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.
• First-time formers: ~50% recurrence within 10 years.
• Stones need supersaturation but not sufficient alone — urinary inhibitors prevent crystallisation.
  • Above the solubility product (metastable) → crystals grow on existing crystals (heterogeneous nucleation).
  • Above the formation product → spontaneous (homogeneous) nucleation.
• Inhibitors (6): citrate (most important)[inhibits Ca growth, nucleation & aggregation], Tamm-Horsfall mucoprotein (most abundant urinary protein)[inhibits Ca, aggregation only], magnesium, nephrocalcin, bikunin, uropontin — none inhibit uric acid.
• Citrate is the most potent complexor of calcium — it inhibits spontaneous precipitation of calcium oxalate and prevents heterogeneous nucleation of CaOx by monosodium urate.
• 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.
• Substance A is a component of matrix in all stone formers and is immunogenically unique.

Mineral Metabolism

• PTH (↓ serum Ca trigger) → ↑ renal Ca reabsorption + ↑ phosphate excretion, ↑ bone Ca release, stimulates 1α-hydroxylase. Does not act on intestine.
• Calcitriol [1,25(OH)₂D₃] → most potent stimulator of intestinal Ca absorption, ↑ renal Ca/PO₄ reabsorption, ↑ bone Ca release, inhibits PTH.
• 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.

Classification (frequency)

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

Metabolic Risk Factors

Hypercalciuria — most common abnormality in Ca stone formers

Type	Serum Ca	PTH	Mechanism
Absorptive	Normal	Normal/↓	↑ gut Ca absorption (type I diet-independent; type II only on normal diet)
Renal (leak)	Normal	↑	Renal Ca wasting → 2° hyperPTH; ↑ fasting urinary Ca
Resorptive	↑	↑	Usually primary hyperPTH (adenoma); 100% brushite recurrence → suspect HPT
Idiopathic	Normal	Normal	No serum abnormality

• ↑ PTH + high fasting urine Ca distinguishes renal from absorptive.

• Glucocorticoid induced hypercalcemia ; alter calcium metabolism , common in cushing syndrome — the glucocorticoid drives hypercalciuria + uricosuria + hypocitraturia

• 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

	Urinary Ca	Serum Ca	PTH
Absorptive	Normal during fasting (high if severe); high non-fasting	Normal — ↑ absorption balanced by ↑ renal excretion	Normal or slightly low
Renal leak	High all the time	Normal	Mildly elevated
Resorptive	High all the time	High	Very high

• 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.
• 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
• 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).
• Dietary — rhubarb, chocolate, nuts, tea, spinach, beets; keep Ca normal, vitamin C ≤2 g/day.

Hyperuricosuria

• Pure uric acid or Ca oxalate (monosodium urate heterogeneous nucleation).
• Most common cause = ↑ dietary purine; also gout, myelo/lymphoproliferative, Lesch-Nyhan (HGPRT).
• Low PH <5.5

Hypomagnesuria

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

Renal Tubular Acidosis (acquired mnemonic A CASH POT)

Type	Defect	Stones	Features
1 (distal)	↓ H⁺ secretion Rx: K citrate or NaHCO3	Common (~70%), Ca phosphate	Urine pH >6.0, non-AG hyperchloraemic acidosis, hypercalciuria, hypocitraturia, hypokalaemia, nephrocalcinosis
2 (proximal)	↓ HCO₃⁻ reabsorption	Uncommon	HCO₃⁻ 15–18, urine pH <5.5 steady state; citrate not low
4 (distal)	↓ mineralocorticoid response	Uncommon	Hyperkalaemia, chronic renal damage

• Incomplete type 1 RTA → confirm with ammonium chloride load; treat with potassium citrate.
• Distal (type 1) RTA — the defect is the H⁺ ATPase in the collecting duct (α-intercalated cells); urine pH > 6.8, hyperchloraemia, hypokalaemia, low serum bicarbonate. 70% develop calcium phosphate stones (brushite) and medullary nephrocalcinosis.

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). Causes (DIRT): Diarrhoea, Idiopathic, type 1 RTA, Thiazides. Severe → suspect RTA.
• Topiramate causes hypocitraturia and recurrent stones → give potassium citrate.
• Urine pH <5.5 → uric acid (and Ca oxalate via nucleation).

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. Diabetics ~6× risk (insulin resistance → ↓ ammoniagenesis → low pH). Radiolucent.
  • 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
  • 20% of gout patients develop uric acid stones. In gout, the commonest compositions are uric acid (52%) then calcium oxalate monohydrate (45%)
  • Risk factors: thalassaemia · myeloproliferative disorders · gout · obesity · Lesch-Nyhan · diabetes · pregnancy · neoplastic disease · purine-rich diet (red meat) · dehydration (diarrhoea, colectomy, ileostomy)
  • Uric acid is the most common bladder stone, followed by struvite
• Calcium phosphate — type 1 RTA, 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). Poorly radio-opaque; nitroprusside spot test (urine turns purple).
  • Average age at first stone is 12.2 years; cystine crystallises above 250 mg/L — the treatment target is to get below that
  • Yellow and waxy in appearance; produces a sulphurous gas on laser lithotripsy
  • Reduce egg, chicken, beef, poultry, fish and pork — animal protein is rich in cystine and methionine, which are metabolised to cystine
  • Alkalinisation 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
• Struvite (Mg-ammonium-phosphate) — only with urease-producing organisms: Proteus (most common), Klebsiella, Pseudomonas, S. aureus (most E. coli don't). Females 2:1; commonly staghorn.
  • 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
• Other: matrix (~65% protein, urea-splitting UTI, radiolucent), xanthine (XDH deficiency ,Allopurinol), 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), indinavir (radiolucent, may be invisible on CT), topiramate (distal-RTA picture,Ca Phosphate ), triamterene, ephedrine, silicates, TMP/SMX.

Hereditary Disorders Associated with Stones

Pattern	Disorders
Autosomal dominant	Distal RTA
Autosomal recessive	Cystinuria · primary hyperoxaluria (oxalosis) · adenine (2,8-DHA) · xanthinuria · Bartter's syndrome
X-linked	XR nephrolithiasis syndrome · Lesch-Nyhan (uric acid) · hypophosphataemic rickets · Dent's disease (calcium stones)

Stones in Special Populations

Why transplant patients form stones

• From the renal failure: hypercalciuria (tubular dysfunction) · hyperoxaluria · dehydration · iatrogenic calcium supplements · hypercalcaemia from secondary hyperparathyroidism
• From the transplant: foreign bodies (suture, stent) · UVJ strictures · steroids · stones transplanted with the kidney

Why urinary diversions form stones

• UTI · mucus · stasis · hypocitraturia · acidosis · dehydration

Causes of stones in neonates

• Dehydration · underweight at birth · TPN · steroids · distal RTA · furosemide · theophylline · cystinuria · sepsis · congenital hyperparathyroidism

• Intestinal bypass surgery produces a urine profile like chronic diarrhoea — low volume, acidic urine, hypocitraturia, hyperoxaluria, and low serum sodium/magnesium/calcium. Treat with potassium citrate and calcium citrate.

Anatomic predisposition

• UPJ obstruction, horseshoe kidney, caliceal diverticulum, medullary sponge kidney — but an underlying metabolic abnormality is still required.

Diagnosis & Imaging

Modality	Sens	Spec	Notes
KUB	57%	76%	Cheap, low dose; misses small stones
Ultrasound	84%	53%	No radiation; misses ureteric stones; poor sizing
Non-contrast CT	95%	98%	Most sensitive; uric acid = low HU
MRI	82%	98%	No radiation; stones = filling defects; most $$

• Radiolucent (KUB): uric acid, matrix, xanthine, triamterene, 2,8-DHA, indinavir.
• Radio-opaque: Ca oxalate, Ca phosphate (densest). Poorly opaque: struvite, cystine.
• Crystal shapes: Ca oxalate = envelope/dumbbell; uric acid = rhomboid/rosette; cystine = hexagonal; struvite = coffin-lid; Ca phosphate = amorphous.

Chemical type	Crystal appearance
Calcium oxalate monohydrate	Hourglass
Calcium oxalate dihydrate	Envelope, tetrahedral
Calcium phosphate apatite	Amorphous
Brushite	Needle-shaped
Struvite	Rectangular, coffin-lid
Cystine	Hexagonal
Uric acid	Amorphous shards, plates

Phlebolith vs stone

Phlebolith	Stone
Target sign — round with a lucent centre	Rim sign — ureteric oedema around the stone
Comet-tail sign — the blood vessel tail	Proximal hydroureter · periureteral fat stranding · ipsilateral renal enlargement · ipsilateral loss of the white pyramid sign

• 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).

Acute Management

• Analgesia + fluids.
• 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).
• Indication for Acute Decompression : Sepsis , Solitary or bilateral obstruction , Refractory Pain with Obstruction, Obstruction with elevated Cr

Metabolic Evaluation

• Screening (all stones): H&P, UA ± culture, electrolytes, Ca, creatinine, uric acid, imaging for burden; stone analysis at least once.
• Extended (24-h urine ×1–2): recurrent, family history, solitary kidney, malabsorption, children, cystine/uric acid/struvite, predisposing conditions.
  • 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.
• 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).

Indications for metabolic evaluation (12)

1. Recurrent stone formers · 2. Strong family history · 3. Intestinal disease, particularly chronic diarrhoea · 4. Pathologic skeletal fractures · 5. Osteoporosis · 6. History of UTI with calculi · 7. Personal history of gout · 8. Infirm health (unable to tolerate repeat episodes) · 9. Solitary kidney · 10. Anatomic abnormalities · 11. Renal insufficiency · 12. Stones of cystine, uric acid or struvite

Low risk	High risk
First-time stone former WITHOUT any of: family history · GI or bone disease · gout · recurrent UTIs · nephrocalcinosis · type II diabetes · obesity	Recurrent stone formers · children or adolescents · solitary kidney · cystine, uric acid or struvite stone · a first-time former WITH any of the factors at left

The extensive evaluation — 2 visits

• 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

Dietary Therapy (6 measures)

• Fluid → urine output >2.5 L/day (cystine ≥4 L/day); RCT 12% vs 27% recurrence at 5 yr.
• Sodium ≤100 mEq (2,300 mg)/day — high Na ↑ urinary Ca.
• Calcium keep at RDA 1,000–1,200 mg/day — low-Ca diet ↑ oxalate absorption (counterproductive).
• Oxalate limit (esp. enteric hyperoxaluria); fruit/veg ↑ (raises citrate); animal protein limit.
• Avoid low-carb/high-protein weight-loss diets (↑ stone + bone loss).
• Calcium citrate is the best supplement — the high urine citrate offsets the higher urine calcium (200 mg calcium, 950 mg citrate). Supplements are safest 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.
• Only 10–15% of urinary oxalate comes from diet — the rest is from the liver.
• Bariatric surgery raises stone risk through increased urinary oxalate.
• A moderate-calcium diet + salt restriction + moderation of animal protein produced 50% fewer stones than a calcium-restricted diet.

Pharmacologic Therapy

Abnormality	First-line	Key points
Ca + hypercalciuria	Thiazide [25 mg BID]	+ Na restriction + K (citrate); chlorthalidone/indapamide preferred
Ca + hypocitraturia	Potassium citrate [20 mEq BID]	First-line for RTA, thiazide-induced, idiopathic
Ca oxalate [Enteric]	Ca supplements +/- cholestyramine	Normal urinary Ca; + limit animal protein
Ca oxalate + hyperuricosuria	Allopurinol + Kcitrate	Normal urinary Ca; + limit animal protein
Uric acid	Potassium citrate	Alkalinise pH >5.5 (6.0- 6.5); avoid >7.0
Cystine	Fluid + alkalinise + Na/protein restriction	Target pH 7.0; add thiol (tiopronin) if refractory
Struvite	Surgical clearance	AHA only after surgery exhausted

• Thiazide side effects: 3 hypers (glucose, lipids, urate), 3 hypos (K, Mg, citrate), metabolic alkalosis → give K citrate.
• Allopurinol 300 mg/day (xanthine oxidase) — adjunct when alkalinisation fails (most uric acid formers have low pH, not hyperuricosuria).
• AHA (urease inhibitor) — toxicity limits use: haemolytic anaemia + DVT (~15% each).
• Follow-up 24-h urine within 6 months of starting therapy, then annually.
• Thiazides cause hypokalaemia AND hyperglycaemia — and the two are linked. A low plasma potassium impairs insulin secretion. Preventing the hypokalaemia — 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.
• For fatigue on a thiazide, check potassium and sodium — largely avoided by starting low and titrating up.
• 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.
• Acetohydroxamic acid 250 mg TID if struvite clearance is incomplete — it blocks the urease enzyme.

Cystine chelators — second line

They raise cystine solubility by binding it through disulphide bonds.

Agent	Profile	Side effects
α-mercaptopropionylglycine (tiopronin, Thiola)	Fewest side effects — first line	Rash, asthenia, GI distress, joint aches, mental status changes
D-penicillamine	More side effects, slightly more effective	Nephrotic syndrome, dermatitis (pemphigus), pancytopenia, impaired taste/smell, fevers, arthralgia
Captopril	Fewest side effects but least effective	Fatigue, hypotension, chronic cough, rash

Side effects of stone-prevention drugs

Medication	Side effects
Thiazides	Potassium wasting, muscle cramps, hyperuricosuria, intracellular acidosis, hypocitraturia
Sodium cellulose phosphate	GI distress, hypomagnesaemia, hyperoxaluria, PTH stimulation
Orthophosphate	Similar to SCP, soft tissue calcification
Potassium citrate	GI upset, hyperkalaemia
Allopurinol	Rash, myalgia
Magnesium gluconate / pyridoxine (B6)	Diarrhoea
D-penicillamine	Nephrotic syndrome, dermatitis, pancytopenia
α-mercaptopropionylglycine	Rash, asthenia, rheumatologic complaints, GI distress, mental status changes
Captopril	Rash, cough, hypotension
Acetohydroxamic acid	Thromboembolic phenomena, tremor, headache, palpitations, oedema, GI distress, loss of taste, rash, alopecia, anaemia

Dissolution Therapy

Alkalinisation dissolves	Acidification dissolves
Uric acid · cystine · xanthine · ammonium acid urate	Calcium phosphate · struvite · indinavir

Contraindications

• Active infection · fever · flank pain · distal obstruction · electrolyte abnormalities · renal insufficiency · immature tract

Complications of urinary alkalinisation

• Calcium phosphate stones · struvite stones · hyperkalaemia (potassium citrate) · volume overload (sodium bicarbonate) · GI upset, flatulence

Treatment Selection

• Non-contrast CT before intervention — defines burden/density/anatomy, guides SWL vs URS (US cannot).
• Worse SWL: attenuation >900–1000 HU, skin-to-stone >10 cm, unfavourable lower-pole anatomy, resistant composition.
• SWL resistance (descending): cystine > brushite > Ca oxalate monohydrate > matrix.
• If purulent urine endoscopically → abort, drain, treat infection.
• 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

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 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

Ureteric stones

Scenario	Approach
Uncomplicated <10 mm	Observation ± MET (α-blocker; recommended distal, option mid/proximal)
Distal/mid >10 mm or failed	URS first-line (SWL 2nd)
Proximal >10 mm or failed	URS or SWL (URS superior <10 mm)

• Spontaneous passage driven by axial diameter; ~50% of distal <10 mm pass; α-blockers add ~23% absolute.
• MET appear to be most effective in distal ureteral stone 5mm or larger
• Intervene if conservative fails by 4–6 weeks (or earlier for pain/↓function/infection).
• 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.
• 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

Stone	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; URS option; not SWL

• 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%.
• PCNL = highest single-procedure stone-free rate (size-independent) but most morbid (~15% complications; transfusion ~7% commonest; haemorrhage most significant).

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.
• Split function <15% → consider nephrectomy.
• Staghorn (mostly struvite) → PCNL (remove — 50% lose function by 2 yr if untreated).
• Transplant → PCNL preferred for >1.5 cm.
• Horseshoe → SWL or URS <1.5 cm, PCNL ≥1.5 cm;
• Calyceal diverticulum → PCNL (direct puncture) first-line; URS for small (<2 cm) upper/mid; anterior calyx → URS (PCNL bleeding risk); SWL seldom works.
• 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
  • 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
• 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, haematuria, or declining renal function
  • 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
• 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
• In spinal deformity or limb contractures, SWL often fails with high retreatment rates. URS is an option; PCNL is best
• 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
• 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

Surgical Modalities (high-yield)

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; 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).
• Chronic SWL changes (4): ↑ blood pressure, ↓ renal function, ↑ stone recurrence, induction of brushite stones.
• Contraindications (6): distal obstruction, pregnancy, uncorrected coagulopathy, untreated UTI, nearby arterial aneurysm, untargetable stone.
• Factors affect negatively; stone composition[ Cystine, Brushite, Ca Ox], >1000HU, Skin to stone distance >10cm, Renal anomalies, Lower pole stone

Generator mechanics

Generator	Mechanism	Foci
Electrohydraulic (spark gap)	Spherically expanding shockwave from an underwater spark discharge	Electrode at F1, stone at F2; reflector focuses energy at F2
Electromagnetic	Plane or cylindrical shockwaves from a magnetic field between coil conductors	F2 only — acoustic lens or parabolic reflector
Piezoelectric	Plane shockwaves from rapid expansion of ceramic elements	F2 only — crystals in a spherical dish

	Advantages	Disadvantages
Electrohydraulic	Effective; subcapsular haematoma < 1%	Short electrode life; pressure fluctuates each shock
Electromagnetic	Less painful (energy over a larger area); controllable and reproducible; long electrode life	Subcapsular haematoma 5–10% — small focal region of high energy
Piezoelectric	Accurate focusing; little pain; long ceramic life; no analgesia needed	Less effective — small F2

Six theories of stone fragmentation

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

Stone density and SWL success

Density	Clearance
< 500 HU	100%
50–1000 HU	85.7%
> 1000 HU	54.5%

• 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)

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 anaesthesia · do NOT use a ureteral stent · consider MET · consider percussion, diuresis, inversion therapy

Complications

• Trauma to liver, skeletal muscle, pancreas, stomach, duodenum, lung, colon
• Subcapsular haematoma 5–10% with newer generators — resolves over ~6 weeks
• Haematuria · intrarenal and perinephric oedema (resolves in days) · AKI
• Steinstrasse 5–10% · UTI/pyelonephritis 5–10% · renal colic requiring admission · failed lithotripsy
• Impaired semen quality with distal ureteric stones — normalises by 3 months
• Cardiac arrhythmias resolve on stopping SWL — stop, resume once settled
• Any patient with a haemoglobin drop or significant flank pain 24 hours after SWL needs imaging (renal US or CT) to separate a perinephric haematoma from obstruction
• SWL in the elderly is feasible but carries a higher risk of perinephric haematoma

Steinstrasse

• Risk factors: large stone burden, staghorn stones, pre-existing ureteric obstruction
• Occurs in 2–10% of SWL cases; 70% in the distal ureter
• Asymptomatic → observe; ~70% clear spontaneously (with antibiotics and repeat ultrasound)
• A nephrostomy allows passage in up to 75%
• URS is the treatment of choice — the leading stone can be shocked

Indications for stenting BEFORE SWL

• Solitary functioning kidney · obstruction proximal to the stone · refractory renal colic · renal insufficiency · size > 1.5 cm · poorly visualised stone · bilateral SWL · infection with obstruction
• Consider ureteroscopy instead in some of these cases

After SWL

• Most fragments pass in the first 3 months, but clearance can continue beyond 24 months
• Residual fragments localise 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

Intracorporeal Lithotripters

Modality	Contact	Mechanism of Action	Tissue Effects	Advantage	Disadvantage	Sizes
EHL	1 mm from stone	Electrical spark produces vapor bubble; subsequent cavitation bubble creates shockwaves that fracture stones	>1 mm from mucosa, <500 mJ — no injury; >1000 mJ — ureteric perforation	Able to reach lower pole; inexpensive	Significant tissue damage at higher energy; durability of probe tip	1.6, 1.9, 3.3, 9
Ultrasonic	Direct	Rapidly vibrating probe tip causes fragmentation, while simultaneous aspiration removes debris	Mucosal stripping; no muscularis damage	Most efficient single modality; in-line suction for simultaneous stone removal	Reduced efficiency in hard stones	2.5, 3, 4.5, 9
Pneumatic	Direct	Ballistic tip repeatedly strikes stone, similar to jackhammer	Focal areas of hemorrhage and mucosal erosions; least traumatic of all intracorporeal lithotripters	Least traumatic; works well on harder stones; least expensive	Least efficient; significant retropulsion	2.4, 3, 4.8, 6, 10.5
Ho:YAG laser	Direct	Photothermal energy transfer rapidly heats and disintegrates stone, producing fine fragments	Thermal injury to depth of 0.5–1.0 mm	Flexible enough to reach lower pole; smallest fragments; works on all stone compositions; can be used for nonstone indications	Mucosal injuries with 0.5–1 mm depth of penetration; fiber breakage can damage flexible scope; high initial cost	200, 365, 550, 1000 μm
Combination, ultrasonic/pneumatic	Direct	Simultaneous pneumatic and ultrasonic lithotripsy	Subepithelial denudation, muscularis rupture	More efficient than pneumatic or ultrasonic alone; works on all stone compositions	Only rigid probes available; requires large-diameter working channel	9.9 (Swiss LithoClast Ultra); 11.25 (CyberWand)

• Holmium:YAG (2140 nm, photothermal vaporisation) — fragments any composition; thermal injury 0.5–1 mm; safe 0.5 mm from urothelium.
• [Dusting]Least fragments + Least retropulsion: ↓ pulse energy, ↑ frequency, long pulse width [0.2-0.4JX50-80Hz] .
• "Popcorn" high energy and high frequency,
• "Fragmenting " high energy and low frequency
• Thulium Yag , less wave length and 0.2mm of depth
• General recommendation in using Laser ; dont exceed 20 W in kidney , 12 W in ureter , 30 W in bladder and maintaining good irrigation.
• In ureteric stone always start as low as possible 0.6JX6Hz , dont exceed 15Hz of frequency in the ureter , be safe

Ureteroscopy (URS)

• Flexible scope needed for proximal stones; full fragmentation below safety-wire diameter (0.035 in) passes spontaneously.
• 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). Avulsion → PCN + delayed reconstruction or immediate repair. Submucosal stone → laser excision + stent (stricture risk).
• Mandatory imaging after instrumentation (0.4–4% silent strictures) — renal ultrasound at ~6 weeks for silent hydronephrosis.
• 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.
• 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 · can dilate a narrow ureteric orifice

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)

1. Infected + obstructed system · 2. Large stone burden with fragments to pass · 3. Impacted stone with significant oedema · 4. Solitary kidney · 5. Planned repeat URS in ~1 week · 6. Ureteric dilation > 10 Fr · 7. Intra-operative perforation

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

• A solitary kidney is NOT an absolute indication to stent after URS

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. Delayed repair is recommended
• Risk factors for ureteric perforation: long operating time · use of EHL · impacted stone · renal stones · surgeon inexperience

Predictors of successful endourologic treatment of a stricture

• Non-ischaemic strictures do well; ischaemic 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

URS in urinary diversions

• Retrograde access to the upper tract succeeds in up to 75% of urinary diversions
• Indiana pouches are the most difficult diversion for retrograde URS
• If the ureteric orifice cannot be seen: loopograms or pouchograms where reflux exists; alternatively IV indigo carmine or contrast
• For patent ureteroenteric anastomoses, an access sheath aids re-entry and protects the anastomosis

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.
• 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 → angioembolisation → partial nephrectomy; delayed bleed (AV fistula/pseudoaneurysm) → selective arteriogram + embolisation.
• Delayed hemorrhage: continuous = AV fistula ; Intermittent: pseudoaneurysm , both Rx: Angio
• 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%
• Sepsis — best predictor = stone or renal-pelvic urine culture (not voided); fragmenting stones releases endotoxin even with sterile urine.
• Venous gas embolism — mill-wheel murmur, hypoxia → head-down, right-side-up. Supracostal puncture → pneumothorax/hydrothorax risk.
• 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
• 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
• Examine the chest at the end of any PCNL using a supracostal puncture

Absolute contraindications

• Uncorrected coagulopathy · active untreated UTI · pregnancy

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
• 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

Perforation and extravasation

• The first sign of significant extravasation of irrigant into the peritoneal cavity is a NARROWED PULSE PRESSURE
• 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 anaesthetist 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

• Place a ureteric stent

• 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

• Post-operative bleeding: ABCs, vitals, pressure dressing, clamp the nephrostomy, IV fluids, transfusion with serial haemoglobin, bed rest, ± angiography ± embolisation

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%).

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.
• 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.

Lower Urinary Tract Calculi

• Primary bladder stones — children, boys 9–33×, low-protein/low-phosphate diet → ammonium acid urate; solitary, rarely recur, diet-prevented.
• Secondary — bladder outlet obstruction (most common), neurogenic bladder, augmentation/diversion (struvite + Ca phosphate). Adults: uric acid (sterile) or struvite (infected).
• Commonest symptom terminal gross haematuria; cystoscopy most accurate; treat endoscopically (holmium laser)if less than 4cm , if larger percutaneous — avoid through continent catheterisable 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.