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Background: The use of extracorporeal shock wave lithotripsy (ESWL) to treat calcium oxalate dihydrate (COD) renal calculi gives excellent fragmentation results. However, the retention of post-ESWL fragments within the kidney remains an important health problem. This study examined the effect of various urinary conditions and crystallization inhibitors on the regrowth of spontaneously-passed post-ESWL COD calculi fragments., Methods: Post-ESWL COD calculi fragments were incubated in chambers containing synthetic urine varying in pH and calcium concentration: pH = 5.5 normocalciuria (3.75 mM), pH = 5.5 hypercalciuria (6.25 mM), pH = 6.5 normocalciuria (3.75 mM) or pH = 6.5 hypercalciuria (6.25 mM). Fragment growth was evaluated by measuring increases in weight. Fragment growth was standardized by calculating the relative mass increase., Results: Calcium oxalate monohydrate (COM) crystals formed on COD renal calculi fragments under all conditions. Under pH = 5.5 normocalciuria conditions, only COM crystals formed (growth rate = 0.22 +/- 0.04 microg/mg x h). Under pH = 5.5 hypercalciuria and under pH = 6.5 normocalciuria conditions, COM crystals and a small number of new COD crystals formed (growth rate = 0.32 +/- 0.03 microg/mg x h and 0.35 +/- 0.05 microg/mg x h, respectively). Under pH = 6.5 hypercalciuria conditions, large amounts of COD, COM, hydroxyapatite and brushite crystals formed (growth rate = 3.87 +/- 0. 34 microg/mg x h). A study of three crystallization inhibitors demonstrated that phytate completely inhibited fragment growth (2.27 microM at pH = 5.5 and 4.55 microM at pH = 6.5, both under hypercalciuria conditions), while 69.0 microM pyrophosphate caused an 87% reduction in mass under pH = 6.5 hypercalciuria conditions. In contrast, 5.29 mM citrate did not inhibit fragment mass increase under pH = 6.5 hypercalciuria conditions., Conclusion: The growth rate of COD calculi fragments under pH = 6.5 hypercalciuria conditions was approximately ten times that observed under the other three conditions. This observation suggests COD calculi residual fragments in the kidneys together with hypercalciuria and high urinary pH values may be a risk factor for stone growth. The study also showed the effectiveness of specific crystallization inhibitors in slowing calculi fragment growth.

Objective: The exact mechanism of renal stone formation is still not totally understood. Thus, the role of crystallization inhibitors at different stages of stone development, the influence of preexisting solid particles and the effects of variations in urine composition require further clarification. The aim of this paper is to clarify some of these questions by studying the regrowth achieved by real spontaneously passed post-extracorporeal shock wave lithotripsy (post-ESWL) fragments of calcium oxalate monohydrate (COM) renal calculi., Material and Methods: An in vitro system was used to study the regrowth of post-ESWL fragments of COM calculi, which was defined as the relative increase in weight of the fragments., Results: It was found that new columnar zones of COM crystals were formed under normal calcium and oxalate urinary conditions and no calcium phosphates were observed, in spite of the urinary pH being >6. The presence of 3.03 microM phytate totally blocked these crystal growth processes. When hypercalciuric urine was used at a pH of 6.5, large brushite crystals and zones totally covered by hydroxyapatite were observed for short periods, and zones containing calcium oxalate dihydrate crystals could be observed for longer periods. In such cases, 9.09 microM phytate totally blocked the growth processes, 69.0 microM pyrophosphate caused a reduction in calculi growth of 93% and 5.35 mM citrate caused no inhibitory effects., Conclusion: The results show that when crystallization inhibitors were absent, the growth of calcium oxalate calculi fragments took place even under normal urine conditions, clearly demonstrating the importance of crystallization inhibitors in avoiding or delaying calculi development.

Objective: To assess the effects of a glycoprotein (mucine) on calcium oxalate crystal development in different conditions and situations, to clarify some of its possible effects., Materials and Methods: Crystallization was assessed using a batch system in presence of mucine suspensions, by kinetic-turbidimetric measurements, and using a flow system in the presence of retained agglomerates of mucine, evaluating the precipitated calcium oxalate., Results: In batch conditions low mucine concentrations (<15 mg/L) inhibited calcium oxalate nucleation and higher concentrations (<250 mg/L) inhibited calcium phosphate nucleation, whereas at high concentrations there was also promotion. The presence of an aggregate of mucine in the flow system provoked calcium oxalate monohydrate crystallization at 0.691 microg/h per mg of mucine. In flow conditions pyrophosphate at 11.5 micromol/L caused a decrease of 84% in the calcium oxalate crystallized on mucine, 1.32 mmol/L of citrate a decrease of a 83%, 20 mg/L of pentosan polysulphate a decrease by 80%, and 7.58 micromol/L phytate totally prevented the crystallization of calcium oxalate on mucine., Conclusion: All substances inhibiting calcium oxalate crystallization with the capacity to interact with calcium ions also have crystallization promoting properties when they are at sufficiently high concentrations, because of their capacity to form agglomerates or the insolubility of their calcium salts.

Due to the absence of HPLC methods to determine myo-inositol using mass detection and considering its sensitivity and selectivity, a high performance liquid chromatography-mass spectrometry method for the analysis of myo-inositol is described and applied to its direct determination in urine and saliva samples. Successful resolution of myo-inositol and its related substances was achieved with a stationary phase Aminex HPX-87C Column with milli-Q water as mobile phase and 5 mM ammonium acetate added post-column. The detector counted positive ions by monitoring m/z=198, which corresponds to the myo-inositol adduct with ammonium cation. Urine and saliva samples were previously purified by passing through an anion-exchange resin. Concentrations as low as 138 and 461 μg/l in saliva and urine could be respectively quantified. Intra-day R.S.D. ranged from 0.83 to 1.02%, whereas inter-day R.S.D. was between 1.54 and 3.58%. [Copyright &y& Elsevier]

Myo-inositol hexakisphosphate (phytate) is a substance present in urine with an important role in preventing calcium renal calculi development. In spite of this, the use of urinary phytate levels on stone-formers’ evaluation and treatment is still notably restricted as a consequence of the enormous difficulty to analyze this substance in urine. In this paper, a simple procedure for routinary urinary phytate determination based on phosphorus determination through inductively coupled plasma atomic emission spectrometry is described.The method only requires a previous separation of phytate from other components by column anion exchange chromatography. The working linear range used was 0–2 mg l−1 phosphorus (0–7 mg l−1 phytate). The limit of detection was 64 μg l−1 of phytate and the limit of quantification was 213 μg l−1. The relative standard deviation (R.S.D.) for 1.35 mg l−1 phytate was 2.4%. Different urine samples were analyzed using an alternative analytical methodology based on gas chromatography (GC)/mass detection used for inositol determination (phytate was previously hydrolyzed), resulting both methods comparable using as criterion to assess statistical significance P<0.05. [Copyright &y& Elsevier]