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Published in Anton Sebastian, A Dictionary of the History of Medicine, 2018
Analgesic Nephropathy The association between prolonged analgesic use and chronic renal failure was pointed out by O. Spuhler and H.U. Zollinger of Germany in 1953. Phenacetin was the first drug to be incriminated in this.
Practice Paper 6: Answers
Published in Anthony B. Starr, Hiruni Jayasena, David Capewell, Saran Shantikumar, Get ahead! Medicine, 2016
Anthony B. Starr, Hiruni Jayasena, David Capewell
Diclofenac is a strong non-steroidal anti-inflammatory drug (NSAID) that is usually prescribed for muscular injury and renal colic. NSAIDs inhibit the production of prostaglandins, which are essential in maintaining renal perfusion. NSAIDs are therefore nephrotoxic and should be avoided in patients with known renal disease and in those at risk of renal disease, e.g. elderly people. Long-term use of NSAIDs may lead to analgesic nephropathy and chronic renal failure.
Why paracetamol (acetaminophen) is a suitable first choice for treating mild to moderate acute pain in adults with liver, kidney or cardiovascular disease, gastrointestinal disorders, asthma, or who are older
Published in Current Medical Research and Opinion, 2022
John Alchin, Arti Dhar, Kamran Siddiqui, Paul J. Christo
There has been speculation that paracetamol may be associated with renal impairment87,88. Historically, realization that classic analgesic nephropathy was caused by phenacetin overuse raised concerns that paracetamol, its primary metabolite, might have similar injurious renal effects88,89; however, this hypothesis has been dismissed88–91. Although acute nephrotoxicity has been documented in rodents given paracetamol doses of ≥500 mg/kg and following overdoses in a few clinical cases87,90,91, there is no evidence that episodic use of paracetamol alone at recommended doses causes renal damage, nor that cumulative lifetime doses exacerbate advanced CKD83,87,88,90–92.
Nonsteroidal anti-inflammatory drugs in end-stage kidney disease: dangerous or underutilized?
Published in Expert Opinion on Pharmacotherapy, 2021
NSAID-related adverse kidney outcomes are similarly well documented. Inhibition of prostaglandin synthesis, particularly of prostaglandin E2 (PGE2) and PGI2, has the net effect of increased sodium reabsorption in the thick ascending loop of Henle and decreased potassium secretion in the distal tubule leading to hyperkalemia and a Type IV renal tubular acidosis [36–38]. Increased sodium and water retention, in turn, is thought to contribute to mild worsening of blood pressure control and decreased response to antihypertensive agents, particularly loop diuretics [36,39]. Acute kidney injury (AKI) is a common complication of NSAID therapy as well, with NSAID-associated AKI accounting for up to 15.5% of all cases of drug-related kidney failure [40,41]. PGI2 is essential in maintaining adequate kidney perfusion in patients with other preexisting health conditions that predispose to decreased actual or effective circulating volume [36]. NSAID use in these individuals may increase the risk of ischemia and acute tubular necrosis. Long-term consumption of NSAIDs is also known to cause analgesic nephropathy, the hallmarks of which are renal papillary necrosis and chronic kidney dysfunction [36,42]. Finally, two rare complications of NSAID therapy are interstitial nephritis and minimal change disease [36,43,44]. While the mechanism of this association is currently unknown, it is hypothesized that COX inhibition shunts arachidonic acid down alternate metabolic pathways to produce pro-inflammatory prostanoids [36].
Effect of hemodialysis on platelet function in end-stage renal disease Egyptian patients using in vitro closure time test (PFA-100 analyzer)
Published in Platelets, 2015
Mohamed A. Mekawy, Deena M. M. Habashy, Waleed A. M. Abd El-Mohsen
This study was carried on 40 patients who were attending Ain Shams University Hospitals after being diagnosed as ESRD undergoing regular hemodialysis. All patients were in the stable phase of disease. The patients were 28 (70%) males and 12 (30%) females, their ages ranged from 20 to 60 years with a mean ± standard deviation (SD) of 39.75 ± 9.89. The duration of the patients’ illness ranged from 1 to 10 years with a mean ± SD of 4.40 ± 2.33. The patient group included: 14/40 (35%) hypertensive patients; 10/40 (25%) diabetic patients; 2/40 (5%) analgesic nephropathy patient; 4/40 (10%) chronic glomerulonephritis patients and 10/40 (25%) renal failure of unknown cause.