Urolithiasis

Kidney stones (nephrolithiasis)

  • ~ 10% prevalence
  • 90% radio-opaque (most common is calcium oxalate)
  • Most common cause: dehydration

Stone composition (in order of frequency)

Composition Urine pH Visible on X-ray Dissolvable Other
Calcium oxalate (80%) Wide range + - Most common
Monohydrate: ovals/dumbbells; very hardˆ
Dihydrate: envelopes, octahedrons
Common cause: dehydration
Uric acid (5-10%) Acidic < 6.0 - + Usually normal serum/urine uric acid levels
Parallelograms, double-headed arrows, rosettes
Common cause: dehydration
Struvite
(Mg NH4 PO3)		 Alkaline + + Most common staghorn composition
Coffin lids
Common cause: UTI
Calcium phosphate Alkaline    

Usually nidus for Ca oxalate stones (Randall's plaque)
Powder-like (cloudy urine)
Common cause: Type I RTA (acidosis → bone demineralization); medullary sponge kidney
Matrix (soft) Alkaline - - a/w Proteus UTI
Cystine Acidic + + Very hardˆ
Hexagonal
Cause: cystinuria (autosomal recessive)
Protease inhibitor
(Indinavir)		 ≥ 5.0 -* -  
  • *Almost all stones will be visible on non-contrast CT EXCEPT protease inhibitor stones
  • ˆHard stones can be resistant to ESWL and pulsed laser, but holmium laser is effective
  • Presentation - acute colicky flank pain radiating to groin or scrotum (constantly moving/writhing); n/v; hematuria
    • Ddx: pyelo, acute abdomen, gonadal (ovarian/testicular torsion)
  • PMH - metabolic risk factors
    • Obesity, DM, HTN, gout (hyperuricemia)
    • History of bowel disease/resection (poor absorption) - Crohn's, celiac, gastric bypass
    • Metabolic acidosis (e.g. Type I RTA, chronic diarrhea)
      • Acidosis causes urine ↑Ca, ↑PO4 (bone demineralization), ↓citrate (using up buffer)
      • Chronic acidosis causes bone demineralization → hypercalciuria
    • **hide**sarcoidosis (vit D), cystinuria, IBD, primary hyperPTH, medullary sponge kidney (Ca phosphate stones), adult polycystic kidney disease
    • UTI increases stone risk (causes hypocitraturia, and urease producing organisms split urea into ammonia + bicarb, alkalinizing the urine)
      • Urease producing: Proteus, Klebsiella, Pseudomonas, corynebacterim, s. aureus, staphylococcus epidermidis
  • Dietary risk factors
    • Low PO fluid intake
    • PRAL (potential renal acid load) - acid reduces urinary citrate
      • High PRAL (↑ stone risk) - cheese, egg yolk
      • Low PRAL - fruits, vegetables
    • High sodium intake; low fiber; high oxalate; carbonated drinks (phosphoric acid)
  • Medications
    • Vitamin C - metabolized to oxalate
    • Vitamin D - ↑ Ca absorption
    • Protease inhibitors/indinavir; triamterene - precipitate in urine
    • Furosemide - hypercalciuria (loops lose calcium)
    • Acetazolamide/carbonic anhydrase inhibitors - metabolic acidosis
    • Uricosurics (salicylates, probenecid)
    • Topiramate (mimics RTA)

Diagnosis of acute stone episode

  • Gold standard of diagnosis - non-contrast CT (PPV 100%, NPV 91%)
    • KUB if CT not available (75-90% are radiopaque); second-line for pediatrics
    • RBUS if pediatric/pregnant (much less sensitive, esp for stones < 2-3 mm)
    • IV contrast is OK, but if wait until the urogram/excretory phase it can obscure a stone
    • Contrast CT only needed for suspected indinivir stone (not visible on non-con CT)
  • On CT, look for:
    • Size, location, skin to stone distance (relevant for PCNL)
    • Density (HU 200-500 ~ uric acid; > 1400 ~ very hard, not amenable to shock wave)
    • Hydronephrosis
    • Abnormal anatomy (horseshoe kidney, ectopic kidney)
  • Low-dose CT
    • Typical noncon CT - 5 mSv; low dose 2-4; ultra low dose: <2, KUB 1-2; CT IVP 8-10
  • MRI does not visualize calcium
    • Stones can be seen as filling defects in urine on T2 images (but not seen on T1)

Metabolic workup

  • Indicated for recurrent or bilateral stones (unilateral stones can be managed with diet/fluid management), or children
  • Previous stone composition
  • BMP, Ca
  • PTH if: ↑Ca or stone is predominantly Ca phosphate (indicating bone demineralization)
    • If ↑Ca and PTH normal but not appropriately suppressed (e.g. > 20) - still refer for hyperPTH workup
  • 24 hr urine test to evaluate efficacy of diet/pharmacologic intervention after 2-6 mo
    • pH, volume, Ca, oxalate, citrate, uric acid, Na, K, Cr
    • Normal urine Cr - Male 14-26 mg/kg/d, Female 11-20 mg/kg/d (less indicates inadequate collection)

Stone prevention

  • First time stone former - risk of 2nd stone in next 1-2 years is 10%; 5 years 20%, 15 years 40%

Dietary management (first-line)

  • ↑ PO fluid intake - produce 2.5 L urine/day
    • ↑ citrate content (lemonade, orange juice), ↓ carbonated drinks
  • Low sodium (< 2000 mg/d), low oxalate, low PRAL diet (e.g. low animal protein/cheese/egg yolks, high fruits/vegetables)
  • Moderate Ca intake (1000-1200 mg/d) - too low or too high increases stone risk
    • Ca is typically chelated by fat in the GI tract
    • Oxalate is freely absorbed in the GI tract, but Ca-oxalate complex is excreted
    • Thus low Ca leads to increased oxalate levels/stone promotion
  • Avoid high vit C/D
  • High fiber, weight loss

Medications

  • Potassium citrate 20 mEq PO BID-TID - urinary alkalinization (citrate converted to bicarb)
    • K citrate can decrease urine Ca (unclear mechanism, through raising bicarb levels)
    • Sodium citrate can increase urine Ca and promote stones
    • Sodium bicarb if risk for hyperkalemia
    • Side effects: diarrhea from the potassium
    • Uric acid stones - alkalinize to pH > 6.5 x 2-6 wks
    • Cystine stones - alkalinize to pH ≥ 7.5
    • Start at 10 mEq TID, check UA and serum K 1 week after. Can increase to 20 mEq BID. Check UA yearly
  • Thiazides - increase Ca reabsorption; correct acidosis
    • Chlorthalidone, indipamide are QD dosing
    • Chlorthalidone more effective than HCTZ (BID dosing)
    • Should be on low sodium diet 
  • Allopurinol (only if hyperuricosuria present) (regardless of hyperuricosemia) - prevent uric acid/calcium oxalate stones
  • Thiola for cystine stones if unresponsive to diet/alkalinization (hydration, low salt, low protein)

Based on metabolic workup

Hypocitraturia
< 350 mg/d

Citrate decreases calcium stone formation by complexing with Ca and inhibiting Ca crystallization
< 100 mg/d: think of Type I RTA

 K citrate
Increase fruits/vegetables, limit non-dairy animal protein
Hyperoxaluria
> 45 mg/d		   Low ox, low fat, normal-high Ca diet (take Ca with meals to chelate oxalate)
Hyperuricosuria
> 600 mg/d		   Limit non-dairy animal protein
K citrate to alkalinize urine
Allopurinol NOT recommended first-line; has many side effects
Hypercalciuria
> 200 mg/d (F)
> 250 mg/d (M)		   Limit sodium
Normal Ca intake
Thiazide, K citrate
(Parathyroidectomy if primary hyper-PTH)
Hypomagnesiuria
< 50 mg/d		 Mg increases solubility of Ca, PO3, oxalate Mg oxide 400-500 mg PO BID (titrate to prevent diarrhea; careful in renal insufficiency)
Hypernatriuria
> 200 meq/d		 Increases urine calcium, decreases citrate Low sodium diet
Urine pH > 6.0 Type I RTA a/w hypokalemia, hyperchloremic metabolic acidosis (inability to excrete H+) Citrate/bicarb

Non-acute stone episode

When to treat

  • < 7 mm OK for surveillance
  • Non-obstructing renal stones: size > 8-10 mm, symptoms (pain/UTI), solitary kidney, special circumstances (e.g. won't be able to access healthcare if has acute episode)

Acute stone episode

Chance of passing stone

  • % chance of stone passage = 100 - (stone size in mm X 10)
Size (mm) Days to pass Requiring intervention
≤ 2 8 3%
3-4 12 14%
4-6 22 50%
> 6 - 99%

Medical management

  • Pain control - Toradol good for urinary tract pain, but keep renal function in mind
  • Medical expulsive therapy - α blocker (tamsulosin 0.4 mg), increase stone passage rate 30%, speed up by 2-4 days and decrease pain
    • Can also give tamsulosin + prednisone (5 mg)
  • Dissolution (PO K citrate, or irrigate urinary tract)
    • Uric acid stones - alkalinize to pH > 6.5 x 2-6 wks
    • Cystine stones - alkalinize to pH ≥ 7.5
  • Follow-up: unless stone is caught and saved, do US/low dose CT at 1 mo to check if stone is passed

Indications for urgent intervention

  • Stent vs PCNL - no difference in outcomes
  • Obstructed upper tract with infection - nephrostomy tube/stent (treat the stone after infection resolves)
  • Impending renal deterioration (prolonged unilateral obstruction, any bilateral obstruction, obstruction in solitary kidney, rising Cr)
    • Renal blood flow decreases after 1.5 hrs of obstruction; ureteral hypertrophy ~ 3 d; ureteral scarring ~ 2 wks; permanent renal damage ~ 1 mo
    • Should treat an obstructing stone in < 6 wks
  • Refractory pain
  • Intractable n/v
  • Patient preference

Treatment

  • Pre-op urine culture
    • Cannot do surgical stone treatment with positive yeast cx (risk of fungemia)

Fluoroscopy tips

Method Contraindications/complications
ESWL (not used too much anymore)
Stone size: < 1 cm (up to 2 cm if favorable composition/location); skin to stone distance < 10 cm
Extracorporeal shock waves focused on stone (visualized with fluoroscopy; must be visible on KUB); patient passes fragments
  • Mechanism - alternating positive/compressive (20-100 MPa) and negative (-5 to -15 MPa) pressure to create shockwaves -> shear, spall, superfocusing, squeezing, cavitation, fatigue of stone
  • Frequency 1-1.5 Hz (60-90/min). May pause for 3-4 min after first 100 shocks to minimize renal injury

Lithotripters - electrohydraulic, electromagnetic, piezoelectric

  • Electromagnetic delivers energy over larger skin surface area = more comfortable, but energy is focused into a smaller area = higher risk of subcapsular hematoma

Benefits: Only sedation needed (outpatient), non-invasive. Lower complication rate (e.g. sepsis) compared to URS, but lower stone free rate for ureteral stones (72% vs. 90% for URS)

Less successful for lower pole clearance (due to gravity) - lower pole stones > 1 cm should be treated with ureteroscopy or PCNL (Lower Pole I/II studies)
Distal ureteral stones aren't visualized well (blocked by iliac bones); also don't want to shock in region of ovaries in young/middle-aged women

Absolute: pregnancy, coagulopathy, UTI, renal/abdominal aorta aneurysm, intrarenal vascular calcifications near stone. solitary kidney (could get obstructed by fragment)
Relative: hard stones (e.g. cystine, brushite, HU > 1000), chronic pancreatitis with calcifications, distal urinary obstruction (cannot pass fragments), poor ability to target stones (e.g. obesity)
Complications:

  • Intraoperative arrhythmia (PVCs) (8-21%) - gate shock wave to R wave (during depolarization/refractory period) to minimize risk. Do not need to abort; wait for arrhythmia to resolve then resume
  • Renal hematoma (HTN is risk factor) (up to 40% presence, but < 1% clinically significant)
  • Steinstrasse (cobblestone) - stone fragments line the ureter afterwards (can stent for stone > 1.5 cm but may as well just do URS at that point)

Ureteroscopy/laser lithotripsy
Stone size: < 2 cm
90% stone-free for ureter, 60-80% for renal stone

  • KTP - good for coagulation
  • Holmium/neodymium - good for coag. "Contact laser" vs distance laser
  • Settings - typically 0.2 J, 80 Hz for dusting, vs 0.4 J, 10 Hz for fragmentation

Benefits: not affected by obesity unlike ESWL/PCNL

If not able to access ureter, can place stent for passive dilation and return in 1 week 

Complications: ureteral avulsion/perforation (most common in proximal ureter - thinnest part; while mid-ureter has poorest blood supply)

  • Stent x 3-6 weeks if perforation

Ultrasound (or low dose CT) within 2 months post treatment to confirm no residual stone, unless very simple

PCNL (more extensive discussion in link)
Stone size: renal > 2 cm; lower pole stones > 1 cm; staghorns; skin to stone distance < 15 cm
Percutaneous renal access through flank for renal stones/large proximal ureteral stone

Relative indications: abnormal collecting system abnormalities, transplant kidneys

  • Pre-op: CT (for anatomy), CBC/coags, UCx. 
  • Access posterolaterally (Brodel's avascular plane; avoid intraperitoneal injury)
  • Perform during end-expiration to avoid lung injury; try for infracostal access
    • CXR afterwards to check for pneumothorax unless below 12th rib/pleural reflection

POD 1: CT to check for stone fragments (wait until contrast has cleared system)

Videos for access - bullseye vs triangulation

Contraindications - pregnancy, UTI, coagulopathy, cannot access kidney safely, cannot appropriately position (prone)

Complications - bleeding (5% major), pneumothorax (10% of supracostal punctures), other organ injury (0.5% bowel injury), infection (~50% get febrile post-op; 1% get septic)

"Tubeless" PCNL OK if: no bleeding, single access, and are stone free

Open/laparoscopic surgery if all else fails/is not feasible

Stone-free rates:

    Stone-free rate
Location Size ESWL Ureteroscopy PCNL Open surgery
Renal Non-staghorn 65-75% 50-80% 80-90%  
Staghorn 54% ? 80% 70%
Proximal u. ≤ 10 mm 85-90% 85% 97%
> 10 mm 70% 80%  
Mid u. ≤ 10 mm 85-90%    
> 10 mm 75-80%  
Distal u. ≤ 10 mm 85% 97%   87%
> 10 mm 75% 93%  
author: admin | last edited: Jan. 1, 2023, 10 p.m. | pk: 25

  1. AUA Guidelines - medical stone management
    1. Soothing narration by Dr Seranio
  2. AUA Guidelines - surgical stone management
  3. AUA Core Curriculum - pathology and evaluation
  4. AUA Core Curriculum - medical stone management
  5. AUA Core Curriculum - surgical stone management
  6. https://www.auanet.org/education/educational-programs/medical-student-education/medical-student-curriculum/kidney-stones
  7. https://www.auanet.org/Documents/education/NMSC-Kidney-Stones.pdf
  8. Albala DM, Assimos DJ, Clayman RV, Denstedt JD, Grasso M, Gutierrez-Aceves J et al: Lower pole I: a prospective randomized trial of extracorporeal shock wave lithotripsy and percutaneous nephrostolithotomy for lower pole nephrolithiasis - initial results. J Urol 2001; 166: 2072-2080
  9. Duffey B, Monga M. Principles of Urologic Endoscopy. Chapter 7, Vol 1. In: Wein AJ, Kavoussi LR, Partin AW and Peters CA, eds. Campbell Walsh-Urology, 11th Edition. Philadelphia, WB Saunders Elsevier; 2016
  10. COViD lecture - Imaging in nephrolithiasis
  11. COViD lecture - Surgical management of Stone Disease
  12. COViD lecture - Kidney stone prevention and diet
  13. COViD lecture - Metabolic stone evaluation and 24 urine
  14. COViD lecture - Metabolic stone evaluation - stone trees