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Overview and Recommendations
Background
- •Nephrolithiasis, the formation of renal calculi, affects nearly 1 in 11 individuals in the U.S., with a rising pediatric incidence of 6% to 10% annually and a high 5-year recurrence rate approaching 50%.
- •The Randall’s plaque hypothesis serves as the central pathophysiologic paradigm for idiopathic calcium oxalate stones, where interstitial calcium phosphate deposits in the thin loops of Henle erode through the urothelium to serve as a nidus for crystal growth.
- •Systemic metabolic health is a primary driver of lithogenesis; metabolic syndrome (OR 1.30), hypertension, and diabetes are independent risk factors, while malabsorptive states like or bariatric surgery drive enteric .
- •Stone composition dictates long-term management: calcium oxalate and phosphate are most common (~80%), followed by uric acid (linked to low urine pH), struvite (infection-related), and rare genetic variants like cystine.
- •Prognostic stakes are high in specific phenotypes; staghorn calculi filling the renal pelvis are associated with chronic inflammation, epithelial-mesenchymal transition, and progressive renal fibrosis if left untreated.
Evaluation
- •Suspect nephrolithiasis in patients presenting with sudden, severe, unilateral flank pain (renal colic) that often radiates to the groin, frequently accompanied by nausea, vomiting, and restlessness.
- •Ask about a personal or family history of stones, recent dietary changes, fluid intake habits, and history of urinary tract infections or malabsorptive bowel disease.
- •Examine for costovertebral angle (CVA) tenderness and assess vital signs for fever or tachycardia, which may signal life-threatening obstructive pyelonephritis.
- •Order a non-contrast CT of the abdomen and pelvis (NCCT) as the gold-standard diagnostic test to determine stone size, location, and density (Hounsfield units).
- •Utilize renal as the mandatory first-line imaging in pediatric and pregnant patients to minimize ionizing radiation, though it may overestimate stone size and has lower sensitivity (54%) than CT.
- •Obtain a urinalysis to screen for microscopic hematuria (present in 70-90% of cases), nitrites (suggesting infection), and urine pH (pH < 5.5 suggests uric acid; pH > 7.2 suggests struvite).
- •Assess renal function with serum creatinine and screen for with serum calcium levels in all first-time stone formers.
- •Perform a 24-hour urine collection (measuring volume, calcium, oxalate, citrate, and sodium) in recurrent or high-risk formers to identify modifiable metabolic drivers.
- •Identify 'red flag' features requiring urgent intervention: fever, solitary kidney with obstruction, bilateral obstruction, or intractable pain/emesis preventing oral hydration.
Management
- •Administer 30 mg IV or other as first-line analgesia; they are non-inferior to opioids and reduce the risk of unplanned ER visits for stent-related symptoms.
- •Initiate medical expulsive therapy (MET) with 0.4 mg daily for distal ureteral stones between 5 mm and 10 mm to facilitate spontaneous passage.
- •Decompress the collecting system immediately via or if the patient has an obstructed, infected kidney; this is a surgical emergency with a 20% mortality rate if delayed.
- •Select (ESWL) or (URS) for most symptomatic stones < 20 mm; URS generally offers higher stone-free rates in a single session.
- •Perform (PCNL) as the gold standard for large stone burdens (> 20 mm) or complex staghorn calculi.
- •Utilize (30-60 mEq/day in divided doses) for patients with hypocitraturia or uric acid stones to alkalinize the urine and inhibit crystal aggregation.
- •Consider thiazide-type diuretics like 25 mg daily to reduce urinary calcium excretion in patients with recurrent calcium stones and hypercalciuria.
- •Prescribe 15 mg/kg/day for the management of refractory struvite (infection) stones, though monitor closely for adverse effects like tremulousness.
- •Mandate high fluid intake to achieve a target urine output of > 2.5 L/day, which reduces recurrence risk by approximately 60%.
- •Refer to a urologist for any stone > 10 mm, failed trial of spontaneous passage, or stones in patients with solitary kidneys or complex anatomy.
- •Monitor residual fragments > 4 mm closely, as they have an 88% progression rate and frequently require secondary intervention.
Board Review — High Yield
- •Randall's Plaque, The subepithelial calcium phosphate nidus on the renal papilla where calcium oxalate stones originate.
- •Struvite Stones, Composed of magnesium ammonium phosphate; caused by urease-producing bacteria (e.g., Proteus, Klebsiella).
- •Uric Acid Stones, Radiolucent on X-ray but visible on CT; treated with urinary alkalinization (target pH 6.5-7.0).
- •Cystinuria, Genetic defect in COLA transporter (Cystine, Ornithine, Lysine, Arginine); stones are hexagonal and 'wax-like'.
- •Indication for Surgery, Stones > 10 mm rarely pass spontaneously; stones < 5 mm pass in ~80% of cases.
- •Infected Obstruction, A surgical emergency requiring immediate drainage (stent or nephrostomy), NOT definitive lithotripsy.
- •Thiazide Mechanism, Increases distal convoluted tubule calcium reabsorption, thereby lowering urinary calcium levels.
- •Enteric Hyperoxaluria, Seen in Crohn's/Bariatric surgery; fat malabsorption leads to calcium binding with fats, leaving free oxalate for absorption.
Deep Dive — Evidence Details
Definition & Classification
- ▸Composition (Calcium vs. Uric Acid) drives long-term medical prevention.
- ▸Stone-Free Rate (SFR) success threshold is typically <3 mm fragments.
Nephrolithiasis refers specifically to stones originating in the kidney, while urolithiasis covers the entire urinary tract [7]D5[8]D5. It is classified by composition (Calcium, Uric Acid, Struvite, Cystine), which dictates medical prevention, and surgical grade (Satava Grades 1-3) [1]A1c[6]C4. Idiopathic Calcium Nephrolithiasis (CN) is defined as stone formation without systemic causes like [1]A1c. The Stone-Free Rate (SFR) is the primary surgical success metric, typically defined as the absence of fragments or residual fragments <3 mm [6]C4. Distinguishing nephrolithiasis from nephrocalcinosis (parenchymal calcification) is vital, as the latter often signals systemic metabolic disease [1]A1c. Pearl: Distinguish between nephrolithiasis and nephrocalcinosis; the former involves stones in the collecting system amenable to passage or extraction, while the latter involves parenchymal calcification that often signals underlying systemic metabolic disease [1]A1c.
Pathophysiology & Mechanism
- ▸Nephrolithiasis results from interaction among urinary supersaturation, crystal growth and aggregation, tubular adhesion, epithelial injury, genetic susceptibility, and systemic or anatomical modifiers. [14][37][233][240]
- ▸Calcium oxalate crystal deposition can trigger oxidative stress, endoplasmic-reticulum stress, apoptosis, inflammation, necroptosis, and fibrosis. [37][38][237]
- ▸AGXT-related primary hyperoxaluria type 1 and CLCN5/OCRL1-related Dent disease demonstrate inherited mechanisms of hyperoxaluria and tubular dysfunction. [229][230][236][242]
- ▸Urinary proteins may promote calcium oxalate crystallization, aggregation, growth, and tubular-cell adhesion. [37]
- ▸Pyelovenous backflow is believed to occur at intrarenal pressures above **30 mmHg**, although its value as a sepsis-prediction threshold remains investigational. [239]
Overview
Nephrolithiasis is a multifactorial process in which urinary supersaturation, crystal nucleation and growth, crystal aggregation, retention within the kidney, and renal tubular injury interact. The clinical phenotype ranges from stable, asymptomatic calculi to stone growth, renal colic, obstruction, infection, and need for intervention; increasing imaging use has increased detection of asymptomatic stones, many of which remain stable. [14]A1a The available evidence supports a model in which metabolic, genetic, urinary, environmental, inflammatory, and anatomical factors modify the balance between crystallization and crystal clearance. [14]A1a[233][240]D
Urinary supersaturation and crystal formation
Calcium oxalate is the predominant stone type addressed by several of the cited mechanistic studies. [233][237] Excess urinary oxalate or calcium, reduced urine volume, and insufficient concentrations of endogenous inhibitors increase the likelihood that urine becomes supersaturated and permits crystal nucleation, growth, and aggregation. [228][233] A machine-learning and multi-omics study of calcium oxalate stone formers identified urinary organic-acid and inorganic-ion profiles as candidate biomarkers of metabolic dysregulation and risk stratification, supporting the concept that stone formation reflects interacting biochemical pathways rather than a single abnormality. [233]
Urinary proteins may have either inhibitory or promoting effects. Proteomic analysis of urine from calcium oxalate stone formers found chromatographic fractions with effects on calcium oxalate crystallization, crystal growth, aggregation, and adhesion to renal tubular cells; almost all tested fractions showed some promoting activity, with the greatest combined promoting scores in fractions SFQ2, SFQ8, and SFQ9. [37]C4 These findings suggest that the urinary proteome can alter not only crystal formation but also crystal retention at the tubular epithelium. [37]C4
Low fluid intake increases urinary concentration and is therefore a plausible contributor to stone risk. [228] In a nationwide retrospective cohort study, symptomatic benign prostatic hyperplasia was investigated as a potential indirect risk factor because men with lower urinary tract symptoms may restrict fluid intake to reduce urinary frequency and urgency. [228] This proposed pathway links behavioral adaptation and reduced urine volume with stone formation, although the cited abstract does not provide the cohort’s incidence estimates. [228]
Genetic and tubular mechanisms
Inherited disorders can produce nephrolithiasis through sustained hyperoxaluria or proximal tubular dysfunction. Primary hyperoxaluria type 1 results from pathogenic variants in AGXT, impairing glyoxylate metabolism and causing excessive oxalate accumulation; the resulting hyperoxaluria can lead to nephrolithiasis, nephrocalcinosis, progressive kidney injury, and end-stage kidney disease. [229]C[242]D The Tunisian study emphasizes that clinically recognized disease may be concentrated in populations with consanguinity, while the computational study identified the G161C and Y260C AGXT variants as potentially damaging to protein stability. [229]C[242]D
Dent disease illustrates how defective tubular transport promotes stones. Loss of CLCN5 function disrupts receptor-mediated endocytosis in the proximal tubule, producing low-molecular-weight proteinuria and hypercalciuria, with subsequent nephrocalcinosis, nephrolithiasis, and progressive kidney failure. [230]C[236]C Dent disease type 2 may arise from pathogenic OCRL1 variants, and clinical expression is variable, contributing to underdiagnosis or delayed diagnosis. [230]C A catalog of CLCN5 pathogenic variants was developed to improve variant interpretation and diagnostic accuracy, reinforcing the importance of genetic mechanisms in selected stone-forming patients. [236]C
Genome-wide and genome-phenome analyses in Taiwanese Han Chinese also identified genetic susceptibility to kidney stone disease and used polygenic risk scores to estimate individual risk, supporting a heritable component within otherwise multifactorial nephrolithiasis. [240]D
Tubular injury, inflammation, and crystal retention
Calcium oxalate crystals can injure renal tubular epithelial cells and activate oxidative stress, endoplasmic-reticulum stress, apoptosis, necroptosis, inflammation, and fibrosis. [37]C4[38]D5[237] Experimental work indicates that serine metabolism may protect against calcium oxalate nephrolithiasis by reducing reactive oxygen species, endoplasmic-reticulum stress, and tubular epithelial-cell apoptosis through an SDSL–IDH2 pathway. [237] In mice, nesfatin-1 mitigated glyoxylate-induced nephrolithiasis or nephrocalcinosis through GPR12 receptor modulation and inhibition of the PKCα/NADPH-oxidase pathway, providing experimental evidence for antioxidant, anti-inflammatory, and antifibrotic mechanisms. [38]D5
Environmental exposures may amplify crystal-induced injury. In an NHANES-based cross-sectional analysis, each unit increase in log-transformed urinary glyphosate concentration was associated with a 25% higher odds of nephrolithiasis (OR 1.25, 95% CI 1.06–1.47); network toxicology and experimental validation implicated PI3K/AKT signaling. [235] These observational and experimental findings indicate an association and a candidate mechanism, but do not establish that glyphosate is a causal determinant of stones in humans. [235]
Obstruction, pressure, and systemic modifiers
Obstruction changes renal hemodynamics and may produce acute kidney injury. A prospective observational study measuring circulating endocannabinoids before and after relief of upper urinary tract obstruction evaluated whether the endocannabinoid system changes during acute renal dysfunction; the system is implicated in renal hemodulation, inflammation, and organ homeostasis, while excessive activation has been linked with chronic injury. [227]C The cited study was designed to compare patients with and without acute kidney injury and to identify possible biomarkers or therapeutic targets. [227]C
During ureteroscopy, pyelovenous backflow is believed to occur when intrarenal pressure exceeds 30 mmHg; continuous pressure monitoring has therefore been studied as a potential predictor of postoperative sepsis. [239]D This mechanism links elevated collecting-system pressure with systemic infectious risk, although the cited pilot study was designed to evaluate the association and does not establish a universal predictive threshold. [239]D
Systemic and anatomical conditions can modify stone risk and composition. Inflammatory bowel disease is associated with nephrolithiasis through gut–kidney interactions involving altered metabolism, intestinal inflammation, and immune dysregulation, with Crohn disease generally carrying greater kidney-complication risk than ulcerative colitis. [241]D Urinary diversion after radical cystectomy may also be followed by late urinary tract infection and nephrolithiasis, particularly among patients undergoing ureterostomy, although the cited institutional study is observational and confounded by differences in age and comorbidity. [232] Renal transplant recipients have distinct metabolic and urological profiles, and a large stone-composition analysis specifically examined whether transplantation is associated with different urinary stone patterns. [231] Nephrocalcinosis may coexist with nephrolithiasis; a feline postmortem study used high-resolution microradiography to test associations between parenchymal mineralization and renal stones, providing comparative evidence relevant to mineral deposition and stone pathogenesis. [234]
Clinical expression
The mechanisms above explain why identical radiographic stones may behave differently: urinary supersaturation determines ongoing crystal production, tubular adhesion and injury promote retention, inherited disorders sustain metabolic drivers, and obstruction or infection determines acute morbidity. [14]A1a[37]C4[38]D5 For asymptomatic stones, subsequent pain, obstruction, infection, growth, and intervention are clinically important possible outcomes, which is why surveillance versus stone-directed treatment requires individualized assessment of metabolic, genetic, anatomical, and patient-specific risks. [14]A1a
| Contributor | Proposed mechanism | Evidence |
|---|---|---|
| Low urine volume | Concentrates lithogenic solutes and may increase urinary supersaturation | [228] |
| Urinary metabolic imbalance | Organic acids and ions reflect calcium oxalate stone-forming risk | [233] |
| Promoting urinary proteins | Enhance crystallization, growth, aggregation, or tubular adhesion | [37]C4 |
| AGXT dysfunction | Impairs glyoxylate metabolism and causes hyperoxaluria | [229]C[242]D |
| CLCN5/OCRL1 dysfunction | Causes proximal tubular abnormalities, including hypercalciuria | [230]C[236]C |
| Crystal-induced injury | Activates ROS, ER stress, apoptosis, inflammation, and fibrosis | [37]C4[38]D5[237] |
| Obstruction | Alters renal hemodynamics and may cause acute kidney injury | [227]C |
| Elevated intrarenal pressure | May permit pyelovenous backflow and contribute to infectious complications | [239]D |
Epidemiology & Risk Factors
- ▸Metabolic syndrome and Vitamin D deficiency (OR 2.29) significantly increase stone risk.
- ▸Radical nephrectomy carries an 18-fold higher risk of subsequent stones compared to partial nephrectomy.
Prevalence is 7-13% in North America [70]D5. Pediatric incidence is rising 6-10% annually [47]D5. Metabolic syndrome (OR 1.30), , and are major risk factors [52]B3b. Environmental heat increases risk (pooled RR 1.31) [65]A1a. Iatrogenic risks include (OR 18.18 vs partial) and use in children (7% incidence) [56]B3b[64]A1a. Genetic susceptibility is ~50% heritable [45]D5. Pearl: Ambient temperature and metabolic health are potent modifiable drivers; every 10% increase in population compliance with high water intake could prevent thousands of stones and save millions in healthcare costs [58]B2b[65]A1a.
Clinical Presentation & Diagnosis
- ▸CT is the gold standard for adults; Ultrasound is mandatory first-line for children/pregnancy.
- ▸Fever in the setting of obstruction is a surgical emergency (obstructive pyelonephritis).
Symptomatic stones present with sudden, paroxysmal flank pain (renal colic) radiating to the groin, often with nausea and hematuria (28-70%) [82]B3b[88]C4. Non-contrast CT is the gold standard [104]D5. Ultrasound is first-line for children/pregnancy but has only 54% sensitivity and tends to overestimate stone size [47]D5[106]B3b. Red flags requiring urgent decompression include fever/chills (infection), anuria (bilateral/solitary kidney obstruction), and intractable emesis [24]C4[113]C4. Pearl: Stone size is a poor predictor of symptoms, but it strongly dictates the need for intervention; stones >5 mm are significantly more likely to require surgical than smaller fragments [77]B2a.
Acute Management & Decompression
- ▸Use the 2026 AUA three-part guideline series as the principal framework for evaluation, treatment, surgical management, and future directions. [9][10][11]
- ▸Urgently involve urology when obstruction is accompanied by infection, systemic illness, AKI, anuria, solitary-kidney risk, or deterioration; the supplied abstracts do not specify a numeric decompression deadline. [9][10][11][136][227]
- ▸The CLAD-MB score predicted surgery within 7 days in a prospective cohort in which 10% of 602 emergency-department patients underwent surgery. [137]
- ▸Treat infection risk as central to instrumentation; positive stone cultures occurred in 56% of PCNL patients and polymicrobial cultures in 25%. [246]
- ▸Do not extrapolate postoperative PCNL or ureteroscopy studies to emergency decompression decisions. [93][140][243][244][249]
Immediate priorities
Acute nephrolithiasis management should first identify patients who may have complicated obstruction, acute kidney injury (AKI), urinary infection, or a need for early intervention. The 2026 AUA surgical-management guideline is presented as a three-part, systematic-review-based framework covering evaluation, treatment, surgical management, and future directions. [9]A1c[10]A1c[11]A1c Recurrent stones may result in kidney damage, sepsis, or invasive procedures, underscoring the importance of recognizing high-risk presentations rather than treating all renal colic as uncomplicated. [136]A1a
A patient with suspected obstructing stone and clinical evidence of infection, systemic illness, or deteriorating renal function requires urgent urologic assessment for drainage and antimicrobial management; definitive stone treatment should be planned after the acute infectious or obstructive threat has been controlled. This principle is consistent with the guideline scope and with evidence linking obstruction and AKI to physiologic changes that improve after relief of upper urinary tract obstruction. [9]A1c[10]A1c[11]A1c[227]C The supplied guideline abstracts do not provide a numeric decompression-time threshold; local emergency-urology protocols should therefore be followed when sepsis, anuria, solitary-kidney obstruction, or progressive renal impairment is suspected. [9]A1c[10]A1c[11]A1c
Analgesia and emergency-department care
Emergency-department pathways can standardize treatment of renal colic, discharge planning, and opioid stewardship. A nine-emergency-department electronic pathway study specifically evaluated opioid utilization, pain-control processes, discharge practices, and repeat visits after presentations for renal colic or ureteral stones. [251] These findings support protocolized assessment and discharge instructions, but the supplied abstract does not report the pathway’s numerical outcome estimates; no specific analgesic regimen or dose should be inferred from that study alone. [251]
Pain management should be individualized according to renal function, gastrointestinal risk, pregnancy status, allergy history, and contraindications. The references supplied for this section do not provide comparative acute-colic efficacy data for nonsteroidal anti-inflammatory drugs, acetaminophen, opioids, or intravenous fluids; treatment choices should therefore follow institutional emergency-medicine and urology protocols rather than extrapolation from postoperative studies. [9]A1c[10]A1c[11]A1c[251]
Deciding who needs early surgery
Most patients presenting with renal colic do not necessarily require immediate surgery, but the probability of intervention can be estimated clinically. In a prospective cohort of 602 emergency-department patients with renal colic, 60 patients (10%) underwent surgery within 7 days. The study prospectively refined and validated the Complicated UroLithiasis and Alternative Diagnoses (CLAD-MB) score for predicting surgery within that interval. [137]B2b The score may assist triage and follow-up planning, but it should complement—not replace—assessment for infection, obstruction severity, renal dysfunction, uncontrolled pain, vomiting, or alternative diagnoses. [137]B2b
The AUA guideline series should guide selection among observation, ureteroscopy, shock-wave lithotripsy, and percutaneous approaches according to stone and patient characteristics. [9]A1c[10]A1c[11]A1c The supplied abstracts do not reproduce the guideline’s individual stone-size, location, or procedural recommendations, so those thresholds should be verified directly in the full guideline before implementation. [9]A1c[10]A1c[11]A1c
Methods of decompression and peri-procedural infection risk
When urgent drainage is required, decompression is generally achieved by placement of a ureteral stent or a percutaneous nephrostomy tube; the supplied guideline abstracts identify surgical treatment of kidney and ureteral stones as their subject but do not provide comparative drainage instructions. [9]A1c[10]A1c[11]A1c Definitive ureteroscopy or other stone treatment should be undertaken only after appropriate evaluation and management of infection risk. Postoperative infection remains a major concern: a multicenter study evaluated flexible, navigable suction ureteral access sheath-assisted retrograde intrarenal surgery under local anesthesia in patients with stones ≤30 mm and persistent asymptomatic bacteriuria or pyuria despite antibiotic therapy, specifically because infection limits retrograde intrarenal surgery and postoperative fever or sepsis are serious complications. [243]
Stone and urine microbiology may be discordant. In a retrospective PCNL cohort, stone cultures were positive in 56% of patients and polymicrobial in 25%; these findings support careful preoperative infection assessment and consideration of intraoperative stone cultures in high-risk procedures. [246] Reported post-ureteroscopy sepsis rates may also be inflated when based solely on administrative or billing codes; one study specifically compared coded events with clinically verified Sepsis-3 cases. [247]C Accordingly, postoperative fever, hypotension, altered mental status, or other systemic deterioration after instrumentation warrants prompt clinical reassessment rather than reliance on diagnostic coding or a single culture result. [246][247]C
Definitive treatment after stabilization
For selected renal stones, less invasive techniques may facilitate recovery. Prospective observational data evaluated total tubeless mini-PCNL for renal stones measuring 10–30 mm, while a randomized trial assessed tract infiltration with 20 mL of 0.25% bupivacaine after tubeless PCNL for solitary renal pelvic stones <3 cm to reduce postoperative pain. These studies address postoperative technique, not emergency decompression, and should not be used to delay drainage in an infected or obstructed system. [249][244]
Pre-stenting before retrograde intrarenal surgery has also been evaluated in a randomized trial assessing access-sheath insertion, operative time, stone-free status, and postoperative complications; the supplied abstract does not provide the comparative results. [140]A1b Novel suction-enabled ureteroscopy has real-world retrospective data from 61 cases involving 106 stones, but this evidence is insufficient to establish superiority over standard approaches in emergency obstruction. [93]C4
Follow-up and safety net
Discharge is appropriate only when the patient is clinically stable, pain and vomiting are controlled, renal function is acceptable, and there is a reliable plan for urologic follow-up and definitive stone management. Delays in follow-up can affect time to surgery and other outcomes; a diverse urban cohort specifically examined language-associated differences in follow-up after emergency-department renal-colic visits. [245] Patients should receive clear return precautions for fever, rigors, worsening pain, persistent vomiting, reduced urine output, or clinical deterioration because obstruction complicated by infection or AKI can become life-threatening. [136]A1a[227]C
| Clinical situation | Management implication |
|---|---|
| Suspected obstructing stone with infection or systemic illness | Urgent urologic assessment for drainage and antimicrobial management; defer definitive stone treatment until stabilization. [9]A1c[10]A1c[11]A1c[136]A1a[227]C |
| AKI, anuria, solitary-kidney obstruction, or progressive renal impairment | Treat as high risk and follow emergency-urology decompression protocols; no numeric timing threshold is provided in the supplied abstracts. [9]A1c[10]A1c[11]A1c[227]C |
| Stable renal colic without high-risk features | Provide protocolized analgesia, discharge education, and timely urologic follow-up. [137]B2b[251][245] |
| Persistent bacteriuria or pyuria before endoscopic treatment | Reassess infection risk and perioperative strategy; postoperative fever and sepsis are important complications. [243][246][247]C |
Definitive Management & Prevention
- ▸PCNL is the gold standard for stones >20 mm.
- ▸Potassium citrate reduces recurrence risk by 79% (high-level evidence).
Treatment choice depends on size: <10 mm (Observation/ESWL), 10-20 mm (URS/ESWL), >20 mm (PCNL) [110]A1a[111]A1a. In children, mini-PCNL is superior to ESWL (93% vs 33% SFR) [60]A1b. Medical prevention includes high fluid intake (urine output >2.5 L/d; RR 0.39) and (1 mEq/kg/day in peds) [62]A1a[165]A1a. Recent data (NOSTONE trial) showed no benefit for over placebo for recurrence [41]A1b. Pearl: For lower pole stones < 2 cm, active displacement to the upper pole during ureteroscopy significantly improves stone-free rates (RR 1.21) without increasing complications [99]A1a.
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