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PubMed1991

[Studies of sodium pentosan polysulphate (SPP) therapy on the urinary stone disease. Experimental studies on the calcium oxalate crystallization and the effects in healthy subjects].

Concerning with the inhibitory activity of sodium pentosan polysulphate (SPP) on calcium oxalate stone formation, the following three experiments were carried out. 1) The inhibitory activities for calcium oxalate crystal formation, aggregation and growth in vitro, 2) the effects on the deposition of calcium oxalate crystals in rats treated with ethylene glycol, and 3) the effects of oral administration to human subjects on the metastable limit of urinary calcium oxalate and on the inhibitory activity of the urine for calcium oxalate crystal growth. The results were as follows: 1. The degree of the calcium oxalate crystal formation measured by an aggregometer was decreased by addition of more than 1 mM of SPP. 2. The inhibitory activity of SPP on calcium oxalate crystal aggregation was measured using a Coulter Counter. The aggregation was inhibited at a low concentration of SPP (0.02 microM). 3. Calcium oxalate crystal growth was measured using a seeded crystal method with [14C] oxalic acid. SPP inhibited the crystal growth proportionally to the concentration of SPP (0.1 microM-100 microM). 4. Renal tubular deposition of calcium oxalate crystals was marked in rats that orally received ethylene glycol (0.4%), which was expected to be suppressed by intramuscular administration of SPP (30 mg/kg/day or 60 mg/kg/day). 5. Oral administration of SPP (500 mg/day) to five healthy male subjects for five days resulted a tendency to increase of the metastable limit of the urinary calcium oxalate as measurement by an aggregometer, but the inhibitory activity of the urine for calcium oxalate crystal growth, which was measured by seeded crystal method with [14C] oxalic acid, showed no variable changes.

Adult↗
PubMed1999

Role of urinary bikunin in the inhibition of calcium oxalate crystallization.

Several urinary macromolecules are known to modulate calcium oxalate (CaOx) crystallization. One of these is urinary bikunin, the light chain of inter-alpha-inhibitor. Bikunin has been demonstrated to be an efficient inhibitor of CaOx crystal growth; however, its inhibitory activity against other events in CaOx crystallization has not been fully investigated. To assess the potential of urinary bikunin as an effective inhibitor, its effects on CaOx crystal nucleation and aggregation were evaluated. Nucleation and aggregation of CaOx crystals were studied by measuring turbidity at 620 nm. In the nucleation assay, crystallization was induced by mixing calcium chloride and sodium oxalate, at final concentrations of 3 and 0.5 mM, respectively. Both solutions were buffered with 0.05 M Tris, 0.15 M NaCl, pH 6.5. Nucleation measurements were performed at 37 degrees C, with stirring at 800 rpm. Inhibition of nucleation was estimated by comparing the induction time in the presence of the inhibitor with control values. In the aggregation assay, the optical density of the solution containing CaOx monohydrate crystals was monitored. Inhibition of aggregation was evaluated by comparing the turbidity slope in the presence of the inhibitor with control values. The data showed that urinary bikunin, at concentrations of 2.5 to 20 microg/ml, retarded crystal nucleation by 67 to 58% and inhibited crystal aggregation by 59 to 80%. According to these results, it seems that urinary bikunin is an efficient inhibitor of crystal nucleation and aggregation. Its presence in the kidneys and urine may protect subjects against CaOx crystallization and kidney stone formation.

Calcium Oxalate↗
PubMed1999

Nucleation, adhesion, and internalization of calcium-containing urinary crystals by renal cells.

Renal tubular fluid in the distal nephron is supersaturated favoring nucleation of the most common crystals in renal stones, which are composed of calcium oxalate and calcium phosphate. The mechanisms whereby these newly formed crystals can be retained in the nephron and develop into calculi are not known. Calcium oxalate monohydrate and hydroxyapatite (calcium phosphate) crystals rapidly adhere to anionic sites on the surface of cultured renal epithelial cells, but this process is inhibited by specific urinary anions such as citrate, glycosaminoglycans, uropontin, or nephrocalcin, each of which can coat the crystals. Therefore, competition for the crystal surface between soluble anions in tubular fluid and anions anchored on the apical cell surface could determine whether a crystal binds to a tubular cell. Crystals of calcium oxalate dihydrate can also nucleate directly on the surface of cultured BSC-1 cells in a face-specific manner, suggesting another potential pathway for crystal deposition in the nephron. Once present on the cell surface, calcium oxalate monohydrate, calcium oxalate dihydrate, and hydroxyapatite crystals are quickly internalized by renal cells; alterations in gene expression and initiation of proliferation may then ensue. Calcium oxalate crystals can also dissolve after renal cells internalize them, but this process may require up to several weeks. Increased knowledge about cell-crystal interactions, including identification of molecules in tubular fluid and on the cell surface that modulate the process, appear critical for understanding the pathogenesis of nephrolithiasis.

Animals↗
PubMed1997

Partial improvement of crystal quality for microgravity-grown apocrustacyanin C1.

The protein apocrustacyanin C1 has been crystallized by vapour diffusion in both microgravity (the NASA space shuttle USML-2 mission) and on the ground. Rocking width measurements were made on the crystals at the ESRF Swiss-Norwegian beamline using a high-resolution psi-circle diffractometer from the University of Karlsruhe. Crystal perfection was then evaluated, from comparison of the reflection rocking curves from a total of five crystals (three grown in microgravity and two earth controls), and by plotting mosaicity versus reflection signal/noise. Comparison was then made with previous measurements of almost 'perfect' lysozyme crystals grown aboard IML-2 and Spacehab-1 and reported by Snell et al. [Snell, Weisgerber, Helliwell, Weckert, Holzer & Schroer (1995). Acta Cryst. D51, 1099-1102]. Overall, the best diffraction-quality apocrustacyanin C1 crystal was microgravity grown, but one earth-grown crystal was as good as one of the other microgravity-grown crystals. The remaining two crystals (one from microgravity and one from earth) were poorer than the other three and of fairly equal quality. Crystal movement during growth in microgravity, resulting from the use of vapour-diffusion geometry, may be the cause of not realising the 'theoretical' limit of perfect protein crystal quality.

Carrier Proteins↗
PubMedDate not supplied

[Synovial fluid crystal identification by electron microscopy].

BACKGROUND: In clinical practice crystal identification in synovial fluid is made by polarized light microscopy and with some specific stainings. Nevertheless, sometimes we are unable to identify crystals by these means, either because they are too small or because they are widespread on the fluid. AIMS: To compare the identification of crystals in synovial fluid from patients with non-infectious monoarthritis but no history of local trauma or articular disease, using polarized light and electronic microscopy. METHODS: We analized synovial fluid samples from patients with non-infectious monoarthritis and no history of local trauma or articular disease. First we used a polarized light microscope and alizarin red staining. Later we used conventional transmission electron microscopy and energy dispersive spectroscopy, in order to identify and characterize crystals. RESULTS: Fourty-five samples from 23 synovial fluids were analyzed. Under polarized light microscopy we identified crystals on 11 samples: 3 with calcium pyrophosphate crystals, 6 with calcium basic phosphate crystals and 2 with sodium monourate crystals. On the remaining 12 samples we were unable to identify crystals. Samples were then analyzed by conventional transmission electron microscopy and energy dispersive spectroscopy confirming the presence of the previously identified crystals. On the remainig 12 samples we were able to identify calcium basic phosphate crystals. DISCUSSION: Microcrystals seem to be an universal finding in synovial fluid of patients with osteoarthritis. The prevention of their deposition in joints might contribute to stop joint damage in this disease.

Arthritis↗
PubMed1991

Crystal growth on enamel in relation to acid etching.

Crystal formation may occur during etching of enamel surfaces with phosphoric acid. In this in vitro study we observed, from a morphological standpoint, some crystals left after etching, on the surfaces, using the scanning electron microscope. More often, after water-spraying, a thin generalized precipitate remains on the surface. This precipitate may be harmful for the retention of composite resins. On few specimens we obtained needle-shaped or petal-like crystals. Crystal deposits were spread evenly, on the surface, or nucleated from different points. We tempted to identify these crystal formations by X-ray diffraction and microprobe analysis. Chemical identification seems very important because calcium phosphates solubility varies. Crystal dissolution in saliva can lead to marginal leakage and impairs the quality of esthetic restorations. On the contrary insoluble crystals may ensure microscopic retentions and crystal growth is now considered as an alternative for enamel pretreatment in bracket bonding. Crystal formation, in these first experiments, is too scarce to be used for crystal bonding. But it appears that two factors may enhance the crystal number: a preliminary topical application of fluoride and adsorption of an acidic protein, on the surface, before etching. However, further investigations are still necessary.

Acid Etching, Dental↗
PubMed1990

Calcium pyrophosphate crystal deposition: a kinetic study using a type I collagen gel model.

Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease is characterized by deposits of triclinic (t) and monoclinic (m) CPPD crystals in articular and fibrocartilage. Many investigators have attempted to model CPPD crystal growth using both solution and a variety of gel systems. We have investigated the effect of type I collagen fibrils on CPPD crystal nucleation and growth using an ionic diffusion model. Collagen was isolated from porcine menisci using a pepsin solubilization procedure and gelled in three layers, with one containing 10 mM pyrophosphate (PPi) plus physiologic ions, the middle containing only the ions, while the third contained 25 mM Ca plus physiologic ions. Initially, amorphorous calcium pyrophosphate formed at the Ca-PPi interface. Monoclinic CPPD crystallized in 6 weeks when the [Ca] was between 2 and 3 mM and the [PPi] was between 50 and 75 microM. At 13 weeks, t-CPPD formed when the [Ca] was also between 2 and 3 mM, but the PPi was less than 25 microM. One of the most striking differences between this system and all previous solution and gel model systems is the total absence of orthorhombic calcium pyrophosphate tetrahydrate (o-CPPT) from the gels made of collagen fibrils in near native conformation. Further, crystals of t-CPPD appear as large single crystals with the classic prismatic growth habit observed in vivo, and crystals of m-CPPD also evidence the in vivo rod habit. In contrast, the crystal growth habits of t-CPPD, m-CPPD, and o-CPPT grown in all of the other model systems never matched that observed in vivo. When compared to the previous studies, these results, particularly the crystal growth habit data, suggest that the native collagen fibrils themselves can nucleate CPPD crystal formation.

Animals↗
PubMed1988

Calcium pyrophosphate crystal deposition in hyaline cartilage. Ultrastructural analysis and implications for pathogenesis.

Using transmission electron microscopy, selected area electron diffraction, and micro x-ray diffraction techniques, we studied calcium pyrophosphate dihydrate (CPPD) deposits from 23 patients with chondrocalcinosis affecting the femoral head to delineate the cellular and matrix environment in which CPPD crystals form, to determine the sequence of crystal deposition, and to address the question of coexistent calcium apatite crystal deposition. We found 2 types of CPPD crystal deposits with few transitional forms. First, small collections of crystals were seen at the border of the territorial matrix at the articular and subarticular poles of the chondron. CPPD crystal deposits were unassociated with collagen or matrix vesicles. Second, and more frequently, large collections of randomly arranged crystals (agglomerates) were observed, the smallest replacing the chondrocyte and adjacent pericellular matrix. Chondrocytes adjacent to crystal deposits were intact. Coexistent apatite crystal deposition was demonstrated in only 2 of 23 cartilages ultrastructurally examined, providing evidence that mixed crystal deposits are possible but not common in CPPD crystal arthropathy.

Aged↗
PubMed1988

Calcium pyrophosphate crystal deposition in model systems.

The chemistry and molecular bonding characteristics of the CaPPi family of compounds are very complex. The unique molecular flexibility of the PPi anion and the potential variability of Ca coordination geometries have allowed for a broad spectrum of CaPPi type structures. The structure of t-CPPD has the smallest P-OB-P angle of the known CaPPi structures, both Ca atoms are 7 coordinate which is the maximum allowable contacts for Ca atoms, and the two water molecules of crystallization not only serve to fill molecular space, but they are also involved in direct contact to the PPi anions and the Ca atoms. The structure of t-CPPD appears to be very stable and the structural characteristics support the observation that the crystals are sparingly soluble in an aqueous environment. Unfortunately, the structure of m-CPPD is not known and comparisons cannot be made. The solution model studies have resulted in the observation that t-CPPD and m-CPPD crystals can be grown in an aqueous environment at conditions far less harsh than those required for the standard synthetic procedure. However, the synthetic procedure, in contrast to the solution models, yields the prismatic crystal growth morphology of t-CPPD and the rod morphology of m-CPPD observed in vivo. The solution models showed that increasing Mg or Pi retarded crystal formation. At physiologic levels of Mg and Pi, a-CaPPi formed, but neither t-CPPD nor m-CPPD would form. In all solution studies, the final Ca and PPi were not determined and therefore a correlation could not be made between the ionic concentrations and crystal type formed. The gel models using silica, polyacrylamide, and biologic grade gelatin all highlighted that the time of incubation of Ca and PPi ions was a critical parameter in determining the type of crystal formed. The biologic grade gelatin model studies that we conducted indicated that the formation of the two in vivo crystals was mediated by the formation of intermediate crystalline materials and the subsequent dissolution of those species. This formation/dissolution/reformation mechanism allows for a very localized ionic concentrating process to occur. In our model system, we measured the final Ca and PPi levels at all points of crystallization and could map the ionic concentration gradients and compare them to the crystal type formed with respect to the time of incubation. However, the crystal growth morphologies for t-CPPD and m-CPPD still did not match the morphologies observed in vivo.(ABSTRACT TRUNCATED AT 400 WORDS)

Anions↗
PubMed1982

Effect of fluoride on crystal growth of calcium apatites in the presence of a salivary inhibitor.

The effect of fluoride on the kinetics of crystal growth of calcium apatites was studied using seed crystals of hydroxyapatite coated with PRP-3, a proline-rich phosphoprotein salivary inhibitor of crystal growth. Initial precipitation rates in the presence of PRP-3, under conditions of partial inhibition, were enhanced by fluoride, effectively counteracting the inhibitory activity of the macromolecule. This rate enhancement is related to an increase in the precipitation driving force, i.e., the degree of supersaturation with respect to the precipitating phase; in this case a fluoridated hydroxyapatite. The growth of this phase takes place at the uncovered crystal growth sites which have been previously shown to be the same sites as the adsorption sites for the protein inhibitors. Explanations based on fluoride activation of secondary crystal growth sites and on the displacement of adsorbed inhibitor by fluoride are not substantiated by the present results. It has been demonstrated that under conditions of maximum coverage of available crystal growth sites by PRP-3, resulting in no apparent crystal growth, measurable crystal growth is observed upon the addition of fluoride (1 ppm). This phenomenon is best explained by the fact that at maximum PRP-3 coverage, a small number (16%) of crystal growth sites remain uncovered, which support an unmeasurable rate of crystal growth. Upon the addition of fluoride, this rate is significantly enhanced. It is suggested that the fraction of uncovered growth sites is related to steric interactions of the PRP-3 molecule in the adsorbed state. Overall, the results presented suggest that fluoride can accelerate crystal growth in an environment such as the enamel surface where the acquired pellicle is formed.

Crystallization↗
PubMed1983

Cholesterol crystal formation and growth in model bile solutions.

Cholesterol monohydrate crystal formation was studied in supersaturated model bile solutions, containing unlabeled cholesterol, sodium cholate and soybean phosphatidylcholine, and tracer amounts of [3H]cholesterol. Solutions were either seeded with cholesterol crystals to initiate growth, or not seeded to allow self-nucleation and subsequent crystal growth to occur. Crystal growth at 37 degrees C was measured by two methods. First, radioactive cholesterol crystals were isolated by filtration, and the mass of cholesterol that had precipitated was calculated. In unseeded solutions, there was a long lag period before crystal growth was detected. This lag time was decreased by increases in the cholesterol concentration, temperature, and lipid concentration. In seeded solutions, crystal growth also was dependent on the cholesterol concentration, temperature, and lipid concentration. The second method used to measure crystal growth involved the Coulter Counter. At 37 degrees C, reproducible results were not obtained using unseeded solutions due to blocking of the counter aperture with large crystals. In seeded solutions, crystal growth could be measured as an increase in total particle volume. However, comparison of growth rate estimates from the Coulter Counter with those obtained radiochemically revealed poor agreement between the two methods. It is probable that the Coulter Counter is inaccurate in measuring the volume of cholesterol monohydrate crystals due to their anisometric shape.

Bile↗
PubMed1993

Compound heterozygosity for hemoglobin C and Korle-Bu: moderate microcytic hemolytic anemia and acceleration of crystal formation [corrected].

We report here that compound heterozygosity for hemoglobin Korle-Bu (HbKB) and HbC (beta 6 Glu-->Lys) is associated with moderate chronic hemolytic anemia with microcytosis. To understand the pathogenesis of this syndrome, we have studied the effect of Hb Korle-Bu (KB = beta 73 Asp-->Asn) on the crystallization of HbC. We have previously established that fetal Hb (HbF) inhibits the crystallization of HbC. In contrast, HbS accelerates crystallization affecting the pathogenesis of SC disease. We now report on in vitro crystallization of mixtures of HbKB, HbC, and various amounts of HbF and the native hemolysate of a child who is a compound heterozygote for HbKB and HbC. At 6 months of age, the propositus' hemolysate contained 55% HbKB, 39% HbC, and 6% HbF. Crystal formed within 2 minutes compared with 30 minutes for the mixture of 40% HbC:60% HbS and with 180 minutes for 40% HbC:60% HbA. The morphology of the crystals formed was cubic, in contrast with the tetragonal crystals observed in CC and SC disease. Early crystals did not exhibit "sharp edges" until 45 minutes. Purified HbKB formed aggregates but not crystals after 24 hours. Isopycnic gradients showed that the KB/C compound heterozygotes have red blood cell (RBC) densities intermediate between the AC and CC phenotype and similar to SC disease. The surface residue beta 73, known to participate in areas of interaction of the deoxy HbS polymer, can now be assigned to areas of contact in HbC containing crystals. The hemolysis observed in the HbKB/C compound heterozygote is likely to be secondary to the acceleration of Hb crystallization. The microcytosis and increased RBC density is clearly the consequence of the presence of HbC, but the basis of the increased RBC pathology compared with AC trait, despite the low proportion of HbC (35% to 40%), remains to be elucidated.

Adolescent↗
PubMed1994

[A role for lipoproteins in the recovery from CPPD crystal-induced arthritis].

Calcium pyrophosphate dihydrate (CPPD) crystal-induced inflammation subsides spontaneously, and there have been few reports on its mechanism. It has recently been proposed that lipoproteins in the inflammatory synovial fluid played a role in the recovery from crystal-induced arthritis. This study investigated the inhibitory effect of lipoprotein on the inflammation-inducing activity of CPPD crystals in vitro and in vivo. Lipoproteins (very low density lipoprotein--VLDL, and low density lipoprotein-LDL) were isolated from human serum (in vitro) and rat serum (in vivo) by the sequential ultracentrifugal technique. In the in vitro studies, saline with lipoproteins was mixed with CPPD crystals, and co-incubated with isolated polymorphonuclear leukocytes (PMN). The production of superoxide anion (O-(2)) was measured as an index of inflammatory activity. In the in vivo studies, suspensions of CPPD crystals and rat lipoprotein solutions, were injected into the rat air pouch. The total number of white blood cells (WBC), crystal-containing WBCs, and concentrations of beta-glucronidase and prostaglandin (PG) E2, were measured. In the in vitro studies, O-(2) production by PMNs was more significantly suppressed after treating the CPPD crystals with VLDL or LDL than when the crystals were not treated with VLDL or LDL. In the in vivo studies, treatment of the CPPD crystals with lipoproteins significantly decreased the number of WBC and crystal-containing WBC, as well as the concentration of beta-glucronidase, and tended to depress the concentration of PGE2. These findings suggested that lipoproteins, especially LDL in inflammatory synovial fluid played an important role in the recovery from CPPD crystal-induced arthritis.

Animals↗
PubMedDate not supplied

Intranuclear Reinke's crystals in a testicular Leydig cell tumor diagnosed by aspiration cytology. A case report.

Fine needle aspiration cytologic findings in a Leydig cell tumor of the testis are described. Besides the rarity of case reports on fine needle aspiration cytologic diagnosis of this tumor, the present case was of interest because of the finding of numerous intranuclear and intracytoplasmic Reinke's crystals as well as some lying free between the cells. In a few cells the intranuclear crystals were seen to orient themselves in a row, with a nipplelike protrusion of the nuclear membrane as if being pushed by the crystals. Besides the well-formed crystals, many nuclei showed irregular, thin, groovelike spaces that may have been earlier stages of crystal formation. These findings suggested the intranuclear formation of Reinke's crystals. Extranuclear crystals were seen to fuse in pairs and hence to appear thicker than the intranuclear crystals. The crystals lying free between the cells also showed a linear arrangement in places. The crystals were more numerous with May-Grünwald-Giemsa (MGG) staining. Intranuclear crystals were seen only in MGG-stained smears.

Adult↗
PubMed1993

Components generated locally as well as serum alter the phlogistic effect of monosodium urate crystals in vivo.

Proteins binding monosodium urate (MSU) crystals alter their phlogistic potential in vitro and in vivo. These proteins and other materials capable of interacting with crystals could enter the joint space from the circulation and/or could be produced locally. Using the rat subcutaneous air pouch synovium-like model, we observed different effects of collected pouch fluid supernatants from acute (6 h) and from subsiding (72 h) inflammation, and from autologous rat serum on MSU crystal induced inflammation in new air pouches. Plain crystals at 6 h produced a mean leukocyte count (WBC) of 18,156/mm3 with 12% of cells showing phagocytosis of MSU; reaction to plain crystals at 72 h had subsided to only 75 WBC/mm3 and 1% phagocytosis; new crystals preincubated in supernatant from acutely inflamed 6 h air pouches produced higher numbers of WBC in new pouches at 6 h (34,044/mm3); while crystals preincubated in 72 h supernatant gave only 9,825/mm3 and 7% phagocytosis; crystals preincubated in rat serum produced similar pouch WBC to plain crystals at 6 h, but resulted in only 2% phagocytosis. Our study provides evidence that components generated locally during subsiding inflammation as well as serum components could bind to MSU crystals and affect the generation of chemotactic factors and/or crystal phagocytosis contributing in the self-limited nature of acute gouty arthritis.

Animals↗
PubMed1996

Strategies for crystallizing membrane proteins.

Crystallizing membrane proteins remains a challenging endeavor despite the increasing number of membrane protein structures solved by X-ray crystallography. The critical factors in determining the success of the crystallization experiments are the purification and preparation of membrane protein samples. Moreover, there is the added complication that the crystallization conditions must be optimized for use in the presence of detergents although the methods used to crystallize most membrane proteins are, in essence, straightforward applications of standard methodologies for soluble protein crystallization. The roles that detergents play in stability and aggregation of membrane proteins as well as the colloidal properties of the protein-detergent complexes need to be appreciated and controlled before and during the crystallization trials. All X-ray quality crystals of membrane proteins were grown from preparations of detergent-solubilized protein, where the heterogeneous natural lipids from the membrane have been replaced by a homogeneous detergent environment. It is the preparation of such monodisperse, isotropic solutions of membrane proteins that has allowed the successful application of the standard crystallization methods routinely used on soluble proteins. In this review, the issues of protein purification and sample preparation are addressed as well as the new refinements in crystallization methodologies for membrane proteins. How the physical behavior of the detergent, in the form of micelles or protein-detergent aggregates, affects crystallization and the adaptation of published protocols to new membrane protein systems are also addressed. The general conclusion is that many integral membrane proteins could be crystallized if pure and monodisperse preparations in a suitable detergent system can be prepared.

Animals↗
PubMed1995

Morphological effects of glycosaminoglycans on calcium oxalate monohydrate crystals.

The effects of individual glycosaminoglycan (GAG) species on calcium oxalate monohydrate (COM) crystal growth were studied in vitro by the observation of crystal morphology grown in a supersaturated calcium oxalate solution in the presence of GAGs using optical and scanning electron microscopes. GAGs affected the morphology of COM crystals differently depending on the species. The growth rates of the crystals formed in the presence of chondroitin-6-sulfate (ChS-C) were higher in length and lower in width and thickness than those of control crystals. The incorporation of dermatan sulfate or heparin into the crystals formed in the presence of these GAGs was revealed by X-ray microanalysis, whereas ChS-C was not detected in the crystals grown with it. The experiment using dicarboxylates, as a simple model of GAG molecules, showed that a distance between the side groups was important for their morphological effects. These findings suggested that the different effects of GAGs on the crystal morphology resulted from the differences in their interaction modes with COM crystal faces, that is, the differences in their binding behavior, their inhibition modes of crystal growth, and other roles played after binding to the crystals.

Calcium Oxalate↗
PubMed1996

Crystallization during volume reduction of solutions with an ion-composition corresponding to that in the distal tubuli.

The effect of macromolecules on the crystallization in solutions with an ion-composition and a pH corresponding to that of urine in the distal part of the distal tubuli was examined by recording the number and volume of crystals in a Coulter Multisizer and by studying the crystal morphology with scanning electron microscopy at different degrees of evaporation. The experiments were carried out with 100 ml samples of salt solutions with and without different concentrations of dialysed urine (dU) from normal subjects. Addition of dU resulted in a greater number of crystals and a reduction in the mean crystal volume (MCV). Under the experimental conditions, the maximal effect of the macromolecules appeared to be accomplished in solutions with an initial dU concentration of 10%. The precipitate was strongly suggestive of calcium phosphate (CaP) as shown by scanning electron microscopy and Raman spectroscopy. This conclusion was further supported by the ion-activity products of calcium oxalate (CaOx) and different CaP salts in those samples in which crystal formation was recorded. The obtained results give support to the view that macromolecules might exert a promotive effect on the nucleation of CaP. The macromolecules also appear to counteract the development of large CaP crystals, but whether this is due to an inhibition of crystal growth, an inhibition of crystal aggregation or both could not be concluded from these experiments. The way in which CaP crystals initially form in the nephron might be of importance for the subsequent crystallization of CaOx and the formation of CaOx containing stones.

Calcium Oxalate↗