Stones

Epidemiology & Pathogenesis

• Lifetime prevalence 1–15%; uncommon <20, peaks 40s–60s; men > women (gap narrowing).
• Highest among White populations and the southeastern US; ↑ with BMI, waist size, weight gain.
• Metabolic syndrome (obesity, hypertension, dyslipidemia, insulin resistance) ↑ stone risk — risk rises with the number of traits present.
  • Impaired ammoniagenesis → ↓ urine pH → uric acid stones; hyperinsulinemia → hypercalciuria → calcium stones.
• First-time formers: ~50% recurrence within 10 years.
• Stones need supersaturation but not sufficient alone — urinary inhibitors prevent crystallization.
  • Above the solubility product (metastable) → crystals grow on existing crystals (heterogeneous nucleation).
  • Above the formation product → spontaneous (homogeneous) nucleation.
  • Concentration product in the metastable range → urine is supersaturated; homogeneous nucleation = nuclei forming in pure solution.
  • Stone-forming propensity = saturation index — the urine's saturation with stone-forming salts, set by pH and the ionic strength of the major ions.
  • Relative saturation ratio (EQUIL 2) has been the standard; newer JESS counts soluble complexes EQUIL 2 misses → likely more accurate.
• Inhibitors (6):
  • citrate (most important)[inhibits Ca growth, nucleation & aggregation]
  • Tamm-Horsfall mucoprotein (most abundant urinary protein)[inhibits Ca, aggregation only]
  • magnesium
  • nephrocalcin [inhibits Ca growth, nucleation & aggregation — like citrate, but citrate is more important]
  • bikunin
  • uropontin
  • None inhibit uric acid.
  • Also pyrophosphate; inhibitors raise the supersaturation needed to trigger nucleation.
  • Tamm-Horsfall (uromodulin) — potent inhibitor of COM crystal aggregation
    • Made in the thick ascending limb and DCT.
    • Inhibits aggregation in alkaline urine but polymerizes into an aggregation-promoting form in acidic urine.
• Citrate is the most potent complexor of calcium
  • It inhibits spontaneous precipitation of calcium oxalate and prevents heterogeneous nucleation of CaOx by monosodium urate.
  • Main protective mechanism = complexing urinary Ca → ↓ ionic Ca → ↓ CaOx saturation.
  • Not via alkalinization — alkalinizing urine ↓ uric acid and cystine stones but does not affect CaOx stone formation.
• Osteopontin (uropontin) inhibits growth, aggregation AND nucleation of CaOx crystals.
• Randall plaques = calcium apatite in basement membrane of thin loops of Henle → anchor for idiopathic calcium oxalate stones.
  • Plaque is invariably apatite
  • Spreads from the thin-limb basement membrane through the medullary interstitium to a subepithelial site where CaOx crystals adhere and grow.
  • Seen at endoscopy in 74% of stone formers vs 43% of controls → supports the fixed-particle theory.
• Substance A is a component of matrix in all stone formers and is immunogenically unique.
  • Not an inhibitor — a stone-matrix mucoprotein found in the urine of 85% of stone formers and no healthy individuals → a marker of stone formation.

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Mineral Metabolism

• PTH (↓ serum Ca trigger) → ↑ renal Ca reabsorption + ↑ phosphate excretion
  • ↑ bone Ca release
  • Stimulates 1α-hydroxylase.
    • 1α-hydroxylase in the proximal tubule converts liver-derived 25(OH)D₃ → 1,25(OH)₂D₃ (most active) → gut Ca absorption via intestinal Ca-binding protein.
  • Does not act on intestine.
  • Acts primarily on the kidney — Ca reabsorption in the ascending loop of Henle, distal and collecting tubules; blocks proximal tubular PO₄ reabsorption.
• Calcitriol [1,25(OH)₂D₃] → most potent stimulator of intestinal Ca absorption
  • ↑ renal Ca/PO₄ reabsorption
  • ↑ bone Ca release
  • Inhibits PTH.
  • 7-dehydrocholesterol and cholecalciferol are only its precursors.
• Dietary Ca: 30–40% absorbed; fractional absorption ↑ on low-Ca diet.
• Dietary oxalate: only 6–14% absorbed; reduced by Oxalobacter formigenes and Ca/Mg binding.
  • H. pylori has no effect on oxalate absorption; Ca restriction ↑ oxalate absorption but typically leaves urinary citrate and pH unchanged.

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Classification (frequency)

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Metabolic Risk Factors

Hypercalciuria — most common abnormality in Ca stone formers

• Definition: > 200 mg urinary calcium/day, measured after 1 week on a 400 mg calcium / 100 mg sodium diet
• Absorptive hypercalciuria is the most common solely-occurring abnormality
• The normal kidney filters 270 mmol of calcium daily and reabsorbs all but 4 mmol
• ↑ PTH + high fasting urine Ca distinguishes renal from absorptive.
• Absorptive: ↑ gut Ca absorption transiently ↑ serum Ca → suppresses PTH + ↑ filtered load.
  • Exam answer: serum Ca normal to mildly ↑.
  • Type I: urine Ca ↑ on both fasting and Ca-load testing; type II normalizes on Ca restriction. Routine subtyping not required.
• Renal leak: primary Ca wasting from impaired tubular reabsorption → compensatory 2° hyperPTH.
  • Chronic 2° hyperPTH → low or low-normal radial bone density; exclude rickets, osteopenia, CKD before diagnosing.
• Resorptive: ↑ serum Ca, ↑ PTH, hypercalciuria, hypophosphatemia — the raised serum Ca, not PTH, separates it from renal leak.
  • Intact PTH assay separates hyperPTH from PTH-independent hypercalcemia — sarcoidosis, vitamin D toxicity, malignancy.
  • Primary hyperPTH → most commonly Ca phosphate stones (PTH-driven phosphaturia + bicarbonaturia alkalinize urine)
  • Recurrent pure brushite → check serum Ca + PTH.
  • Primary hyperPTH ≈ 5% of nephrolithiasis; suspect when serum Ca > 10.1 mg/dL.
  • Optimal Rx = parathyroidectomy — only removing the adenoma is definitive.
• Glucocorticoid induced hypercalcemia; alter calcium metabolism, common in cushing syndrome
  • The glucocorticoid drives hypercalciuria + uricosuria + hypocitraturia
  • Exam answer: serum Ca stays normal — glucocorticoid excess promotes bone resorption and PTH release but inhibits gut Ca absorption → hypercalciuria without hypercalcemia.
  • Stones in 50% of active Cushing syndrome → stone former with cushingoid features: low-dose dexamethasone suppression test or late-night salivary cortisol.
• Sarcoidosis — granulomatous disease most commonly causing hypercalcemic urolithiasis:
  • Macrophage 1α-hydroxylase → extrarenal 1,25(OH)₂D₃ → ↑ gut Ca absorption → ↑ serum and urine Ca (mixed absorptive + resorptive hypercalciuria).
  • PTH suppressed (vs primary hyperPTH); resolves quickly once corticosteroids are started.

Therapy

• Orthophosphate — no convincing RCTs; contraindicated in UTI
• Sodium cellulose phosphate — not preferred, and not available in the USA
• Check potassium within 1–2 weeks of starting or adjusting a thiazide
• Fish oil is an effective first-line therapy for mild-to-moderate hypercalciuria
• Medullary sponge kidney with hypercalciuria → start a thiazide

Hyperoxaluria (4 types)

• Urinary oxalate > 40 mg/day; glycine and ascorbic acid are the precursors of oxalate.
  • Hyperoxaluric Ca stones = 2–15% of stone formers: oxalate overproduction (primary), ↑ dietary oxalate, or ↑ intestinal absorption (enteric).
• Primary
  • AR glyoxylate defect
  • Urine oxalate >75 mg/day without bowel dysfunction → genetic referral.
  • If untreated, 50% have ESRD by age 15, with a ~30% death rate
  • Medical: hydration, low-oxalate diet, potassium citrate, magnesium, vitamin B6
  • Definitive treatment is a combined liver and kidney transplant
  • Rare; the defect overproduces oxalate → renal Ca deposition is only indirect — Ca handling itself is unaffected.
• Chronic antibiotic use can wipe out Oxalobacter formigenes, the oxalate-degrading gut bacterium → hyperoxaluria and recurrent calcium oxalate stones.
  • Treatment is probiotics.
• Enteric
  • Fat malabsorption (IBD, celiac, resection, Roux-en-Y) → fatty acids saponify Ca, free oxalate absorbed; + hypocitraturia/hypomagnesuria → Ca supplement with meals (not oxalate restriction alone).
  • Any cause of fat malabsorption — small bowel resection, intrinsic bowel disease, jejunoileal bypass
  • Saponification binds luminal Mg as well as Ca, and poorly absorbed bile salts and fatty acids ↑ colonic mucosal permeability to oxalate.
  • ↑ colonic absorption of free oxalate = risk factor most tied to recurrent stones in IBD; short bowel syndrome and Crohn's → CaOx stones.
  • Ca with meals binds gut oxalate; also correct fluid and alkali losses, and on Ca supplements monitor 24-h urine for hypercalciuria.
  • Roux-en-Y gastric bypass: hyperoxaluria = most common urinary abnormality, appears ≥ 6 months postop, sometimes > 100 mg/day → Ca supplementation.
  • Stone risk confined to malabsorptive procedures (long-arm Roux-en-Y, duodenal switch) — not restrictive ones (gastric banding, sleeve gastrectomy).
• Dietary
  • Rhubarb, chocolate, nuts, tea, spinach, beets
  • Keep Ca normal, vitamin C ≤2 g/day.
  • Vitamin C: 10–20% of ascorbate → oxalate; 2 g/day ↑ urine oxalate 20–30% without changing urine pH, citrate, Ca or Mg.
  • Vitamin C–related stones → stop the supplement; Ca restriction would ↑ gut oxalate absorption.

Hyperuricosuria

• Pure uric acid or Ca oxalate (monosodium urate heterogeneous nucleation).
• Most common cause = ↑ dietary purine; also gout, myelo/lymphoproliferative, Lesch-Nyhan (HGPRT).
  • Lesch-Nyhan → hyperuricemia + hyperuricosuria → uric acid stones
    • By contrast hyperPTH, malignancy (hypercalcemic), primary hyperoxaluria and medullary sponge kidney → calcium stones.
  • Excess dietary protein can cause uric acid stones but usually ↑ urinary sulfate and urea nitrogen — normal values argue against it.
• Low PH <5.5

Hypomagnesuria

• Urinary magnesium < 40 mg/day
• Due to poor dietary intake or reduced intestinal absorption — diarrheal states, IBD
• Treatment: magnesium oxide (side effect — diarrhea) or potassium-magnesium citrate

Renal Tubular Acidosis (acquired mnemonic A CASH POT)

• Incomplete type 1 RTA → confirm with ammonium chloride load; treat with potassium citrate.
  • Suspect distal RTA when urine pH stays > 5.8 with UTI excluded; the NH₄Cl load confirms it by inadequate acidification, even with normal bicarbonate.
• Distal (type 1) RTA
  • The defect is the H⁺ ATPase in the collecting duct (α-intercalated cells)
    • Defective apical H⁺-ATPase → protons cannot be excreted despite systemic acidosis.
  • Urine pH > 6.8, hyperchloremia, hypokalemia, low serum bicarbonate.
    • Exam answer: persistently alkaline urine, pH > 6.0 (e.g. 6.7 with CaP stones, hypocitraturia, hypokalemia, low serum HCO₃⁻).
  • 70% develop calcium phosphate stones (brushite) and medullary nephrocalcinosis.
  • Chronic acidosis → hypercalciuria (↓ proximal tubular Ca reabsorption + bone mineral dissolved to buffer the acid load) → associated bone disease.
  • Hyperchloremia + hypokalemia in a recurrent stone former → think type 1
  • Key urinary abnormality = hypocitraturia from acidosis-driven proximal citrate reabsorption.
  • Potassium citrate = treatment of choice — corrects acidosis and hypokalemia and restores urinary citrate; sodium alkali add an unwanted sodium load.
  • Alkali still given despite already-alkaline urine — it corrects intracellular acidosis and restores citrate excretion.
• Urinary citrate separates the types:
  • Type 1 → profound hypocitraturia → frequent stones
  • Type 2 → near-normal citrate, rarely stones.
    • Type 2 is also hypercalciuric — preserved citrate (not Ca, Na or PO₄ handling) is what protects it.
• Type 2: hyperchloremic non-AG acidosis + hypokalemia but urine pH < 5.5
  • Intact distal proton secretion acidifies urine once serum HCO₃⁻ falls to 15–18 mEq/L.
• Type 3 is not a recognized RTA type.

Hypocitraturia & Urine pH

• Urinary citrate < 320 mg/day — or < 550 mg in women, < 450 mg in men.
• Acid-base state is primary determinant (acidosis ↓ citrate).
  • Dietary citric acid adds little — absorbed citrate → bicarbonate, neutralized by citric acid's own proton (no net alkali load).
• Causes (DIRT):
  • Diarrhea
    • IBD / chronic diarrhea: multifactorial — bicarbonate loss, hypokalemia, metabolic and intracellular acidosis → ↑ tubular citrate reabsorption + ↓ citrate synthesis.
  • Idiopathic
  • Type 1 RTA
  • Thiazides.
• Severe → suspect RTA.
  • RTA hallmark = low urine citrate with inappropriately high urine pH.
• Topiramate causes hypocitraturia and recurrent stones → give potassium citrate.
  • Typical 24-h urine finding = hypocitraturia → counsel on stone risk, especially prior stone formers.
  • Stop the drug if possible; if it must continue → potassium citrate, preferred over sodium bicarbonate (sodium load).
• Urine pH <5.5 → uric acid (and Ca oxalate via nucleation).

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Stone Types

Calcium Oxalate

• Most common, caused by IBD, interstitial bypass, furosemide, dehydration
• Wide range of PH

Uric acid

• 3 determinants: low pH (<5.5, most important) > low volume > hyperuricosuria.
  • At pH < 5.5, even LOW concentrations of uric acid exceed the formation product
  • At pH > 6.5, even concentrations above 1200 mg/L remain soluble
  • Solubility is governed by pH, not concentration
  • Below pH 5.5 poorly soluble undissociated uric acid predominates → alkalinization, not urate reduction, is the primary therapy.
  • Uric acid is > 10× more soluble at pH 7 than at pH 5
  • Low urine pH is the key factor in gouty diathesis (now termed idiopathic low urine pH) and the commonest abnormality in uric acid stone formers
• Diabetics ~6× risk (insulin resistance → ↓ ammoniagenesis → low pH).
  • Type 2 diabetes: the insulin resistance is renal
  • Less ammonia from glutamine and ↓ proximal Na+/H+ exchanger → defective ammonium excretion.
  • Uric acid stones in 34% of diabetic vs 6% of nondiabetic stone formers
• Radiolucent.
• 20% of gout patients develop uric acid stones.
  • In gout, the commonest compositions are uric acid (52%) then calcium oxalate monohydrate (45%)
• Risk factors:
  • Thalassemia
  • Myeloproliferative disorders
  • Gout
  • Obesity
  • Lesch-Nyhan
  • Diabetes
  • Pregnancy
  • Neoplastic disease
  • Purine-rich diet (red meat)
  • Dehydration (diarrhea, colectomy, ileostomy)
• Obesity ↑ uric acid excretion; hyperuricosuria + low urine pH together = the greatest risk factor for uric acid stones
• Uric acid is the most common bladder stone, followed by struvite

Calcium phosphate

• Type 1 RTA
  • Distal (type 1) RTA — failed proton secretion keeps urine persistently alkaline
• Primary hyperPTH
• Medullary sponge kidney
• Carbonic anhydrase inhibitors.

Cystine

• Cystinuria, AR (SLC3A1 chromosome 2 / SLC7A9 chromosome 19), impairs reabsorption of COLA (Cystine, Ornithine, Lysine, Arginine).
  • An epithelial transport defect, not a metabolic disorder
  • Impairs proximal tubular reabsorption and intestinal absorption of the 4 dibasic amino acids
  • Only cystine forms stones (poor urinary solubility)
• Poorly radio-opaque
• Nitroprusside spot test (urine turns purple).
  • Screen with the sodium nitroprusside (cyanide-nitroprusside) spot test, alongside a 24-hour urine
• Average age at first stone is 12.2 years
• Cystine crystallizes above 250 mg/L — the treatment target is to get below that
  • Exam answer: cystine crystallizes above ~300 mg/L (1.33 mmol/L at pH 6.0); solubility depends strongly on pH → treatment pairs alkalinization with aggressive dilution
• Yellow and waxy in appearance; produces a sulfurous gas on laser lithotripsy
• Reduce egg, chicken, beef, poultry, fish and pork
  • Animal protein is rich in cystine and methionine, which are metabolized to cystine
• Alkalinization to pH 7.0–7.5 is often not realistic and risks calcium phosphate stones
• If on maximal oral therapy and still forming stones, repeat the stone analysis to look for an additional metabolic abnormality
  • e.g. still forming stones despite potassium citrate, alpha-MPG, lower cystine excretion and urine pH 7–7.5 → hypercalciuria, hypocitraturia or hyperuricosuria can cause non-cystine stones

Struvite (Mg-ammonium-phosphate)

• Only with urease-producing organisms:
  • Proteus (most common)
  • Klebsiella
  • Pseudomonas
  • S. aureus (most E. coli don't).
    • > 90% of S. aureus organisms produce urease, whereas E. coli, the commonest urinary pathogen, only rarely does
• Females 2:1
• Commonly staghorn.
• Urease splits urea → ammonium + carbon dioxide → alkaline urine
• Recurrent UTI is the key risk factor.
• Struvite forms in alkaline urine, pH > 7.2; may also contain carbonate apatite
• Staghorn formers, by frequency: struvite (> 67%) > cystine > uric acid > Ca oxalate monohydrate.
  • Isolated calcium phosphate is the LEAST likely to form a staghorn.

Ammonium Acid Urate

• Laxative abuse, IBD
• < 1% of stones
• Classically laxative abuse and anorexia nervosa
• Also morbid obesity and recurrent UTIs
• Laxative abuse:
  • Chronic dehydration → intracellular acidosis with abundant urinary ammonium, while laxative sodium loss lowers urinary sodium → urate complexes with ammonium → AAU.
  • The urine is low-volume and persistently acidic — the classic uric acid environment
  • Uric acid is metabolically continuous with AAU, the most characteristic laxative-abuse stone
• Two routes: metabolic (laxative abuse, malnutrition, phosphate deficiency) and infective (urease-splitting organisms also generate ammonium)

Other

• Matrix (~65% protein, urea-splitting UTI, radiolucent)
  • Matrix: noncrystalline mucoprotein concretions; invariably form with UTI (usually Proteus or E. coli); commonly cause obstruction
• Xanthine (XDH deficiency ,Allopurinol)
  • Xanthine: inherited disorder of xanthine dehydrogenase or xanthine oxidase, or rarely high-dose allopurinol (inhibits xanthine dehydrogenase).
  • Highly insoluble and completely radiolucent → often mistaken for uric acid
  • Lesch-Nyhan (HGPRT deficiency): high-dose allopurinol blocks xanthine oxidase → hypoxanthine and xanthine accumulate → the less soluble xanthine forms stones
• 2,8-DHA (APRT deficiency)
• Ammonium acid urate (laxative abuse,Ileostomy).

Medication-associated (Lotta Good Drugs Cause Calculi FIT TEST)

• Furosemide
• Guaifenesin
• Vitamin D
• Vitamin C (→oxalate)
• Carbonic anhydrase inhibitors (acetazolamide → Ca phosphate)
  • Carbonic anhydrase inhibitors (acetazolamide, topiramate, zonisamide) mimic distal (type 1) RTA:
    • Hyperchloremic metabolic acidosis
    • Urine pH > 6.0
    • Very low urinary citrate
    • Hypercalciuria → Ca phosphate stones
• Indinavir (radiolucent, may be invisible on CT)
  • Indinavir — radiolucent on both plain film and CT (unlike uric acid) → in HIV, obstruction without a visible stone on CT suggests indinavir.
  • Incidence 4–13%
  • Treat first with drug discontinuation + hydration, not surgery
• Topiramate (distal-RTA picture, Ca Phosphate)
• Triamterene
• Ephedrine
• Silicates
• TMP/SMX.

Hereditary Disorders Associated with Stones

Stones in Special Populations

Why transplant patients form stones

• From the renal failure:
  • Hypercalciuria (tubular dysfunction)
  • Hyperoxaluria
  • Dehydration
  • Iatrogenic calcium supplements
  • Hypercalcemia from secondary hyperparathyroidism
• From the transplant:
  • Foreign bodies (suture, stent)
  • UVJ strictures
  • Steroids
  • Stones transplanted with the kidney
• Allograft stones: ~1% of recipients, mean onset 28 months
  • Calcium-based 67% > struvite 20% > uric acid 13%
• Immunosuppressants that cause stones: calcineurin inhibitors and steroids
• Denervated allograft → no typical renal colic
  • After ureteral instrumentation, watch for silent hydronephrosis presenting as a rising creatinine

Why urinary diversions form stones

• UTI
• Mucus
• Stasis
• Hypocitraturia
• Acidosis
• Dehydration
• Kock pouch = highest stone rate
  • Staples holding the intussuscepted nipple valve can erode into the reservoir → foreign-body nidus for struvite encrustation
• Bowel reservoirs make mucus and cannot inhibit bacterial proliferation as urothelium does → colonized alkaline urine deposits struvite
• Pouch stone incidence rises steadily with time

Causes of stones in neonates

• Dehydration
• Underweight at birth
• TPN
• Steroids
• Distal RTA
• Furosemide
• Theophylline
• Cystinuria
• Sepsis
• Congenital hyperparathyroidism

Intestinal disease and spinal cord injury

• Intestinal bypass surgery produces a urine profile like chronic diarrhea
  • Low volume, acidic urine, hypocitraturia, hyperoxaluria, and low serum sodium/magnesium/calcium.
  • Treat with potassium citrate and calcium citrate.
  • Give both alongside fluids — calcium citrate alone typically fails to correct the acidosis and hypocitraturia
• Crohn's disease with chronic diarrhea
  • Hyperoxaluria + hypocitraturia (stool bicarbonate loss)
  • Low urine volume
  • Acidic urine
  • Low urinary Ca and Mg
• Total colectomy + end ileostomy
  • Urine oxalate is LOW (oxalate is absorbed only in the colon)
  • Dehydration + stool bicarbonate loss → low volume, low pH
• Spinal cord injury (quadriplegia)
  • Acute phase: immobilization hypercalciuria → calcium stones
  • Later, persistent infection (poor bladder emptying, catheters) dominates, aided by alkaline urine and hypocitraturia

Anatomic predisposition

• UPJ obstruction
• Horseshoe kidney
• Caliceal diverticulum
  • Exam answer: in caliceal diverticular stone formers the 24-hour urine is typically normal — the stone results mainly from urinary stasis
• Medullary sponge kidney
• But an underlying metabolic abnormality is still required.

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Diagnosis & Imaging

• Radiolucent (KUB):
  • Uric acid
  • Matrix
  • Xanthine
  • Triamterene
  • 2,8-DHA
  • Indinavir.
  • These need non-contrast CT to be seen (except indinavir, often invisible on CT too); cystine and struvite are not radiolucent
• Radio-opaque: Ca oxalate, Ca phosphate (densest).
• Poorly opaque: struvite, cystine.
• ~300–500 HU suggests uric acid → check urinalysis next:
  • Urine pH < 5.5 + HU < 500 = 90% PPV for uric acid.
• MRI cannot see calcium
  • Ca oxalate stones show only as filling defects against high-signal urine on T2, and not at all on T1.
• Crystal shapes:
  • Ca oxalate = envelope/dumbbell
    • Dihydrate (weddellite) envelope = a square with intersecting diagonals
    • Monohydrate (whewellite) = dumbbell or spindle, and lithotripsy-resistant
  • Uric acid = rhomboid/rosette
  • Cystine = hexagonal
  • Struvite = coffin-lid
  • Ca phosphate = amorphous.
  • Only the cystine, struvite and brown spiculated 2,8-DHA crystals are pathognomonic; otherwise crystalluria is generally not diagnostic

Phlebolith vs stone

• Ultrasound correlates with CT stone size about two-thirds of the time.
  • It overestimates one-third of stones < 10 mm, and underestimates one-third of stones > 10 mm.
• KUB underestimates over 90% of stones > 10 mm
  • Partly because it cannot measure in three dimensions.
• Nephrocalcinosis
  • Medullary (type 1 RTA, hyperPTH, MSK, hypervitaminosis D, sarcoid) vs cortical (cortical necrosis, primary hyperoxaluria, Alport).
• DMSA (cortical agent) best predicts renal functional recovery after relief of prolonged obstruction
  • Superior to the tubular agents DTPA and MAG-3.

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Acute Management

• Analgesia + fluids.
  • NSAIDs are first-line and superior to opioids
  • They block the prostaglandin synthesis that drives raised intrarenal pressure and ureteric spasm
• Obstruction + suspected infection = emergency → urgent decompression (stent or PCN) + defer definitive stone treatment until sepsis controlled.
• Forniceal extravasation
  • Manage like any ureteric stone (intervene for fever/vomiting/unrelenting pain).
  • CT: perinephric stranding + contrast tracking along the psoas border = forniceal rupture → it decompresses the collecting system and carries no adverse prognosis → a small, uninfected stone is observed
• Indication for Acute Decompression:
  • Sepsis
  • Solitary or bilateral obstruction
  • Refractory Pain with Obstruction
    • Colic not controlled by medical analgesia → decompression or ureteroscopic stone removal
  • Obstruction with elevated Cr
• Hydronephrosis after reconstructive vascular surgery
  • 5% of at-risk ureters
  • Cause: localized retroperitoneal fibrosis (70%), anterior graft placement (30%) → grafts belong posterior to the ureter
  • Early obstruction from secondary retroperitoneal fibrosis within 6 months of graft surgery → a 4-week course of oral steroids can resolve it
  • Ureterolysis only if that fails

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Metabolic Evaluation

• Screening (all stones): H&P, UA ± culture, electrolytes, Ca, creatinine, uric acid, imaging for burden; stone analysis at least once.
  • This basic evaluation also includes blood count, CRP and a urine dipstick; the specific (extended) evaluation is only for high-risk formers
• Extended (24-h urine ×1–2): recurrent, family history, solitary kidney, malabsorption, children, cystine/uric acid/struvite, predisposing conditions.
  • Any uric acid content — even 20–30% of a mixed calcium stone — mandates it; recurrent stone formation is the strongest indication
  • Predisposing conditions that escalate to it: gout, RTA type 1, primary hyperPTH, type 2 diabetes
  • Measure: volume, pH, creatinine, Na, K, Ca, oxalate, uric acid, citrate (+cystine if suspected).
  • Adequacy by 24-h creatinine: male 20–25 mg/kg, female 15–20 mg/kg.
  • Check creatinine before interpreting any 24-h urine.
    • Low → most likely undercollection → repeat; every total is underestimated, so a 'normal' Ca, oxalate or uric acid may hide true hypercalciuria or hyperoxaluria
    • High (e.g. 47 mg/kg in a man) → overcollection (e.g. a 48-hour sample by mistake) → raised Ca, oxalate, uric acid, Na and K are unreliable
• Urine pH: normal 5.8–6.2; >7.0 → infection/RTA; <5.5 → uric acid.
• Check PTH if primary hyperPTH suspected (mid-range PTH + high-normal Ca + Ca phosphate stones).
  • Still suggestive when serum Ca is frankly high, not just high-normal; also measure vitamin D, since low vitamin D may mask primary hyperPTH

Indications for metabolic evaluation (12)

• Recurrent stone formers
• Strong family history
• Intestinal disease, particularly chronic diarrhea
• Pathologic skeletal fractures
• Osteoporosis
• History of UTI with calculi
• Personal history of gout
• Infirm health (unable to tolerate repeat episodes)
• Solitary kidney
• Anatomic abnormalities
• Renal insufficiency
• Stones of cystine, uric acid or struvite

• Low risk (healthy, first-time, single stone, no family history) → extended metabolic evaluation only if the patient requests it

The extensive evaluation — 2 visits

• Timing: no earlier than 20 days after the acute episode, preferably at ~3 months — once stable, infection-free and back on the usual diet
• Stop everything that interferes with calcium, uric acid or oxalate metabolism — vitamin D, calcium supplements, antacids, diuretics, acetazolamide, vitamin C
• Stop all stone-treatment medications — thiazides, phosphate, allopurinol, magnesium
• Two 24-hour urine samples, collected on the patient's usual diet (not a restricted diet)
• Discard the first morning void, then collect for 24 hours including the next morning's sample

Stone analysis

• Repeat the analysis if stone formation continues, particularly if not responding to treatment
• Most common method — X-ray diffraction or Fourier-transform infrared spectroscopy
• MicroCT is an emerging non-destructive method

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Dietary Therapy (6 measures)

• Fluid → urine output >2.5 L/day (cystine ≥4 L/day); RCT 12% vs 27% recurrence at 5 yr.
  • For all stone formers, preferably water — the target is urine output, not intake, because insensible losses and food water content vary.
  • The RCT was in recurrent calcium oxalate formers. In practice → intake 2.5–3.0 L/day, urine specific gravity <1.010.
  • Exam answer (cystinuria): hydration ≥3 L/day (1.5 L/m² in children).
• Sodium ≤100 mEq (2,300 mg)/day — high Na ↑ urinary Ca.
  • The key dietary restriction for calcium oxalate formers — high Na also ↑ urine pH and ↓ citrate; RCTs show benefit.
• Calcium keep at RDA 1,000–1,200 mg/day — low-Ca diet ↑ oxalate absorption (counterproductive).
  • Too little calcium to bind oxalate in the gut → ↑ intestinal oxalate absorption → ↑ urinary oxalate. Dietary calcium ≥1,000 mg/day is linked to lower stone risk.
  • Calcium citrate and potassium citrate are the best supplements
    • The high urine citrate offsets the higher urine calcium (200 mg calcium, 950 mg citrate).
    • Both are taken WITH meals.
  • Give calcium as food rather than a supplement
    • EXCEPT in enteric hyperoxaluria from intestinal disease or bowel resection, where supplements with meals are added and a low-fat diet is also advised.
  • A moderate-calcium diet + salt restriction + moderation of animal protein produced 50% fewer stones than a calcium-restricted diet.
• Oxalate limit (esp. enteric hyperoxaluria); fruit/veg ↑ (raises citrate); animal protein limit.
  • The protein to limit is non-dairy animal protein.
  • Only 10–15% of urinary oxalate comes from diet — the rest is from the liver.
  • Bariatric surgery raises stone risk through increased urinary oxalate.
• Avoid low-carb/high-protein weight-loss diets (↑ stone + bone loss).
  • Atkins/keto-type diets put an acid load on the kidney → ↓ urinary citrate + pH, ↑ urinary calcium + uric acid.
  • Urinary sulfate = marker of animal protein intake (↑ on a high-protein diet).
    • Urinary sodium is unaffected by protein itself but may ↑ from the salt added to most animal proteins.

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Pharmacologic Therapy

• Enteric hyperoxaluria (bowel disease/resection) →
  • ↑ oral fluids + potassium citrate 60–120 mEq/day (reverses acidosis + hypocitraturia) + calcium supplements with meals (bind intestinal oxalate).
  • Calcium citrate is the ideal supplement → ↓ urinary oxalate and ↑ urinary citrate. Thiazides may worsen the metabolic acidosis + hypokalemia.
  • No hypocitraturia → calcium supplementation takes priority over potassium citrate.
    • (Sodium restriction mainly targets hypercalciuria; animal protein restriction targets hyperuricosuria.)
  • Rapid intestinal transit → liquid potassium citrate if tablets are poorly absorbed. Avoid magnesium supplements (diarrhea).
• Uric acid pH target
  • Exam answer: alkaline citrate 3–10 g/day, titrated by dipstick → urine pH 6.2–6.8 for prevention, 6.5–7.2 for dissolution; pH above ~7.0–7.2 promotes calcium phosphate stones.
• Mixed calcium oxalate + uric acid stones (after complete clearance) → potassium citrate is best:
  • Alkalinization prevents uric acid crystallization
  • Citrate inhibits calcium oxalate crystallization.
• Cystinuria — Exam answer: alkalinize to urine pH >7.5; never acidify the urine.
• Thiazide side effects: 3 hypers (glucose, lipids, urate), 3 hypos (K, Mg, citrate), metabolic alkalosis → give K citrate.
  • Up to 1 in 6 stop thiazides for side effects (ALLHAT) → co-prescribe potassium citrate; monitor serum potassium, glucose, lipids.
  • Intracellular acidosis despite systemic metabolic alkalosis: hypokalemia drives H⁺ into proximal tubular cells → ↑ citrate reabsorption + metabolism → hypocitraturia.
  • Recurrent calcium stones despite a compliant thiazide → most likely thiazide-induced hypocitraturia → check serum K + 24-h urine citrate
    • Pair the thiazide with potassium citrate.
• Thiazides cause hypokalemia AND hyperglycemia — and the two are linked.
  • A low plasma potassium impairs insulin secretion.
  • Preventing the hypokalemia — potassium citrate, a potassium-sparing agent such as triamterene, or a banana a day — prevents or lessens the glucose intolerance.
    • Start it at the onset of thiazide therapy, or as soon as glucose intolerance appears.
  • Up to 30% develop hypokalemia and 3–5% new hyperglycemia after starting a thiazide; glucose rises significantly once serum K falls <3.5 mEq/L.
  • New hyperglycemia → start potassium citrate rather than stopping the thiazide.
  • Exam answer: avoid triamterene — triamterene stones have been reported.
    • Use potassium citrate or potassium chloride instead
    • Amiloride or spironolactone may avoid the need for supplementation.
• For fatigue on a thiazide, check potassium and sodium — largely avoided by starting low and titrating up.
  • Weakness, cramps or fatigue soon after starting → diuretic-induced hyponatremia or hypokalemia.
    • Muscle cramps + fatigue on hydrochlorothiazide (25 mg BID or 50 mg once daily) for hypercalciuria → hypokalemia + hypomagnesemia.
  • Lassitude and sleepiness = the most common thiazide side effects — even without hypokalemia, usually at initiation, resolving with continued therapy.
  • Hypokalemia → potassium supplements or a combined thiazide + potassium-sparing diuretic.
  • Hyponatremia → stop the thiazide, cation repletion, oral fluid restriction; 3% IV saline if severely symptomatic.
• Allopurinol 300 mg/day (xanthine oxidase)
  • Adjunct when alkalinization fails (most uric acid formers have low pH, not hyperuricosuria).
  • Offer to recurrent calcium oxalate formers with hyperuricosuria (urine uric acid >800 mg/day) and normal urinary calcium
    • Hyperuricemia is not required.
    • Benefit in hypercalciuria is unproven; limiting non-dairy animal protein may maximize its efficacy.
  • After a uric acid stone dissolves on allopurinol + potassium citrate + purine restriction → 24-h urine shows hypouricosuria (xanthine oxidase inhibition ↓ uric acid production).
• Stones forming in a patient already ON allopurinol are calcium oxalate monohydrate (45%), then uric acid (30%), then xanthine (15%).
  • Allopurinol lowers uric acid so CaOx predominates — but a NEW stone appearing after allopurinol was started is most likely xanthine.
  • Xanthine stones, like uric acid stones, are radiolucent on plain film.
• Acetohydroxamic acid 250 mg TID if struvite clearance is incomplete — it blocks the urease enzyme.
  • Oral urea analog → competitively inhibits bacterial urease by binding its nickel-containing active site → no ammonia, urine pH doesn't rise, struvite can't crystallize.
  • Prevents new infection stones and inhibits growth of existing ones. The DVT risk is with long-term use; nausea and vomiting also occur.
  • AHA (urease inhibitor) — toxicity limits use: hemolytic anemia + DVT (~15% each).
  • Other adjuncts after struvite clearance:
    • Antibiotics for persistent bacteriuria
    • Urinary acidification with ammonium chloride 1 g two to three times daily or methionine 200–500 mg one to three times daily.
• Follow-up 24-h urine within 6 months of starting therapy, then annually.

Cystine chelators — second line

They raise cystine solubility by binding it through disulfide bonds.

• α-MPG (Thiola) → forms a more soluble mixed-disulfide (drug–cystine rather than cystine–cystine) complex
  • It does not work by diuresis, alkalinization or lowering cystine excretion.
• Recurrence on α-MPG even though measured cystine excretion has fallen = continued supersaturation:
  • 250 mg/day in 775 mL/day is still >300 mg/L, above the 200–250 mg/L solubility limit → urine output must also rise.
• Urine pH already 7–7.5 → more potassium citrate risks calcium phosphate stones.
  • Captopril (↓ cystine excretion) suits ongoing cystine stones
  • Restrict dietary methionine (a cystine precursor).

Side effects of stone-prevention drugs

• Nausea/abdominal pain on potassium citrate with urine pH on target (e.g. 6.7) → take it during or after meals; don't change the dose or the drug.

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Dissolution Therapy

• Uric acid stones → dissolve with potassium citrate:
  • Suspected uric acid stone, asymptomatic + non-obstructing → trial of potassium citrate alkalinization instead of ureteroscopy or mini-PCNL.
  • Gout + low-attenuation stone (400 HU) + urine pH 5.0 = uric acid → potassium citrate, target urine pH ~6.5.
    • Add allopurinol for prevention if hyperuricemia + hyperuricosuria.
  • Dissolution fails → ureteroscopy or SWL (SWL needs ultrasound or contrast to target the radiolucent stone).
  • Measured urinary uric acid rises after starting potassium citrate — pH above the uric acid pKa (5.5) redissolves crystals that had precipitated in acidic urine.

Contraindications

• Active infection
• Fever
• Flank pain
• Distal obstruction
• Electrolyte abnormalities
• Renal insufficiency
• Immature tract

Complications of urinary alkalinization

• Calcium phosphate stones
  • CaP stones on alkali with urine pH 7.4 = excess alkalization → keep pH 6.5–7.0 in gouty diathesis; pH >7.0 promotes CaP stones.
• Struvite stones
• Hyperkalemia (potassium citrate)
• Volume overload (sodium bicarbonate)
• GI upset, flatulence

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Treatment Selection

• Non-contrast CT before intervention — defines burden/density/anatomy, guides SWL vs URS (US cannot).
• Before any planned stone removal → confirm sterile urine with urine culture or urinary microscopy, not dipstick urinalysis.
• Worse SWL:
  • Attenuation >900–1000 HU
  • Skin-to-stone >10 cm
  • Unfavorable lower-pole anatomy
  • Resistant composition.
• Single-treatment stone-free rate increasingly favors URS over SWL once maximum stone diameter is ≥10 mm.
• SWL resistance (descending): cystine > brushite > Ca oxalate monohydrate > matrix.
  • After Ca oxalate monohydrate (COM), descending resistance: hydroxyapatite > struvite > Ca oxalate dihydrate > uric acid
  • Exam answer: brushite = most SWL-resistant; cystine and COM also fairly resistant; Ca oxalate dihydrate and hydroxyapatite more fragile
• If purulent urine endoscopically → abort, drain, treat infection.
  • At URS → drain with a ureteral stent, send urine culture, continue antibiotics
    • Nephrostomy only if a stent cannot be advanced
  • At PCNL access → do NOT dilate the tract
    • Culture urine, place a nephrostomy tube, give broad-spectrum antibiotics, stage the PCNL later
• Staghorn need to be treated as its associated with recurrent UTI, and functional deterioration
  • Complete renal function loss can occur after 2 years without treatment
• Ureteric colic is mediated by prostaglandins released by the obstructed ureter
• Medication stones: the average interval between starting the drug and the stone event is 21.5 weeks

Clinically insignificant residual fragments (CIRF)

• ≤ 2–4 mm, non-obstructive, non-infectious, in an otherwise asymptomatic patient
• 43% of fragments initially deemed insignificant became symptomatic at a mean follow-up of 23 months
• Routine radiologic follow-up of asymptomatic patients after SWL can be limited to abdominal radiography and ultrasound

Ureteric stones

• Spontaneous passage driven by axial diameter
  • ~50% of distal <10 mm pass
  • α-blockers add ~23% absolute.
  • Passage predictors: size, location, side, symptom duration, degree of hydronephrosis
    • → smaller, more distal, right-sided stones pass more readily
    • Composition does NOT predict passage
• MET appear to be most effective in distal ureteral stone 5mm or larger
  • α-blockers raise expulsion mainly for stones >5 mm
    • Unproven <4 mm, where tamsulosin may still ease pain.
  • Steroids and NSAIDs do not independently increase expulsion
• Intervene if conservative fails by 4–6 weeks (or earlier for pain/↓function/infection).
  • e.g. 3 mm distal stone, pain and vomiting controlled, no fever → observe; no urgent intervention
• URS preferred for childbearing-age women and suspected cystine/uric acid stones.
• The exact duration of obstruction beyond which irreversible kidney damage begins is unknown in humans.
  • Exam answer: complete ureteral obstruction → irreversible function loss begins at 2–4 weeks (not before 2 weeks) and can progress to total renal unit loss by up to 6 weeks
• A semi-rigid ureteroscope proximal to the iliac vessels is NOT contraindicated.
• Mid-ureteric stones may need oblique or prone positioning for SWL, to see the stone away from the adjacent bones.
• In a NON-obstructed megaureter, MET, SWL and URS are all viable initial strategies.
• Calcium channel blockers are NO LONGER recommended for medical expulsive therapy.

In an OBSTRUCTED megaureter

• Retropulse the stone to the kidney → PCNL → reposition to perform ureteroneocystostomy
• Or ureterolithotomy with ureteroneocystostomy, open or minimally invasive
• Or ureteroscopy with endoureterotomy in short-segment cases (< 3 cm), allowing concomitant stone treatment
• If an endoureterotomy was done for a stricture, delay stone management to a separate session

Renal stones

• Total stone burden (size + number) = single most important factor in choosing SWL vs URS vs PCNL
  • The >20 mm PCNL-not-SWL cutoff applies to total burden.
• Symptomatic non-lower-pole <2 cm:
  • SWL = fewer complications
  • URS = higher stone-free rate.
• Lower pole 10–20 mm and >1000 HU → mini-PCNL beats RIRS and SWL on stone-free rate, even at low BMI
  • At the cost of more bleeding and longer hospital stay.
• Surveillance: ~50% progress, 10–20% need surgery by 3–4 yr .
• Management recommended in:
  • Stone growth
  • Stone in high risk patient for stone formation
  • Obstructed stone
  • Infection
  • Symptomatic
  • More than 15mm.
• SWL success: renal pelvis/UPJ 80–88%, upper/mid calyx ~70%, lower pole 35–69%.
  • Exam answer: SWL lower pole stone-free rate 25–95% — poor clearance because fragments stay in the calyx and seed recurrence, not because disintegration fails
• PCNL = highest single-procedure stone-free rate (size-independent) but most morbid (~15% complications; transfusion ~7% commonest; hemorrhage most significant).
  • Lower Pole Stone Study Group (10–25 mm lower pole stones):
    • Stone-free at 3 months 76% PCNL vs 40% URS
    • → e.g. 25 mm lower pole stone in a brushite former → PCNL

Treat an asymptomatic calyceal stone in:

• Children
• Solitary kidney
• High-risk professions (e.g. pilots)
• Women considering pregnancy

Anatomic factors that make lower-pole clearance less likely

• Gravity-dependent position
• Multiple infundibula
• Narrow infundibulum (< 5 mm)
• Infundibulopelvic angle < 90°
• Long infundibulum (> 3 cm)

Special scenarios

• Anticoagulation → URS safe.
• High BMI → URS/PCNL unaffected; SWL falls.
  • e.g. symptomatic 1.1 cm middle calyx stone, BMI 41 → flexible URS (RIRS):
    • Obesity hampers SWL targeting and success, and raises anesthetic risk for PCNL
• Split function <15% → consider nephrectomy.
• In spinal deformity or limb contractures, SWL often fails with high retreatment rates.
  • URS is an option; PCNL is best
• Retrorenal colon → PCNL risks colon injury
  • e.g. 2.2 cm, 1100 HU lower pole stone → staged URS safest (size, location and density disfavor SWL, even with a favorable 9 cm skin-to-stone distance)
• Laparoscopic surgery is first-line for anatomic abnormalities with large or complex stones (e.g. malrotated pelvic kidney)
• In XGP with distorted renal parenchyma, proceed to nephrectomy

Staghorn

• Staghorn (mostly struvite) → PCNL (remove — 50% lose function by 2 yr if untreated).
  • Untreated struvite staghorn → 10–30% mortality (28% at 10 yr) vs 7.2% after surgical treatment
  • Complete removal is essential
    • Residual fragments harbor urease-producing bacteria → ongoing infection and stone growth
    • Even 3–4 mm post-SWL struvite fragments → ureteroscopic clearance

Transplant

• Transplant → PCNL preferred for >1.5 cm.
• Asymptomatic renal stones in NATIVE kidneys need no pre-transplant intervention.
• In a transplanted kidney, manage conservatively if the stone is < 4–5 mm with near-baseline function

Horseshoe kidney

• Horseshoe → SWL or URS <1.5 cm, PCNL ≥1.5 cm;
• Horseshoe kidney — 15–20% incidence of stone disease
  • Most are calcium oxalate, commonest in the renal pelvis and posterior lower pole calyces
  • Before SWL, exclude UPJO and poor pelvicalyceal drainage
    • Both common in horseshoe kidneys (elongated pelvis, high ureteric insertion) and they severely limit SWL success
  • If skin-to-stone distance falls outside the focal zone, use the "blast path" technique
  • In PCNL, access is the upper posterior calyx.
    • Traditional posterior access is hampered by the bony pelvis and can cause debilitating femoral neuropathy

Calyceal diverticulum

• Calyceal diverticulum → PCNL (direct puncture) first-line
  • URS for small (<2 cm) upper/mid
  • Anterior calyx → URS (PCNL bleeding risk)
  • SWL seldom works.
• Calyceal diverticula — urothelium-lined, non-secretory cystic dilations, thought to arise embryonically.
  • Distribution: 50% upper pole · 30% mid pole or renal pelvis · 20% lower pole.
  • Treat when there is pain, recurrent infection, hematuria, or declining renal function
  • Asymptomatic diverticular stone (e.g. 15 mm, anterior upper pole diverticulum) → observation only
    • Intervene for pain or recurrent UTIs
  • URS is reasonable first-line for small (< 2 cm) stones in an UPPER or MIDDLE calyx with a SHORT-NECK diverticulum
    • The holmium laser incises the neck, fragments the stone, and ablates the diverticular lining
  • Laparoscopic/robotic is for anteriorly located symptomatic diverticula with thin overlying parenchyma
    • Used when large diverticula or stone burdens make endoscopy unreasonable
    • Fulguration helps obliterate larger cavities
  • PCNL access: puncture directly onto the stone inside the diverticulum
    • Entering via a normal calyx leaves you working across the narrow neck
    • Retrograde URS is a useful adjunct to find the diverticulum during PCNL
  • Lower pole diverticulum (e.g. symptomatic 1.5 cm stone) → PCNL + fulguration
    • Best stone-free and symptom-free chance; reduces diverticulum recurrence

UPJO + stone

• UPJO + stone → PCNL + antegrade endopyelotomy,then URS + retrograde endopyelotomy, or pyeloplasty + pyelolithotomy.
  • Establish which caused which — is the UPJO the cause of the stone, or the reverse?
  • If UPJO is suspected, re-image 4–6 weeks AFTER the stone is treated
    • If hydronephrosis persists, get a diuretic renogram.
    • If a nephrostomy is in place and it remains equivocal, do a Whitaker test.
    • Only repair the UPJ once obstruction is confirmed
  • Exam answer: suspected UPJO + stone + recurrent UTIs → diuretic renal scan first to quantify obstruction; retrograde pyelography is invasive and does not quantify it
  • Scan confirms UPJO → dismembered pyeloplasty + pyelolithotomy possible
    • For a borderline lower pole stone, PCNL ± antegrade endopyelotomy (per the scan) is preferred over URS
  • Clear the stones FIRST, then address the UPJO
    • Stone incorporation near the endopyelotomy site causes granuloma and fibrosis (unavoidable in retrograde endopyelotomy with URS)
  • Discourage endopyelotomy when:
    • Strictures are long (> 2 cm)
    • There is a high UPJ insertion
    • A prior endopyelotomy has failed
  • Recurrence after endopyelotomy responds well to pyeloplasty
  • Recurrence after pyeloplasty responds well to endopyelotomy
  • Laparoscopic/robotic pyeloplasty short-term success exceeds 90%, and appears superior to antegrade endopyelotomy

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Surgical Modalities

Shock Wave Lithotripsy (SWL)

• Generators (3):
  • Electrohydraulic/spark-gap (largest focal zone, short electrode life)
  • Electromagnetic
  • Piezoelectric (insufficient power).
• 60 shocks/min > 120 → better fragmentation + more renal-protective
• GA improves stone-free rate (less stone motion)
• "Ramping up" energy is renoprotective.
• Unmodified Dornier HM3 = gold standard
• No antibiotic prophylaxis if no UTI
  • Holds with sterile urine even with a ureteral catheter or nephrostomy in place
  • Reserve prophylaxis for suspected or confirmed infected stones or bacteriuria
• No routine pre-stenting — see the stenting indications below.
• Post-SWL hematoma risk (TD COACH):
  • Thrombocytopenia
  • Diabetes
  • Coagulopathy
  • Obesity
  • Age
  • Coronary disease
  • Hypertension (greatest risk).
    • Especially poorly controlled hypertension
• Perinephric hematoma follows 1–20% of SWL
• Stone size and location affect fragmentation but not hematoma risk, and a slow 1 Hz rate does not raise it
• BMI > 30 or < 21.5 kg/m² → increased risk of renal hemorrhage
• Chronic SWL changes (4):
  • ↑ blood pressure
  • ↓ renal function
    • Renal insufficiency after unmodified Dornier HM3 SWL: 63–85% show renal injury within 24 hours
    • Repeated or high-energy exposure scars the parenchyma
  • ↑ stone recurrence
  • Induction of brushite stones.
• Contraindications (6):
  • Distal obstruction
  • Pregnancy
  • Uncorrected coagulopathy
  • Untreated UTI
  • Nearby arterial aneurysm
  • Untargetable stone.
    • An untargetable stone includes skeletal malformation preventing targeting
  • Untreated or severe hypertension is also an absolute contraindication
• Pediatric age is NOT a contraindication
• Factors affecting SWL negatively: stone composition (cystine, brushite, CaOx), >1000 HU, skin-to-stone distance >10 cm, renal anomalies, lower-pole stone.
  • Attenuation of ≥ 1000 HU · unfavorable lower-pole anatomy
• Stone size is the most predictive factor for SWL outcome
  • Its largest linear dimension is likely as predictive as more complex volumetric estimates.

Generator mechanics

Advantages and disadvantages

• Electrohydraulic delivers the most powerful SWL
  • The original Dornier HM3 used one, and no later machine has matched it
  • Its largest focal zone eases targeting and may improve stone-free rates
• Piezoelectric: wide aperture → minimal discomfort but often lower stone-free rates
• Electromagnetic: smaller focal zone but higher pressures

Six theories of stone fragmentation

• Spall fracture — the wave hits impedance mismatch and reflects as a tensile (negative) wave
• Superfocusing — internal reflections focus energy at a point of very high stress
• Shear stress — transverse waves create areas of high shear
• Compression (squeezing-splitting) — the wave travels faster through stone than fluid
• Acoustic cavitation — bubble collapse raises pressure on the stone
• Accumulated damage — cumulative tensile and shear stress

Stone density and SWL success

• 970 HU is the most sensitive and specific cut-off — 96% success below, 38% above
• Strongly consider SWL for non-lower-pole stones < 2 cm with HU < 500
• Mean shocks needed: cystine 5937 · brushite 1681 · uric acid 400 (the least)
• A stone denser than the adjacent transverse process or 12th rib is more SWL-resistant
• Cystine appears as GROUND GLASS on plain radiography — if seen pre-operatively, choose something other than SWL

Factors affecting the degree of renal trauma

• Aggravating:
  • Number of shocks
  • A shorter administration period increases damage
  • Higher voltage
  • Generator type
  • Juvenile kidney
  • Pre-existing renal impairment
• Mitigating:
  • Pre-treatment with 100–500 low-energy shocks
  • Slow delivery (≤ 60 shocks/min)
  • To lower post-SWL bleeding, also control blood pressure beforehand
• Primary insult: vascular
  • Rupture of thin-walled veins, small-artery walls, and glomerular and peritubular capillaries

Ways to improve outcomes

• Appropriate coupling, water-soluble lubricant applied by hand
• Slow (60–70/min) or intermediate (80–90/min) rate
• Image frequently and stop once fragmented — do not use a preset number of shocks
• Ramping protocol
• General anesthesia
• Do NOT use a ureteral stent
• Consider MET
• Consider percussion, diuresis, inversion therapy

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Complications

• Trauma to liver, skeletal muscle, pancreas, stomach, duodenum, lung, colon
• Subcapsular hematoma 5–10% with newer generators — resolves over ~6 weeks
• Hematuria
• Intrarenal and perinephric edema (resolves in days)
• AKI
• Steinstrasse 5–10%
• UTI/pyelonephritis 5–10%
• Renal colic requiring admission
• Failed lithotripsy
• Impaired semen quality with distal ureteric stones — normalizes by 3 months
• Cardiac arrhythmias resolve on stopping SWL — stop, resume once settled
• Any patient with a hemoglobin drop or significant flank pain 24 hours after SWL needs imaging (renal US or CT) to separate a perinephric hematoma from obstruction
  • Most hematomas → conservative: hemodynamic monitoring, IV fluids or transfusion
  • Renal angiography only for significant bleeding that conservative care cannot control
• SWL in the elderly is feasible but carries a higher risk of perinephric hematoma
  • Elderly bedridden patient (e.g. 1 cm upper-pole calcium stone): the drawback is physical condition
    • Age increases shock wave renal injury and immobility hampers fragment clearance

Steinstrasse

• Risk factors: large stone burden, staghorn stones, pre-existing ureteric obstruction
• Occurs in 2–10% of SWL cases; 70% in the distal ureter
  • Exam answer: steinstrasse (a build-up of stone fragments in the ureter) is most typically an SWL complication, in 4% of cases, with stone size the main risk factor
• Asymptomatic → observe; ~70% clear spontaneously (with antibiotics and repeat ultrasound)
  • Medical expulsive therapy increases stone expulsion and reduces the need for endoscopic intervention
• A nephrostomy allows passage in up to 75%
  • Likely more successful than a ureteral stent alone
  • Percutaneous antegrade ureteroscopy is a salvage option
  • Fever or UTI → percutaneous nephrostomy first
    • Definitive clearance (URS or SWL) waits until the infection resolves
• URS is the treatment of choice — the leading stone can be shocked
  • Persistent asymptomatic steinstrasse at 4 weeks, once expectant management has failed → ureteroscopic laser lithotripsy (immediate success approaching 100%)
    • Repeat SWL is less predictable
• In adults, stenting before SWL reduces steinstrasse but does not improve stone-free rates
• Obstruction is silent in up to 23% → follow-up imaging even without symptoms

Indications for stenting BEFORE SWL

• Solitary functioning kidney
• Obstruction proximal to the stone
• Refractory renal colic
• Renal insufficiency
• Size > 1.5 cm
• Poorly visualized stone
• Bilateral SWL
• Infection with obstruction

Consider ureteroscopy instead in some of these cases

• Proximal ureteral stone → treat in situ
  • Push-back, stenting or nephrostomy beforehand does not improve stone-free rates, and stents lower quality of life
• A ureteral catheter placed up to the stone helps only with targeting radiolucent stones

After SWL

• Most fragments pass in the first 3 months, but clearance can continue beyond 24 months
• Residual fragments localize to the lower pole calyces regardless of where the stone was treated
• Percussion, diuresis and inversion therapy improve stone-free rates for lower pole stones

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Intracorporeal Lithotripters

• Holmium:YAG (2140 nm, photothermal vaporization)
  • Fragments any composition
  • Thermal injury 0.5–1 mm
  • Safe 0.5 mm from urothelium.
  • Pulsed; 2140 nm sits at a water absorption peak, so it vaporizes the stone rather than shattering it
  • Will also cut guidewires and basket wires
• Dusting — least fragments + least retropulsion:
  • ↓ pulse energy, ↑ frequency, long pulse width (0.2–0.4 J × 50–80 Hz).
  • Lowering pulse energy and lengthening pulse width reduce retropulsion the most
    • Frequency matters less, though raising it typically decreases retropulsion
• Popcorn — high energy and high frequency.
• Fragmenting — high energy and low frequency.
• Thulium:YAG — shorter wavelength, 0.2 mm depth of penetration.
• General laser limits:
  • Don't exceed 20 W in the kidney, 12 W in the ureter and 30 W in the bladder
  • Maintain good irrigation.
• Ureteric stones: always start as low as possible (0.6 J × 6 Hz) and don't exceed 15 Hz in the ureter.
• Pneumatic (ballistic): highest retropulsion
  • The jackhammer impact pushes the stone → place antiretropulsion devices proximal to the stone in rigid and semirigid ureteroscopy
  • Significantly lower ureteral perforation risk than EHL, ultrasonic or laser
• EHL: greatest risk of ureteral injury
  • Its shock wave is unfocused, and at higher energies (hard stones) it can injure the ureter even when fired several millimeters from the wall
  • Impacted stones also raise perforation risk

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Ureteroscopy (URS)

• Flexible scope needed for proximal stones
  • Needs ≥ 180° of deflection to reach the lower-pole calyx; modern scopes deflect up to 270°
  • A laser fiber or basket in the working channel reduces actual deflection
  • Pass a small (200-μm) holmium fiber with the scope straight, then deflect
    • Inserting it through a deflected scope is the main cause of cumulative working-channel damage
  • Durability protocol (fiber only through a straight scope, no lasering in maximal deflection) doubled uses before damage, from 10 to 20
• Full fragmentation below safety-wire diameter (0.035 in) passes spontaneously.
• No specific contraindications beyond untreated UTI and general anesthetic issues
• RIRS can treat stones up to 3 cm, depending on operator skill.
• Post-URS stent indications (5):
  • Ureteric injury
  • Stricture/edema
  • Burden >1.5 cm
  • Solitary/impaired kidney
  • Planned second-look.
• Otherwise omit; if placed, 3–7 days.
• Perforation → stop, stent ~4 weeks (± PCN).
  • Persisting with stone basketing after a ureteral tear worsens the injury — stop once perforation is recognized
• Avulsion → PCN + delayed reconstruction or immediate repair.
• Submucosal stone → laser excision + stent (stricture risk).
  • Submucosal stone = one pushed into the ureteral wall during a procedure
  • Excision + stent is for a symptomatic one, and if that fails → segmental ureteral resection and repair
  • SWL is ineffective
• Mandatory imaging after instrumentation (0.4–4% silent strictures)
  • Renal ultrasound at ~6 weeks for silent hydronephrosis.
  • Exam answer: renal ultrasound within 8 weeks of any ureteroscopy (e.g. at 6 weeks); silent ureteral stricture in 1–4%
• The POOREST holmium fragmentation is calcium oxalate monohydrate; moderate for uric acid and cystine.
• URS is the most cost-effective strategy for ureteric stones at all locations once observation fails
  • SWL carries a higher retreatment rate.
• URS does not add surgical risk in the elderly.
• In cystinurics, URS should take a prominent role to limit cumulative renal damage from repeated intervention
  • Even for stones > 2 cm, as long as clearance is achievable in 1–2 sessions.
  • e.g. an asymptomatic 11 mm upper-pole cystine stone → URS
    • Cystinuria is high-risk so removal is indicated, and cystine resists SWL and is only faintly radiopaque for targeting
• Post-URS: dietary instructions, remove the JJ at 1–2 weeks, metabolic workup if indicated.

Benefits of a ureteral access sheath

• Shorter operating time
• Higher stone-free rates
• Easier ureteric re-entry
• Less damage to the ureteroscope
• Lower intrapelvic pressures
  • The sheath lowers intrarenal pressure whatever the irrigation method; warming the irrigant does not affect intrarenal pressure
• Can dilate a narrow ureteric orifice
• Irrigation: a single-action hand pump gives the highest peak intrarenal pressure (> 300 cm H2O) while keeping a low baseline

Reducing radiation exposure

• Grid-controlled fluoroscopy
• Aim more midline
• Last-image-hold
• Collimation
• Place the fluoroscopy head/beam UNDER the table — this reduces exposure to the surgeon, not the patient
• Lead aprons and thyroid shields · dosimeters

Indications to leave a stent after URS (7)

• Infected + obstructed system
• Large stone burden with fragments to pass
• Impacted stone with significant edema
• Solitary kidney
• Planned repeat URS in ~1 week
• Ureteric dilation > 10 Fr
• Intra-operative perforation

Purpose: prevent colic from stones or edema · facilitate stone passage · prevent stricture formation

• A solitary kidney is NOT an absolute indication to stent after URS
• Balloon dilation of a narrowed ureteral segment → JJ stent mandatory, splinting 4–6 weeks to prevent re-stenosis
• Routine stenting after uncomplicated URS with complete stone removal is unnecessary
• Also stent higher-risk patients — bleeding, residual fragments, UTI, pregnancy — and any doubtful case
  • Not indications by themselves:
    • Access-sheath use
    • Basketing
    • Ureteral duplication
    • Advanced age

Complications

• Drain a urinoma if present; give antibiotics
• Complete extrusion of a calculus can happen with a ureteric perforation
  • The stone can be left in place
• Avulsion
  • From forceful basketing or withdrawing a large scope forced up the ureter.
  • The PROXIMAL third is at greatest risk, having the least muscular support.
    • The proximal ureter also has the lowest tensile strength
  • Delayed repair is recommended
  • Avulsion with the stone still trapped in the basket and no safety guidewire → divert immediately with a percutaneous nephrostomy
• Risk factors for ureteric perforation:
  • Long operating time
  • Use of EHL
  • Impacted stone
  • Renal stones
  • Surgeon inexperience
• Three risk factors for later ureteral stricture: perforation · impacted stones · submucosal stones
  • After a perforation, imaging after stent removal is mandatory to confirm healing

Predictors of successful endourologic treatment of a stricture

• Non-ischemic strictures do well; ischemic ones do poorly
• Length < 2 cm does better
• Urine flow through the incised area is necessary
• Poor renal function (< 25% of total) is more likely to fail
• < 2 cm, no prior intervention → ureteroscopic endoureterotomy
  • More durable than balloon dilation
  • Incise anteromedially, away from the iliac vessels
• Recurrent, or > 2 cm at presentation → ureteroureterostomy or reimplantation with psoas hitch
  • A failed balloon dilation can leave a much longer stricture

Stones in urinary diversions — treatment

• Ileal conduit — observe if asymptomatic; treat endoscopically if symptomatic.
• Neobladder — small stones: transurethral; large stones: percutaneous.
  • e.g. a 3 cm + 2 cm burden → percutaneous, sparing the rhabdosphincter on which continence depends
  • Map the reservoir before puncture to avoid bowel or pouch vascular pedicle injury
  • Single-sitting success 89–100%
  • Recurrence 10–42%, independent of method
• Continent cutaneous pouch — percutaneous.

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PCNL

• Access: posterior calyx through the papilla, along calyceal axis
  • Upper-pole preferred for staghorn/complex (line with kidney axis, allows endopyelotomy) but risks pleura/liver/spleen.
  • Lower-pole access avoids thoracic injury but carries a slightly higher colonic risk, especially on the left
• Absolute CI: untreated UTI.
• Flexible nephroscopy every case
• Normal saline irrigation
• Overadvancing the dilator/sheath = commonest serious access error.
• Hemorrhage = most significant complication → nephrostomy tube → clamp → Kaye balloon → angioembolization → partial nephrectomy
  • A nephrostomy tamponade catheter or fulguration treats immediate bleeding, not delayed
  • Renal exploration only for failed angioembolization or life-threatening hemorrhage
• Delayed hemorrhage:
  • Delayed bleed (AV fistula/pseudoaneurysm) → selective arteriogram + embolization.
  • Continuous = AV fistula
  • Intermittent: pseudoaneurysm
  • Both Rx: Angio
  • Typically ~1 week post-op as bright-red bleeding · angiography is indicated even if hemodynamically stable
• Post-operative bleeding:
  • ABCs
  • Vitals
  • Pressure dressing
  • Clamp the nephrostomy
  • IV fluids
  • Transfusion with serial hemoglobin
  • Bed rest
  • ± angiography ± embolization
• Pelvic perforation injury: sign of collapsed pelvicalyceal system
  • Rx: Nephro U stent or PCN and DJ for 7 days then repeat nephrogram
• Pleural injury
  • If Insertion supra 12 =4%
  • If insertion supra11=24%
  • Supracostal puncture → pneumothorax/hydrothorax risk.
• Sepsis — best predictor = stone or renal-pelvic urine culture (not voided)
  • Fragmenting stones releases endotoxin even with sterile urine.
  • A negative preoperative culture does not exclude infection in a staghorn stone → give a 1-week course of broad-spectrum antibiotics before PCNL
  • About one third of stented patients with sterile preoperative urine are still colonized (mostly Enterococcus and Staphylococcus epidermidis) → culture urine proximal to the stone and stone fragments
  • Staphylococcus epidermidis is the commonest cause of secondary infection after percutaneous stone removal → cephalosporins are the prophylaxis of choice for noninfected stones
• Venous gas embolism — mill-wheel murmur, hypoxia → head-down, right-side-up.
  • Also hypotension and dysrhythmias; immediately place the patient left lateral decubitus
• Tubeless PCNL acceptable if presumed stone-free, no active bleeding, no planned second look.

Anatomic considerations for access

• Ideally through Brodel's line — between the anterior and posterior divisions of the main renal artery
• Avoid direct infundibular access and direct puncture of the renal pelvis
  • A nonpapillary puncture risks the interlobar arteries running beside the infundibula → safest entry is through the calyceal fornix (papillary tip)
• A simple calyx (single papilla) most likely lies in the interpolar region; compound calyces (two or three papillae) sit at the upper and lower poles
• Subcostal access (below the 12th rib) where possible — fewer pleural complications, less pain
• Attempt access during the EXPIRATORY phase — lower risk of pleural complications
• Use an Amplatz-type open sheath to reduce fluid absorption

Gaining access once the calyx is chosen

1. Cystoscopy + ureteric catheter + Foley catheter
2. 18-gauge needle into the calyx under fluoroscopy, adjusting with the C-arm
3. Aspirate urine to confirm position
4. Pass a hydrophilic guidewire ideally into the ureter, otherwise curl it in the renal pelvis (a Cobra catheter can direct the wire through the UPJ from lower-pole access)
5. 8–10 Fr coaxial dilators to dilate the track
6. Safety guidewire through a double-lumen catheter
7. Dilate to accept the working sheath — balloon dilators (expensive, fast, safe) · semirigid Amplatz · metal fascial dilators

Indications for PCNL on a URETERIC stone

• Large, complex proximal stones
• Distal ureteric stricture
• Urinary diversion
• Concomitant renal stone
• Failed URS or SWL

Indications for a SUPRACOSTAL puncture

• Most of the stone is in the upper calyces
• Associated UPJO needing endopyelotomy
• Multiple lower-pole calyces with stones
• Associated ureteric stone
• Staghorn with substantial upper-pole component

Supracostal puncture

• Examine the chest at the end of any PCNL using a supracostal puncture
• Left supracostal: the pleura is the structure most at risk (pneumothorax, pleural effusion, hydrothorax) → puncture only in full expiration

Absolute contraindications

• Uncorrected coagulopathy · active untreated UTI · pregnancy
  • Stop anticoagulants and correct the INR first
  • Horseshoe kidney, solitary kidney and obesity are NOT absolute contraindications
  • Other contraindications: tumor in the presumed access tract · possibly malignant kidney tumor

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Performance

• PCNL gives higher stone-free rates and fewer auxiliary procedures than SWL or URS for renal stones between 1 and 2 cm
• PCNL is the preferred approach for most MATRIX renal stones
  • Gelatinous and minimally mineralized → SWL is ineffective and ureteroscopy has a lower success rate
• In the elderly, surgical success is essentially unchanged but complication rates are higher
• Post-PCNL drainage is the standard of care
• Flexible nephroscopy is the gold standard for assessing residual stones after PCNL
• Transplant kidneys — use CT or ultrasound guidance (risk of intervening bowel)
  • A fibrous capsule may require metal fascial dilators
• Retrorenal colon occurs in < 1% overall, but is commoner after jejunoileal bypass, in nursing-home residents, in spinal cord injury, and in advanced scoliosis
  • Exam answer: on CT, a retrorenal colon is seen in 10% of prone vs 1.9% of supine patients → favors the supine position to lower colonic injury risk

Perforation and extravasation

• The first sign of significant extravasation of irrigant into the peritoneal cavity is a NARROWED PULSE PRESSURE
  • From reduced venous return; it precedes ventilatory difficulty and hypercarbia
• Extraperitoneal perforation shows as medial displacement of the kidney on fluoroscopy
• Intraperitoneal extravasation is less common but more serious.
  • The patient is prone, so distension is hard to see — the anesthetist typically notes a rising diastolic BP and rising CVP
  • Treat with vigorous diuresis; otherwise peritoneal drainage or laparotomy
  • Place a nephroureterostomy, or a nephrostomy plus JJ stent
• Sepsis (T > 38.5 °C) occurs in 25%

Colonic injury

• Rare, and usually retroperitoneal
  • About 0.1% of PCNLs; the left colon is injured twice as often as the right — colon–kidney apposition is greatest on the left at the lower pole
• Recognition: greenish, feculent nephrostomy drainage
• Risk factors:
  • Puncture lateral to the posterior axillary line
  • Anterior calyceal puncture
  • Horseshoe kidney
  • Kyphoscoliosis
  • Jejunoileal bypass
    • Jejunoileal bypass predisposes via previous bowel surgery + a thin, malabsorptive habitus, and also causes enteric hyperoxaluria stones
  • Thin or elderly patients
  • Not upper-pole puncture
• Place a ureteric stent
  • Retrograde stent → drains the kidney separately from the colon
• Pull the nephrostomy back into the colon — it becomes a colostomy tube.
  • Leave at least 1 week; remove after imaging shows no communication with the colon
• Antibiotics · NPO, consider TPN
• Laparotomy if obviously intraperitoneal, or for sepsis, peritonitis, or failed conservative management
  • Transcolonic nephrostomy with sepsis + hemodynamic instability → urgent open repair after antibiotics and resuscitation
  • Tube withdrawal + ureteral stent + Foley suits only stable patients

Sequence of tube removal after PCNL

Nephrostomy + JJ stent + Foley

1. Clamp the nephrostomy → observe for pain or fever
2. If none, remove the nephrostomy and keep the Foley until the next day — this lets the percutaneous wound heal without urine refluxing through it
3. Remove the Foley, observing the flank wound — if it stays dry, discharge; if not, replace the Foley
4. The JJ stent is removed last

With a chest tube in place

• First get a CXR and check chest tube output. If the CXR is clear and there is no output:

1. Clamp the nephrostomy → observe for pain, fever, shortness of breath, or increased chest tube output
2. If all negative, remove the nephrostomy, keeping the Foley and chest tube
3. If chest tube output stays nil, remove the Foley and keep watching the chest tube
4. If still nil, remove the chest tube
5. The JJ stent is removed last

Open / laparoscopic / nephrectomy

• Reserved for failed PCNL/SWL/URS or anatomy needing reconstruction (UPJO, infundibular stenosis)
• Nephrectomy for negligibly functioning kidney (split function <15%).
• Robotic pyelolithotomy is more invasive than ureteroscopy → reserve for cases needing simultaneous reconstruction or larger complex stones with aberrant anatomy.

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Stones in Pregnancy

• Incidence unchanged; ~74% calcium phosphate (reverse of non-pregnant).
• Pregnancy → ↑ GFR 30–50% (creatinine ~25% lower), lithogenic hypercalciuria + hyperuricosuria; metabolic work-up deferred until after delivery.
  • ↑ GFR → ↑ filtered calcium load; placental 1,25(OH)₂D₃ → ↑ intestinal calcium absorption → secondarily suppresses PTH.
  • Hypercalciuria of pregnancy is reversible and offset by ↑ excretion of inhibitors (citrate, magnesium, glycoproteins) → overall stone risk similar to non-pregnant women.
• Physiologic hydronephrosis — gravid uterus compression (main) + progesterone
  • Right > left
  • Resolves 4–6 wk postpartum.
• Colic → risk of preterm delivery + PROM.
• Imaging: US first-line → MRI 2nd → low-dose CT/limited IVP; fetal exposure <5 rads (ACOG).
• Observation first-line (50–80% pass).
• NSAIDs contraindicated.
• Stent/PCN (exchange q4–6 wk) or URS; elective surgery in 2nd trimester.
• During URS in pregnancy, use a below-table x-ray source and shield the fetus with a lead apron placed below the patient.

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Lower Urinary Tract Calculi

• Primary bladder stones — children, boys 9–33×, low-protein/low-phosphate diet → ammonium acid urate
  • Solitary, rarely recur, diet-prevented.
  • Form without any predisposing cause; linked to nutritional deficiency (deficient animal protein); arise within the first 5 years of life.
  • Primary idiopathic (endemic) — North Africa, Middle East, Asia:
    • Cereal-based diet → low urinary phosphate + high urinary ammonia → ammonium acid urate (commonest stone).
• Secondary — bladder outlet obstruction (most common), neurogenic bladder, augmentation/diversion (struvite + Ca phosphate).
  • Adults: uric acid (sterile) or struvite (infected).
  • Without infection, obstruction, neurological problems or a foreign body, bladder stones rarely form.
  • Homogeneous nucleation rarely responsible → heterogeneous nucleation around a foreign body as a result of infection, or from obstruction → supersaturation.
  • Spinal cord injury — more prone than other neurogenic bladder patients:
    • Bladder stone risk peaks 3 months after injury
    • 15–30% of adults form ≥1 stone within 10 years
    • Risk quadruples after the first stone.
• Commonest symptom terminal gross hematuria
• Cystoscopy most accurate
• Treat endoscopically (holmium laser)if less than 4cm, if larger percutaneous — avoid through continent catheterizable channel.
• No medical therapy — relieve obstruction.
• Prostatic calculi — inspissated secretions; asymptomatic; don't affect PSA.
• Female urethral calculi → almost always urethral diverticulum (risk fistula).
• Preputial calculi → circumcision + removal.