Non-steroidal anti-inflammatory drugs (NSAIDs) in at-risk patients with decreased renal function.

Non-steroidal anti-inflammatory drugs (NSAIDs) in at-risk patients with decreased renal function.

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Inhibition of renal prostaglandin synthesis by non-steroidal anti-inflammatory drugs (NSAIDs) causes various electrolyte and acid-base disturbances including sodium retention (edema, hypertension), hyponatremia, hyperkalemia, and decreased renal function. Decreased sodium excretion can result in weight gain, peripheral edema, attenuation of the eff...

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... a PG-dependent, complex, intrarenal short-loop feedback, as well as possible extrarenal mechanisms, may be involved in the renal regulation of water balance (Fig. 4) 21) . Removal of the inhibitory ef- fect of PGs on antidiuretic hormone (ADH) activity can diminish free water excretion 21) , of which cellular mechanisms is still unclear. The ensuing water reten- tion can promote the development of hyponatremia when there are high and relatively nonsuppressible levels of ADH due to syndrome of ...

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... Previous studies have shown that high doses of xenobiotic compounds, toxins or drugs could cause kidney damage, which may result in electrolytes imbalance (Al-Asmari et al., 2020;Rajakrishnan et al., 2017). The inhibition of renal prostaglandin synthesis by non-steroidal anti-inflammatory drugs (NSAIDs) causes various electrolyte and acid-base disturbances including sodium retention, hyponatremia (reduced blood sodium levels), hyperkalemia (elevated blood potassium levels), and decreased renal function (Kim & Joo, 2007). The marked decreases in the levels of sodium, chloride and bicarbonate ions, and marked increase in the level of potassium ions, by treatment of rats with DF may indicate disruption of electrolyte balance, which might be attributed to the adverse effects of this drug. ...
... Thus, when there is acute or chronic kidney damage, it may result in electrolyte imbalance, evident by alteration in the concentrations of electrolytes (sodium, potassium, chloride, and bicarbonate ions) in the blood of rats (Imo et al., 2019). Our findings of hyponatremia and hyperkalemia in DF-administered rats are in disagreement with Rajakrishnan et al. (2017) who reported elevated levels of sodium ions and decreased levels of potassium ions in the serum of druginjected rats, but are in agreement with Kim and Joo (2007), who reported that NSAIDs may cause hyponatremia and hyperkalemia in susceptible patients. ...
... Sodium ion, as the major cation of the extracellular fluid, is regulated by the kidney, so the extremes in blood sodium ion levels may cause cells of the kidney to malfunction and could result in tissue damage (Imo et al., 2019). Though it may occur rarely, but NSAIDs can cause hyponatremia by decreasing the renal free water clearance (Kim & Joo, 2007). Chloride ion is important in the maintenance of cation/ anion balance between the intra and extra-cellular fluids. ...
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Abstract Background The medicinal potential of plant extracts for the management of liver and kidney disorders in humans has been harnessed for the past several centuries. However, the abundant plant resources have not been fully investigated, thus this study was initiated to evaluate the influence of Cassia spectabilis leaves extract (CSE) on diclofenac-induced oxidative stress and hepatorenal damage in Wistar rats. The rats in the 1st group were injected with normal saline, and rats in the 2nd group were injected with diclofenac sodium (DF) by intramuscular route. Rats in the 3rd to 5th groups were treated with graded doses of CSE by oral gavages, and injected with DF. The serum markers of oxidative stress and hepatorenal damage in rats were estimated by biochemical assays. In addition, histological examinations of liver and kidney tissues were evaluated. Results There was significant (p
... Nonsteroidal anti-inflammatory drugs: Inhibition of renal prostaglandin synthesis can cause electrolyte and acidbase disturbances (sodium retention, hyponatremia, hyperkalemia, and decreased renal function). 5 Renin-angiotensin-aldosterone system (RAAS) inhibitors: may lead to higher incidence of hypotension, acute renal failure, or hyperkalemia. RAAS inhibitors may cause hyponatremia due to their anti-aldosterone action. ...
... Failure in the regulatory functions of the kidney leads to abnormally high or low levels of these ions in the blood, due to reduced GFR and rate of secretion of these ions. The inhibition of renal prostaglandins synthesis by NSAIDs causes various disturbances in the electrolytes and acid-base including sodium retention, and decreased renal function (Kim and Joo, 2007). Whereas the FA and LE significantly improved these changes induced by DS in the renal failure and electrolytes levels (Sakr et al., 2018). ...
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Excessive intake of non-steroidal anti-inflammatory drugs such as, diclofenac sodium (DS) may lead to toxicity in the rats. In this work, we aimed to examine the protective impact of lentil extract (LE) and folic acid (FA) on the hematological markers, the kidney tissue oxidative stress and the renal function against diclofenac sodium (DS) in male albino rats. The rats (120-150 g) were divided into four equal groups randomly, the first group kept as the untreated control. The second group was administrated with DS (11.6 mg/kg b.wt. orally once/day). The third group was received DS+FA (11.6 mg/kg b.wt.+76.9 microgram/kg b.wt.) orally once/day. The fourth group was treated with DS+LE (11.6 mg/kg b.wt.+500 mg/kg b.wt.) orally once/day. After four weeks, the results revealed that DS produced a significant decrease in the values of red blood cells (RBCs), hemoglobin concentration (Hb), hematocrit (HCT) and white blood cells (WBCs). On the other hand, there was a significant increase in the platelets count. Also, DS induced a renal deterioration; this was evidenced by the significant increase in the serum levels of urea, creatinine, uric acid, Na, Ca, Mg as well as the nitric oxide (NO) level in the kidney tissue. Also, there were a significant reduction in the serum levels of potassium (K) and reduced glutathione (GSH) in the kidney homogenates. Moreover, the findings in the rats treated by DS+LE or DS+FA showed a potential protection on the hematological markers, oxidative stress in the kidney tissue and the renal function disturbed by DS. LE and FA could play a potent role for the prevention the adverse hematological, the kidney tissue oxidative stress and the renal dysfunction caused by DS via their anti-oxidative and bioactive phytochemicals.
... The researchers suggested that the "prolonged compression of scalp arteries" accounted for saline efficacy, likely affecting pain receptors in "the periarterial nociceptive afferents." Moreover, pain and inflammation is relieved by nonsteroidal antiinflammatory drugs (NSAIDs) [27], and these substances can cause sodium retention and edema [28]. ...
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This paper examines evidence implicating migraine headache as a withdrawal symptom of excessive sodium chloride intake. Emerging research in food addiction posits that food and drug addictions share common features, such as withdrawal symptoms. Salt (sodium chloride) meets the criteria for the diagnosis of substance dependence, including withdrawal in which the substance is used to relieve withdrawal symptoms. The premonitory symptoms of migraine include food cravings for salty foods, which can alleviate migraine pain. Edema, possibly related to large amounts of salt consumed in binge eating, can cause approximately four pounds of retained fluid. This amount of fluid is similar to the fluid retained before the onset of migraine headache, which may be accompanied by polyuria. This paper proposes that inhibited withdrawal from highly processed food intake, rich in salt, mediates an association between increased sodium chloride intake and relief from migraine headache pain. The relief from withdrawal symptoms could also be a mediating factor that explains the controversial findings inversely associating dietary sodium intake with migraine history. Moreover, the withdrawal of retained sodium and edema related to the use of nonsteroidal anti-inflammatory drugs may elucidate a potential mechanism in medication overuse headache. Further research is needed to investigate the pain experienced from sodium chloride withdrawal in migraine headache.
... 29 Non-steroidal anti-inflammatory drugs inhibit renal prostaglandin synthesis and cause various electrolyte and acid-base disturbances, including hyponatremia and hyperkalemia. 30 Besides the analgesics, several drugs that might be used for comorbid diseases might induce electrolyte disorders. 31 This study showed cancer patients taking medications had two times the risk to develop hypocalcemia compared with 31 The study determines the magnitude and influencing factors in cancer patients; this study is the first of its kind in the area. ...
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Objective: The objective of this study was to determine the magnitude of electrolyte disorders and influencing factors among cancer patients in Southwest Ethiopia. Methods: Facility-based cross-sectional study was conducted in Jimma Medical Center (JMC). Eighty-four cancer patients admitted to JMC were recruited for this study. A structured questionnaire and serum electrolyte measurements were used for data collection. Bivariate and multiple logistic regression was employed to determine the association between electrolyte disorders and associated factors among admitted cancer patients. P value ⩽ 0.05 was used as a cut point to declare statistical significance. Result: The overall prevalence of electrolyte disorders was 60.7%. The presence or absence of comorbid diseases, age, body mass index (BMI), nutritional status, and current prescribed medication use were associated with electrolyte disorders. Younger patients had lower odds for electrolyte disorders (odds ratio (OR) = 0.128 (P value = 0.05) and OR = 0.08 (P value = 0.033)) for the first and the second quartile, respectively. Underweight patients had a threefold likelihood to develop electrolyte disorders (OR = 3.13 (P value = 0.043)) than having normal BMI. Compared with those in need of nutritional intervention, patients not in need of nutritional intervention had lower odds for the disorders (OR = 0.109 (P value = 0.006)). Medication had increased the likelihood of electrolyte disorders by 5.5 times than with no medication (P value = 0.023). Those who had comorbid disease had 10 times likely to develop electrolyte disorders than those who did not have comorbid diseases (P value = 0.004). Conclusion: Electrolyte disorders were prevalent in cancer patients. Age, BMI, nutritional condition, comorbid disease, and prescribed drugs were the predictors of electrolyte disorders in cancer patients. Authors recommend routine screening of electrolyte disorders in cancer patients and special emphasis on controlling and managing risk factors. Keywords Cancer, electrolyte disorders, Ethiopia, influencing factors
... 29 Non-steroidal anti-inflammatory drugs inhibit renal prostaglandin synthesis and cause various electrolyte and acid-base disturbances, including hyponatremia and hyperkalemia. 30 Besides the analgesics, several drugs that might be used for comorbid diseases might induce electrolyte disorders. 31 This study showed cancer patients taking medications had two times the risk to develop hypocalcemia compared with 31 The study determines the magnitude and influencing factors in cancer patients; this study is the first of its kind in the area. ...
Article
Full-text available
Objective: The objective of this study was to determine the magnitude of electrolyte disorders and influencing factors among cancer patients in Southwest Ethiopia. Methods: Facility-based cross-sectional study was conducted in Jimma Medical Center (JMC). Eighty-four cancer patients admitted to JMC were recruited for this study. A structured questionnaire and serum electrolyte measurements were used for data collection. Bivariate and multiple logistic regression was employed to determine the association between electrolyte disorders and associated factors among admitted cancer patients. P value ⩽ 0.05 was used as a cut point to declare statistical significance. Result: The overall prevalence of electrolyte disorders was 60.7%. The presence or absence of comorbid diseases, age, body mass index (BMI), nutritional status, and current prescribed medication use were associated with electrolyte disorders. Younger patients had lower odds for electrolyte disorders (odds ratio (OR) = 0.128 (P value = 0.05) and OR = 0.08 (P value = 0.033)) for the first and the second quartile, respectively. Underweight patients had a threefold likelihood to develop electrolyte disorders (OR = 3.13 (P value = 0.043)) than having normal BMI. Compared with those in need of nutritional intervention, patients not in need of nutritional intervention had lower odds for the disorders (OR = 0.109 (P value = 0.006)). Medication had increased the likelihood of electrolyte disorders by 5.5 times than with no medication (P value = 0.023). Those who had comorbid disease had 10 times likely to develop electrolyte disorders than those who did not have comorbid diseases (P value = 0.004). Conclusion: Electrolyte disorders were prevalent in cancer patients. Age, BMI, nutritional condition, comorbid disease, and prescribed drugs were the predictors of electrolyte disorders in cancer patients. Authors recommend routine screening of electrolyte disorders in cancer patients and special emphasis on controlling and managing risk factors.
... Of relevance, the viral clearance was delayed and clinical outcomes did not improve when corticosteroids were used to treat SARS-1 patients [139], and corticosteroids cause retention of sodium [140]. Likewise, the French Health Ministry suggested that ibuprofen aggravates infection in COVID-19 [139], and non-steroid anti-inflammatory drugs (NSAIDs) like ibuprofen cause sodium and water retention [141]. ...
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Dietary factors in the etiology of COVID-19 are understudied. High dietary sodium intake leading to sodium toxicity is associated with comorbid conditions of COVID-19 such as hypertension, kidney disease, stroke, pneumonia, obesity, diabetes, hepatic disease, cardiac arrhythmias, thrombosis, migraine, tinnitus, Bell’s palsy, multiple sclerosis, systemic sclerosis, and polycystic ovary syndrome. This article synthesizes evidence from epidemiology, pathophysiology, immunology, and virology literature linking sodium toxicological mechanisms to COVID-19 and SARS-CoV-2 infection. Sodium toxicity is a modifiable disease determinant that impairs the mucociliary clearance of virion aggregates in nasal sinuses of the mucosal immune system, which may lead to SARS-CoV-2 infection and viral sepsis. In addition, sodium toxicity causes pulmonary edema associated with severe acute respiratory syndrome, as well as inflammatory immune responses and other symptoms of COVID-19 such as fever and nasal sinus congestion. Consequently, sodium toxicity potentially mediates the association of COVID-19 pathophysiology with SARS-CoV-2 infection. Sodium dietary intake also increases in the winter, when sodium losses through sweating are reduced, correlating with influenza-like illness outbreaks. Increased SARS-CoV-2 infections in lower socioeconomic classes and among people in government institutions are linked to the consumption of foods highly processed with sodium. Interventions to reduce COVID-19 morbidity and mortality through reduced-sodium diets should be explored further.
... The deficiency of prostaglandin induces hyperaldosteronism, which would potentially cause decreased secretion of potassium. This is the basic phenomenon of NSAID-triggered hyperkalemia [13]. When less sodium chloride is supplied to the distal nephron, the electrochemical gradient for potassium excretion is also disturbed [13], meanwhile, the less active potassium channel also plays a role [14]. ...
... This is the basic phenomenon of NSAID-triggered hyperkalemia [13]. When less sodium chloride is supplied to the distal nephron, the electrochemical gradient for potassium excretion is also disturbed [13], meanwhile, the less active potassium channel also plays a role [14]. Hyperkalemia has been reported to cause fatal cardiac dysrhythmia. ...
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Introduction The association between continuous use of nonsteroidal anti-inflammatory drugs (NSAIDs) and hyperkalemia is not consistent in the literature and creates grounds for further large-scale trials, particularly in patients with a chronic disease that affects renal function, such as diabetes mellitus (DM). In this study, we will compare mean serum potassium level and the prevalence of hyperkalemia in diabetic and non-diabetic patients based on their use of NSAIDs. Methods This case-control study was conducted in the internal medicine unit of a tertiary care hospital from May 2019 to December 2020. After taking informed consent, 700 patients with a confirmed diagnosis of type 2 DM, of either gender, were enrolled in the study via consecutive convenient non-probability technique. Another set of 700 participants from the public were enrolled as the reference or control group. Continuous NSAID use was defined as NSAID used for a minimum of 20 days in the last 30 days. Blood was drawn via phlebotomy and sent to the laboratory to test for potassium level. Results Serum potassium level was significantly higher in diabetic patients with continuous NSAID use compared to the diabetic patients without continuous use (4.8 ± 0.8 mmol/L vs. 4.5 ± 0.7 mmol/L; p-value: 0.0001). Additionally, serum potassium level was significantly higher in non-diabetic patients with continuous NSAID use compared to non-diabetic patients without continuous use (4.3 ± 0.7 mmol/L vs. 3.9 ± 0.5 mmol/L; p-value: 0.0001) Conclusion In this study, the patients with continuous use of NSAIDs had higher levels of serum potassium level compared to patients without continuous use of NSAIDs. This difference was even higher in diabetic patients.
... Prostaglandins have a diversity of physiological effects, acting as important mediators of inflammation [2]. NSAIDs reduce prostaglandin production by the inhibition of both COX−1 and COX−2, as a result, eliciting various electrolyte disturbances, acute renal failure and chronic renal effects [2][3][4][5][6]. ...
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Nonsteroidal anti-inflammatory drugs (NSAIDs) belong to a class of universally and commonly used anti-inflammatory analgesics worldwide. A diversity of drawbacks of NSAIDs have been reported including cellular oxidative stress, which in turn triggers the accumulation of unfolded proteins, enhancing endoplasmic reticulum stress, and finally resulting in renal cell damage. Cordyceps cicadae (CC) has been used as a traditional medicine for improving renal function via its anti-inflammatory effects. N6-(2-hydroxyethyl)adenosine (HEA), a physiologically active compound, has been reported from CC mycelia (CCM) with anti-inflammatory effects. We hypothesize that HEA could protect human proximal tubular cells (HK−2) from NSAID-mediated effects on differential gene expression at the mRNA and protein levels. To verify this, we first isolated HEA from CCM using Sephadex® LH−20 column chromatography. The MTT assay revealed HEA to be nontoxic up to 100 µM toward HK−2 cells. The HK−2 cells were pretreated with HEA (10–20 µM) and then insulted with the NSAIDs diclofenac (DCF, 200 µM) and meloxicam (MXC, 400 µM) for 24 h. HEA (20 µM) effectively prevented ER stress by attenuating ROS production (p < 0.001) and gene expression of ATF−6, PERK, IRE1α, CDCFHOP, IL1β, and NFκB within 24 h. Moreover, HEA reversed the increase of GRP78 and CHOP protein expression levels induced by DCF and MXC, and restored the ER homeostasis. These results demonstrated that HEA treatments effectively protect against DCF- and MXC-induced ER stress damage in human proximal tubular cells through regulation of the GRP78/ATF6/PERK/IRE1α/CHOP pathway.
... Alteration of renal hemodynamics due to decreased production of PG through COX-1 inhibition results in electrolytes and acid-base disturbances, and renal insufficiency. [2] The effects are more pronounced in conditions with augmented PG production like preexisting renal disease, heart failure, cirrhosis of liver, or concomitant diuretic therapy. In a large study looking at naive NSAID users, the risk of hyperkalemia was reported with relatively selective COX 2 inhibitors (rofecoxib and celecoxib), diclofenac, and indomethacin. ...