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Calcium oxalate crystal localization and osteopontin immunostaining in genetic hypercalciuric stone-forming rats.
Kidney Int. 2004 Jan; 65(1):154-61.KI

Abstract

BACKGROUND

The inbred genetic hypercalciuric stone-forming (GHS) rats develop calcium phosphate (apatite) stones when fed a normal 1.2% calcium diet. The addition of 1% hydroxyproline to this diet does not alter the type of stone formed, while rats fed this diet with 3% hydroxyproline form mixed apatite and calcium oxalate stones and those with 5% hydroxyproline added form only calcium oxalate stones. The present study was designed to determine the localization of stone formation and if this solid phase resulted in pathologic changes to the kidneys.

METHODS

GHS rats were fed 15 g of the standard diet or the diet supplemented with 1%, 3%, or 5% hydroxyproline for 18 weeks. A separate group of Sprague-Dawley rats (the parental strain of the GHS rats), fed the standard diet for a similar duration, served as an additional control. At 18 weeks, all kidneys were perfusion-fixed for structural analysis, detection of crystal deposits using the Yasue silver substitution method, and osteopontin immunostaining.

RESULTS

There were no crystal deposits found in the kidneys of Sprague-Dawley rats. Crystal deposits were found in the kidneys of all GHS rats and this Yasue-stained material was detected only in the urinary space. No crystal deposits were noted within the cortical or medullary segments of the nephron and there was no evidence for tubular damage in any group. The only pathologic changes occurred in 3% and 5% hydroxyproline groups with the 5% group showing the most severe changes. In these rats, which form only calcium oxalate stones, focal sites along the urothelial lining of the papilla and fornix of the urinary space demonstrated a proliferative response characterized by increased density of urothelial cells that surrounded the crystal deposits. At the fornix, some crystals were lodged within the interstitium, deep to the proliferative urothelium. There was increased osteopontin immunostaining in the proliferating urothelium.

CONCLUSION

Thus in the GHS rat, the initial stone formation occurred solely in the urinary space. Tubular damage was not observed with either apatite or calcium oxalate stones. The apatite stones do not appear to cause any pathological change while those rats forming calcium oxalate stones have a proliferative response of the urothelium, with increased osteopontin immunostaining, around the crystal deposits in the fornix.

Authors+Show Affiliations

Anatomy Department, Indiana University School of Medicine, Indianapolis, Indiana, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

14675046

Citation

Evan, Andrew P., et al. "Calcium Oxalate Crystal Localization and Osteopontin Immunostaining in Genetic Hypercalciuric Stone-forming Rats." Kidney International, vol. 65, no. 1, 2004, pp. 154-61.
Evan AP, Bledsoe SB, Smith SB, et al. Calcium oxalate crystal localization and osteopontin immunostaining in genetic hypercalciuric stone-forming rats. Kidney Int. 2004;65(1):154-61.
Evan, A. P., Bledsoe, S. B., Smith, S. B., & Bushinsky, D. A. (2004). Calcium oxalate crystal localization and osteopontin immunostaining in genetic hypercalciuric stone-forming rats. Kidney International, 65(1), 154-61.
Evan AP, et al. Calcium Oxalate Crystal Localization and Osteopontin Immunostaining in Genetic Hypercalciuric Stone-forming Rats. Kidney Int. 2004;65(1):154-61. PubMed PMID: 14675046.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Calcium oxalate crystal localization and osteopontin immunostaining in genetic hypercalciuric stone-forming rats. AU - Evan,Andrew P, AU - Bledsoe,Sharon B, AU - Smith,Susan B, AU - Bushinsky,David A, PY - 2003/12/17/pubmed PY - 2004/9/29/medline PY - 2003/12/17/entrez SP - 154 EP - 61 JF - Kidney international JO - Kidney Int. VL - 65 IS - 1 N2 - BACKGROUND: The inbred genetic hypercalciuric stone-forming (GHS) rats develop calcium phosphate (apatite) stones when fed a normal 1.2% calcium diet. The addition of 1% hydroxyproline to this diet does not alter the type of stone formed, while rats fed this diet with 3% hydroxyproline form mixed apatite and calcium oxalate stones and those with 5% hydroxyproline added form only calcium oxalate stones. The present study was designed to determine the localization of stone formation and if this solid phase resulted in pathologic changes to the kidneys. METHODS: GHS rats were fed 15 g of the standard diet or the diet supplemented with 1%, 3%, or 5% hydroxyproline for 18 weeks. A separate group of Sprague-Dawley rats (the parental strain of the GHS rats), fed the standard diet for a similar duration, served as an additional control. At 18 weeks, all kidneys were perfusion-fixed for structural analysis, detection of crystal deposits using the Yasue silver substitution method, and osteopontin immunostaining. RESULTS: There were no crystal deposits found in the kidneys of Sprague-Dawley rats. Crystal deposits were found in the kidneys of all GHS rats and this Yasue-stained material was detected only in the urinary space. No crystal deposits were noted within the cortical or medullary segments of the nephron and there was no evidence for tubular damage in any group. The only pathologic changes occurred in 3% and 5% hydroxyproline groups with the 5% group showing the most severe changes. In these rats, which form only calcium oxalate stones, focal sites along the urothelial lining of the papilla and fornix of the urinary space demonstrated a proliferative response characterized by increased density of urothelial cells that surrounded the crystal deposits. At the fornix, some crystals were lodged within the interstitium, deep to the proliferative urothelium. There was increased osteopontin immunostaining in the proliferating urothelium. CONCLUSION: Thus in the GHS rat, the initial stone formation occurred solely in the urinary space. Tubular damage was not observed with either apatite or calcium oxalate stones. The apatite stones do not appear to cause any pathological change while those rats forming calcium oxalate stones have a proliferative response of the urothelium, with increased osteopontin immunostaining, around the crystal deposits in the fornix. SN - 0085-2538 UR - https://www.unboundmedicine.com/medline/citation/14675046/Calcium_oxalate_crystal_localization_and_osteopontin_immunostaining_in_genetic_hypercalciuric_stone_forming_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0085-2538(15)49686-3 DB - PRIME DP - Unbound Medicine ER -