Safe and appropriate use of diclofenac in chronic kidney disease

Abstract

Pain is most common symptom associated with progressive disorder, chronic kidney disease (CKD), and is usually undertreated during the early stages of CKD. So, present review was conducted to evaluate the challenges for the management of pain in CKD patients and addresses the scope for considering Diclofenac as suitable alternative for pain management in CKD patient. The database PubMed and Google Scholar were searched from 1970 to Dec 2020 for literature published in English and all studies, review articles that examined the use of Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) in pain management in CKD patients were included. Literatures revealed that there is a considerable challenge in appropriate management of pain in CKD patients include understanding the altered pharmacokinetics and pharmacodynamics of analgesics in CKD patients and the risk of acute interstitial nephritis. The shorter duration of analgesics is acceptable and considered to pose a low risk of acute interstitial nephritis in patients. Considering that Diclofenac has a shorter half-life and high efficacy, it may be well tolerated in patients with CKD. The acceptance of Diclofenac is partly attributed to being a potent COX-2 inhibitor with the lowest IC50 and its rapid onset of action at lowest effective dose. In conclusion, diclofenac may be well tolerated in patients of renal impairment when used at lowest effective dose for shortest dose duration. Diclofenac is worthy of consideration in mild to moderate cases of CKD. For effective pain management, it is vital to evaluate the tolerability and efficacy of the available analgesics critically.

Histopathological effects on kidney of diclofenac potassium and diazepam used in an experimental epilepsy model

“…The notable acceptance of diclofenac can be attributed to being a potent COX-2 inhibitor while maintaining similar activity to some other popular non-selective NSAIDs. Tests have shown that diclofenac inhibits COX-2 enzyme with higher potency than COX-1 [14]. Since specific and robust expressions of KCNQ2/3 channels in neurons and loss of function can lead to neuronal hyperexcitability, pharmacological activation of KCNQ2/3 channels is the basis of epilepsy and pain treatment [32].…”

“…Common mode of action for all NSAIDs is the inhibition of COX enzymes resulting in reduced prostanoid synthesis [13]. Diclofenac potassium is a compound with non-steroid anti-inflammatory, analgesic and antipyretic effects [14]. It is a benzene acetic acid derivative showing COX-2 enzyme inhibition.…”

“…Chemical name for diclofenac potassium is 2-[(2,6dichlorophenyl)amino]-benzene acetic acid [15]. It has a quick elimination rate and a two-hour biological half-life [14]. In this study, we aimed to investigate the histopathological effects of diclofenac potassium and diazepam on the kidneys in an experimental epilepsy model with penicillin in rats.…”

Prevention, diagnosis, and treatment of urolithiasis in geriatric patients - differences, similarities and caveats in comparison to the general population

“…Even though the prudent use of short plasma half-life NSAIDs may be taken into consideration, regular renal function monitoring is crucial. This is especially necessary if dialysis was not necessary prior to treatment [24][25][26]. Apart from renal considerations, diclofenac and ibuprofen increase the risk of severe coronary events.…”

Prevalence of Periodontal Tissue Diseases in Patients With Chronic Kidney Disease

“…Chronic kidney disease is a large group of diseases that have different causes but are united by the fact that they have a long course and a tendency to progress until complete loss of kidney function [5,6]. In renal pathology, one of the pathogenetic chains is associated with impaired calcium (hypo-or hypercalcaemia) and phosphorus (hyperphosphatemia) metabolism [7]. A deficiency of active vitamin D and impaired parathyroid hormone secretion (secondary or tertiary hyperparathyroidism) lead to bone metabolism disorders (renal osteodystrophy) and calcification of blood vessels and other soft tissues, accompanied by progressive bone structure disorders due to too fast (caused by hyperparathyroidism) or too slow (socalled adynamic bone disease) bone metabolism.…”