• Shivani Megh Pal
• Seemha Rai

Hyperoxaluria leads to extensive damage to the tubules and causes renal inflammation and fibrosis; and it further advances to nephrolithiasis, nephrocalcinosis as well as renal parenchymal disease. Oxalate synthesis takes place in liver and there is no further metabolism of oxalate in humans. A significant share of oxalate load is caused by metabolism of ingested oxalate precursors. The exposure of renal epithelial cells to oxalate causes ROS generation which is predominantly responsible for renal epithelial cell injury. The injury to the kidney tissue paves the way for crystal nucleation, aggregation and consequently stone deposition in the renal tissue. CST, by virtue of its oxalate binding property, decreased oxalate burden to the renal cells leading to amelioration of renal injury and improvement in renal function. Moreover, the role of CST in minimizing hyperoxaluria induced liver injury was established by a decline in the activities of enzymes SGOT, SGPT and GGT, which were otherwise enhanced by EG and ammonium chloride administration. Our study confirms that in hyperoxaluric animals, CST treatment reduced renal injury and nephrocalcinosis, improved renal function, in renal tissue.

Hyperoxaluria; Cholestyramine; Calcium oxalate; Oxidative stress

"Cholestyramine reduces oxalate mediated renal injury and its manifestations in hyperoxaluric rats.", International Journal of Emerging Technologies and Innovative Research (www.jetir.org), ISSN:2349-5162, Vol.6, Issue 4, page no.912-925, April-2019, Available :http://www.jetir.org/papers/JETIR1904V81.pdf

"Cholestyramine reduces oxalate mediated renal injury and its manifestations in hyperoxaluric rats.", International Journal of Emerging Technologies and Innovative Research (www.jetir.org | UGC and issn Approved), ISSN:2349-5162, Vol.6, Issue 4, page no. pp912-925, April-2019, Available at : http://www.jetir.org/papers/JETIR1904V81.pdf