MicrobiologyTier 1Medical Sciences concept

Urease-producing organisms and struvite renal stones

Core concept

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Urease-producing organism in urine

urea -> 2 NH3 + CO2
-> urine pH rises above 7.2
-> ammonium, magnesium and phosphate become supersaturated
-> struvite = magnesium ammonium phosphate, usually mixed with carbonate apatite
-> rapid growth into the collecting system -> STAGHORN calculus

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The stone and the infection are one problem: bacteria live within the stone matrix, so the infection cannot be cured while the stone remains
Struvite is the only stone type in which infection is the cause rather than the consequence

Urease producers - "PPUNCH"

Proteus mirabilis (the classic), Providencia, Ureaplasma urealyticum, Nocardia, Klebsiella (some), Staph saprophyticus / Staph aureus, Morganella, Corynebacterium urealyticum, Helicobacter pylori (same enzyme, different organ - the basis of the urea breath test and of ammonia generation in hepatic encephalopathy)
E. coli is NOT a urease producer - the commonest UTI organism does not cause struvite stones

Stone types

Stone	~%	Urine pH	Radiology	Notes
Calcium oxalate	~70-80%	Any/acid	Radio-opaque	Hypercalciuria, hyperoxaluria, hypocitraturia
Calcium phosphate	~10%	Alkaline	Radio-opaque	Distal (type 1) RTA, hyperparathyroidism
Struvite	~10-15%	>7.2, alkaline	Radio-opaque, staghorn	F>M, recurrent UTI, neurogenic bladder, catheter, spinal cord injury
Uric acid	~5-10%	<5.5, acid	RADIOLUCENT on plain film (seen on CT)	Gout, high purine, chronic diarrhoea, T2DM/metabolic syndrome
Cystine	~1%	Acid	Faintly opaque	AR cystinuria; hexagonal crystals; young, recurrent, bilateral

Struvite crystals are "coffin-lid" shaped on microscopy
Non-contrast CT KUB is the imaging investigation of choice for all stone types

Definitive treatment is complete stone clearance - percutaneous nephrolithotomy is the standard for staghorn calculi
- Any residual fragment harbours organisms -> recurrence. "Stone-free" is the therapeutic target.
Antibiotics alone will not sterilise the urine; culture-directed therapy peri-operatively, and acetohydroxamic acid (urease inhibitor) only where surgery is impossible - poorly tolerated
An untreated struvite staghorn destroys the kidney and can cause xanthogranulomatous pyelonephritis; long-term risk of urosepsis and SCC of the renal pelvis
Obstruction plus infection is a urological emergency - decompress (nephrostomy or stent) before definitive stone treatment; do not wait
Prevention: eradicate and prevent UTI, treat the underlying urinary stasis (neurogenic bladder, catheter care), maintain fluid intake >2.5 L/day
Send every stone for analysis, and do a metabolic work-up in recurrent stone formers (serum calcium, urate, PTH; 24 h urine calcium, oxalate, citrate, urate, volume, pH)

Urinary tract pathogens - nitrite and biochemical identification
Causes of hyperchloraemic metabolic acidosis (distal RTA and calcium phosphate stones)
Urinalysis and dipstick testing
Helicobacter pylori and urease-based testing
Obstructive uropathy and acute kidney injury

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