Mechanisms of crystal collision being the first step of aggregation (AGN) were analyzed for calcium oxalate monohydrate (COM) directly produced in urine. COM was produced by oxalate titration in urine of seven healthy men, in solutions of urinary macromolecules and in buffered distilled water (control). Crystal formation and sedimentation were followed by a spectrophotometer and analyzed by scanning electron microscopy. Viscosity of urine was measured at 37 degrees C. From results, sedimentation rate (v (S)), particle diffusion (D) and incidences of collision of particles in suspension by sedimentation (I (S)) and by diffusion (I (D)) were calculated. Calculations were related to average volume and urinary transit time of renal collecting ducts (CD) and of renal pelvis. v (S) was in urine 0.026 +/- 0.012, in UMS 0.022 +/- 0.01 and in control 0.091 +/- 0.02 cm min(-1) (mean +/- SD). For urine, a D of 9.53 +/- 0.97 mum within 1 min can be calculated. At maximal crystal concentration, I (S) was only 0.12 and I (D) was 0.48 min(-1) cm(-3) which, even at an unrealistic permanent and maximal crystalluria, would only correspond to less than one crystal collision/week/CD, whereas to the same tubular wall being in horizontal position 1.3 crystals/min and to a renal stone 624 crystals/cm(2) min could drop by sedimentation. Sedimentation to renal tubular or pelvic wall, where crystals can accumulate and meet with a tissue calcification or a stone, is probably essential for stone formation. Since v (S) mainly depends on particle size, reducing urinary supersaturation and crystal growth by dietary oxalate restriction seems to be an important measure to prevent aggregation.