Renal Physiology of the Prostaglandins and the Effects of Nonsteroidal Anti-Inflammatory Agents on the Kidney

Hart, Denise; Lifschitz, Meyer D.

doi:10.1159/000167510

Cited by 33 publications

(4 citation statements)

References 43 publications

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“…Conversely, PGl 2 and PGE 1 have the effect of relaxing blood vessels and preventing hypoxia-mediated renal tissue damage. More importantly, in the case of renal artery stenosis, PGl 2 and PGE 1 selectively prevent tissue contraction and inhibit the decline of GFR [87,88].…”

Section: Mechanism Of Aa-induced Renal Inflammationmentioning

confidence: 99%

Arachidonic Acid Metabolism and Kidney Inflammation

Wang

Chen

et al. 2019

IJMS

248

171

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As a major component of cell membrane lipids, Arachidonic acid (AA), being a major component of the cell membrane lipid content, is mainly metabolized by three kinds of enzymes: cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome P450 (CYP450) enzymes. Based on these three metabolic pathways, AA could be converted into various metabolites that trigger different inflammatory responses. In the kidney, prostaglandins (PG), thromboxane (Tx), leukotrienes (LTs) and hydroxyeicosatetraenoic acids (HETEs) are the major metabolites generated from AA. An increased level of prostaglandins (PGs), TxA2 and leukotriene B4 (LTB4) results in inflammatory damage to the kidney. Moreover, the LTB4-leukotriene B4 receptor 1 (BLT1) axis participates in the acute kidney injury via mediating the recruitment of renal neutrophils. In addition, AA can regulate renal ion transport through 19-hydroxystilbenetetraenoic acid (19-HETE) and 20-HETE, both of which are produced by cytochrome P450 monooxygenase. Epoxyeicosatrienoic acids (EETs) generated by the CYP450 enzyme also plays a paramount role in the kidney damage during the inflammation process. For example, 14 and 15-EET mitigated ischemia/reperfusion-caused renal tubular epithelial cell damage. Many drug candidates that target the AA metabolism pathways are being developed to treat kidney inflammation. These observations support an extraordinary interest in a wide range of studies on drug interventions aiming to control AA metabolism and kidney inflammation.

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Section: Mechanism Of Aa-induced Renal Inflammationmentioning

confidence: 99%

Arachidonic Acid Metabolism and Kidney Inflammation

Wang

Chen

et al. 2019

IJMS

248

171

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“…7 PGE 2 also acts directly on renal tubules to increase excretion of Na and water and stimulates renin secretion from the macula densa. 8 Therefore, another potential adverse effect of NSAID administration and decreased renal PG production can be Na and water retention leading to edema.…”

Section: Renal Hemodynamicsmentioning

confidence: 99%

The Renal Effects of NSAIDs in Dogs

Lomas

Grauer

2015

Journal of the American Animal Hospital Association

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The quality of life for dogs with osteoarthritis can often be improved with nonsteroidal anti-inflammatory drugs (NSAIDs); however, the number of adverse drug events associated with NSAID use reported to the Federal Drug Administration Center for Veterinary Medicine is higher than that for any other companion animal drug. Of those events, adverse renal reactions are the second most reported. NSAIDs produce pharmacologic effects via inhibition of cyclooxygenase (COX), which decreases production of prostanoids. Prostaglandins are synthesized by both the COX-1 and COX-2 enzymes in the healthy kidney and influence renal blood flow, glomerular filtration rate, renin release, and Na excretion. There are important species differences in the renal expression of COX-1 and COX-2. For example, dogs have higher basal levels of COX-2 expression in the kidney compared with humans. In addition, in dogs with chronic kidney disease, an increase in COX-2 expression occurs and synthesis of prostaglandins shifts to the COX-2 pathway. For those reasons, NSAIDs that target COX-2 may be expected to adversely affect renal function in dogs, especially dogs with chronic kidney disease. The purpose of this review was to evaluate the literature to report the renal effects of NSAIDs in dogs.

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“…If possible, given the patient's cardiopulmonary condition, a normal blood pressure should be achieved and main tained by application of oncotically effective macromole cules instead of catecholamine doses that exceed the renally protective dopamine dose [36,37], This concept does not promote a shift of volume from the intravascular to the interstitial compartment. Application of nonsteroi dal anti-inflammatory drugs (NSAIDs) should be avoided [21,38], as they nonselectively block vasoconstricting and vasodilating prostaglandins.…”

Section: Loss Of Renal Functionmentioning

confidence: 99%