Urinary calculi are solid particles in the urinary system. They may cause pain, nausea, vomiting, hematuria, and chills and fever due to secondary infection. Diagnosis is based on radiologic imaging, usually noncontrast CT. Treatment is with analgesics, antibiotics for infection, medical expulsive therapy, and, sometimes, minimally invasive surgical procedures (shock wave lithotripsy or endoscopic stone removal).
The annual incidence of renal calculi in adults in the United States is approximately 1 to 2% (1–3); approximately 1 of every 1000 (4) adults in the United States is hospitalized annually because of urinary calculi. Up to 19% of men and 10% of women will develop a urinary calculus by age 70 (2). Calculi vary from microscopic crystalline foci to calculi several centimeters in diameter. A large calculus, called a staghorn calculus, can fill an entire renal calyceal system.
DR. E. WALKER / SCIENCE PHOTO LIBRARY
References
1. Hill AJ, Basourakos SP, Lewicki P, et al. Incidence of Kidney Stones in the United States: The Continuous National Health and Nutrition Examination Survey. J Urol. 2022;207(4):851-856. doi:10.1097/JU.0000000000002331
2. Tundo G, Vollstedt A, Meeks W, Pais V. Beyond Prevalence: Annual Cumulative Incidence of Kidney Stones in the United States. J Urol. 2021;205(6):1704-1709. doi:10.1097/JU.0000000000001629
3. Ghani KR, Roghmann F, Sammon JD, et al. Emergency department visits in the United States for upper urinary tract stones: trends in hospitalization and charges. J Urol. 2014;191(1):90-96. doi:10.1016/j.juro.2013.07.098
4. Scales CD Jr, Curtis LH, Norris RD, et al. Changing gender prevalence of stone disease. J Urol. 2007;177(3):979-982. doi:10.1016/j.juro.2006.10.069
Etiology of Urinary Calculi
Risk factors include metabolic disorders that increase urinary salt concentration, either by increasing excretion of calcium or uric acid salts or by decreasing excretion or urinary citrate. Examples of such disorders include hyperparathyroidism (causing hypercalciuria), renal tubular acidosis, gout, and type 2 diabetes. Dietary factors such as high sodium intake or insufficient fluid intake resulting in increased urinary concentration can also contribute to stone formation.
Approximately 85% of calculi in the United States are composed of calcium, mainly calcium oxalate (see table Composition of Urinary Calculi); 5 to 10% are composed of uric acid, 1 to 2% of cystine; and 5 to 15% of magnesium ammonium phosphate (struvite).
Composition of Urinary Calculi
Composition | Percentage of All Calculi* | Common Causes |
|---|---|---|
Calcium oxalate | 40–80 | Hypercalciuria Hypocitruria |
Calcium phosphateCalcium phosphate | 18–24 | Hypercalciuria Hyperparathyroidism Hypocitruria |
Cystine | 1–2 | |
Magnesium ammonium phosphate (struvite) | 5–15 | Urinary tract infection caused by urea-splitting bacteriacaused by urea-splitting bacteria |
Uric acid | 5–10 | Urine pH < 5.5 Hyperuricosuria (occasionally) |
*Total percentages add up to more than 100% because approximately 40% of calculi are mixed in composition. Data adapted from the following sources: Singh P, Enders FT, Vaughan LE, et al. Stone Composition Among First-Time Symptomatic Kidney Stone Formers in the Community. Mayo Clin Proc. 2015;90(10):1356-1365. doi:10.1016/j.mayocp.2015.07.016; Moe OW. Kidney stones: pathophysiology and medical management. Lancet. 2006;367(9507):333-344. doi:10.1016/S0140-6736(06)68071-9 Zreik R, Pilosov Solomon I, Saliba W, et al. The relationship between patients' kidney stone type and demographics in Israel: analysis of 10 K patients. World J Urol. 2023;41(6):1641-1646. doi:10.1007/s00345-023-04424-w Zhang D, Li S, Zhang Z, et al. Urinary stone composition analysis and clinical characterization of 1520 patients in central China. Sci Rep. 2021;11(1):6467. Published 2021 Mar 19. doi:10.1038/s41598-021-85723-3 Scales CD Jr, Curtis LH, Norris RD, et al. Changing gender prevalence of stone disease. J Urol. 2007;177(3):979-982. doi:10.1016/j.juro.2006.10.069 Tundo G, Vollstedt A, Meeks W, Pais V. Beyond Prevalence: Annual Cumulative Incidence of Kidney Stones in the United States. J Urol. 2021;205(6):1704-1709. doi:10.1097/JU.0000000000001629 | ||
For calcium calculi, risk factors vary by population. The main risk factor in the United States is hypercalciuria, a hereditary condition present in 50% of men and 75% of women with calcium calculi (1); thus, patients with a family history of calculi are at increased risk of recurrent calculi. These patients have normal serum calcium, but urinary calcium is elevated > 250 mg/day (> 6.2 mmol/day) in men and > 200 mg/day (> 5.0 mmol/day) in women.
Hypocitruria (urinary citrate < 350 mg/day [1820 micromol/day]), present in approximately 40 to 50% of calcium calculi–formers, promotes calcium calculi formation because citrate normally binds urinary calcium and inhibits the crystallization of calcium salts.
More than 10% of calcium calculi may be caused by renal tubular acidosis (2). Up to 5% of patients with calcium calculi may have primary hyperparathyroidism (3). Rare causes of hypercalciuria are sarcoidosis, vitamin D intoxicationvitamin D intoxication, hyperthyroidism, multiple myeloma, metastatic cancer, and primary hyperoxaluria.
Elevated urinary oxalate levels (hyperoxaluria, urinary oxalate > 40 mg/day [> 440 micromol/day]) may cause calcium oxalate calculus formation (hyperuricosuric calcium oxalate nephrolithiasis). Hyperoxaluria can be primary or caused by excess ingestion of oxalate-containing foods (eg, rhubarb, spinach, cocoa, nuts, pepper, tea) or by excess oxalate absorption due to various enteric diseases (eg, bacterial overgrowth syndromes, Crohn disease, ulcerative colitis, chronic pancreatic or biliary disease) or ileojejunal (eg, bariatric) surgery.
Other risk factors include taking high doses of vitamin C (ie, > 2000 mg/day), a calcium-restricted diet (possibly because dietary calcium binds dietary oxalate), and mild hyperuricosuria. Mild hyperuricosuria, defined as urinary uric acid > 800 mg/day (> 5 mmol/day) in men or > 750 mg/day (> 4 mmol/day) in women, is almost always caused by excess intake of purine (in proteins, usually from meat, fish, and poultry).
Uric acid calculi most commonly develop as a result of increased urine acidity (urine pH < 5.5), or very rarely with severe hyperuricosuria (urinary uric acid > 1500 mg/day [> 9 mmol/day]), which crystallizes undissociated uric acid. Uric acid crystals may comprise the entire calculus or, more commonly, provide a nidus on which calcium or mixed calcium and uric acid calculi can form.
Cystine calculi occur only in the presence of cystinuria.
Magnesium ammonium phosphate calculi (struvite, infection calculi) indicate the presence of urinary tract infection caused by urea-splitting bacteria (eg, Proteus species, Klebsiella species). These calculi must be treated as infected foreign bodies and removed in their entirety. Unlike other types of calculi, magnesium ammonium phosphate calculi occur 3 times more frequently in women.
Rare causes of urinary calculi include indinavir, melamine, triamterene, and xanthine.Rare causes of urinary calculi include indinavir, melamine, triamterene, and xanthine.
ANDREW BEZEAR, REED BUSINESS PUBLISHING / SCIENCE PHOTO LIBRARY
Etiology references
1. Coe FL, Evan A, Worcester E. Kidney stone disease. J Clin Invest. 2005;115(10):2598-2608. doi:10.1172/JCI26662
2. Dessombz A, Letavernier E, Haymann JP, Bazin D, Daudon M. Calcium phosphate stone morphology can reliably predict distal renal tubular acidosis. . Calcium phosphate stone morphology can reliably predict distal renal tubular acidosis.J Urol. 2015;193(5):1564-1569. doi:10.1016/j.juro.2014.12.017
3. Sharma S, Rastogi A, Bhadada SK, et al. Prevalence and predictors of primary hyperparathyroidism among patients with urolithiasis. Endocr Pract. 2017;23(11):1311-1315. doi:10.4158/EP171759.OR
Pathophysiology of Urinary Calculi
Urinary calculi may remain within the renal parenchyma or renal collecting system or be passed into the ureter and bladder. During passage, calculi may irritate the ureter and may become lodged, obstructing urine flow and causing hydroureter and sometimes hydronephrosis. Common sites of lodgment include the following:
Ureteropelvic junction
Distal ureter (at the level of the iliac vessels)
Ureterovesical junction
Larger calculi are more likely to become lodged. Typically, a calculus that becomes lodged has a diameter > 5 mm, whereas calculi ≤ 5 mm are more likely to pass spontaneously.
Even partial obstruction causes decreased glomerular filtration, which may persist briefly after the calculus has passed. With hydronephrosis and elevated glomerular pressure, renal blood flow declines, further worsening renal function. Generally, however, in the absence of infection, permanent renal dysfunction occurs only after approximately 28 days of complete obstruction.
Secondary infection can occur with long-standing obstruction, but most patients with calcium-containing calculi do not have infected urine.
Symptoms and Signs of Urinary Calculi
Large calculi remaining in the renal parenchyma or renal collecting system are often asymptomatic unless they cause obstruction and/or infection. Severe pain, often accompanied by nausea and vomiting, usually occurs when calculi pass into the ureter and cause acute obstruction. Gross hematuria also occurs, but not in all patients with urinary tract stones.
Pain (renal colic) is of variable intensity but is typically excruciating and intermittent, often occurs cyclically, and lasts 20 to 60 minutes. Nausea and vomiting are common. Pain in the flank or kidney area that radiates across the abdomen suggests upper ureteral or renal pelvic obstruction. Pain that radiates along the course of the ureter into the genital region suggests lower ureteral obstruction. Suprapubic pain along with urinary urgency and frequency suggests a distal ureteral, ureterovesical, or bladder calculus (see Symptoms and Signs of Obstructive Uropathy).
On examination, patients may be in obvious extreme discomfort, often ashen and diaphoretic. Patients with renal colic may be unable to lie still and may pace, writhe, or constantly shift position. The abdomen may be somewhat tender on the affected side as palpation increases pressure in the already-distended kidney (costovertebral angle tenderness), but without peritoneal signs (guarding, rebound, rigidity).
For some patients, the first symptom is hematuria or either gravel or a calculus in the urine. Other patients may have symptoms of a urinary tract infection, such as fever, dysuria, or cloudy or foul-smelling urine.
Diagnosis of Urinary Calculi
Clinical differential diagnosis
Urinalysis
Imaging
Identification of the cause
The symptoms and signs may suggest other diagnoses, such as
Peritonitis (eg, due to appendicitis, diverticulosis, ectopic pregnancy, or pelvic inflammatory disease): Pain is usually constant, and patients lie still because movement worsens pain; patients often also have rebound tenderness or rigidity.
Cholecystitis: May cause colicky pain, usually in the epigastrium or right upper quadrant, often with Murphy sign.
Bowel obstruction: May cause colicky abdominal pain and vomiting, but the pain is usually bilateral and not located primarily in the flank or along the ureter. Obstipation or constipation and decreased flatus are common.
Pancreatitis: May cause upper abdominal pain and vomiting, but the pain is usually constant, may be bilateral, often radiates through to the back, and is usually not along the flank or ureter.
With most of these disorders, urinary symptoms are uncommon and other symptoms may suggest which organ system is actually involved (eg, vaginal discharge or bleeding in pelvic disorders among females). Dissecting aortic aneurysm must be considered, particularly in older patients, because, if a renal artery is affected, it can cause hematuria, pain that radiates along a ureteral distribution, or both. Other considerations in the general evaluation of acute abdominal pain are discussed elsewhere (see Evaluation of Acute Abdominal Pain).
Patients suspected of having a calculus causing colic require urinalysis and usually an imaging study. If a calculus is confirmed, evaluation of the underlying disorder, including calculus composition testing, is required.
Urinalysis
Macroscopic or microscopic hematuria is common, but urine may be normal despite having multiple calculi. Pyuria with or without bacteria may be present. Pyuria suggests infection, particularly if combined with suggestive clinical findings, such as foul-smelling urine or a fever. A calculus and various crystalline substances may be present in the sediment. If so, further testing via 24-hour urine collections is usually necessary to identify the cause because the composition of the calculus and crystals cannot be determined conclusively by microscopy. The only exception is when typical hexagonal crystals of cystine are found in a concentrated, acidified specimen, confirming cystinuria.
Imaging tests
Noncontrast CT is the preferred initial imaging study in most patients. This study can detect the location of a calculus as well as the degree of obstruction. Moreover, CT may also reveal other causes of the pain (eg, aortic aneurysm). For patients who have recurrent calculi, cumulative radiation exposure from multiple CT scans is a concern. However, the routine use of low-dose renal CT can meaningfully reduce cumulative radiation dose with little loss of sensitivity (1). For patients with typical symptoms, ultrasonography or abdominal radiographs can usually confirm presence of a calculus with minimal or no radiation exposure. MRI may not identify calculi.
Although most urinary calculi can be visualized on radiograph, more definitive imaging is still needed regardless of their presence, so taking a radiograph can be avoided except in some patients with suspected recurrent calculi. Both renal ultrasonography and excretory urography (previously called intravenous urography or intravenous pyelography) can identify calculi and hydronephrosis. However, ultrasonography is less sensitive for small or ureteral calculi in patients without hydronephrosis, and excretory urography is time-consuming and exposes the patient to the risk of IV contrast agents. These studies are generally used when CT is unavailable.
Identifying the cause
The calculus is obtained by straining the urine (or, if necessary, during operative removal) and sent to the laboratory for stone analysis. Some calculi are brought in by patients. Urine specimens that show microscopic crystals are sent for crystallography.
In patients with a single calcium calculus and no additional risk factors for calculi, evaluation to exclude hyperparathyroidism is sufficient. Evaluation entails urinalysis and determination of plasma calcium concentration on 2 separate occasions. Predisposing factors, such as recurrent calculi, a diet high in animal protein, or use of vitamin C or D supplements, should be sought.
Patients with a strong family history of calculi, conditions that might predispose to calculi formation (eg, sarcoidosis, bone metastases, multiple myeloma), or conditions that would make it difficult to treat calculi (eg, solitary kidney, urinary tract anomalies) require evaluation for all possible causative disorders and risk factors. This evaluation should include serum electrolytes, uric acid, and calcium . Follow-up determination of parathyroid hormone levels is performed if necessary. Urine tests should include routine urinalysis and 2 separate 24-hour urine collections with the patient on their routine diet to determine urine volume, pH, and excretion of calcium, uric acid, citrate, oxalate, sodium, and creatinine. For further information on the medical management of kidney stones, see the guideline of the American Urological Association (), or conditions that would make it difficult to treat calculi (eg, solitary kidney, urinary tract anomalies) require evaluation for all possible causative disorders and risk factors. This evaluation should include serum electrolytes, uric acid, and calcium . Follow-up determination of parathyroid hormone levels is performed if necessary. Urine tests should include routine urinalysis and 2 separate 24-hour urine collections with the patient on their routine diet to determine urine volume, pH, and excretion of calcium, uric acid, citrate, oxalate, sodium, and creatinine. For further information on the medical management of kidney stones, see the guideline of the American Urological Association (2).
Diagnosis references
1. Zilberman DE, Tsivian M, Lipkin ME, et al. Low dose computerized tomography for detection of urolithiasis—its effectiveness in the setting of the urology clinic. J Urol. 185(3):910-914, 2011. doi: 10.1016/j.juro.2010.10.052
2. Pearle MS, Goldfarb DS, Assimos DG, et al. Medical management of kidney stones—AUA guideline. doi: 10.1016/j.juro.2014.05.006 J Urology. 92(2):316-24, 2014. doi: 10.1016/j.juro.2014.05.006
Treatment of Urinary Calculi
See also
Analgesia
Facilitate calculus passage, eg, with alpha-receptor blockers such as tamsulosin (described as medical expulsive therapy)Facilitate calculus passage, eg, with alpha-receptor blockers such as tamsulosin (described as medical expulsive therapy)
For persistent or infection-causing calculi, complete removal using primarily endoscopic techniques
Analgesia
Renal colic may be relieved with opioids, such as morphine and, for a rapid onset, fentanyl. Ketorolac is rapidly effective and nonsedating. Vomiting usually resolves as pain decreases, but persistent vomiting can be treated with an antiemetic (eg, ondansetron).Renal colic may be relieved with opioids, such as morphine and, for a rapid onset, fentanyl. Ketorolac is rapidly effective and nonsedating. Vomiting usually resolves as pain decreases, but persistent vomiting can be treated with an antiemetic (eg, ondansetron).
Expulsive therapy
Although increasing fluids (either oral or IV) has traditionally been recommended, increased fluid administration does not appear to speed passage (1). Patients with calculi < 1 cm in diameter who have no infection or obstruction, whose pain is controlled with analgesics, and who can tolerate liquids can be treated at home with analgesics and alpha-receptor blockers (eg, tamsulosin) to facilitate calculus passage. Calculi that have not passed within 6 to 8 weeks typically require removal. In patients with suspected infection and obstruction, initial treatment is relief of obstruction as soon as possible with a cystoscopically placed ureteral stent or percutaneous nephrostomy tube and treatment of the infection, followed by removal of calculi once feasible. 1 cm in diameter who have no infection or obstruction, whose pain is controlled with analgesics, and who can tolerate liquids can be treated at home with analgesics and alpha-receptor blockers (eg, tamsulosin) to facilitate calculus passage. Calculi that have not passed within 6 to 8 weeks typically require removal. In patients with suspected infection and obstruction, initial treatment is relief of obstruction as soon as possible with a cystoscopically placed ureteral stent or percutaneous nephrostomy tube and treatment of the infection, followed by removal of calculi once feasible.
Pearls & Pitfalls
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Calculus removal
The technique used for removal depends on the location and size of the calculus. Techniques include extracorporeal shock wave lithotripsy and, to ensure complete removal or for larger calculi, endoscopic techniques. Endoscopic techniques may involve rigid or flexible ureteroscopes (endoscopes) and may involve direct-vision removal (basketing), fragmentation with one of several types of lithotripsy device (eg, pneumatic, ultrasonic, laser), or both. Short-term ureteral stenting (eg, 4 to 7 days) is commonly used until resolution of any inflammation or edema caused by the stone or the procedure. Patients who have incurred ureteral trauma from either the obstructing stone or during stone removal may be stented for 1 to 2 weeks.
For symptomatic calculi < 1 cm in diameter in the renal collecting system or proximal ureter, shock wave lithotripsy is a reasonable first option for therapy.
For larger calculi or if shock wave lithotripsy is unsuccessful, ureteroscopy (performed in a retrograde fashion) with holmium or thulium laser lithotripsy is usually used. Sometimes removal is possible using an endoscope inserted anterograde through the kidney. For renal stones > 2 cm, percutaneous nephrolithotomy, with insertion of a nephroscope directly into the kidney, is the treatment of choice.
For midureteral calculi, ureteroscopy with holmium laser lithotripsy is usually the treatment of choice. Shock wave lithotripsy is an alternative.
For distal ureteral calculi, endoscopic techniques (ureteroscopy), such as direct removal and use of intracorporeal lithotripsy (eg, holmium or thulium laser, pneumatic), are considered by many to be the procedures of choice. Shock wave lithotripsy can also be used.
(See also the American Urological Association/Endourological Society Guideline, Part I.)
Calculus dissolution
Uric acid calculi in the upper or lower urinary tract occasionally may be dissolved by prolonged alkalinization of the urine with potassium citrate 20 mEq (20 mmol/L) orally 2 to 3 times a day, but chemical dissolution of calcium calculi is not possible and of cystine calculi is difficult.Uric acid calculi in the upper or lower urinary tract occasionally may be dissolved by prolonged alkalinization of the urine with potassium citrate 20 mEq (20 mmol/L) orally 2 to 3 times a day, but chemical dissolution of calcium calculi is not possible and of cystine calculi is difficult.
Treatment reference
1. Springhart WP, Marguet CG, Sur RL, et al. Forced versus minimal intravenous hydration in the management of acute renal colic: a randomized trial. J Endourol. 2006;20(10):713-716. doi:10.1089/end.2006.20.713
Prevention of Urinary Calculi
In a patient who has passed a first urinary calculus, the likelihood of forming a second calculus ranges from 11% at 2 years to 39% at 15 years (1). Drinking large amounts of fluids—8 to 10 ten-ounce (300-milliliter) glasses a day—is recommended for prevention of all stones. Patients who form stones (those with a history of recurrent stones and those with stones newly diagnosed via imaging) should drink enough fluid to produce at least 2.5 liters of urine daily. Recovery and analysis of the calculus, measurement of calculus-forming substances in the urine, and the clinical history are needed to plan other prophylactic measures.
In < 3% of patients, no metabolic abnormality is found. These patients seemingly cannot tolerate normal amounts of calculus-forming salts in their urine without crystallization. Thiazide diuretics, potassium citrate, and increased fluid intake may reduce their calculus production rate.3% of patients, no metabolic abnormality is found. These patients seemingly cannot tolerate normal amounts of calculus-forming salts in their urine without crystallization. Thiazide diuretics, potassium citrate, and increased fluid intake may reduce their calculus production rate.
For hypercalciuria, patients may receive long-acting thiazide diuretics (eg, chlorthalidone or indapamide) to lower urine calcium excretion and thus prevent urinary supersaturation with calcium oxalate. Patients are encouraged to increase their fluid intake to patients may receive long-acting thiazide diuretics (eg, chlorthalidone or indapamide) to lower urine calcium excretion and thus prevent urinary supersaturation with calcium oxalate. Patients are encouraged to increase their fluid intake to≥ 3 L/day. A diet that is low in sodium and high in potassium is recommended. Even with a high potassium intake, supplementation with potassium citrate is recommended to prevent 3 L/day. A diet that is low in sodium and high in potassium is recommended. Even with a high potassium intake, supplementation with potassium citrate is recommended to preventhypokalemia. Restriction of dietary animal protein is also recommended (2).
For patients with hypocitruria, potassium citrate enhances citrate excretion. A normal calcium intake (eg, 1000 mg or approximately 2 to 3 dairy servings per day) is recommended, and calcium restriction is avoided. Alternative alkaline agents (eg, sodium or potassium bicarbonate) can be used to enhance citrate excretion if potassium citrate cannot be tolerated. potassium citrate enhances citrate excretion. A normal calcium intake (eg, 1000 mg or approximately 2 to 3 dairy servings per day) is recommended, and calcium restriction is avoided. Alternative alkaline agents (eg, sodium or potassium bicarbonate) can be used to enhance citrate excretion if potassium citrate cannot be tolerated.
Hyperoxaluria prevention varies. Patients with small-bowel disease can be treated with a combination of high fluid intake, calcium loading (usually in the form of calcium citrate), cholestyramine, and a low-oxalate, low-fat diet. Hyperoxaluria may respond to pyridoxine, possibly by increasing transaminase activity, because this activity is responsible for the conversion of glyoxylate, the immediate oxalate precursor, to glycine.prevention varies. Patients with small-bowel disease can be treated with a combination of high fluid intake, calcium loading (usually in the form of calcium citrate), cholestyramine, and a low-oxalate, low-fat diet. Hyperoxaluria may respond to pyridoxine, possibly by increasing transaminase activity, because this activity is responsible for the conversion of glyoxylate, the immediate oxalate precursor, to glycine.
In hyperuricosuria, intake of animal protein should be reduced. If the diet cannot be changed, allopurinol lowers uric acid production. For uric acid calculi, the urine pH must be increased to between 6 and 6.5 by giving an oral alkalinizing medication that contains potassium (eg, potassium citrate) along with increased fluid intake.intake of animal protein should be reduced. If the diet cannot be changed, allopurinol lowers uric acid production. For uric acid calculi, the urine pH must be increased to between 6 and 6.5 by giving an oral alkalinizing medication that contains potassium (eg, potassium citrate) along with increased fluid intake.
Infection with urea-splitting bacteriaurea-splitting bacteria requires culture-specific antibiotics and complete removal of all calculi. If eradication of infection is impossible, long-term suppressive therapy (eg, with nitrofurantoin) may be necessary. In addition, acetohydroxamic acid can be used to reduce the recurrence of struvite calculi.requires culture-specific antibiotics and complete removal of all calculi. If eradication of infection is impossible, long-term suppressive therapy (eg, with nitrofurantoin) may be necessary. In addition, acetohydroxamic acid can be used to reduce the recurrence of struvite calculi.
To prevent recurrent cystine calculi, urinary cystine levels must be reduced to < 250 mg cystine/L of urine. Any combination of increasing urine volume along with reducing cystine excretion (eg, with alpha-mercaptopropionylglycine [tiopronin] or penicillamine) should reduce the urinary cystine concentration.-mercaptopropionylglycine [tiopronin] or penicillamine) should reduce the urinary cystine concentration.
Prevention references
1. Rule AD, Lieske JC, Li X, Melton LJ 3rd, Krambeck AE, Bergstralh EJ. The ROKS nomogram for predicting a second symptomatic stone episode. J Am Soc Nephrol. 2014;25(12):2878-2886. doi:10.1681/ASN.2013091011
2. Ferraro PM, Bargagli M, Trinchieri A, et al. Risk of kidney stones: Influence of dietary factors, dietary patterns, and vegetarian–vegan diets. Nutrients. 12(3): 779, 2020. doi: 10.3390/nu12030779
Key Points
85% of urinary calculi are composed of calcium, mainly calcium oxalate (see table Composition of Urinary Calculi); 5 to 10% are composed of uric acid,1 to 2% of cystine; and 5 to 15% of magnesium ammonium phosphate (struvite).
Larger calculi are more likely to obstruct; however, obstruction can occur even with small ureteral calculi (ie, 2 to 5 mm).
Symptoms include hematuria, symptoms of infection, and renal colic.
Test usually with urinalysis, CT scan, and—if the calculus can later be retrieved—determination of calculus composition.
Give analgesics and other medications to facilitate calculus passage (eg, alpha-receptor blockers) acutely, and remove calculi that cause infection or persist endoscopically.
Decrease the risk of subsequent calculus formation by treating with thiazide diuretics, potassium citrate, increased fluid intake, and decreased dietary animal protein, depending on calculus composition.Decrease the risk of subsequent calculus formation by treating with thiazide diuretics, potassium citrate, increased fluid intake, and decreased dietary animal protein, depending on calculus composition.
