Factors affecting calcium oxalate dihydrate fragmented calculi regrowth

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 μg/mg·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 μg/mg·h and 0.35 ± 0.05 μg/mg·h, respectively). Under pH = 6.5 hypercalciuria conditions, large amounts of COD, COM, hydroxyapatite and brushite crystals formed (growth rate = 3.87 ± 0. 34 μg/mg·h). A study of three crystallization inhibitors demonstrated that phytate completely inhibited fragment growth (2.27 μM at pH = 5.5 and 4.55 μM at pH = 6.5, both under hypercalciuria conditions), while 69.0 μM 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

Role of Agglomeration in the Early Stages of Papillar Stone Formation

Possible effects of crystal agglomeration on the early stages of calcium oxalate papillar stone formation are evaluated. The collecting ducts are filled with liquid that flows laminarly as established through hydrodynamical and physicochemical considerations. Under such conditions, agglomeration due to laminar shear forces proceeds. Agglomeration of calcium oxalate monohydrate crystals present in urine at a concentration typical for clinically observed crystalluria cannot result in the formation of a particle sufficiently large enough to be retained in the Bellini\u27s duct and become a papillar stone nidus (nucleus). Formation of such an aggregate during the passage time of urine through the duct requires an unrealistically high concentration of crystals in urine, one that exceeds the normal content of urinary oxalate by several orders of magnitude. Aggregates obstructing the Bellini\u27s duct as assumed in the free particle theory cannot represent a major factor in stone formation. This conclusion is corroborated by experimental results and other observations

Studies on Structure of Calcium Oxalate Monohydrate Renal Papillary Calculi. Mechanism of Formation

A scanning electron microscopy study of the ultrastructure of 18 calcium oxalate monohydrate papillary calculi was performed with the purpose of establishing the main steps in calculus formation. It is concluded that these calculi originate in a core located near the central part of the calculus. Significant quantities of organic matter as well as calcium phosphates can be found in the core and at the surface of adhesion to the papilla and, in some cases, fibers and calcified tubules can also be found in the contact zone. In no case did this material affect the crystalline structure of the calculi, indicating that its formation follows the calculus genesis. The study of the compact columnar zone revealed that its formation starts in a practically continuous surface formed by organic matter and crystals that surround the core. This layer favors the growth of oriented calcium oxalate monohydrate crystals upon it. Based on these observations, a feasible mechanism of papillary calcium oxalate monohydrate calculus formation is proposed

An automatic system for crystal growth studies at constant supersaturation

An automatic system for growing crystals from seeded supersaturated solutions at constant supersaturation is described. Control of burettes and data acquisition are controlled by computer. The system was tested with a study of the calcium oxalate kinetics of crystal growth

Do mammals make all their own inositol hexakisphosphate?

A highly specific and sensitive mass assay for inositol hexakisphosphate (InsP6) was characterized. This centres around phosphorylating InsP6 with [32P]ATP using a recombinant InsP6 kinase from Giardia lambia, followed by HPLC of the 32P-labelled products with an internal [3H]InsP7 standard. This assay was used to quantify InsP6 levels in a variety of biological samples. Concentrations of InsP6 in rat tissues varied from 10–20 μM (assuming 64% of wet weight of tissue is cytosol water), whereas using the same assumption axenic Dictyostelium discoideum cells contained 352±11 μM InsP6. HeLa cells were seeded at low density and grown to confluence, at which point they contained InsP6 levels per mg of protein similar to rat tissues. This amounted to 1.952±0.117 nmol InsP6 per culture dish, despite the cells being grown in serum shown to contain no detectable (less than 20 pmol per dish) InsP6. These results demonstrate that mammalian cells synthesize all their own InsP6. Human blood was analysed, and although the white cell fraction contained InsP6 at a concentration comparable with other tissues, in serum and platelet-free plasma no InsP6 was detected (<1 nM InsP6). Human urine was also examined, and also contained no detectable (<5 nM) InsP6. These results suggest that dietary studies purporting to measure InsP6 at micromolar concentrations in human plasma or urine may not have been quantifying this inositol phosphate. Therefore claims that administrating InsP6 in the diet or applying it topically can produce health benefits by increasing extracellular InsP6 levels may require reassessment

Estudio paleopatológico de la necrópolis mudéjar de la calle Colón, 3 (Novelda, Alicante)

X Congreso Nacional de Paleopatología. Univesidad Autónoma de Madrid, septiembre de 200

Dos embarazadas de la maqbara de la Calle Herrerías (Tudela, Navarra) (s. IX-XI)

X Congreso Nacional de Paleopatología. Univesidad Autónoma de Madrid, septiembre de 200

Reduction of ureteral stent encrustation by modulating the urine pH and inhibiting the crystal film with a new oral composition: a multicenter, placebo controlled, double blind, randomized clinical trial

Background: Encrustation of ureteral double J stents is a common complication that may affect its removal. The aim of the proposed study is to evaluate the efficacy and safety of a new oral composition to prevent double J stent encrustation in indwelling times up to 8 weeks. Methods: A double-blinded, multicenter, placebo-controlled trial was conducted with 105 patients with indwelling double J stents enrolled across 9 public hospitals in Spain. The patients were randomly assigned (1:1) into intervention (53 patients) or placebo (52 patients) groups for 3 to 8 weeks and both groups self-monitored daily their morning urine pH levels. The primary outcome of analysis was the degree of stent ends encrustation, defined by a 4-point score (0 - none; 3 - global encrustation) using macroscopic and electron microscopy analysis of crystals, after 3 to 8-w indwelling period. Score was exponentially transformed according to calcium levels. Secondary endpoints included urine pH decrease, stent removal, and incidence of adverse events. Results: The intervention group benefits from a lower global encrustation rate of stent ends than placebo group (1% vs 8.2%; p < 0.018). Mean encrustation score was 85.12 (274.5) in the placebo group and 18.91 (102.27) in the intervention group (p < 0.025). Considering the secondary end points, treated patients reported greater urine pH decreases (p = 0.002). No differences in the incidence of adverse events were identified between the groups. Conclusions: Our data suggest that the use of this new oral composition is beneficial in the context of ureteral double J indwelling by decreasing mean, as well as global encrustation