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J R Asplin

Publications and source records attributed to J R Asplin.

26 records · Page 2Linked to original sources
PubMed1998

Metabolic urinary correlates of calcium oxalate dihydrate in renal stones.

PURPOSE: We determined what metabolic features of the 24-hour urine predict calcium oxalate dihydrate in kidney stones. Prior studies have suggested that low urine magnesium, high urine calcium, high calcium-to-oxalate ratio and high urine supersaturation with respect to calcium oxalate monohydrate predict calcium oxalate dihydrate. MATERIALS AND METHODS: Stone analyses and results from 2, 24-hour pretreatment urine collections from 96 patients with nephrolithiasis were drawn from 3 kidney stone prevention centers. Standard stone risk measurements were made on the urine, including supersaturation for calcium oxalate monohydrate, brushite and uric acid. RESULTS: The main differences in metabolic urine findings were between patients with no calcium oxalate dihydrate and those with any calcium oxalate dihydrate in stones. Percent calcium oxalate dihydrate itself did not correlate with urine findings. Patients with no calcium oxalate dihydrate in stones showed a biphasic pattern of urine calcium oxalate monohydrate supersaturation, about half had values below almost any found among patients with calcium oxalate dihydrate in stones (less than 7) and the rest overlapped with the calcium oxalate dihydrate group. Except for higher calcium oxalate monohydrate supersaturation, patients with calcium oxalate dihydrate in stones had higher urine calcium excretion and lower urine citrate concentrations, even after calcium oxalate monohydrate supersaturation was considered. CONCLUSIONS: Patients with low calcium oxalate monohydrate supersaturation (less than 7) are unlikely to have calcium oxalate dihydrate in renal stones. However, many patients with no calcium oxalate dihydrate have higher calcium oxalate monohydrate supersaturation values, and so prediction of calcium oxalate dihydrate or its absence from urine findings is imperfect. Urine magnesium and the calcium-to-oxalate ratio are unrelated to calcium oxalate dihydrate.

Calcium Oxalate↗
PubMed1998

Medical reduction of stone risk in a network of treatment centers compared to a research clinic.

PURPOSE: We determined whether a network of 7 comprehensive kidney stone treatment centers supported by specialized stone management software and laboratory resources could achieve reductions in urine supersaturation comparable to those in a single research clinic devoted to metabolic stone prevention. MATERIALS AND METHODS: Supersaturation values for calcium oxalate, calcium phosphate and uric acid in 24-hour urine samples were calculated from a set of kidney stone risk factor measurements made at a central laboratory site for the network and research laboratory for the clinic. Individual results and group outcomes were presented to each center in time sequential table graphics. The decrease in supersaturation with treatment was compared in the network and clinic using analysis of variance. RESULTS: Supersaturation was effectively reduced in the network and clinic, and the reduction was proportional to the initial supersaturation value and increase in urine volume. The clinic achieved a greater supersaturation reduction, higher fraction of patient followup and greater increase in urine volume but the treatment effects in the network were, nevertheless, substantial and significant. CONCLUSIONS: Given proper software and laboratory support, a network of treatment centers can rival but not quite match results in a dedicated metabolic stone research and prevention clinic. Therefore, large scale stone prevention in a network system appears feasible and effective.

Adult↗
PubMed1997

Dependence of upper limit of metastability on supersaturation in nephrolithiasis.

Formation of renal stones requires supersaturation (SS) high enough to induce crystallization; such a SS is referred to as the upper limit of metastability (ULM). The ULM for calcium oxalate (CaOx) or calcium phosphate can be measured by adding oxalate or calcium to urine, respectively, and noting the point at which overt crystallization occurs as evidenced by clouding. In principle, the urine should be more prone to form stone crystals as its SS approaches the ULM, and the SS ULM distance has been used as an index of stone forming potential. In addition, one would expect the ULM and initial SS to be unrelated, as the starting urine SS has no apparent link to the amount of calcium or oxalate that urine can dissolve without leading to crystal formation. However, in rats, we have found a surprising correlation between ULM and SS, such that ULM appears to rise with initial SS, for CaOx, and, to a lesser extent, for brushite (Br), a typical calcium phosphate initial phase. In this study, we measured CaOx and Br ULM, and SS, in urine of 50 patients and 11 normal people, to determine if ULM and SS were correlated, as in rats, and to explore the relationship between SS and ULM. We found the same dependence of ULM on SS as in rats, for both CaOx and Br, and found no differences between patients and normal people with respect to this dependency. However, for Br, patients showed a lower ULM than normals, but the same initial SS, meaning that patients were closer to their crystal formation threshold than normals. Treatments for stones had no apparent effect on the SS-ULM dependency. We conclude that in humans, as in rats, ULM is related to initial SS, and that this relationship is the same in patients as in normals for CaOx, but shifted in a stone forming direction for Br among patients. The ULM-SS interaction is unaffected by contemporary conventional stone treatments, and is more marked for CaOx than Br. The mechanisms of the dependence are unknown. The smaller difference between ULM and initial SS for Br in patients than normal supports prior evidence suggesting a defect in stone patients that could lead to calcium phosphate crystallization, subsequent nucleation of CaOx, and stone disease.

Calcium↗
PubMed1997

Relationship between supersaturation and crystal inhibition in hypercalciuric rats.

Calcium oxalate (CaOx) and calcium phosphate (CaP) crystals do not precipitate in large amounts in normal urine despite considerable supersaturation (SS), partly because urine inhibits crystal nucleation, aggregation, and growth. In normal rats and rats bred for hypercalciuria (GHS), we varied SS by varying calcium intake to test the hypothesis that increased SS might deplete inhibitors and reduce inhibition of crystal formation. In normal rats when compared to a low calcium diet (0.02% Ca), a high calcium diet (1.2% Ca) raised the SS of CaOx from 0.8 to 8.2. The high calcium diet also raised the upper limit of metastability (ULM) of CaOx (the SS at which crystals form in urine) from 11.8 to 36. In GHS rats, diet change altered CaOx SS from 1.5 to 12, and ULM from 17 to 50 (all differences, P < 0.001). Because ULM rose with SS, the increased SS had little potential to increase CaOx stone risk. For CaP, however, SS rose from 0.6 to 2.4 and 1.1 to 8 in normal and GHS rats (P < 0.001 for both), respectively, whereas ULM for CaP did not increase significantly (8 vs. 7 and 7 vs. 11; P = NS, both changes). Therefore, CaP SS rose close to the ULM, posing a high stone risk. The stones formed by these rats are composed of CaP. Increasing CaOx SS by diet raises ULM for CaOx thereby offsetting the risk of CaOx stones in rats.

Animals↗
PubMed1996

Evidence of calcium phosphate supersaturation in the loop of Henle.

We have used published rat micropuncture data to construct a matrix of ion concentrations along the rat nephron. With an iterative computer model of known ion interactions, we calculated relative supersaturation ratios in all nephron segments. The collecting ducts and urine showed expected supersaturation with stone-forming salts. Fluid in the thin segment of the loop of Henle may be supersaturated with calcium carbonate and calcium phosphate under certain conditions. Because calculations cannot predict the actual course of crystallization, we made solutions to mimic, in vitro, presumed conditions in the loop of Henle. The solid phases that formed were analyzed by X-ray powder diffraction, electron microprobe, and infrared spectroscopy. All samples were identified as poorly crystallized or immature apatite. The descending limb of Henle's loop creates a unique condition as it extracts water but not sodium, bicarbonate, calcium, or phosphate, giving a calcium concentration at the bend of 3 mM, pH 7.4, and a phosphate concentration that varies from 0.8 to 48 mM, depending on parathyroid hormone and dietary phosphate. We conclude that conditions in the thin segment potentially could create a solid calcium phosphate phase, which may initiate nucleation of calcium oxalate salts in the collecting ducts, potentiating nephrolithiasis and nephrocalcinosis.

Animals↗
PubMed1996

Normal calcium oxalate crystal growth inhibition in severe calcium oxalate nephrolithiasis.

Urine from mammalian kidneys is regularly supersaturated with respect to calcium oxalate monohydrate, the most common solid phase in human nephrolithiasis, and also inhibits the nucleation, growth, and aggregation of calcium oxalate crystals. Nephrolithiasis is often associated with increased supersaturation, and it is assumed that this increase overbalances the inhibition effects, causing stones. However, some patients form stones in the absence of increased supersaturation, and in those patients, one might assume that reduced inhibition is the cause of their stones. This hypothesis was tested in 25 patients who formed at least ten stones each, yet lacked the usual metabolic abnormalities that increase supersaturation. Compared with 25 age- and sex-matched control subjects, urine supersaturation among the patients was not increased; this is an expected result of this study's selection criteria. Compared with the same age- and sex-matched control subjects, urine from the patients showed no evidence for reduced inhibition of calcium oxalate crystal growth, so low inhibition of growth did not contribute to pathogenesis of stones in our highly selected study population, despite their otherwise unexplained and active stone formation. These results do not support the hypothesis that growth inhibition defects are a cause of stone disease.

Calcium Oxalate↗
PubMed1996

Uric acid stones.

Uric acid is the end product of purine degradation in humans. It is a weak acid with a pK of 5.35 in urine. In acidic urine the undissociated form of uric acid predominates and is poorly soluble, leading to crystalluria and stone formation. Uric acid stones account for 5% to 10% of all stones in the United States. Acidic urine, hyperuricosuria, and low urine volume are the risk factors for uric acid stone formation. Uric acid stones may be idiopathic or secondary to a systemic disease such as gout. Treatment includes alkalinization of the urine, high fluid intake, and reduction of uric acid excretion if it is abnormal.

Gout↗