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Drugs, accidents and poisoning
Published in Jagdish M. Gupta, John Beveridge, MCQs in Paediatrics, 2020
Jagdish M. Gupta, John Beveridge
15.7. Recognized side effects of phenytoin (Dilantin) administration includeataxia.hirsutism.hypertrophy of the gums.lymphadenopathy.renal papillary necrosis.
Haematological problems
Published in Catherine Nelson-Piercy, Handbook of Obstetric Medicine, 2020
SCD leads to: Anaemia; chronic haemolytic (not marked in women with HbSC disease).Painful vaso-occlusive crises.Infections. The increased risk of infections is partly due to loss of splenic function from auto-infarction.Acute chest syndrome. This is characterized by fever, tachypnoea, pleuritic chest pain, leukocytosis, worsening anaemia and pulmonary infiltrates. It may be caused by pulmonary infection or infarction from intravascular sickling or thrombosis.Splenic sequestration.Gallstones.Retinopathy.Leg ulcers.Aseptic necrosis of bone.Renal papillary necrosis.Stroke.Pulmonary hypertension.
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].
Ibuprofen-based advanced therapeutics: breaking the inflammatory link in cancer, neurodegeneration, and diseases
Published in Drug Metabolism Reviews, 2021
Arun Upadhyay, Ayeman Amanullah, Vibhuti Joshi, Rohan Dhiman, Vijay Kumar Prajapati, Krishna Mohan Poluri, Amit Mishra
Reportedly, increased use of selective inhibitors of COX-2 in the past few decades have led to an increased occurrence of coronary heart disease and myocardial infarction (Graham et al. 2005; Hippisley-Cox and Coupland 2005). Similarly, inhibition of the renal prostaglandins by excessive use of COX inhibitors is another area of significant concern regarding the use of these drugs that lead to the abnormal retention of ions and water molecules followed by destabilized blood pressure and formation of peripheral edema (Adams et al. 1986; Komers et al. 2001). It has been observed that functions of both the COX isoforms are crucial for the proper functioning of the kidneys; PGI2 is involved in potassium secretion, while PGE2 is implicated in suppressing sodium reabsorption (Harris 2002). Therefore, inhibition of prostaglandins caused due to diminished COX activities has been reported with deleterious consequences in elderly individuals or people with compromised health conditions (Brater 2002). The complications may include renal papillary necrosis, along with acute or chronic kidney disease (Bennett et al. 1996; Gooch et al. 2007; Winkelmayer et al. 2008). There are several other physiological complications that the NSAIDs may present, e.g. causing a delay in fracture healing response or exacerbating asthma, etc. (Szczeklik and Stevenson 2003; Wheeler and Batt 2005; Geusens et al. 2013).
Renal papillary necrosis, an endoscopic vision
Published in Scandinavian Journal of Urology, 2019
Jorge Panach-Navarrete, María Medina-González, Lorena Alarcón-Molero, Eduardo Sánchez-Cano, Francisco Pastor-Hernández, José María Martínez-Jabaloyas
Renal papillary necrosis is an infrequent pathology, which has been etiologically related to an infection of the renal pyramids associated with renal vasculopathy or obstruction of the upper urinary tract. Patients with diabetes, sickle cell anemia, chronic alcoholism and vascular disease are especially susceptible to this complication [2]. Even though tests such as urinary sediment (where papillary fragments can be observed) or culture (to check for the presence of infection) are important for the diagnosis, its basis will be made with imaging tests.