Impact Of Renal Ischemia On Formation Of Calcium Oxalate Stone In Rat

Objective:To investigate the impact and the mechanism of renal ischemia on formation of calcium oxalate stone in rat.Methods:100male wistar rats were randomly divided into4groups (25each group), group A and group B were given0.75%ethylene glycol to induce the renal calcium oxalate stone. Group C and group D were given ordinary water.5in each group fed for2,4,7,14,21days. After given0.75%ethylene glycol to group A and group B for1day, group A and group C were clamped their left renal artery for30minute by blood vessel clip, and cut off the right kidney. Dissociated the left kidney in group B and group D and cut off the right side. Some of each group were collected24h urine samples by the metabolic cage on days2,4,7,14and21. Blood samples were collected by heart puncture and then cut off the left kidney. Examine the blood biochemistry. Use automatic biochemical analyzer to determine the urinalysis biochemistry of rat. And High Performance Liquid Chromatography to detect the the content of oxalic acid, calcium in urine samples. Hematoxylin-eosinn staining and Von-Kossa’s staining to observe the quantity and the location of renal calcium oxalate crystal.Results:(1) At2d and4d, the BUN and Cr values in blood samples:group A was significantly higher than group B (P<0.05) and group D (P<0.05); group C was singnificantly higher than group B (P<0.05) and group D.But there was no significant difference between group A and group C, and also between group B and group D.(2) The calcium and oxalic acid values in urine samples:group A was significantly higher than group C (P<0.05) and group D (P<0.05); group B was singnificantly higher than group C (P<0.05) and group D. But there was no significant difference between group A and group B, and also between group C and group D.(3) Group A:On the days4, we can see the focal inflammatory response and calcification within the kidney by microscope. Within one week the kidney shows a gradual increase crystalline deposition in interstitial and tubular basement. When the two weeks, we can see a large number calcification and crystal deposition within the tubular. Group B:No significant calcium deposition in the kidney within7days. After two weeks, tubular epithelial calcification can be seen. Group C:The glomerular is normal, and the tubular epithelial cell swelling, partial necrosis, neutrophil infiltration seen in the tubular, no calcification, crystal deposition. Chronic inflammatory cells can be seen in stroma, no calcification. Group D:The rat renal cartex and medulla are normal, the cell arranged in neat rows, no inflammatory response, calcification and calulus deposition within the tubular and the interstitial cells. Renal tubular epithelial cells without edema.Conclusion: (1) At the early stage of renal ischemia, there was significant difference in renal funcation between ligation groups and non-ligation groups. That indicate renal ischemia for30minutes can lead to renal insufficiency.(2) There was no significant difference in the content of oxalic acid and calcium in urine between ligation groups and non-ligation groups. That indicate renal vascular factors does not effect the calcium oxalate metabolism.(3) In the high oxalic acid concentration, renal ischemia caused the hypoxia and hypercapnia injure the renal tubular epithelial cell and interstitial cells in rat. That promoted the early calcium oxalate crystal adhesion and deposition in the kidney and the renal calcium oxalate stone formation. And stone formation earlier than in the high oxalic acid concentration only.(4) In the normal oxalic acid concentration, renal ischemia does not effect the calcium oxalate stones formation in rat.(5) The renal calcium oxalate stone formation is more than one factor involved in the complex process. Oxalic acid, calcium and renal vascular factors are likely to play an important role in the process.