A nidus, crystalluria and aggregation: key ingredients for stone enlargement

Saw, N.K.; Rao, P. N.; Kavanagh, John P.

doi:10.1007/s00240-007-0121-5

Cited by 24 publications

(20 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Existing theories such as nucleation and supersaturation can only partly explain the formation of CaOx stones. However, both in vitro and animal studies have demonstrated that high levels of oxalate and/or calcium oxalate monohydrate (COM) is a major risk factor for the formation of stone nuclei [16][17][18]. In addition, previous studies indicated that renal tubular damage is tightly associated with the formation of kidney stones [2].…”

Section: Discussionmentioning

confidence: 98%

“…*P < 0.05 more accurate method to measure low concentrations of molecules in a minimal specimen volume [22]. Ox, a small dicarboxylate ion, is freely filtered at the glomerulus, and its active secretion by renal proximal tubule cells contributes to the overall urinary excretion of Ox [17]. Detecting Ox amounts in urine is a simple way to evaluate the Ox metabolism [18].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Renal tubular injury induced by ischemia promotes the formation of calcium oxalate crystals in rats with hyperoxaluria

et al. 2016

View full text Add to dashboard Cite

Hyperoxaluria and cell injury are key factors in urolithiasis. Oxalate metabolism may be altered by renal dysfunction and therefore, impact the deposition of calcium oxalate (CaOx) crystals. We investigated the relationship of renal function, oxalate metabolism and CaOx crystal deposition in renal ischemia. One hundred male Sprague-Dawley rats were randomly divided into four groups. Hyperoxaluria model (Group A and B) was established by feeding rats with 0.75 % ethylene glycol (EG). The left renal pedicle was clamped for 30 min to establish renal ischemia Groups (B and C), while Groups A and D underwent sham operation. Then, serum and urine oxalate (Ox), creatinine (Cr) and urea nitrogen (UN) levels were evaluated by liquid chromatography mass spectrometry (LCMS) and ion mass spectrum (IMS) at days 0, 2, 4, 7, and 14. CaOx crystallization was assessed by transmission electron microscope (TEM). A temporal and significant increase of serum Cr and UN levels was observed in Groups B and C compared to values obtained for Groups A and D (P < 0.05). Ox levels in serum and urine were significantly higher in Groups A and B than in the other two groups from day 7 (P < 0.05). In addition, CaOx crystallization was observed in both Groups A and B, but Group B showed earlier and more pronounced crystal deposition in the renal tissue. Our results indicated that renal tubular injury induced by renal ischemia might not affect Ox levels but could promote CaOx crystal retention under hyperoxaluria.

show abstract

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Renal tubular injury induced by ischemia promotes the formation of calcium oxalate crystals in rats with hyperoxaluria

et al. 2016

View full text Add to dashboard Cite

show abstract

“…The observed correlation between protein aggregate formation and CaOx crystal aggregation is likely to be critical to stone formation, because addition of preformed crystals to stone aggregates has been demonstrated repeatedly. [22–24] Since most urine proteins are anionic and demonstrate similar CaOx crystal interactions, stone formation will likely be driven by highly abundant rather than trace urinary proteins, or possibly the summation of contributions from many urine proteins in the mixture.…”

Section: Introductionmentioning

confidence: 99%

Stone former urine proteome demonstrates a cationic shift in protein distribution compared to normal

et al. 2017

View full text Add to dashboard Cite

Many urine proteins are found in calcium oxalate stones, yet decades of research have failed to define the role of urine proteins in stone formation. This urine proteomic study compares the relative amounts of abundant urine proteins between idiopathic calcium oxalate stone forming and non-stone forming (normal) cohorts to identify differences that might correlate with disease. Random mid-morning urine samples were collected following informed consent from 25 stone formers and 14 normal individuals. Proteins were isolated from urine using ultrafiltration. Urine proteomes for each sample were characterized using label-free spectral counting mass spectrometry, so that urine protein relative abundances could be compared between the two populations. A total of 407 unique proteins were identified with the 38 predominant proteins accounting for >82% of all sample spectral counts. The most highly abundant proteins were equivalent in stone formers and normals, though significant differences were observed in a few moderate abundance proteins (immunoglobulins, transferrin, and epidermal growth factor), accounting for 13% and 10% of the spectral counts respectively. These proteins contributed to a cationic shift in protein distribution in stone formers compared to normals (22% vs. 18%, p = 0.04). Our data showing only small differences in moderate abundance proteins suggest that no single protein controls stone formation. Observed increases in immunoglobulins and transferrin suggest increased inflammatory activity in stone formers, but cannot distinguish cause from effect in stone formation. The observed cationic shift in protein distribution would diminish protein charge stabilization, which could lead to protein aggregation and increased risk for crystal aggregation.

show abstract

“…However, for the transformation of kidney calcifications to a clinically symptomatic stone, further crystal apposition is necessary. It probably occurs during crystalluria by crystal aggregation (AGN) [4, 5]. Crystallization processes involved in stone formation are, apart from urinary supersaturation, essentially influenced by crystallization inhibitors like citrate and urinary macromolecules (UM), the latter comprising a large group of proteins and some glycosaminoglycans [6].…”

Section: Introductionmentioning

confidence: 99%

Crystal sedimentation and stone formation

Baumann¹,

Affolter²,

Meyer³

2009

Urol Res

View full text Add to dashboard Cite

Mechanisms of crystal collision being the first step of aggregation (AGN) were analyzed for calcium oxalate monohydrate (COM) directly produced in urine. COM was produced by oxalate titration in urine of seven healthy men, in solutions of urinary macromolecules and in buffered distilled water (control). Crystal formation and sedimentation were followed by a spectrophotometer and analyzed by scanning electron microscopy. Viscosity of urine was measured at 37°C. From results, sedimentation rate (vS), particle diffusion (D) and incidences of collision of particles in suspension by sedimentation (IS) and by diffusion (ID) were calculated. Calculations were related to average volume and urinary transit time of renal collecting ducts (CD) and of renal pelvis. vS was in urine 0.026 ± 0.012, in UMS 0.022 ± 0.01 and in control 0.091 ± 0.02 cm min−1 (mean ± SD). For urine, a D of 9.53 ± 0.97 μm within 1 min can be calculated. At maximal crystal concentration, IS was only 0.12 and ID was 0.48 min−1 cm−3 which, even at an unrealistic permanent and maximal crystalluria, would only correspond to less than one crystal collision/week/CD, whereas to the same tubular wall being in horizontal position 1.3 crystals/min and to a renal stone 624 crystals/cm2 min could drop by sedimentation. Sedimentation to renal tubular or pelvic wall, where crystals can accumulate and meet with a tissue calcification or a stone, is probably essential for stone formation. Since vS mainly depends on particle size, reducing urinary supersaturation and crystal growth by dietary oxalate restriction seems to be an important measure to prevent aggregation.

show abstract

A nidus, crystalluria and aggregation: key ingredients for stone enlargement

Cited by 24 publications

References 19 publications

Renal tubular injury induced by ischemia promotes the formation of calcium oxalate crystals in rats with hyperoxaluria

Renal tubular injury induced by ischemia promotes the formation of calcium oxalate crystals in rats with hyperoxaluria

Stone former urine proteome demonstrates a cationic shift in protein distribution compared to normal

Crystal sedimentation and stone formation

Contact Info

Product

Resources

About