Sections View Full Chapter Figures Tables Videos Annotate Full Chapter Figures Tables Videos Supplementary Content + Download Section PDF Listen ++ For further information, see CMDT Part 23-05: Urinary Stone Disease + Key Features Download Section PDF Listen +++ +++ Essentials of Diagnosis ++ Severe flank pain Nausea and vomiting Identification on noncontrast CT scan or ultrasonography +++ General Considerations ++ Affects 240,000–720,000 Americans per year The prevalence of kidney stones has increased to 8.8%, or 1 in 11 Americans, representing a 70% increase over the last 15 years Males > females (1.5:1) Initial presentation usually occurs in the third through fifth decades; more than 50% of patients will have recurrent stones Incidence is greatest during hot summer months Contributing factors to urinary stone formation Geographic factors High humidity Elevated temperatures Genetic factors Cystinuria Distal renal tubular acidosis Excess animal protein and salt intake (over 3500 mg daily) Restricted dietary calcium intake Persons in sedentary occupations have a higher incidence than manual laborers Increasing evidence is revealing that urinary stone disease may be a precursor to subsequent cardiovascular disease Five major types of urinary stones Calcium oxalate Calcium phosphate Struvite (magnesium ammonium phosphate) Uric acid Cystine Most urinary stones contain calcium (85%) and are radiopaque; uric acid stones are radiolucent Hypercalciuric calcium nephrolithiasis (> 250 mg/24 h) can be caused by absorptive, resorptive, and renal disorders (eTable 23–1) Absorptive hypercalciuria Secondary to increased absorption of calcium at the level of the small bowel, predominantly in the jejunum Can be further subdivided into types I, II, and III Type I: Independent of calcium intake. There is increased urinary calcium on a regular or even a calcium-restricted diet Type II: Dependent on dietary calcium intake Type III: Secondary to a renal phosphate leak, which results in increased vitamin D synthesis and secondarily increased small bowel absorption of calcium Resorptive hypercalciuria Secondary to hyperparathyroidism Hypercalcemia, hypophosphatemia, hypercalciuria, and an elevated serum parathyroid hormone level are found Renal hypercalciuria Occurs when the renal tubules are unable to efficiently reabsorb filtered calcium Hypercalciuria and secondary hyperparathyroidism result Hyperuricosuric calcium nephrolithiasis is secondary to dietary excesses or uric acid metabolic defects Hyperoxaluric calcium nephrolithiasis is usually due to primary intestinal disorders, including chronic diarrhea, inflammatory bowel disease, or steatorrhea Hypocitraturic calcium nephrolithiasis is secondary to disorders associated with metabolic acidosis including chronic diarrhea, type I (distal) renal tubular acidosis, and long-term hydrochlorothiazide treatment Uric acid calculi: Contributing factors include Low urinary pH Myeloproliferative disorders Malignancy with increased uric acid production Abrupt and dramatic weight loss Uricosuric medications Struvite calculi (magnesium-ammonium-phosphate, "staghorn" calculi) Occur with recurrent urinary tract infections with urease-producing organisms, including Proteus, Pseudomonas, Providencia and, less commonly, Klebsiella, Staphylococcus, and Mycoplasma (but not Escherichia coli) Urine pH ≥ 7.2 Cystine calculi: Inherited disorder with recurrent stone disease ++Table Graphic Jump LocationeTable 23–1.Laboratory findings suggestive of systemic diseases presenting with kidney stones.View Table||Download (.pdf)eTable 23–1. Laboratory findings suggestive of systemic diseases presenting with kidney stones. Disease Serum Laboratory Abnormalities Acute or chronic kidney disease Elevated serum creatinine, decreased eGFR Renal tubular acidosis Elevated serum chloride, decreased serum bicarbonate, hypokalemia Hyperuricemia with uric acid precipitation in tissues Chronic and severely elevated serum uric acid Hyperuricemia with gout Elevated serum uric acid Primary hyperparathyroidism Elevated serum calcium with elevated serum parathyroid hormone level Confirmed by sestamibi scan, neck ultrasound, or surgical exploration Vitamin D deficiency Normal serum calcium, elevated serum parathyroid hormone Confirmed by low serum 25-hydroxy vitamin D level Hypercalcemia of malignancy Elevated serum calcium, low serum parathyroid hormone Confirmed by elevated PTH-related protein or elevated 1,25-dihydroxyvitamin D and imaging eGFR, estimated glomerular filtration rate; PTH, parathyroid hormone. + Clinical Findings Download Section PDF Listen +++ +++ Symptoms and Signs ++ Acute, unremitting, and severe colic Typically localized to the flank Nausea and vomiting Patients constantly moving—in sharp contrast to those with an acute abdomen Pain episodic and radiates anteriorly over the abdomen With stone in the ureter, pain may be referred into the ipsilateral groin With stone at the ureterovesical junction, marked urinary urgency and frequency; in men pain may radiate to the tip of the penis After the stone passes into the bladder, there typically is minimal pain with passage through the urethra Stone size does not correlate with severity of symptoms + Diagnosis Download Section PDF Listen +++ +++ Laboratory Tests ++ Serum chemistries and urinalysis should be obtained for all patients with newly diagnosed nephrolithiasis Urinalysis Microscopic or gross hematuria (~90%) Absence of microhematuria does not exclude urinary stones Urinary pH Persistent urinary pH < 5.5 is suggestive of uric acid Persistent urinary pH > 7.2 is suggestive of a struvite (infection-related) or calcium phosphate stone +++ Metabolic evaluation ++ Stone analysis on recovered stones Patients with uncomplicated first-time stones: serum calcium, electrolytes, and uric acid For patients with recurrent stones or patients with a family history of stone disease Sodium intake and animal protein intake should be reduced Adequate fluid should be ingested After these changes have been made, obtain 24-h urine collection for urinary volume, pH, calcium, uric acid, oxalate, phosphate, sodium, and citrate excretion A serum parathyroid hormone (PTH) level should be checked when hyperparathyroidism is suspected as the cause of calcium oxalate or calcium phosphate stones A serum uric acid should be obtained to exclude severe hyperuricemia, which can lead to uric acid stones as well as crystal deposition in the kidneys or heart +++ Imaging Studies ++ Plain film of the abdomen (KUB, kidney-ureter-bladder) and renal ultrasonography will detect most stones Noncontrast CT is the most accurate imaging tool for evaluating flank pain given its increased sensitivity and specificity over other tests All stones whether radiopaque or radiolucent on KUB are visible on noncontrast CT, except the rare calculi due to indinavir therapy However, ultrasound is a safe and effective alternative for initial evaluation of renal colic and can be used in the emergency department with good accuracy + Treatment Download Section PDF Listen +++ +++ Medications ++ Renal hypercalciuria: Thiazides (effective long-term) Hyperuricosuric calcium nephrolithiasis Most cases (85%) can be treated with dietary purine restrictions In those cases not reversed with dietary restriction, give allopurinol, 300 mg once daily orally Hyperoxaluric calcium nephrolithiasis Adherence to a diet containing moderate calcium intake (1000–1200 mg daily), and avoiding high-oxalate containing foods Low-dose calcium carbonate (250 mg) can be consumed with meals if dietary calcium increases are not successful to reach the 1000 mg daily mark If the diarrhea or steatorrhea cannot be effectively curtailed, oral calcium should be increased with meals, either by ingesting dairy products or taking low-dose calcium carbonate supplements (250 mg) Excess ascorbic acid (> 2000 mg/day) substantially increases urinary oxalate levels Hypocitraturic calcium nephrolithiasis Potassium citrate, 40–60 mEq total daily intake, divided either into two or three times daily Oral lemonade Has been shown to modestly increase urinary citrate However, it must be consumed several times every day as oral citrate is cleared from the urine in 6–8 hours Uric acid calculi Patients should monitor their urinary alkalinization with Nitrazine pH paper If hyperuricemia is present in addition to hyperuricosuria, give allopurinol, 300 mg once daily orally Struvite calculi Relatively soft and amenable to percutaneous removal Appropriate perioperative antibiotics are required Cystine calculi Exceptionally challenging to manage medically Prevention is centered around Marked increase in fluid intake during the day and night to achieve a urinary volume of 3–4 L/day Decrease in dietary sodium and cystine intake Urinary alkalinization (typically with high-dose potassium citrate) with a goal urinary pH > 7.0 (monitored with Nitrazine pH paper), Refractory stone formers may be treated with disulfide inhibitors such as tiopronin (alpha-mercaptoproprionylglycine) or penicillamine There are no known inhibitors of cystine calculi Difficult to manage medically +++ Surgery ++ Resorptive hypercalciuria: surgical resection of the parathyroid adenoma Infection with ureteral obstruction: a medical emergency requiring both antibiotics and prompt drainage by a ureteral catheter or a percutaneous nephrostomy tube Ureteral stones Stones < 5–6 mm in diameter will usually pass spontaneously Active medical expulsive therapy with appropriate pain medications is appropriate for first few weeks Medical expulsive therapy (eg, tamsulosin, 0.4 mg orally once daily, plus ibuprofen, 600 mg orally three times per day on a full stomach, with or without a short course of a low-dose oral corticosteroid [such as prednisone 10 mg orally daily for 5–10 days]) increases rate of spontaneous stone passage Therapeutic intervention is required if spontaneous passage does not occur or if patient has intolerable pain or persistent nausea and vomiting Indications for earlier intervention include Severe pain unresponsive to medications Fever Persistent nausea and vomiting requiring intravenous hydration Distal ureteral stones: ureteroscopic stone extraction or extracorporeal shock wave lithotripsy (SWL) Proximal ureteral stones—those above the superior margin of the sacroiliac joint—as well as intrarenal stones can be treated with SWL or ureteroscopy Renal calculi Conservative observation for patients presenting without pain, urinary tract infections, or obstruction Intervention if calculi become symptomatic or grow in size SWL is most effective for stones < 1 cm in the lower pole of the kidney or < 2 cm elsewhere in the kidney SWL is less effective for stones that are very hard (cystine stones, calcium oxalate stones > 1000–1200 Hounsfield units on CT scan) and for obese patients (skin-to-stone distance > 10–12 cm) Ureteroscopy and laser lithotripsy is effective for multiple stones and larger stones, though very large stones may require multiple treatment sessions Stones > 15–20 mm and staghorn stones (large branched stones occupying at least two renal calices) are best treated via percutaneous nephrolithotomy Perioperative antibiotics given as indicated by preoperative urine cultures +++ Therapeutic Procedures ++ Forced intravenous fluid diuresis is not productive and exacerbates pain + Outcome Download Section PDF Listen +++ +++ Follow-Up ++ Routine follow-up every 6–8 months and annual imaging (preferably with ultrasonography) Helps encourage medical compliance Assesses for interval stone formation or growth Permits adjustments in medical therapy based on repeat metabolic studies +++ Prevention ++ To reduce stone recurrences, patients are encouraged to: Increase fluid intake to void 2.5 L/day Ingest fluids during meals, 2 h after each meal, prior to going to sleep in the evening, and during the night Reduce sodium intake Reduce animal protein intake during individual meals +++ When to Refer ++ Evidence of urinary obstruction Urinary stone with associated flank pain Anatomic abnormalities, solitary kidney, or chronic kidney disease Concomitant pyelonephritis or recurrent infection +++ When to Admit ++ Intractable nausea/vomiting or pain Obstructing stone with fever or other signs of infection + References Download Section PDF Listen +++ + +Alelign T et al. Kidney stone disease: an update on current concepts. Adv Urol. 2018 Feb 4;2018:3068365. [PubMed: 29515627] + +Corbo J et al. Kidney and ureteral stones. Emerg Med Clin North Am. 2019 Nov;37(4):637–48. [PubMed: 31563199] + +Diri A et al. Management of staghorn renal stones. Ren Fail. 2018 Nov;40(1):357–62. [PubMed: 29658394] + +Hernandez N et al. Cessation of ureteric colic does not necessarily mean that a ureteral stone has been expelled. J Urol. 2018 Apr;199(4):1011–4. [PubMed: 29107030] + +Kim D et al. Hydroxycitrate: a potential new therapy for calcium urolithiasis. Urolithiasis. 2019 Aug;47(4):311–20. [PubMed: 30915494] + +Li JK et al. Updates in endourological management of urolithiasis. Int J Urol. 2019 Feb;26(2):172–83. [PubMed: 30575154] + +Mayans L. Nephrolithiasis. Prim Care. 2019 Jun;46(2):203–12. [PubMed: 31030821] + +Skolarikos A. Medical treatment of urinary stones. Curr Opin Urol. 2018 Sep;28(5):403–7. [PubMed: 29939860] + +Song L et al. 24-hour urine calcium in the evaluation and management of nephrolithiasis. JAMA. 2017 Aug 1;318(5):474–5. [PubMed: 28763529] + +Strilchuk L et al. Safety and tolerability of available urate-lowering drugs: a critical review. Expert Opin Drug Saf. 2019 Apr;18(4):261–71. [PubMed: 30915866] + +Zumstein V et al. Surgical management of urolithiasis—a systematic analysis of available guidelines. BMC Urol. 2018 Apr 10;18(1):25. [PubMed: 29636048]