Stone Formation (Pathogenesis)
Every stone forms by the same physicochemical story: supersaturation → nucleation → growth and aggregation → retention/anchoring → stone, all modulated by promoters versus inhibitors.
The big picture
Every stone, of every type, forms by the same physicochemical story: the urine becomes over-saturated with a salt, crystals nucleate and grow, they aggregate and become anchored in the kidney, and there isn't enough inhibitor to stop them. Understanding this single cascade is what makes the rest of stone disease coherent — each stone type, each metabolic abnormality, and each treatment is just an intervention at one step of it.
The framework: supersaturation → nucleation → crystal growth and aggregation → retention/anchoring (Randall's plaque) → stone, all modulated by the balance of promoters versus inhibitors.
Mechanism pathway
Tap any step to see why it happens.
Diagnostic algorithm
Each step answers one question. Tap to expand.
Board traps
The cascade: supersaturation → nucleation → growth/aggregation → retention/anchoring → stone.
Supersaturation is driven by high solute, low urine volume, and pH — all therapeutic targets.
Heterogeneous nucleation (on a surface) is far easier than de novo — one crystal seeds another.
Randall's plaque on the renal papilla is the anchoring site for calcium oxalate stones (fixed-particle mechanism).
Citrate is the key inhibitor — hypocitraturia promotes stones; potassium citrate prevents them.
Stone formation is a promoter–inhibitor balance — supersaturated urine need not form stones if inhibitors suffice.