Pathogenesis of Urolithiasis

Pathophysiology of Stone Formation

“…A period of further crystal growth and agglomeration on top of the trapped particle in conjunc tion with the adsorption of urinary mucosubstances on to the growing crystal faces may produce a fully devel oped calculus. In support of this hypothesis, it has been shown that periods of spontaneous crystalluria may trig ger off stone formation both in animals [6] and in man [7,9], In the latter, it has also been demonstrated that the severity of the disorder in a given patient is proportional to the volume of abnormally large crystals and agglomer ates excreted in his or her urine [5]. This so-called 'free-particlc' model of stone formation may be shown to account for the formation of cystine, uric acid and infection stones [5], where supersaturation with respect to the salt or acid concerned is the dominant chemical risk factor.…”

“…Apart from their ability to complex with calcium and oxalate, respectively, citrate and magnesium are relatively weak inhibitors under nor mal urinary conditions [16][17][18], Table II also shows that urine contains a number of promoters of crystal agglomeration including the poly merized form of THM [20,21] which competes with the polyanionic inhibitors mentioned above [ 18] for binding sites on the crystal surface. In addition, hyperuricosuria, by increasing the risk of formation of colloidal urate, may lead to adsorption of some of the polyanionic inhib itors and thereby reduce the concentrations of these modifiers of crystallization which are available to inhibit the growth and agglomeration of calcium oxalate crystals in urine [22], Unlike cystine stone disease, where there is a com plete divide between the frequency distributions of uri nary cystine in stone formers and normals, calcium stone disease shows no such clear-cut separation between the respective groups [5]. In the case of each urinary risk factor there is a considerable overlap between the data of the stone formers and those of normal subjects.…”

“…The simplest model of stone formation describes it as being due to the precipitation of sparingly soluble sub stances in the urinary tract following an increase in their excretion in urine [5]. In chemical terms, the main uri nary risk factor for the disorder is supersaturation with respect to one of these substances, which leads to spon taneous crystalluria of the salt concerned.…”

“…This is essential to calculate accurately not only the degree of supersaturation of urine with respect to calcium oxalate and calcium phos phate but also the relative levels of inhibitory and promotive activity. A few years ago, we [5,15] proposed an alternative approach to the assessment of the biochemi cal risk of stones based on Bayes' theorem and probabil ity theory. This significantly reduced the number of nec essary chemical measurements in urine.…”

Induction of Renal Nuclear Oxalate Binding Activity in Experimental Hyperoxaluric Rats

“…Hyperoxaluria is one of the main risk factors of human idiopathic calcium oxalate stone disease [1]. The mechanism involved in stone for mation is not well understood [2], Several experimental models, such as calculus-producing [3] or vitamin B6-deficient diets [4] or administration of sodium oxalate [5], ethylene glycol (EG) [6] or dehydro-ascorbic acid [7], have been used to study the stone disease.…”