Uric acid calculi: types, etiology and mechanisms of formation.

The study of the composition and structure of 41 stones composed of uric acid was complemented by in vitro investigation of the crystallization of uric acid. Uric acid dihydrate (UAD) precipitates from synthetic urine under physiological conditions when the medium is supersaturated with respect to this compound, though uric acid anhydrous (UAA) represents the thermodynamically stable form. Solid UAD in contact with liquid transforms into UAA within 2 days. This transition is accompanied by development of hexagonal bulky crystals of UAA and appearance of cracks in the UAD crystals. Uric acid calculi can be classified into two groups, differing in outer appearance and inner structure. Type I includes stones with a little central core and a compact columnar UAA shell and stones with interior structured in alternating densely non-columnar layers developed around a central core; both of them are formed mainly by crystalline growth at low uric acid supersaturation. Type II includes porous stones without inner structure and stones formed by a well developed outermost layer with an inner central cavity; this type of stones is formed mainly by sedimentation of uric acid crystals generated at higher uric acid supersaturation.

Uric acid urolithiasis and crystallization inhibitors.

An in vitro study of the inhibitory effects that some substances occasionally present in urine can provoke on the crystallization of uric acid has been performed. The most remarkable crystallization inhibitory effects were produced by mucine at concentrations of >0.5 mg/l. Pentosan polysulfate and chondroitin sulfate also clearly increased the uric acid crystallization times at concentrations of >100 mg/l. Saponins, such as escin and glycyrrhizic acid, also produced a notable delay in uric acid crystallization times at concentrations of >10 mg/l. Similar effects were observed in the presence of a surfactant substance, lauryl sulfate. N-Acetyl-L-cysteine caused crystallization perturbations only when it was present at concentrations of >50 mg/l. Citric acid and phytic acid caused no effects on uric acid crystallization even at the highest concentrations assayed (1,000 and 5 mg/l, respectively). From the results obtained it can be deduced that mainly glycoproteins, glycosaminoglycans and surfactant substances can exert protective effects against uric acid crystallization.

Ammonium and sodium urates precipitating from synthetic urine and fine structure of urate renal calculi.

A study of ammonium and sodium urate precipitation in vitro and the fine structure of several urate renal calculi was carried out to contribute to an understanding of the participation of ammonium and sodium urates in urolithiasis. Ammonium urate precipitated in vitro in two different morphologies: a typical spherulite morphology formed at high supersaturation and disorganized needle-like crystals formed at low supersaturation. In all cases sodium urate precipitated in vitro as bundles of curved fibrils, its crystallization being inhibited by calcium in concentrations between 20 and 60 mg/l depending on the sodium urate supersaturation. From a collection of 1300 renal calculi, only three had ammonium urate as their main component (0.2%), three were mixed calculi (0.2%) consisting of ammonium urate and calcium oxalate (two) or uric acid (one), and in one calculus ammonium urate was present as a minor component. Only in a mixed calculus of uric acid and calcium oxalate was sodium urate detected in a very low quantity. The study of the fine structure of the renal calculi constituted mainly by ammonium urate demonstrated similar patterns in which spherulites, needle-like individual crystals and an amorphous mass of ammonium urate with abundant organic matter in non-organized structures coexist. As minor components, struvite or calcium oxalate crystals were found. A general mechanism of the formation of such calculi is proposed.

Structure of uric acid concretion developed around a catheter.

A uric acid concretion formed round a catheter (JJ stent) in the bladder and removed intact from the body together with the catheter was studied using an electron scanning microscope. The concretion was composed of anhydrous uric acid, some uric acid dihydrate (< 5 wt.%) and individual particles of calcium oxalate monohydrate. The stone interior was porous with frequent occurrence of differently sized cavities that were either empty or partially filled with particles of uric acid and/or calcium oxalate monohydrate. Calcium oxalate particles were not of crystalluria origin but developed in the cavity. The succession of processes leading to the stone formation was deduced from its inner structure. The stone was formed due to a crystalline growth with minor, if any, participation of sedimentation. The estimated average rate of the calculus development, 2 x 10(-9) m/s, confirms the predominant role of crystalline growth in stone formation and indicates a relatively low urinary supersaturation with respect to uric acid prevailing during the period of calculogenesis.