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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possibility that hypercalciuria could cause calcium stone formation through a mechanism other than by increasing urinary saturation of stone-forming calcium salts was explored. The effect of increasing calcium concentration on the inhibitor activity against the spontaneous precipitation of calcium oxalate was examined in whole urine (in the presence of naturally occurring inhibitors) and in synthetic media (with added inhibitors). In 11 patients with calcium nephrolithiasis, the induced hypercalciuria from calcium supplementation (600 mg/day) caused a significant fall in the urinary inhibitory activity against calcium oxalate precipitation, as shown by a decline in the formation product ratio from 12.6 +/- 1.1 SEM to 9.6 +/- 1.4 (P less than 0.005). In order to more fully explore this observation, the effect of increasing calcium concentration on the inhibitory activities of citrate (2 mM), chondroitin sulfate (0.05 mg/liter) and a heterogeneous group of naturally-occurring urinary inhibitors (1.0 mg/liter) against calcium oxalate precipitation was examined in vitro in synthetic solutions. The inhibitory actions of both citrate and chondroitin sulfate were significantly attenuated by increasing calcium concentration from 0.25 mM to 6.0 mM (P less than 0.01). However, raising the calcium concentration in synthetic media containing a mixture of partially purified urinary inhibitors produced a significant rise in the urinary inhibitory activity of this macromolecular mixture (P less than 0.01). We conclude that hypercalciuria can attenuate the inhibitory activities of citrate and chondroitin sulfate against calcium oxalate precipitation while at the same time accentuating the inhibitory activity of naturally-occurring urinary inhibitors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation by calcium of the inhibitor activity of naturally occurring urinary inhibitors. 313 70

The aim of this study was to evaluate the effect of magnesium on calcium oxalate crystal formation, both in physiological conditions and at slightly higher oxalate concentrations, using a mixed suspension mixed product removal crystallizer and scanning electron microscopy. True supersaturation ratios were calculated by allowing for complexation in solution. Magnesium inhibited the nucleation rate at all oxalate concentrations. It also inhibited the growth rate at oxalate concentrations of less than approximately 2.0 mmol/l but promoted the growth rate at higher concentrations. This suggests that, provided the oxalate concentration is sufficiently high, increase of magnesium concentration can increase the crystal growth rate. At physiological concentrations of oxalate, however, magnesium decreases both nucleation and growth rates. The SEM photographs showed that the predominant crystal was calcium oxalate trihydrate at low magnesium concentrations, with calcium oxalate dihydrate being observed in larger quantities at high magnesium concentrations.
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PMID:The role of magnesium in calcium oxalate urolithiasis. 334 76

Microscopic crystals were found by SEM analysis in kidneys of stone forming patients as well as in kidneys of non-stone formers. In most samples calcifications were intratubular in the collecting ducts near the papillary tip. 1-2 micron sized particles lay in a gelatinous substance on the epithelium. The only difference in crystal composition is the higher phosphate content in the kidneys of the non-stone forming group. A correlation between the element concentration of the tissue and the occurrence of microliths is given by the cadmium content of the kidney samples. Both groups showed higher cadmium values in the cortex or medulla when crystals were found in the corresponding papillary samples. Urine supersaturation with respect to calcium oxalate was higher in the stone forming group caused by a higher calcium and oxalate but a lower magnesium excretion.
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PMID:Stone formation in human kidney. 359 Apr 31

Serum oxalate rises in uremia because of decreased renal clearance, and crystals of calcium oxalate occur in the tissues of uremic patients. Crystal formation suggests that either uremic serum is supersaturated with calcium oxalate, or local oxalate production or accumulation causes regional supersaturation. To test the first alternative, we ultrafiltered uremic serum and measured supersaturation with two different methods previously used to study supersaturation in urine. First, the relative saturation ratio (RSR), the ratio of the dissolved calcium oxalate complex to the thermodynamic calcium oxalate solubility product, was estimated for 11 uremic (before and after dialysis) and 4 normal serum samples using a computer program. Mean ultrafiltrate oxalate predialysis was 89 +/- 8 microM/liter (+/- SEM), 31 +/- 4 postdialysis, and 10 +/- 3 in normals. Mean RSR was 1.7 +/- 0.1 (predialysis), 0.7 +/- 0.1 (postdialysis), and 0.2 +/- 0.1 (normal), where values greater than 1 denote supersaturation, less than 1, undersaturation. Second, the concentration product ratio (CPR), the ratio of the measured calcium oxalate concentration product before to that after incubation of the sample with calcium oxalate monohydrate crystal, was measured in seven uremic and seven normal serum ultrafiltrates. Mean oxalate was 91 +/- 11 (uremic) and 8 +/- 3 (normal). Mean CPR was 1.4 +/- 0.2 (uremic) and 0.2 +/- 0.1 (normal). Predialysis, 17 of 18 uremic ultrafiltrates were supersaturated with respect to calcium oxalate. The degree of supersaturation was correlated with ultrafiltrate oxalate (RSR, r = 0.99, r = 29, P less than 0.001; CPR, r = 0.75, n = 11, P less than 0.001). A value of ultrafiltrate oxalate of 50 microM/liter separated undersaturated from supersaturated samples and occurred at a creatinine of approximately 9.0 mg/dl.
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PMID:Evidence that serum calcium oxalate supersaturation is a consequence of oxalate retention in patients with chronic renal failure. 371 39

Male Wistar rats were treated by ethylene glycol (0.8 Vol% in water) or a diet low in magnesium (70 mg/kg). The intrarenal crystallisation and stone formation of calcium oxalate was investigated by SEM, TEM and energy dispersive X ray analysis. The first stage in crystallisation was amorphous deposits of calcium surrounding microvilli of the lower part of the nephron, followed by multicentric, intratubular calcium crystals. Finally calcium plaques of the papilla seemed to be precursors of the urinary stone.
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PMID:[Intrarenal calcium crystallization. An electron microscopy study]. 371 39

Infrared spectroscopic analysis of 741 canine urinary calculi revealed that struvite stones, 58% of the total, were the ones most commonly to be found. Cystine stone disease, 21%, is also of great significance for dogs, whereas calcium oxalate, urate and brushite calculi occur only seldom. 3 cases of xanthine stone formation were also noted. SEM examination revealed structures similar to human stones such as bipyramidal weddellite, pseudomorphs from whewellite to weddellite, apatite deposits in cystine stones and characteristic mono-ammonium-urate needles. Other, unknown, structures were also discovered such as closely-knit intergrowths of cystine and brushite strata, mono-Na-urate and mono-K-urate intergrowths and Ca-urate. Of particular interest are the various forms of xanthine from compact spherical to lance-shapes in sheath-like arrangement.
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PMID:Analysis of canine urinary stones using infrared spectroscopy and scanning electron microscopy. 381 33

Measurement of oxalate levels in 14 patients with chronic renal failure, treated by maintenance hemodialysis, revealed elevated plasma oxalate concentrations in all patients 1,075.7 +/- (SEM) 253 micrograms/dl. In 7 of these subjects the oxalate concentration was more than three times higher than the upper limit of normal. Furthermore, a strong positive correlation (r = 0.75) between serum creatinine and plasma oxalate concentration was found. A combination of hemodialysis and hemoperfusion procedure was carried out in a dialysis patient with primary oxalosis as a cause of renal failure. The average oxalate clearance of the hemodialyzer during seven hemodialysis/hemoperfusion procedures was 91 ml/min and that of the charcoal detoxifier was 24 ml/min. The amount of oxalate removed during 4 1/2 h of the hemodialysis/hemoperfusion procedure was 429 mg. This amount was calculated to be produced in about 87 h, with an oxalate generation rate of 4.9 mg/h.
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PMID:Hyperoxalemia in renal failure and the role of hemoperfusion and hemodialysis in primary oxalosis. 405 24

Ionic calcium, calcium binding sites, and other urinary variables were measured in 58 patients with idiopathic calcium nephrolithiasis and 36 normal subjects. The patients showed higher urinary concentrations of calcium. The mean calcium excretion (mmole/24 hr) was 4.45 +/- 0.56 (+/- 1 SEM) in patients and 2.19 +/- 0.22 (+/- 1 SEM) in normal subjects. This difference was highly significant (P less than 0.001). The mean ionic calcium excretion (mmole/24 hr) was 1.90 +/- 0.21 (+/- 1 SEM) for patients and 0.97 +/- 0.12 (+/- 1 SEM) for control subjects. The normal subjects showed significantly higher (P less than 0.01) concentrations and total excretions of magnesium and citrate. Excretory patterns for sodium, potassium, phosphate, and oxalate were not significantly different. The normal subjects had higher mean urinary concentrations of binding sites for calcium ions (23.2 +/- 4.8 mM) than the patients (18.5 +/- 2.9 mM). However, as the patients had higher urinary volumes the difference in the 24-hr excretion of calcium binding sites was not significant statistically. Out of 58 patients 43 (74%) were hypercalciuric. Twenty patients (46%) were categorized as an absorptive group and one patient as a resorptive type, and for the rest of the patients (51%) the mechanism of hypercalciuria remained unidentified. Only two of the control subjects (5%) were found to be hypercalciuric under calcium restricted diet conditions. Though these "control" subjects excreted a high amount of calcium there was no associated increase in the fraction of the calcium in the ionic form (0.37). Patients, however, still had relatively high fractions of ionic calcium (0.48 +/- 0.03).
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PMID:Calcium dynamics in idiopathic calcium stone formers. 630 23

Tubular transport of oxalate is thought to be an energy-mediated process which may contribute to the renal deposition of calcium oxalate in a variety of pathologic states. In order to examine this possibility, the renal handling of oxalate was investigated in rat renal cortical slices in vitro. Slices incubated in vitro with 1 microM [14C]oxalate in Krebs-Ringer bicarbonate buffer at 25 degrees C for 180 min achieved a mean slice to medium ratio of 2.8 +/- 0.08 (SEM) and a mean tissue concentration of 7.7 +/- 0.2 mumol/kg dry wt (N = 64). Section freeze-dry autoradiographs demonstrated maximum uptake within proximal tubule cells but no crystals were evident. Substituting N2 for O2, adding KCN, or removing Ca2+ increased uptake of 14C-oxalate. Dinitrophenol (DNP) and iodoacetamide (IoAc), however, significantly decreased, and O degrees C eliminated slice uptake. Slices incubated with 100 microM [14C]oxalate showed a further increase in tissue accumulation and the appearance of [14C]oxalate crystals. Crystals formed in vitro were deposited throughout the tissue. Oxalic acid did not appear to share the organic acid by renal cortical slices in vitro is largely independent of energy-mediated mechanisms.
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PMID:Oxalate accumulation in rat renal cortical slices. 647 47

Increasing attention is being given to oxalate as a risk factor in urinary calcium stone disease. The accuracy of some methods for measuring urine oxalate is uncertain. Using gas chromatography urine oxalate levels were 0.36 +/- 0.02 and 0.31 +/- 0.02 (mmol/24 h +/- 1 SEM) for men and women respectively of a reference population. In recurrent stone formers urinary oxalate was 0.43 +/- 0.03 in males and 0.38 +/- 0.04 for females whilst solitary stone forming females excreted only 0.31 +/- 0.04 mmol/24 h. The difference between males and females of the reference population was significant (p less than 0.05) as was the difference between reference males and male stone formers.
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PMID:Urine oxalate levels in a New Zealand reference population and renal stone formers. 657 12


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