Stones

Epidemiology and Pathogenesis

Urolithiasis forms when urine becomes supersaturated with stone-forming salts and the balance of promoters and inhibitors tips toward crystallisation. Stone type is driven by specific metabolic derangements, urine pH, and — for struvite — infection, and understanding these underpins both prevention and treatment.

Epidemiology

• Lifetime prevalence is roughly 1–15%, varying by age, sex, race, geography, and BMI.
• Uncommon before age 20; incidence peaks in the 40s–60s.
• More common in men, though the gap is narrowing; highest among White populations and in the southeastern US.
• BMI, waist size, and weight gain correlate positively with stone risk. Asymptomatic renal stones are found in ~10% of screened populations.

Stone Formation and Inhibitors

Urine must be supersaturated for stones to form, but supersaturation alone is insufficient because of urinary inhibitors. The solubility product is the equilibrium point of saturation; above it (the metastable state) crystals grow on pre-existing crystals (heterogeneous nucleation), and only when the formation product is exceeded does spontaneous (homogeneous) nucleation occur. Inhibitors prevent or delay crystallisation in the supersaturated state.

Inhibitors of calcium oxalate/phosphate crystallisation (6): nephrocalcin, magnesium (complexes oxalate), bikunin, citrate (the most important), Tamm-Horsfall mucoprotein (the most abundant urinary protein), and uropontin. No known inhibitors affect uric acid crystallisation. Citrate acts by complexing calcium (lowering calcium oxalate saturation), inhibiting spontaneous precipitation and crystal agglomeration, inhibiting calcium oxalate and (more strongly) calcium phosphate crystal growth, and preventing heterogeneous nucleation of calcium oxalate by monosodium urate.

Stones have a crystalline component (calcium is the most common constituent) and a non-crystalline matrix (≈2.5% of stone weight, ~65% protein). Randall plaques — calcium apatite originating in the basement membrane of the thin loops of Henle — extend to a subepithelial location and anchor calcium oxalate stone formation.

Mineral Metabolism

Calcium — 30–40% of dietary calcium is absorbed (mostly small intestine, ~10% colon), with fractional absorption rising on a low-calcium diet and falling on a high-calcium diet. Oxalate, citrate, phosphate, sulfate, and fatty acids complex calcium and reduce its absorption.

• PTH (secreted in response to low serum calcium): increases renal calcium reabsorption and phosphate excretion (primary effect), stimulates 1α-hydroxylase (converting 25-OH-vitamin D to calcitriol; also stimulated by hypophosphataemia), and increases calcium release from bone.
• Calcitriol [1,25(OH)₂D₃, active vitamin D]: the most potent stimulator of intestinal calcium absorption (PTH does not target the intestine), increases renal calcium and phosphate reabsorption, increases bone calcium release, and inhibits PTH release.

Oxalate — only 6–14% of ingested oxalate is absorbed (throughout the gut). Absorption is reduced by oxalate-degrading bacteria (Oxalobacter formigenes) and oxalate-binding cations (calcium, magnesium). Absorbed oxalate is nearly completely excreted in urine; about half of urinary oxalate is dietary and the rest endogenous (hepatic, from ascorbic acid and glycine).

Classification

Stone	Frequency
Calcium oxalate	60%
Hydroxyapatite	20%
Uric acid	7%
Struvite	7%
Calcium phosphate / brushite	2%
Cystine	1–3%
Triamterene, silica, 2,8-dihydroxyadenine	<1% each

Metabolic Risk Factors

Hypercalciuria

The most common abnormality in calcium stone formers (and the most common cause of microscopic haematuria in children).

Type	Serum Ca	PTH	Mechanism
Absorptive	Normal	Normal/suppressed	↑ intestinal calcium absorption → transient ↑ serum Ca → suppressed PTH → ↑ urinary Ca. Type I: hypercalciuria regardless of diet; type II: only on a normal diet
Renal (leak)	Normal	Elevated	Impaired renal calcium reabsorption → urinary loss → secondary hyperparathyroidism; high fasting urinary calcium
Resorptive	Elevated	Elevated	Usually primary hyperparathyroidism (adenoma) → bone resorption + ↑ calcitriol, with hypophosphataemia. Recurrent 100% brushite stones should raise suspicion for primary HPT
Idiopathic	Normal	Normal	Hypercalciuria without a serum abnormality

Elevated PTH with high fasting urinary calcium differentiates renal from absorptive hypercalciuria. Rare resorptive causes include malignancy (PTHrP), sarcoidosis (macrophage 1α-hydroxylase), thyrotoxicosis, and vitamin D toxicity.

Hyperoxaluria

Four types: primary (rare autosomal recessive defect of glyoxylate metabolism), enteric, dietary, and idiopathic. In enteric hyperoxaluria (fat malabsorption — IBD, celiac, bowel resection, Roux-en-Y bypass), unabsorbed fatty acids saponify calcium, leaving more free oxalate for absorption, and bile salts increase colonic permeability to oxalate; the result is calcium oxalate stones with hypocitraturia and hypomagnesuria from chronic metabolic acidosis. Manage with calcium supplementation timed with meals (not oxalate restriction alone). Dietary hyperoxaluria comes from oxalate-rich foods (rhubarb, chocolate, pepper, nuts, tea, spinach, beets, berries); keep calcium intake moderate (do not severely restrict) and limit vitamin C to ≤2 g/day (a substrate for oxalate).

Hyperuricosuria

May cause pure uric acid stones or calcium oxalate stones (heterogeneous nucleation by monosodium urate). The most common cause is increased dietary purine intake; others include gout, myelo-/lymphoproliferative disorders, multiple myeloma, thalassaemia, haemolytic disorders, pernicious anaemia, haemoglobinopathies, secondary polycythaemia, HGPRT deficiency (Lesch-Nyhan), PRPP-synthetase overactivity, and hereditary renal hypouricaemia.

Renal Tubular Acidosis

A metabolic acidosis, acquired (mnemonic A CASH POT: Analgesic nephropathy, idiopathic hyperCalciuria, ATN, Sarcoidosis, Hyperparathyroidism, Pyelonephritis, Obstructive uropathy, renal Transplant) or inherited.

Type	Defect	Stones	Features
1 (distal)	Impaired H⁺ secretion (α-intercalated cells)	Common (up to 70%); calcium phosphate	Urine pH >6.0, hyperchloraemic non-anion-gap acidosis, hypercalciuria, hypocitraturia, hypokalaemia, nephrocalcinosis
2 (proximal)	Impaired HCO₃⁻ reabsorption	Uncommon	Serum HCO₃⁻ 15–18, urine pH <5.5 at steady state; citrate not low
4 (distal)	Impaired mineralocorticoid response	Uncommon	Chronic renal damage; hyperkalaemia

Incomplete type 1 RTA is confirmed by inadequate urinary acidification after an ammonium chloride load; potassium citrate corrects the acidosis and hypokalaemia.

Hypomagnesiuria, Hypocitraturia, and Urine pH

• Hypomagnesiuria — rare; most often from IBD malabsorption or chronic thiazide therapy. Low magnesium reduces inhibitory activity and lowers urinary citrate.
• Hypocitraturia — acid-base state is the primary determinant (acidosis lowers citrate, alkalosis raises it). Causes (mnemonic DIRT): chronic Diarrhoea, Idiopathic, type 1 RTA, Thiazides. Severe hypocitraturia should raise suspicion for RTA.
• Urine pH — at low pH (<5.5) undissociated uric acid predominates, promoting uric acid and (via heterogeneous nucleation) calcium oxalate stones. Chronic metabolic acidosis lowers urine pH and citrate while raising calcium.

Stone Types

Calcium

Urinary calcium and oxalate are equal contributors to calcium oxalate stones, driven by the metabolic derangements above (hypercalciuria, hyperoxaluria, hyperuricosuria, hypocitraturia).

Uric Acid

Three determinants: low urine pH (<5.5, most important), low urine volume, and hyperuricosuria. Diabetics form uric acid stones ~6× more often (insulin resistance impairs renal ammoniagenesis → low urine pH; 34% of diabetic vs 6% of non-diabetic stone formers). Other causes: obesity, metabolic syndrome, tumour lysis, volume depletion, high animal protein, chronic diarrhoea, and uricosuric drugs.

Calcium Phosphate

Associated with type 1 RTA, primary hyperparathyroidism, medullary sponge kidney, and carbonic anhydrase inhibitors.

Cystine

From cystinuria — autosomal recessive (SLC7A9 or SLC3A1), impairing renal tubular and intestinal reabsorption of Cystine, Ornithine, Lysine, Arginine (COLA). Poorly radio-opaque; the sodium nitroprusside spot test turns urine purple and is used for screening.

Struvite (Infection)

Magnesium ammonium phosphate stones form only with infection by urease-producing organisms — Proteus (most common), Klebsiella, Pseudomonas, Staphylococcus aureus (most E. coli do not produce urease). Urease hydrolyses urea to ammonium and CO₂, raising urine pH and precipitating struvite. More common in females (2:1) and those prone to recurrent UTI (diabetics, elderly, urinary stasis, neurogenic bladder, spinal-cord injury). Commonly form staghorn calculi (as can cystine, calcium oxalate monohydrate, and uric acid).

Other Stones

• Matrix — rare; ~65% organic protein; associated with urea-splitting UTI, prior stones/surgery, and obstruction; radiolucent and can mimic a soft-tissue mass.
• Xanthine — inherited xanthine dehydrogenase deficiency; high-dose allopurinol can rarely precipitate it; radiolucent.
• 2,8-dihydroxyadenine — adenine phosphoribosyltransferase deficiency (autosomal recessive); radiolucent.
• Ammonium acid urate — laxative abuse, recurrent UTI/uric acid stones, IBD; rare in industrialised nations.

Medication-Associated Stones

Mnemonic Lotta Good Drugs Cause Calculi FIT TEST: laxatives, guaifenesin, vitamin D, vitamin C (→ oxalate), carbonic anhydrase inhibitors (acetazolamide → calcium phosphate), furosemide, thiazides (intracellular acidosis → hypocitraturia), indinavir (HIV protease inhibitor — radiolucent, may not be seen on CT), topiramate (carbonic anhydrase inhibitor → distal-RTA-like picture; treat with potassium citrate or stop), triamterene (radiolucent), ephedrine, silicates, and TMP/SMX.

Anatomic Predisposition

UPJ obstruction, horseshoe kidney, caliceal diverticulum, and medullary sponge kidney (congenital cystic dilatation of collecting tubules → stasis, nephrocalcinosis, and a distal-RTA-like picture; hyperechoic papillae with clustered small stones on imaging). For UPJO and horseshoe kidney an underlying metabolic abnormality is still required for stone formation, and correcting the UPJO does not prevent recurrence in most patients.

Diagnosis and Evaluation

Non-contrast CT is the most sensitive test for stones, but management hinges on recognising the obstructed, infected kidney (an emergency) and — for recurrent or high-risk formers — a metabolic work-up built on stone analysis and the 24-hour urine.

Imaging

Modality	Sensitivity	Specificity	Notes
Plain film (KUB)	57%	76%	Cheapest, low radiation (~0.7 mSv); misses small stones and underestimates >90% of stones >10 mm
Ultrasound	84%	53%	No radiation (~5× KUB cost); misses most ureteric stones; poor size correlation (underestimates <10 mm, overestimates >10 mm)
Non-contrast CT	95%	98%	Most sensitive; low-dose ~3 mSv, standard ~10 mSv (~10× KUB cost). Uric acid stones have much lower Hounsfield units than calcium
MRI	82%	98%	No radiation; stones appear as filling defects; most expensive (~30× KUB)

Radiolucent stones (invisible on KUB): uric acid, matrix, and the medication stones (xanthine, triamterene, 2,8-dihydroxyadenine, indinavir). Radio-opaque: calcium oxalate and calcium phosphate (densest). Poorly radio-opaque: struvite and cystine.

Forniceal extravasation (usually from a small distal ureteric stone) is managed like any ureteric stone — intervene for fever, vomiting, or unrelenting pain, otherwise observe.

Nephrocalcinosis — diffuse renal calcium deposition, usually medullary (type 1 RTA, hyperparathyroidism, medullary sponge kidney, hypervitaminosis D, milk-alkali syndrome, sarcoidosis) or, less commonly, cortical (cortical necrosis, primary hyperoxaluria/oxalosis, Alport syndrome, chronic glomerulonephritis).

Acute Presentation and Management

New urgency/frequency suggests a stone at the UVJ irritating the bladder; sudden relief of flank pain suggests stone passage or forniceal rupture. Examine for costovertebral-angle tenderness and check urinalysis ± culture, CBC, and creatinine.

• Analgesia — ketorolac 30 mg IV, IV lidocaine 1.5 mg/kg (max 200 mg) over 10 minutes, acetaminophen 1000 mg PO, and a fluid bolus.
• Obstruction with suspected infection is an emergency — urgently drain the collecting system (ureteric stent or percutaneous nephrostomy) and defer definitive stone treatment until sepsis is controlled and antibiotics are completed.

Metabolic Evaluation

Screening evaluation (all newly diagnosed stones, AUA): history and physical, laboratory (urinalysis ± culture, serum electrolytes, calcium, creatinine, uric acid), and imaging to quantify stone burden. Obtain a stone analysis at least once — a calcium phosphate composition points to type 1 RTA, primary hyperparathyroidism, medullary sponge kidney, or carbonic anhydrase inhibitors.

Extended evaluation — one or two 24-hour urine collections, indicated for recurrent formers, family history, solitary kidney, malabsorptive intestinal disease, obesity, recurrent UTIs, predisposing conditions (RTA type 1, primary hyperparathyroidism, gout, diabetes), anatomic abnormalities, cystine/uric acid/struvite stones, and children. Analyse at minimum volume, pH, creatinine, sodium, potassium, calcium, oxalate, uric acid, and citrate (add cystine if suspected). First-time formers have a ~50% recurrence risk within 10 years.

• Collection adequacy is judged by 24-hour creatinine (males 20–25 mg/kg, females 15–20 mg/kg). Primary hyperoxaluria is suspected when urinary oxalate exceeds 75 mg/day without bowel dysfunction — refer for genetic testing.
• Urine pH — normal 5.8–6.2; >7.0 suggests infection lithiasis or RTA; <5.5 suggests uric acid stones / gouty diathesis.
• PTH — check if primary hyperparathyroidism is suspected (mid-range PTH with high/high-normal calcium, hypercalciuria, calcium phosphate stones); low vitamin D can mask it.
• Diet and drugs — assess fluid, protein, calcium, sodium, oxalate, and supplement intake; stone-provoking agents include triamterene, carbonic anhydrase inhibitors (topiramate, acetazolamide, zonisamide), probenecid, protease inhibitors, lipase inhibitors, chemotherapy, and high-dose vitamin C/D. Roux-en-Y bypass raises stone risk, whereas restrictive bariatric surgery (sleeve, band) does not.

Diet and Pharmacologic Management

Targeted prevention rests on stone composition and the 24-hour urine. Dietary measures apply to all stone formers, while drug therapy is matched to the specific metabolic abnormality.

Dietary Therapy

Six measures reduce recurrence: increase fluid, limit sodium, keep calcium intake normal, limit oxalate, increase fruit and vegetables, and limit non-dairy animal protein.

• Fluid — target urine output >2.5 L/day (an RCT showed 12% vs 27% recurrence at 5 years). The absolute volume matters more than the type of fluid; citrate-rich citrus juices and citric-acid-based sodas may help, whereas phosphoric-acid colas and sugar-sweetened drinks raise risk (coffee, tea, and alcohol are associated with lower risk).
• Sodium — limit to ≤100 mEq (2,300 mg)/day; high sodium raises urinary calcium and pH and lowers citrate.
• Calcium — keep at the RDA (1,000–1,200 mg/day); a low-calcium diet leaves unbound gut oxalate, increasing oxalate absorption and urinary oxalate. Calcium citrate supplements taken with meals are preferred.
• Oxalate — limit oxalate-rich foods (spinach, beets, chocolate, nuts, tea) while maintaining normal calcium; most useful in enteric hyperoxaluria. Limit vitamin C (a substrate for oxalate).
• Fruit and vegetables — increase to raise urinary citrate (for low-citrate calcium formers).
• Animal protein — limit (it raises urinary calcium, oxalate, and uric acid); high-purine foods include anchovies, sardines, and organ meats.
• Cystine formers need a higher fluid target (≥4 L/day) plus sodium and protein restriction.

A low-carbohydrate, high-protein weight-loss diet increases both stone and bone-loss risk. Vitamin D supplementation is controversial — monitor 24-hour urinary calcium during repletion.

Pharmacologic Therapy

Stone / abnormality	First-line drug	Key points
Calcium + hypercalciuria	Thiazide	Pair with dietary sodium restriction; add potassium (citrate)
Calcium + hypocitraturia	Potassium citrate	First-line for RTA, thiazide-induced, and idiopathic hypocitraturia
Calcium oxalate + hyperuricosuria (normal urinary Ca)	Allopurinol	Also limit animal protein; hyperuricaemia not required
Uric acid	Potassium citrate (alkalinise)	Target pH >5.5 (AUA 6.0, CUA 6.5); avoid >7.0 (calcium phosphate risk)
Cystine	Fluid + alkalinisation + Na/protein restriction	Target pH 7.0; add a thiol (tiopronin) if refractory
Struvite	Surgical clearance	AHA only after surgical options exhausted

Calcium Stones

Thiazides stimulate distal calcium reabsorption and, via mild volume depletion, enhance proximal sodium/calcium reabsorption. Chlorthalidone (25 mg/day) and indapamide (2.5 mg/day) are preferred over hydrochlorothiazide (long-acting, once daily). Always combine with sodium restriction (a sodium load blunts the hypocalciuric effect). Adverse effects: lassitude (most common) and a metabolic cluster — three "hypers" (hyperglycaemia, hyperlipidaemia, hyperuricaemia), three "hypos" (hypokalaemia, hypomagnesaemia, hypocitraturia), and metabolic alkalosis. Give potassium (preferably potassium citrate) to offset hypokalaemia and glucose intolerance, or add amiloride/spironolactone (avoid triamterene). A thiazide challenge can unmask primary hyperparathyroidism, and thiazides lose efficacy in ~25% over the long term (calcitonin escape).

Potassium citrate corrects hypocitraturia and the acidosis/hypokalaemia of distal RTA, and is preferred over sodium citrate (a sodium load promotes hypercalciuria); raising urine pH too far risks calcium phosphate stones. For patients with no identified risk factor, potassium citrate is a reasonable first-line agent given its low side-effect profile.

Uric Acid Stones

Potassium citrate is first-line — alkalinise the urine above pH 5.5 (AUA target 6.0, CUA 6.5) to keep uric acid dissolved, without exceeding 7.0. Allopurinol (300 mg/day; xanthine oxidase inhibitor) is reserved as an adjunct when alkalinisation fails, since most uric acid formers have low urine pH rather than hyperuricosuria. Acetazolamide can further raise urine pH in patients already on citrate (up to 50% stop it for side effects).

Cystine Stones

First-line is high fluid intake (≥4 L/day), urinary alkalinisation (potassium citrate to pH 7.0), and sodium/protein restriction. Cystine-binding thiols — tiopronin (α-mercaptopropionylglycine, preferred for lower toxicity), D-penicillamine (causes pyridoxine/B6 deficiency — supplement), and captopril (ineffective) — are added for refractory disease or large stone burdens; they form a more soluble cystine–drug mixed disulfide.

Struvite Stones

Management is primarily surgical (complete stone clearance); medical therapy aims to prevent recurrence. Acetohydroxamic acid (AHA), a urease inhibitor, is offered only after surgical options are exhausted — its serious toxicity (haemolytic anaemia and deep vein thrombosis, each ~15%) limits use. Phosphate therapy is contraindicated.

Other Situations

Fish oil is a first-line option for mild–moderate hypercalciuria; primary hyperparathyroidism with stones is treated by adenoma excision; enteric hyperoxaluria is managed with fluids, calcium, and potassium citrate (60–120 mEq/day); and hypomagnesuric calcium nephrolithiasis with magnesium plus potassium citrate. In neonates, furosemide-induced nephrolithiasis is managed by stopping furosemide; childhood stones should raise suspicion of an inherited disorder (cystinuria, distal RTA, primary hyperoxaluria).

Follow-Up

Obtain a 24-hour urine within 6 months of starting therapy, then annually (or more often by activity). Monitor bloods for drug toxicity — thiazides (hypokalaemia, glucose intolerance), allopurinol/tiopronin (liver enzymes), AHA/tiopronin (anaemia), potassium citrate (hyperkalaemia) — and image periodically for stone growth.

Treatment Selection

Modality choice — SWL, ureteroscopy, or PCNL — is driven by stone burden, location, composition, and patient factors. Non-contrast CT is obtained before intervention: it defines burden, density, and anatomy and (unlike ultrasound) guides the choice between SWL and URS. For operative detail see the procedure pages: Shock Wave Lithotripsy, Ureteroscopy and Laser Lithotripsy, and Percutaneous Nephrolithotomy.

Pre-Treatment Investigations

• Mandatory: urinalysis ± culture — treat infection first, and obtain intra-operative cultures from urine proximal to the stone if infection is suspected (voided cultures may be discordant).
• Selective: serum electrolytes/creatinine (suspected renal impairment), CBC (PCNL or suspected anaemia/infection), and coagulation studies (only with a clinical indication).
• Imaging: non-contrast CT before PCNL and to select SWL vs URS; ultrasound should not be used to choose (no density, inaccurate sizing). Functional imaging (DTPA/MAG-3) if loss of split function is suspected; contrast studies for complex anatomy.

Worse SWL outcomes are predicted by stone attenuation >900–1000 HU and a skin-to-stone distance >10 cm.

General Principles

Weigh symptoms, stone factors (burden, location, composition), and patient factors (anticoagulation, BMI, renal function, anatomy). If purulent urine is encountered endoscopically, abort, drain, and treat the infection. Send stone material for analysis (unless the composition is reliably known from prior identical stones).

Ureteric Stones

Scenario	Recommended approach
Uncomplicated <10 mm	Observation ± medical expulsive therapy (α-blocker — recommended for distal, an option for mid/proximal)
Distal or mid, >10 mm or failed conservative	URS first-line (SWL second-line)
Proximal, >10 mm or failed conservative	URS or SWL (URS superior for <10 mm; equivalent for >10 mm)

• The chief determinant of spontaneous passage is axial stone diameter, then location; ~50% of distal stones <10 mm pass spontaneously, and α-blockers add an absolute ~23% (77% vs 54%). MET is off-label, and SUSPEND (2015) found no benefit of tamsulosin or nifedipine (this trial was not included in the AUA meta-analysis).
• Intervene if conservative treatment fails by 4–6 weeks, or earlier for intractable pain, worsening renal function, or infection (continued obstruction beyond ~6 weeks risks permanent damage). Re-image before surgery if passage is suspected.
• SWL is the least morbid option with the lowest complication rate, but URS has the higher single-procedure stone-free rate and is the most cost-effective. URS is first-line for mid/distal stones (and preferred for women of childbearing age, given uncertain shock-wave effects on the ovary) and for suspected cystine or uric acid stones (poor SWL targeting and fragmentation).

Renal Stones

Stone	Recommended approach
Asymptomatic, non-obstructing caliceal	Active surveillance
Symptomatic <20 mm, non-lower-pole	SWL or URS (preferred over PCNL)
Lower pole ≤10 mm	SWL or URS
Lower pole 10–20 mm	PCNL (first-line) or URS; not SWL
>20 mm (any location)	PCNL (first-line) or URS (option); not SWL

• Active surveillance — ~50% of asymptomatic stones progress and ~10–20% need surgery by 3–4 years (lower-pole and ≥4 mm stones fail observation more often). Treat asymptomatic stones in a solitary kidney, women considering pregnancy, infection, vocational settings (pilots, military), poor healthcare access, children, or with rapid growth. The Sorensen trial (2022) showed removing small asymptomatic secondary stones cut relapse to 16% vs 63%.
• SWL success is location-dependent — renal pelvis/UPJ 80–88%, upper/middle calyces ~70%, lower pole 35–69%. Unfavourable lower-pole anatomy (infundibulum <4 mm, infundibulopelvic angle <90°, multiple infundibula) reduces clearance.
• PCNL gives the highest single-procedure stone-free rate (least affected by stone size) but the most morbidity (~15% complications, mostly Clavien I; transfusion ~7% is the commonest).

Special Scenarios

• Stone composition mainly affects SWL (URS/PCNL are largely unaffected); most resistant: cystine > brushite > calcium oxalate monohydrate > matrix. PCNL is preferred for matrix stones.
• Anticoagulation — URS can be performed safely on anticoagulant/antiplatelet therapy.
• BMI — URS and PCNL outcomes are BMI-independent; SWL success falls with obesity.
• Renal function — a unit with <15% split function should be considered for nephrectomy rather than stone-specific treatment; SWL, multiple URS, and single-tract PCNL do not impair long-term function.
• UPJ obstruction — treat stone and obstruction together: PCNL with antegrade endopyelotomy, URS with retrograde endopyelotomy, or pyeloplasty with pyelolithotomy.
• Calyceal diverticulum — PCNL (direct puncture) is first-line; URS for small (<2 cm) upper/middle or anterior diverticula (PCNL carries a bleeding risk for anterior calyces); SWL is seldom effective.
• Horseshoe / ectopic kidney — SWL if <1.5 cm with no UPJO; URS (basket the fragments out) for <2 cm; PCNL or laparoscopy for ≥2 cm. A retrorenal colon warrants preoperative CT.
• Renal transplant — SWL <1.5 cm, URS (antegrade or retrograde), or PCNL (preferred for >1.5 cm); the denervated graft presents like rejection or ATN rather than colic.
• Staghorn calculi (mostly struvite) — remove them (observation is discouraged; 50% lose renal function by 2 years untreated); PCNL is the method of choice via polar access. Open/laparoscopic surgery is reserved for anatomic abnormalities needing reconstruction, and nephrectomy for a negligibly functioning kidney (avoid in pregnancy).

Stones in Pregnancy

Pregnancy does not change stone incidence, but physiologic hydronephrosis, altered urinary chemistry, and the constraints on imaging and treatment make management distinctive. Most stones pass spontaneously, and intervention is coordinated with obstetrics.

Physiologic Changes

• Increased renal blood flow raises GFR by 30–50% (serum creatinine and BUN run ~25% lower) and increases the filtered load of sodium, calcium, and uric acid — producing lithogenic hypercalciuria and hyperuricosuria. Placental 1,25(OH)₂D₃ further enhances hypercalciuria and suppresses PTH. Filtered inhibitors (citrate, magnesium) and urine output also rise, so a metabolic work-up is deferred until after delivery.
• Hydronephrosis of pregnancy — from progesterone-mediated ureteric smooth-muscle relaxation and, chiefly, compression by the gravid uterus; the right side dilates more, it resolves 4–6 weeks postpartum, and it is absent when the ureter does not cross the pelvic brim (ileal conduit, renal ectopia).
• Composition — in pregnancy ~74% of stones are calcium phosphate and 26% calcium oxalate, the reverse of the non-pregnant pattern.

Renal colic in pregnancy raises the risk of preterm delivery and premature rupture of membranes.

Presentation and Imaging

Flank pain (usually with haematuria) is the commonest presentation, though the gravid state can mask signs.

• Ultrasound is first-line (transvaginal US images the distal ureter).
• MRI is second-line when US is non-diagnostic — no radiation, but stones appear only as filling defects and small ones are hard to see.
• Low-dose CT (<0.19 rad) or a limited IVP (0.1–0.2 rad/film) may be used; conventional CT is avoided. Total fetal exposure should stay below the ACOG maximum of 5 rads.

Management

• Observation is first-line — 50–80% of stones pass spontaneously; follow closely given the maternal/fetal risk.
• Intervention (coordinated with obstetrics): MET (off-label; NSAIDs are contraindicated), a temporising ureteric stent or percutaneous nephrostomy (exchange every 4–6 weeks for encrustation; risks bacteriuria and stent pain), or ureteroscopy.
• Minimise fetal radiation during URS: low-dose/pulsed fluoroscopy, tight collimation, last-image-hold, a below-table x-ray source, and a lead apron beneath the pelvis. ACOG advises non-urgent surgery in the second trimester.

Lower Urinary Tract Calculi

Bladder stones in adults usually mark bladder outlet obstruction, a foreign body, or a diversion; in children they reflect a low-protein diet. Prostatic, urethral, and preputial calculi are less common and have characteristic associations.

Bladder Stones

Primary bladder calculi form without any functional, anatomic, or infectious factor — 9–33× more common in boys, classically in children on low-protein, low-phosphate diets (producing ammonium acid urate stones). They are usually solitary, rarely recur, and are prevented by dietary modification.

Secondary bladder calculi arise from:

• Bladder outlet obstruction — the most common cause (concentrated, acidic urine).
• Neurogenic bladder / spinal-cord injury — intermittent catheterisation carries a lower risk than an indwelling catheter, and suprapubic offers no advantage over urethral.
• Augmentation or urinary diversion (incidence 10–52.5%; mostly struvite and calcium phosphate; females exceed males after augmentation), transplant, and foreign bodies (suture or clips from prior surgery).

In adults, bladder stones are usually uric acid (non-infected urine) or struvite (infected urine); calcium oxalate or cystine suggests a passed renal stone. The commonest symptom is terminal gross haematuria, and cystoscopy is the most accurate diagnostic test. Management is endoscopic (holmium laser is the modality of choice) or percutaneous cystolithotomy; endoscopy through a continent catheterisable channel is avoided because it can disrupt the continence mechanism. There is no role for medical therapy — recurrence is prevented by relieving the outlet obstruction.

Prostatic, Urethral, and Preputial Calculi

• Prostatic calculi — from inspissated prostatic secretions in the large ducts (posterior/posterolateral zones); composed of calcium phosphate and carbonate; usually asymptomatic and do not affect PSA.
• Urethral calculi — in females, nearly all are associated with a urethral diverticulum; delayed diagnosis can produce urethrocutaneous or urethrorectal fistulae. Posterior-urethral stones can be pushed back into the bladder for fragmentation, whereas anterior-urethral stones cannot.
• Preputial calculi — associated with severe phimosis; resolved by circumcision and stone removal.