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.
• Randall plaques = calcium apatite in basement membrane of thin loops of Henle → anchor for idiopathic calcium oxalate stones.

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

Hyperoxaluria (4 types)

• Primary — AR glyoxylate defect; urine oxalate >75 mg/day without bowel dysfunction → genetic referral.
• 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

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.

Hypocitraturia & Urine pH

• Acid-base state is primary determinant (acidosis ↓ citrate). Causes (DIRT): Diarrhoea, Idiopathic, type 1 RTA, Thiazides. Severe → suspect RTA.
• 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.
• Calcium phosphate — type 1 RTA, primary hyperPTH, medullary sponge kidney, carbonic anhydrase inhibitors.
• Cystine — cystinuria, AR (SLC7A9 / SLC3A1), impairs reabsorption of COLA (Cystine, Ornithine, Lysine, Arginine). Poorly radio-opaque; nitroprusside spot test (urine turns purple).
• 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.
• Staghorn formers: struvite, cystine, Ca oxalate monohydrate, uric acid.
• 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.

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.
• 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: ♂ 20–25 mg/kg, ♀ 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).

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).

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.

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

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.

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).

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.

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 (stent if renal stone >20 mm to avoid steinstrasse).
• 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

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 0.8JX6Hz , 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).

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.

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.

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.