Immunohistochemical distribution and quantification of crystal matrix protein

Stapleton, Andrew J.; Seymour, A. E.; Brennan, James S.; Doyle, Ian; Marshall, Villis R.; Ryall, Rosemary L.

doi:10.1038/ki.1993.316

Cited by 44 publications

(45 citation statements)

References 36 publications

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“…Although this would suggest that, on a microglobulin. This is reinforced by immunohistochemical studies demonstrating that urinary PTF1 is present in the most molar basis, the inhibitory potency of PTF1 is almost eightfold that of nephrocalcin and more than double that of bikunin, it is lithogenic regions of the human nephron [40].…”

Section: With Itsmentioning

confidence: 73%

Inhibition of growth and aggregation of calcium oxalate crystals in vitro

Grover

Moritz

Simpson

et al. 1998

European Journal of Biochemistry

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The aim of this study was to compare directly, in the absence of interfering contaminants, the inhibitory effects of Tamm-Horsfall glycoprotein (THG), human serum albumin (HSA), A 1 -microglobulin and prothrombin fragment 1 (PTF1) on calcium oxalate crystallization. These proteins have been detected in urinary calculi, and with the exception of THG in calcium oxalate crystals generated from undiluted human urine. THG was isolated from the urine of healthy men, while PTF1 was purified from Prothrombinex-HT, a human blood concentrate; HSA and A 1-microglobulin were obtained from commercial sources. The effects of these proteins were determined, separately, at the same final concentration (32 nM) on calcium oxalate crystallization in a seeded, inorganic reaction system, using Coulter Counter and [ 14 C]oxalate analysis. Analysis of [ 14 C]oxalate data showed that THG, HSA and A1-microglobulin had no measurable effect on deposition of calcium oxalate. However, PTF1 significantly inhibited mineral deposition by 19.6 %. The average size of the particles precipitated was reduced from the control value of 8.6 µm to 7.3, 5.9, 5.6 and 4.0 µm in the presence of A 1-microglobulin, HSA, THG and PTF1 respectively. These findings were confirmed by scanning electron microscopy, which also revealed that the smaller particles deposited in the presence of the proteins resulted from reduced crystal aggregation rather than a decrease in the size of the individual crystals. It was concluded that, on a molar basis, PTF1 is a more potent inhibitor of calcium oxalate crystal aggregation than THG, HSA and A 1 -microglobulin. Moreover, unlike those proteins it significantly inhibits the deposition of calcium oxalate. These findings have implications for the putative role of urinary proteins in the formation of calcium oxalate stones.Keywords : urolithiasis; calcium oxalate crystals ; Tamm-Horsfall glycoprotein ; human serum albumin ; A 1 -microglobulin.Two factors can be considered largely responsible for the have been fortuitous, or may have resulted from the injurious effects of the stone itself. For instance, haemoglobin is almost current interest in the role of proteins in the pathogenesis of urinary stones, namely the predominance of proteins in the or-certainly the product of the haematuria that almost inevitably accompanies the presence of a stone in the urinary tract. ganic matrix of calculi and the availability of technology enabling their isolation, purification and identification. Proteins deOne approach to identify possible functions for proteins in stone formation is to test their individual effects on calcium oxatected in calcium oxalate stones include Tamm-Horsfall glycoprotein (THG), albumin, A and γ-globulins, haemoglobin, neu-late crystallization, but this has been attempted for relatively few stone proteins. Probably the major reason for this is the trophil elastase, transferrin, A 1-microglobulin, CD59 protein (protectin), superoxide dismutase, A 1 -antitrypsin, uropontin (os-requirement of the experimental systems emp...

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Section: With Itsmentioning

confidence: 73%

Inhibition of growth and aggregation of calcium oxalate crystals in vitro

Grover

Moritz

Simpson

et al. 1998

European Journal of Biochemistry

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“…Verkoelen and coworkers reported on nephrolithasisrelated proteins being synthesized in the kidney [30,31] . These proteins are also known for their role in wound healing [32,33] .…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Urolithiasis: A Link between Stone Formation and Diabetes Mellitus?

Zimmerer¹,

Weiß²,

Hammes³

et al. 2009

Urol Int

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Introduction: The pathogenesis of calcium oxalate stone formation is not completely understood. Recently, an influence of vascular phenomena like arteriosclerosis on the crystallization process was hypothesized. Thus, stone formation should be more common in patients with diabetes mellitus (DM) who are at risk of developing angiopathy. The aim of the study was to determine the prevalence of urolithiasis (UL) in patients with DM and to identify specific risk factors. Material and Methods: 350 patients with DM were evaluated with respect to DM-related history, and a total of 179 patients was included (83 female, 96 male; age 23–84 years). All patients were interviewed to assess the history of stone formation. These data were compared to epidemiological data in Germany. Results: The overall prevalence of UL in the diabetic group was 7.82% (vs. 4.73% in Germany, p = 0.0485; binominal test). The prevalence was significantly higher in patients with coronary heart disease (25%; p < 0.0001; Fisher‘s exact test). We could not demonstrate an increased prevalence of UL for patients with occlusive arterial disease or arterial hypertension as diabetic nephropathy was not a risk factor for developing urinary lithiasis (p = 0.7184, p = 1.000, p = 0.6266, respectively; Fisher’s exact test). Thiazide medication lowered the prevalence of stone formation (p = 0.0399; Fisher’s test). Calcium or magnesium supplementation did not influence stone formation significantly (p = 0.5279; p = 1.000; respectively; Fisher’s test). Conclusions: In Germany, patients with DM are at higher risk of UL compared with patients without diabetes. We demonstrated a significantly higher prevalence of urinary stones in patients with coronary heart disease. These findings are consistent with the hypothesis that urinary stone formation has a vascular pathogenesis in part.

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“…HMM forms (Ͼ40 kDa) are likely to be other PF1-containing activation peptides of prothrombin, primarily prothrombin fragment 1ϩ2, with a molecular mass of 43 kDa (40). Immunohistochemical analysis of human kidneys has shown that PF1 is synthesized in the proximity of renal stones and is more abundant in the kidneys of SF than in healthy individuals (41). However, to date no differences have been found in the relative amounts of any prothrombin forms in the urine of CaOx SF vs. normal controls (14).…”

Section: Discussionmentioning

confidence: 99%

Urine protein markers distinguish stone-forming from non-stone-forming relatives of calcium stone formers

Bergsland

Kelly²,

Coe³

et al. 2006

American Journal of Physiology-Renal Physiology

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We have investigated urine protein inhibitors of calcium oxalate crystallization to determine whether variations in these proteins are associated with kidney stone disease and whether protein measurements improve the identification of stone formers compared with conventional risk factors (RF). Using Western blotting, we studied variations in the electrophoretic mobility patterns and relative abundances of crystallization-inhibitory proteins in urine from 50 stone-forming (SF) and 50 non-stone-forming (NS) first-degree relatives of calcium SF patients, matched by gender and age. Standard urine chemistry stone risk measurements were also made. Multivariate discriminant analysis was used to test the association of these proteins with nephrolithiasis. Differences in form and abundance of several urine proteins including inter-␣-trypsin inhibitor (ITI), prothrombin fragment 1 (PF1), CD59, and calgranulin B (calB) were found to be associated with stone formation. By multivariate discriminant analysis, measurements of forms of PF1, ITI, and calB in men and ITI and CD59 in women, classified 84% of men and 76% of women correctly by stone status. In contrast, standard urine chemistry RF identified only 70% of men correctly and failed to distinguish female SF from NS. Thus a small subset of protein measurements distinguished SF from NS far better than conventional RF in a population of relatives of calcium SF,

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Immunohistochemical distribution and quantification of crystal matrix protein

Cited by 44 publications

References 36 publications

Inhibition of growth and aggregation of calcium oxalate crystals in vitro

Inhibition of growth and aggregation of calcium oxalate crystals in vitro

Evaluation of Urolithiasis: A Link between Stone Formation and Diabetes Mellitus?

Urine protein markers distinguish stone-forming from non-stone-forming relatives of calcium stone formers

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