of stone formation by 40% (Am J Epidemiol 1999;150:187). Consumption of Gatorade neither increases nor decreases urinary stone risk factors according to research supported by the Gatorade Sports Science Institute (J Urology 2009;182:992-997)......"water consumption (>2 L /day), which still remains first-line treatment for the prevention of nephrolithiasis."

Diet: Low salt, low protein. Increase fruit and vegetable intake, which are rich in potassium, result of increasing citrate excretion (Kidney Int 2004;66:2402). A 5 years study on 120 men found a significantly lower risk of stone recurrence among the group assigned to the normal-calcium (1200 mg/day = 30 mmol/day), low animal-protein (52 g/day), low-salt diet (2900 mg/day = 50 mmol/day NaCl) (unadjusted relative risk of 0.49)(NEJM 2002;346:77).

The (DASH) diet: (See ICU-FEN Module: DASH Diet) --> high: fruit/ veges/ fiber/ Ca/ Mg/ K, +low fat dairy = 2100 kcal/d, 27% fat, 6% saturated fat, 31g/d of fiber, 4,700mg/d of potassium, 500mg/d Mg, 1,240mg/d Ca). DASH consists of an eating plan low in total fat, saturated fat, and cholesterol and rich in fruits, vegetables, and low-fat dairy products. The underlying nutrient targets are reduced fat, saturated-fat, and cholesterol intake and increased protein, fiber, calcium, magnesium, and potassium intake The DASH diet may help protect against kidney stones according to the results of a prospective study (J Am Soc Nephrol. 2009;Published online August 13)(decreases the risk of calcium oxalate stone recurrence by 51%)......."Although we think it reasonable for calcium oxalate stone formers with high levels of urinary oxalate to avoid intake of some individual foods very high in oxalate (such as spinach and almonds), our data do not support the common practice of dietary oxalate restriction in calcium stone formers, particularly if such advice results in lower intake of fruits, vegetables, and whole grains.

High Dietary Phytates: High phytate diet (myoinositol hexaphosphate) best. Phytate is found in cold cereal, dark bread, wheat fiber, bran, rice, nuts and beans. Dietary phytate (the most abundant form of phosphate in plants) binds tightly to double charged ions such as calcium (and zinc, iron, magnesium and manganese) in the GI tract to reduce absorption and enhance urinary excretion, which may reduce stone formation (37%) (Arch Intern Med 2004;164:885-891). Calcium oxalate crystal formation is strongly inhibited in vitro by phytate.

Calcium: A normal-calcium, low animal protein and low-salt diet reduce the risk of recurrence (NEJM 2002;346:77-84). A low calcium intake, which acts by increasing the absorption and subsequent excretion of oxalate due to less complexing with calcium in the intestinal lumen (J Am Soc Nephrol 2004;15:1567).....The effect on oxalate more than counterbalances the decrease in calcium absorption and excretion. Avoid soft drinks (promotes natriuresis and hypercalcuria). Dietary calcium and supplemental calcium are not associated with increased risk of kidney stones and may even be protective in younger (27-44 yo) women (Arch Intern Med 2004;164:885-891). Recommendation for calcium intake cannot be generalized since the effect of calcium intake on stone formation depends on the type of stone, oxalate intake, presence of stones and the efficiency of calcium absorption from the bowel. Calcium restriction recommended in pt’s who have moderately to severely elevated intestinal calcium absorption and urinary calcium levels. Pt’s with calcium phosphate stones may need to carefully monitor their calcium dietary intake. Except for absorptive hypercalciuria, calcium restriction in nephrolithiasis pt’s is not recommended (Curr Opin Urology. 2005;15:119–126).

Limit Protein: A high animal protein diet, which can lead to hypercalciuria, hyperuricosuria, hypocitraturia, and elevated urinary acid excretion. Increased intake of oxalate-containing foods is controversial and likely varies considerably from person to person. Reducing animal protein intake will reduce urinary calcium, uric acid, and citrate excretion as the metabolism of sulfur-containing amino acids increases the daily acid load by generating sulfuric acid. Vegetable protein has a lower sulfur content.

Limit Salt intake: Calcium is reabsorbed passively in the proximal tubule down, thus, a low sodium diet (80-100 meq/day) can enhance proximal sodium and calcium reabsorption, leading to a reduction in calcium excretion (NEJM 2002;346:77).

Thiazied Diuretic: Thiazide therapy can lower calcium excretion by as much as 150 mg/day (3.75 mmol/day). Start at 25 mg/day of chlorthalidone or hydrochlorothiazide, some will require 50 to 100 mg/day to achieve adequate lowering of the urine calcium.

Weight: Obese people (BMI above 30) are more likely to develop kidney stones than normal weight individuals, but severe obesity doesn't seem to further increase risk (J Urology 2010;2010)......"Dietary modification and weight loss should be encouraged in the obese population for a multitude of reasons but also to reduce stone risk" they conclude.

Avoid excess: Protein (restrict to 1g/kg/d or ~<52g/d), salt (restrict to 2-3g/d by avoiding processed foods), oxalates (if have Ca-oxalate stones, particularly if have hyperoxaluria on testing – not the same as oxalate stones), prevent recurrent infections. A high salt diet, which increases urinary calcium excretion. Obesity and weight gain increase the risk of kidney stones (JAMA. 2005;293:455-462) as a larger body size may result in increased urinary excretion of calcium, oxalate, and uric acid. Higher sucrose intake is associated with an increased risk of stone formation in younger and older women (Arch Intern Med 2004; 164:885). High fructose intake is associated with an increase risk (37% with women, 27% with men) of kidney stones compares to those with lower intake (Kidney Int 2008;73:207-12)(avoid excessive soda's, fruit punch, apple juice, canned fruits etc). Cranberry juice does not seem to increase urinary citrate levels. Orange juice is not reccomended at it does not lower calcium excretion, it modestly raises oxalate excretion; and the increase in caloric intake (J Urol 1993; 149:1405). High dose vitamin C appears to increases urine oxalate excretion in certain individuals, thus high dose supplements should be avoided (J Urol 2003;170:397).

Oxalobacter formigenes: a Gram-negative, anaerobic microbe common in normal adults. Presence of O formigenes in the intestinal tract is associated with a 70% decreased likelihood of developing calcium oxalate kidney stones according to a case-control study with 247 patients with a recurrent calcium oxalate stones (J Am Soc Nephrol 2008;March).....The bacteria were more prevalent in healthy controls than in patients with a history of calcium oxalate stones (38% versus 17%).....The bacterium consumes oxalate, and its absence could result in "higher oxalate excretion in the urine and thus predisposition to [calcium oxalate] calculus formation"....Among the healthy controls, prevalence of O. formigenes was lowest (29%) in those who took antibiotics to which the bacterium is sensitive -- for example, macrolides, tetracyclines, chloramphenicol, rifampin, or metronidazole -- at any time in the past. Prevalence was highest (59%) in controls who had never used these antibiotics or taken any others in the past five years -- the non-users. This bacterium might one day be used as a probiotic to prevent stone formation. O. formigenes metabolizes oxalate in the gastrointestinal tract, which could reduce its absorption.

Citrate (Polycitra-K, Urocit-K, Bicitra, Oracit, Polycitra, Polycitra-LC): Prevention of calcium and urate kidney stones: 1 packet in water/juice PO tid-qid with meals. 15-30 mL PO solution tid-qid with meals. Tabs 10-20 mEq PO tid-qid with meals. Max 100 mEq/day.

Urinary alkalinization: 5-15 mL PO qid with meals. Polycitra-K packet 3300 mg potassium citrate/ea, Polycitra-K oral solution (1100 mg potassium citrate / 5 mL, 480 mL). Oracit oral solution (490 mg sodium citrate / 5 mL, 15, 30, 480 mL). Bicitra oral solution (500 mg sodium citrate / 5 mL, 480 mL). Urocit-K wax (potassium citrate) Tabs 5, 10 mEq. Polycitra-LC oral solution (550 mg potassium citrate/500 mg sodium citrate per 5 mL, 480 mL). Polycitra oral syrup (550 mg potassium citrate/500 mg sodium citrate per 5 mL, 480 mL. Increases urinary free bases thereby increasing pH.

SE: Hyperkalemia. Frequent: N/V, diarrhea, dyspepsia

W/u: All pt’s should have stone analysis. Detailed metabolic evaluation should be postponed until after the acute stone event has resolved.

Limited evaluation if first stone: Because the rate of recurrence is variable, most recommend only a limited evaluation after a first stone. Ck routine blood chemistries, including multiple measurements of serum calcium and phosph. A low serum phosphorus warrants further eval as well. Complete evaluation after the first stone may be warranted in individuals willing to make dietary changes or to take medical therapy (if warranted by the work-up), because of the potentially high rate of recurrence and potential morbidity from recurrent stones (BMJ 2004;328:1420).

Further eval indicated if: Recurrent, multiple stones, younger, FHx or pt requests eval. Pt’s with stones composed of cystine, uric acid, calcium phosphate or struvite.

Patients at moderate to high risk for recurrent disease: Middle-aged, white males with a family history of stones. Patients with chronic diarrheal states and/or malabsorption, pathologic skeletal fractures, osteoporosis, urinary tract infection, and gout.

Tests to order: Can simply order a “24 hour urine stone risk panel”(done by “Speacialty labs”).

24-hour urine collections: urine volume, pH, and excretion of calcium, uric acid, citrate, oxalate, sodium, creatinine, urinary supersaturation. At lease 2 or 3 separate collections may required given the high variability of this test or to obtain all of this information. If there is a substantial discrepancy between two results, a third collection may be required. Pt should maintain their usual diet and physical activities. Some even suggest waiting several months after the initial stone episode since the pt may have temporarily modified their diet. A 2-day food diary may be helpful.

Check serum for: Ca, P, uric acid, creatinine, alkaline phosphatase, intact PTH. A recent study found no significant association between stone recurrence and initial phosphate levels in serum or urine, thus may not be necessary to check (Scan J Urol 2002;36:368-72). In pt's with first-time kidney stones, conservative therapy (dietary modification only) is the most cost-effective strategy, but for pt's with recurrent kidney stones, empiric therapy (dietary modification and potassium citrate) and a modified simple metabolic evaluation (a single 24-hour urine collection for renal stone risk factors, with potassium citrate and HCTZ for pt's with hypercalciuria and potassium citrate alone for pt’s with normocalciuria) are equally cost-effective (J Urol 2004;172(6 pt 1):2275-81).

UroRisk & StoneRisk diagnostic profiles: measures 10 urine risk factors for stone formation (Calcium oxalate - Brushite - Sodium urate - Uric acid). It offers a urine collection and preservation system and is recommended for initial and recurrent stone formers who test positive for a UTI. Calculates the "relative supersaturation. Give a choice of three customized profiles. (800) 330-6565, ext. 7308

Normal values:

Calcium: For a pt with a history of renal stone formation, urinary calcium results will be more meaningful if the pt’s usual diet is followed for 3 days before specimen collection. Do not stop medications. If the urine calcium test is done because of a metabolic disorder, the pt should eat a low-calcium diet and calcium medications should be restricted for 1 to 3 days before specimen collection. Obtain multiple measurements of serum calcium (at least 2 in patients with high-normal values) to r/o primary hyperparathyroidism, which is a surgically correctable disease While stone analysis is not a good clinical guide to diagnosis of hyperparathyroidism, hypercalcemia is prevalent in this curable disease and should be monitored closely (BJU Int 2009;103:670-678)......"The hypercalcemia of hyperparathyroidism was modest, but hypercalciuria was far more marked than in (stone formers without systemic disease), because the fractional calcium excretion of hyperparathyroidism exceeded that of (stone formers without systemic disease)."......"Surgical cure of hyperparathyroidism did not completely eradicate either hypercalciuria or hypophosphatemia, suggesting that these patients have some additional mineral disorder."....."When faced with severe hypercalciuria (above 300 mg/day) it is prudent to get at least a few fasting serum calciums."

Normal diet: Men <300 (7.5 mmol/day). Women <250 (6.25 mmol/day). Child <4mg/kg.

Low-calcium diet: 50–150 mg/24 h or 1.25–3.75 mmol/d. The bulk of calcium excreted is eliminated in the stool. Increased calcium in urine results from an increase in intestinal calcium absorption, a lack of renal tubule reabsorption of calcium, resorption or loss of calcium from bone, or a combination of these mechanisms.

Ddx increased urine Ca: Hyperparathyroidism (30% to 50% of cases). Sarcoidosis. Primary cancers of breast and bladder. Osteolytic bone metastases. Multiple myeloma. Paget’s disease. Renal tubular acidosis. Fanconi’s syndrome. Vit-D intoxication. Idiopathic hypercalcuria. Diabetes mellitus. Crohn’s disease and some cases of ulcerative colitis. Thyrotoxicosis. Increased urinary calcium almost always accompanies increased blood calcium levels. Ca excretion levels > calcium intake levels are always excessive; urine excretion values >450 mg/24 hours are reliably abnormal. Increased Ca excretion occurs whenever Ca is mobilized from the bone, as in metastatic cancer or prolonged skeletal immobilization. When Ca is excreted in increasing amounts, the situation creates the potential for nephrolithiasis or nephrocalcinosis, especially with high protein intake.

Falsely elevated Ca levels: drugs (calcitonin, vitamins A, K, and C, corticosteroids), meals high in Ca (milk), increased exposure to sunlight, immobilization (especially in children).

Ddx decreased urine Ca: Hypoparathyroidism. Familial hypocalciuria hypercalcemia. Vit-D def. Preeclampsia. Acute nephrosis, nephritis, renal failure. Renal osteodystrophy. Vit D–resistant rickets. Metastatic carcinoma of prostate. Malabsorption syndrome—celiac-sprue disease, steatorrhea. Urine calcium decreases in late normal pregnancy.

Falsely decreased Ca levels: increased ingestion of phosphate, bicarbonate, antacids. Alkaline urine. Thiazide diuretics. Oral contraceptives, estrogens. Lithium.

Uric acid: Men <800 (4.8 mmol/day). Women <750 (4.5 mmol/day). High uric acid is thought to act as a nidus for calcium stone formation in calcium oxalate-stone formers.

Oxalate: Men <45 (0.5 mmol/day). Women <45 (0.5 mmol/day).

Citrate: normal is 320-1300mg for men and women. Alkalinization raises citrate excretion by diminishing the uptake of filtered citrate by the proximal tubular cells (Kidney Int 1990;38:728)(raising the pH in the tubular lumen converts the divalent form into the less reabsorbable trivalent form).

Phosphorus (360-1600mg).

Na (52-380mEq).

Mg (28-180mg/d).

Urinary Creatinine excretion: permits assessment of the completeness of the 24-hour collection. Low level suggest an incomplete collection (need repeat) except for older subjects or malnourished pt’s with decreased muscle mass.

Normal in <50 yo: 20-25 mg/kg (177-221 µmol/kg) lean body weight in men and 15-20 mg/kg (133-177 µmol/kg) in women.

Normal in >50yo: 10-12 mg/kg/d for men. 8-10mg/kg/d in women.

If normal, calculate the ratio of “measured-to-estimated creatinine clearance”. If <0.75 then repeat as inaccurate.

If 0.75-0.9 the inaccurate, but still may be useful. If 0.9-1.1 then accurate urine collection.

If 1.1-1.25 then inaccurate, but still may be useful. If >1.25 then inaccurate, needs repeat.

Sodium excretion: increased sodium intake can contribute to hypercalciuria.

24hr Urine (commercial kits are available) initially while pt on a random diet. Evaluate for volume (>2L), pH (Ca-phos stones form if pH >7, may be due to distal RTA if low urinary citrate, vegetarian diet if high citrate. If pH >7.5 suspect infection. If pH <5.5 suspect uric acid, cysteine, chronic diarrhea or strenuous physical exercise). Can repeat 24hr Ur after modified diets (Ca restriction to see if hypercalcuria is dependent on dietary intake), acid load test or on meds.

Bicarb: A low plasma bicarbonate concentration is suggestive of type 1 renal tubular acidosis or chronic diarrhea.

Underlying Causes of Stones:

Urine pH: Uric acid and cystine stones associated with acid urine. Renal tubular acidosis (type I), and infection related stones associated with alkaline urine. Tx of uric acid and cystine stones includes alkalinization of urine, limit proteins

Hypercalciuria:

Idiopathic hypercalciuria (IH) is the most common cause of calcium-containing kidney stones. Excessive urinary calcium excretion, occurs in about 5%-10% of the population (J Urol. 2008;179:1676-82) and is one of the most common (50% of cases) identifiable causes of calcium kidney stone disease.

Definition: urinary excretion of >250 mg of calcium per day in women or >275-300 mg/day in men while on a regular unrestricted diet. IH is defined as excessive urinary calcium excretion (hypercalciuria) in the setting of normocalcemia and in the absence of secondary causes of hypercalciuria. The disorder is familial, was initially thought to exhibit an autosomal dominant pattern of inheritance, but may be polygenetic. About 80% of all kidney stones contain calcium, and at least one third of all calcium stone formers are found to have hypercalciuria when tested. Hypercalciuria contributes to kidney stone disease and osteoporosis.

• It also can be defined as the excretion of urinary calcium in excess of 4 mg/kg/day or as a urinary concentration of >200 mg of calcium/L.

• An alternate definition is daily urinary excretion of >3 mg/kg or >200 mg of calcium per day while on a restricted (400 mg calcium and 100 mEq sodium) diet.

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