Objective: Increased levels of Angiotensin II (Ang II) are responsible for the development of hypertension and diabetesinduced nephropathy. In addition, the preventability of renal fibrosis with Ang II blockade is a known entity. Although
mast cells are not present in normal kidney, increased mast cell density in the specimens examined for fibrosis has
attracted attention and it is thought that fibrotic agents released from these cells and may contribute to the process.
Therefore, an experimental study was planned to decrease the ang II levels with captopril, an angiotensin converting
enzyme (ACE) inhibitor and to prevent the development of renal scarring due to pyelonephritis using ketotifen, a mast
Material and Methods: Fifty rats were divided into five equal groups. In Group A, the renal cortex was injected with
SF. In Group B, acute pyelonephritis was induced by 107 E. coli injections into the renal cortex. Group C received
antibiotic treatment with E. coli injection, Group D received antibiotic and captopril with E. coli injection, Group E.
received antibiotic and ketotifen with E. coli injection. In order to represent the chronic process, rats were sacrificed after
6 weeks, and the contralateral kidney was included in pathological examination and statistical evaluation.
Results: Inflammatory scores were significantly higher in group B compared to group A (p = 0.001). Captopril or
ketotifen treatment were the only factors that reduced scar development (p = 0.007). However, when captopril or
ketotifen treatments were compared in preventing scar development, no superiority was found (p> 0.05).
Conclusion: We found that captopril and ketotifen has a protective effect in the development of renal fibrosis in a rat
model of acute pyelonephritis. We believe that our study may contribute to clinical trials in the prevention of renal scar