Effects of non-steroidal anti-inflammatory drug treatment on the kidney

image of Effects of non-steroidal anti-inflammatory drug treatment on the kidney
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The population of animals that develop kidney disease are often elderly with multiple problems. It is not uncommon to have a clinical need to provide pain relief, often on a chronic basis, for dogs and cats with chronic kidney disease. This chapter provides information on pharmacology of NSAIDs; the role of COX enzyme products in normal kidney physiology; renal toxicity of NSAIDs; and benefit/harm assessment of the use of NSAIDs in patients with kidney disease.

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20.1 Arachidonic acid cascade from membrane phospholipids to intracellular effects of its metabolites (with particular focus on prostaglandin E). Enzyme actions are represented by a curved green arrow. The actions of enzyme inhibitors or receptor blockers are represented along the cascade by red arrows with flat ends. COX = cyclooxygenase; COXIB = COX-2 inhibitor; EP = G protein-coupled eicosanoid receptor; G, G, G = alpha-subunits of the G protein-coupled receptor; NSAIDs = non-steroidal anti-inflammatory drugs; PG = prostaglandin; PLC = phospholipase C; TX = thromboxane. (Reproduced from Nasrallah . 2014 with permission from the )
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20.4 Chemical formulae of non-steroidal anti-inflammatory drugs (NSAIDs) authorized for use in the UK. (a) Chemical formulae for arachidonic acid and traditional NSAIDs: aspirin (salicylate), ketoprofen/carprofen (aryl propionic acid family; (*) denotes the presence of an asymmetrical carbon), tolfenamic acid (fenamate family) and meloxicam (oxicam family). (b) Chemical formulae for COX-2 inhibitors (COXIBs) authorized for use in companion animals: firocoxib (methylsulphone family), mavacoxib/cimicoxib (sulphonamide family) and robenacoxib (carboxylic acid family).
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20.5 Integration of pharmacokinetic (PK) and pharmacodynamic (PD) data applied to the administration of an original dose of 0.3 mg/kg of meloxicam subcutaneously in the cat. (a) feline whole blood assays for meloxicam ( ). Cyclooxygenase inhibition potencies were 4.1 μM for IC COX-1 (1440 ng/ml) and 1.35 μM for IC COX-2 (474 ng/ml). From the graph, one can extrapolate to the IC COX-1 and IC COX-2. (b) Spectrum of NSAID selectivity based on the IC COX-1:COX-2 potency ratio. COX-1 selective compounds are on the left and COX-2 selective COXIBs are on the right. (c) Plasma concentration–time curve of meloxicam (0.3 mg/kg s.c.) in the cat ( ). The time during which plasma meloxicam remains above IC COX-1 and IC COX-2 can be visualized directly on the figure. IC = 50% inhibitory concentration; Tx = thromboxane.
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20.8 Flowchart summarizing the relationship between hypotension, renin–angiotensin–aldosterone system (RAAS) activation, cyclooxygenase (COX) dependency and renal injury mechanisms. GFR = glomerular filtration rate; MD = macula densa.
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20.9 Gross pathology of naproxen-mediated renal papillary necrosis in a dog. (Reproduced from with permission from )
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