Short-term Administration of Diclofenac Sodium Affects Renal Function After Laparoscopic Radical Nephrectomy in Elderly Patients

Abstract

Objective: Non-steroidal anti-inflammatory drugs decrease the glomerular filtration rate. However, few studies have been conducted on renal function in patients treated with nonsteroidal anti-inflammatory drugs during the first week after laparoscopic radical nephrectomy. The purpose of this study is to determine whether short-term administration of non-steroidal anti-inflammatory drugs during the first week after laparoscopic radical nephrectomy is a risk factor for impaired renal function. Methods: Renal carcinoma patients undergoing laparoscopic radical nephrectomy in Nagoya University Hospital from April 2004 to July 2010 were identified in a retrospective cohort study. The 164 patients were divided into non-non-steroidal anti-inflammatory drug-treated (n ¼ 50) and non-steroidal anti-inflammatory drug-treated (n ¼ 114) groups. Results: Elderly patients (.60 years old) in the non-steroidal anti-inflammatory drug-treated group showed a significant correlation between the residual renal function ratio and the total dose of diclofenac sodium (r ¼ 20.277, P , 0.05). There was no significant correlation between the residual renal function ratio and the total dose of loxoprofen sodium. The time to doubling of the serum creatinine level was significantly shorter in elderly patients treated with diclofenac sodium compared with that in patients treated with non-non-steroidal anti-inflammatory drugs (P ¼ 0.034). These results suggest that renal ischemia induced by short-term administration of diclofenac sodium impairs renal function in elderly patients after laparoscopic radical nephrectomy. Conclusions: In the present study, we found the first evidence that short-term administration of diclofenac sodium is one risk factor for renal impairment after laparoscopic radical nephrectomy in elderly patients. To prevent renal impairment after laparoscopic radical nephrectomy in elderly patients, the use of loxoprofen sodium, which has a negligible effect on renal function compared with diclofenac sodium, is recommended.

Diclofenac induced-acute kidney injury is linked with oxidative stress and pro-inflammatory changes in Sprague Dawley rats

“…raising in the renal biomarkers. The induced AKI in this study as well showed significant reduction in the estimated GFR which was due to the development of acute tubular necrosis and glomerular damage since; Tomohiro et al, 34 exposed that short-term administration of diclofenac leads to proximal renal tubular damage and significant glomerular damage due to potential inhibition of renal prostaglandins which per se reduce renal blood flow and causing renal ischemia. BMI of the experimental rats was higher compared with the control group this might due to daily body weight gain or fluid retention which caused by renal damage.…”

Protective effect of curcumin on the kidney of diclofenac sodium-challenged mice: apoptotic, redox potential and histopathological outcomes

“…Taken into account the plenty of polyunsaturated fatty acids in renal tissues, DS specifically invades the renal microenvironment to induce oxidative and nitrosative stress compromising the renal cytological patterns, blood flow in addition to glomerular capillary ultrafiltration coefficient (Aycan et al, 2018;Garcia-Cohen et al, 2000;Kubo et al, 1997). The renal microvasculature is constricted and perfusion is impaired owing to the ability of DS to suppress generation of vasodilator prostaglandins in the kidneys (Mizuno et al, 2012). This pathological condition promotes renal tubular damage and impairs regenerative ability, which is the leading cause of renal interstitial fibrosis (Wang et al, 2012).…”

Synergistic effect of berberine and pentoxifylline in attenuation of acute kidney injury

“…Our findings illustrated that induced AKI was associated with a significant reduction in the eGFR due to the development of acute tubular necrosis and glomerular damage since; high dose of diclofenac leads to AKI due to inhibition of renal prostaglandins. [17]…”