Crystallisation properties in stone forming and normal subjects' urine diluted using a standardised procedure to match the composition of urine in the distal part of the distal tubule and the middle part of the collecting duct

Abstract

Using a standardised procedure, we assessed the crystallisation properties of calcium phosphate in urine with a composition matching that in the distal part of the distal tubules (DTd) and of calcium oxalate in urine with a composition matching that in the mid-collecting duct (CDm). We used 8-h urine samples collected between 2200 h and 0600 h with sodium azide as preservative. Urine from ten patients with recurrent CaOx stone formation and from ten normal subjects was used for the measurements. The DTd and CDm samples were obtained by diluting the voided 8-h urine to 3000 ml and 1750 ml per 1.73 m2 body surface area, respectively. The nucleation was studied in DTd urine following supersaturation with CaP. The crystal size distribution was assessed with a Coulter counter both following supersaturation of DTd urine with CaP and of CDm urine with CaOx. The crystallisation of CaP in DTd urine as well as that of CaOx in CDm urine, in the presence of CaP crystals that had been precipitated in DTd urine, was measured with the isotope technique. The inhibition of CaOx and brushite crystal aggregation in standardised diluted aliquots of DTd and CDm urine was assessed spectrophotometrically as the rate of sedimentation. There was a slightly increased sedimentation rate and a lower initial absorbance in DTd urine from stone formers supersaturated with CaP. Although these findings might reflect a state of increased crystal aggregation in stone formers' urine, this could not be confirmed by crystal size measurements in the Coulter counter. The inhibition of brushite crystal aggregation in DTd urine was significantly in stone formers' urine than in normal subjects' urine (P < 0.001). Moreover, all inhibition values in DTd samples from stone formers were negative, suggesting a promoter effect on crystal aggregation. The inhibition of CaOx crystal aggregation in CDm urine also was significantly higher in CDm urine from normal subjects than in CDm urine from stone formers (P < 0.05). For all other variables the level was similar when urine samples from the two groups were compared. Although this series of crystallisation assessments was carried out on a small number of standardised diluted urine samples only, the results nevertheless emphasise a defect in aggregation inhibition as one important determinant for an abnormal calcium salt crystallisation in patients with recurrent stone formations. This difference obviously includes aggregation of both CaP crystals in DTd urine and CaOx crystals in CDm urine. The results also show that assessment of crystallisation properties of this kind can be carried out in standardised, diluted 8-h night urine samples, which accordingly can be used in the routine work-up of patients with calcium stone disease. Such an approach might prove useful in order to get information on the combined effects of the driving force of supersaturation and crystallisation modifying properties accomplished by urinary macromolecules and other modifying agents.

How elevated oxalate can promote kidney stone disease: changes at the surface and in the cytosol of renal cells that promote crystal adherence and growth

“…Perhaps of more importance is the possibility that the sites of production of these macromolecules and/or the characteristics of the secreted proteins may be altered in stone disease. Studies in experimental stone-forming animals (19,(42)(43)(44) and in human kidney stone patients (45,46) have supported this possibility. Nonetheless, it is not clear whether such changes are a cause or a consequence of the disease process, since 'stone-forming conditions' in vitro (e g. exposure to elevated oxalate levels or to calcium oxalate crystals) have been shown to increase the expression of many of these compounds (see below and 47).…”

Antiurolithic effect of Bergenia ligulata rhizome: An explanation of the underlying mechanisms

“…asis to happen in most of the individuals, whereas, this natural inhibition is in deficit in stone formers (Tiselius et al, 2001). Studies have also shown that tubular cell injury facilitates CaC 2 O 4 crystal formation and deposition in the renal tubules (Khan and Hackett, 1991).…”

Berberis vulgaris root bark extract prevents hyperoxaluria induced urolithiasis in rats

“…The mechanisms involved in the formation of calcifi c stones are not fully understood but it is generally agreed that urinary lithiasis is a multifaceted process involving events leading to crystal nucleation, aggregation and the growth of insoluble particles (Hess and Kok, 1996). Urine is always supersaturated with common stone forming minerals, however, the crystallization inhibiting capacity of urine does not allow urolithiasis to happen in most individuals, whereas this natural inhibition is in defi cit in stone formers (Tiselius et al, 2001). Studies have also shown that tubular cell injury facilitates CaOx crystal formation and deposition in the renal tubules (Khan and Hackett, 1991;Selvam, 2002).…”