★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★★Open research. Global perspectives.
Featured OPEN ACCESS

EXPLORING RENAL HEALTH: HISTOPATHOLOGY AND BIOCHEMICAL ANALYSIS IN RATS WITH UNILATERAL URETERAL OBSTRUCTION

Nofan Arifianto
Department of Clinical Pathology Faculty of Veterinary Medicine Universitas Gadjah Mada, Indonesia
tajvswd 2023
VOL. 5 / NO. 05 SEPTEMBER
VOLUME 5
ISSUE 05
YEAR 2023
PAGES 11-16

Abstract

This study investigates renal health in a rat model of unilateral ureteral obstruction (UUO) by assessing renal histopathology and analyzing blood urea nitrogen (BUN) and creatinine levels. UUO is a well-established model for studying obstructive nephropathy and provides insights into renal function and structural changes. Rats with surgically induced UUO were compared to control rats. Renal histopathology revealed significant alterations, including interstitial fibrosis and tubular damage, in the UUO group. Biochemical analysis showed a marked increase in BUN and creatinine levels, indicating impaired renal function. These findings underscore the importance of UUO as a model for renal research and highlight the utility of histopathological and biochemical assessments in understanding renal health.

Keywords

Renal histopathology Unilateral ureteral obstruction (UUO) Renal health

Downloads

Download data is not yet available.

References

  1. Chevalier, R. L. (2006). Obstructive nephropathy: towards biomarker discovery and gene therapy. Nature Clinical Practice Nephrology, 2(3), 157-168.
  2. Eddy, A. A. (1996). Molecular insights into renal interstitial fibrosis. Journal of the American Society of Nephrology, 7(12), 2495-2508.
  3. Zager, R. A., Johnson, A. C., & Becker, K. (2005). Renal cortical pyruvate depletion during AKI. Journal of the American Society of Nephrology, 16(7), 1756-1766.
  4. Thomson, S. C., Deng, A., Bao, D., Satriano, J., Blantz, R. C., & Vallon, V. (2001). Ornithine decarboxylase, kidney size, and the tubular hypothesis of glomerular hyperfiltration in experimental diabetes. Journal of Clinical Investigation, 107(2), 217-224.
  5. Vallon, V., Wyatt, A. W., Klingel, K., Huang, D. Y., Hussain, B., Berchtold, S., & Thomson, S. C. (2002). SGK1-dependent cardiac CTGF formation and fibrosis following DOCA treatment. Journal of Molecular Medicine, 80(3), 103-114.
  6. Liu, Y. (2011). Cellular and molecular mechanisms of renal fibrosis. Nature Reviews Nephrology, 7(12), 684-696.
  7. Lameire, N., Van Biesen, W., & Vanholder, R. (2005). Acute renal failure. The Lancet, 365(9457), 417-430.
  8. Huo, W., Zhang, K., Nie, Z., Li, Q., Jin, F., & Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. (2019). KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney International Supplements, 2(1), 1-63.
  9. Bonventre, J. V., & Yang, L. (2011). Cellular pathophysiology of ischemic acute kidney injury. Journal of Clinical Investigation, 121(11), 4210-4221.
  10. Nath, K. A. (1992). Tubulointerstitial changes as a major determinant in the progression of renal damage. American Journal of Kidney Diseases, 20(1), 1-17.
DISCOVER RELATED RESEARCH

Similar Articles

Explore published articles on related topics and research interests.