see also:

• renal colic
• nephrocalcinosis
• urinary tract infections (UTIs) / cystitis
• acute pyelonephritis
• gout
• calcium

• 75% are composed of calcium with oxalate and/or phosphate
• 10% are urate stones (radio-lucent)
• 10% are struvite stones
• 90% are radio-opaque
• those who have had a ureteric stone have a 1/3rd chance of recurrence within a year due to persistent underlying abnormality.
• 7% are in children under 16yrs of age, and in this age group there are some unique patterns:
  • male:female ratio 1:1
  • 50% have metabolic abnormalities
  • 20% have urologic abnormalities
  • 15% have UTI
  • 5% are due to immobilisation syndrome

• Calcium oxalate stones
  • yellow/brown, rough, v.hard, laminated. (+ acid urine);
  • due to dietary oxalates and hyperoxaluria and low urinary citrate concentrations:
    • high dietary oxalate intakes (see dietary oxalates and hyperoxaluria)
    • steatorrhoea / inflammatory bowel disease, small bowel bypass surgery;
    • primary hyperoxaluria (a genetic disease)
  • pathogenesis:
    • in normal people, millions of microcrystals form each day in the kidneys, the amount of which is determined by diet and disease
      • molecules like osteopontin, nephropontin and Tamm-Horsfall protein (THP) reduce crystal formation and growth and thus in normal people, these microcrystals are flushed out
    • urinary calcium concentrations are typically 10 times higher than oxalate, thus, even minor increases in urinary oxalate concentrations can significantly increase the saturation of calcium oxalate
    • urinary citrate is a major inhibitor of calcium oxalate and calcium phosphate crystal formation, and low urine citrate levels are a risk factor for kidney stone formation
    • in many people, a crystal may lodge in a renal tubule and begin to grow, or a number of microcrystals join to start a nidus for growth of a larger crystal which then becomes a stone.
    • when there are calcium oxalate crystals within the kidney, the mTOR and the Src/STAT3 signaling pathways become active, leading to the prompt dilation of the affected renal tubule along the whole length up to and including the collecting duct, and, in people with polycystic kidney disease, this activation appears to be the trigger that initiates renal cyst development ¹⁾
    • inhibition of the mTOR molecule causes stone formation as tubules fail to dilate, and microcrystals build up at the bottleneck where the proximal tubule ends and the thin descending loop of Henle begins.
• CaPO₄/oxalate stones
  • due to:
    • hypercalciuria + decreased sodium concentration in urine?
    • high phosphate diet
    • low urinary citrate concentrations
• Na/NH₄ urate
  • smooth, hard, brown with concentric lamination;
  • usually radio-lucent
  • generally forms in acid urine;
  • with hyperuricaemia
    • gout
    • leukaemia
    • polycythaemia
    • chronic metabolic acidosis eg. glycogen storage disease
    • Lesch-Nyhan syndrome
  • with normouricaemia
    • idiopathic
    • concentrated acid urine
• Cystine:
  • honey color, maple sugar crystal surface & very firm;
  • due to hereditary cystinuria + acid urine;
  • congenital cystinuria
  • hereditary cystinosis
• Xanthine
  • Red/yellow-brown, smooth, friable, laminated & easily cut;
  • due to:
    • hereditary xanthinuria;
    • allopurinol Rx in patients with high uric acid production;
• Silica
  • white/yellow, extremely hard;
  • due to XS Mg trisilicate in antacids;

• the presence of a solid mass nidus around which the crystalloids precipitate
• nidus may be FB, fibrin, necrosed cells, organism clumps, or a 1° stone;
• Mixed stones
  • around 1° stone nidus - Ca oxalate/PO₄;
• struvite
  • 10% of all urinary calculi
  • the most common cause of staghorn calculi which are large stones cast in the renal pelvis
  • esp. in UTI due to Proteus → urease → NH3 → “triple phosphate ”
    • → MgNH₄PO₄ (struvite) + Ca₁₀(PO₄)6 CO₃(carbonate apatite)
    • white, smooth, soft, friable;

• 3x more common in males
• usually in 3rd to 5th decades of life
• 50% of recurrent stone formers have just one lifetime recurrence
• 10% of patients have highly recurrent disease
• stone type and disease severity determine low- or high risk of recurrence
• urobiome:
  • urine is rarely sterile, it usually has low numbers of bacteria which form the renal microbiome
  • it seems that the ATCC 43886 strain of E.coli promotes calcium oxalate stone formation whereas Lactobacillus crispatus inhibits stone formation and that long term antibiotic Rx such as cefazolin may promote stone formation by reducing Lactobacilli numbers ²⁾
  • Proteus is assosciated with the formation of struvite stones
• higher risk in those with:
  • type I renal tubular acidosis (RTA)
  • hyperparathyroidism
  • cystinuria
• lifestyle factors increasing risk:
  • low relative water intake results in more concentrated urine
    • higher risk in those in mountainous, desert or tropical regions
    • sedentary jobs?
    • warm months of the year
    • at risk persons should avoid the urine becoming dark orange (too concentrated) by drinking 2.5L water/day including a large glass before bed and another glass over night if they wake up
  • dietary factors / supplements
    • high oxalate diet increases risk of oxalate stones - see dietary oxalates and hyperoxaluria for foods high in oxalates
    • Mediterranean diet appears to lower risk³⁾
    • caffeine intake appears to lower risk⁴⁾
    • daily oral supplements of 200 mg of MgO and 10 mg of pyridoxine seems to reduce recurrence⁵⁾
  • increased calcium excretion:
    • increased calcium intake
    • immobilisation
      • calciuria increases within 2 weeks of immobilisation, reaching a maximum at 1-6 months after injury⁶⁾
      • immobilisation following Mx of Perthe's disease in children who previously ambulated results in:
        • 2.3x baseline urinary calcium excretion by 1 week but no evidence of stone formation was seen on US after even 16 weeks⁷⁾
    • excess vitamin D in susceptible patients although evidence does not seem to support this theoretical risk in general populations ⁸⁾⁹⁾
• urinary stasis may provide the environment of urolith growth:
  • physical anomalies
  • neurogenic bladder
  • catheter placement (IDC)
  • presence of a foreign body (eg. surgical suture)

• asymptomatic:
  • may have no symptoms until at least partial obstruction
• flank pain
  • dull ache or severe colicky flank pain usually radiating to testicle or labia majora - renal colic
  • passage of stone near the bladder may also cause urinary frequency and urgency.
• painless haematuria
  • this is a more common presentation in children (20-30% of paed. presentations of urolithiasis)
• ureteric obstruction:
  • initial rise in renal blood flow & intraureteral pressure
  • subsequent fall in both renal blood flow & intraureteral pressure
  • proportional increase in renal blood flow in contralateral kidney
  • after 5-14 days of obstruction, increasing potentially reversible deterioration of ipsilateral renal function
  • after 8wks, relief of obstruction results in rapid increase in ipsilateral renal blood flow, with at least partial return of renal function.
  • after 16wks obstruction, only slight recovery of ipsilateral renal function can be expected
  • serum urea and creatinine are POOR markers for impaired unilateral renal function as the contralateral kidney is usually adequate to maintain serum urea and creatinine levels.
• passage of the calculus:
  • tends to be delayed or obstructed at points of narrowing or bending - from proximal to distal:
    • renal calyx
    • pelvi-ureteric junction (PUJ) - where the ureter passes over the pelvic brim and arches over the iliac vessels
    • vesico-ureteric junction (VUJ) - the entrance into the bladder & usually the smallest diameter of the ureter and thus the most common location for impacted stones.
  • stones larger than 7mm are unlikely to pass and should be referred to urology for early Mx