Agaricus Subrufescens ameliorates ovarian dysfunction and regulates altered biochemical parameters in rats with Letrozole induced polycystic ovarian syndrome.

OBJECTIVE: The objective of this study is to investigate the effects of an ethanolic extract derived from Agaricus subrufescens on rat models exhibiting Polycystic Ovarian Syndrome (PCOS) induced by Letrozole. METHODS: A total of thirty female Wistar rats were divided into five groups, each consisting of six rats. The negative control group was administered a volume of 1 mL of a 0.5% solution of carboxy methylcellulose (CMC). Letrozole (1 mg/kg) was administered to additional groups for a duration of 21 days in order to induce polycystic ovary syndrome (PCOS). Animals designated as positive controls were euthanized on the 22nd day. Both the test group and the standard group were subjected to treatment from the 22nd day to the 36th day. The experimental group was administered ethanolic extract of Agaricus subrufescens at doses of 200 mg/kg and 400 mg/kg p.o, while the control group received clomiphene citrate at a dose of 1 mg/kg. The study observed various physiological markers in individuals with polycystic ovarian disease, including estimated blood glucose levels, total cholesterol levels, triglyceride levels, and hormonal fluctuations such as increased testosterone and estrogen levels, as well as decreased progesterone levels. The presence of menstrual irregularities was confirmed through the examination of vaginal smears and histopathological changes in the ovaries. RESULTS: The consumption of Agaricus subrufescens was found to have a significant impact on various physiological parameters, including blood glucose levels, testosterone levels, anovulation, and menstrual irregularity. All therapeutic interventions significantly normalized the levels of serum glutamic-oxaloacetic transaminase (SGOT) and serum glutamic-pyruvic transaminase (SGPT). The rats with polycystic ovary syndrome (PCOS) that were induced by Letrozole exhibited increased levels of urea and creatinine. The findings of this study indicate that the administration of Agaricus subrufescens therapy has a protective effect on renal function, as evidenced by a reduction in serum levels of urea and creatinine. In rats with polycystic ovary syndrome (PCOS) induced by Letrozole, the inhibition of hepatic synthesis, promotion of ovarian follicle immaturity, and elevation of androgen secretions result in an increase in the weight of the liver and ovaries. The weight of endocrine organs exhibited a decrease across all treatment groups. The histopathological examination of PCOS specimens revealed an increased presence of cysts and theca lutein cells. The group of rats with polycystic ovary syndrome (PCOS) that did not receive treatment exhibited a higher number of cysts compared to the groups that received treatment. CONCLUSION: This study demonstrated that the administration of Letrozole orally resulted in the development of polycystic ovarian disease. The results indicated heightened levels of blood glucose, total cholesterol, and triglycerides, as well as alterations in hormone levels such as increased testosterone and estrogen, and decreased progesterone. These hormonal changes were accompanied by menstrual irregularities, which were confirmed through the examination of vaginal smears and histopathological analysis of the ovaries in the control group with polycystic ovarian disease. The treatment groups that received Agaricus subrufescens exhibited a decrease in blood glucose, total cholesterol, and testosterone levels.

Pre-treatment risk factors to predict early cisplatin-related nephrotoxicity in locally advanced head and neck cancer patients treated with chemoradiation: A single Institution experience.

OBJECTIVES: Cisplatin is essential in the curative treatment of locally advanced head and neck squamous cell carcinoma (LA-HNSCC) patients. The assessment of risk factors to predict an early cisplatin-induced nephrotoxicity could help in better managing one of the most relevant cisplatin-related dose-limiting factors. MATERIAL AND METHODS: We retrospectively collected data of LA-HNSCC patients treated at our Institution from 2008 to 2019. Patients received cisplatin in a curative setting concurrently with radiation. Acute Kidney Injury (AKI) was assessed as a dichotomous variable (CreaIncr) based on pre-treatment values, and values recorded at days 6-20 post-first cycle of cisplatin. Univariable logistic regression models were performed to investigate associations between CreaIncr and clinical characteristics. A multivariable logistic model on a priori selected putative covariates was performed. RESULTS: Of the 350 LA-HNSCC treated patients, 204 were analyzed. Ninety (44 %) suffered from any grade AKI (grade I 51.1 %): out of them, 84.4 % received high-dose cisplatin (100 mg/m2 q21). On the univariable logistic regression model, male sex, age, serum uric acid, creatinine, concomitant drugs, and cisplatin schedule were significantly associated with a higher rate of AKI. At multivariable model, age (p = 0.034), baseline creatinine (p = 0.027), concomitant drugs (p = 0.043), and cisplatin schedule (one-day bolus or fractionated high-dose vs. weekly; p = 0.001) maintained their significant association. CONCLUSIONS: Identifying pre-treatment risk factors in LA-HNSCC patients may improve decision-making in a setting where cisplatin has a curative significance. A strict monitoring of AKI could avoid cisplatin dose adjustments, interruptions, and treatment delays, thus limiting a negative impact on outcomes.

Value of systemic inflammation-response index in predicting contrast-induced nephropathy in patients with ST-elevation myocardial infarction.

BACKGROUND: Contrast induced nephropathy (CIN) is one of the feared complications of contrast medium-using procedures. Present study was conducted in order to evaluate the value of systemic inflammatory-response index (SIRI) for development of CIN among patients who underwent primary percutaneous intervention. METHODS: Six hundred seventy-six patients with the diagnosis of ST elevation myocardial infarction were included. The patients were divided into two groups according to the presence of CIN. Patients without (n = 530) and with (n = 146) CIN constituted group 0 and group 1, respectively. Clinical and biochemical features of the patients were recorded. Calculation of SIRI was made for each patient. RESULT: CIN patients were older, had higher prevalence of hyperlipidaemia, higher values of pre- and post-procedural creatinine levels, neutrophil and monocyte counts, neutrophil/lymphocyte ratio (NLR) and monocyte/lymphocyte ratio (MLR) and SIRI. They had lower values of left ventricular ejection fraction (LVEF), haemoglobin and high-density lipoprotein-cholesterol levels. SIRI had the highest area under the curve (AUC) for prediction of CIN. Pairwise analyses of the AUC's demonstrated that SIRI had statistically significantly higher AUC compared to NLR and MLR. Multivariate logistic regression analysis showed that besides from LVEF and pre-procedural creatinine, NLR and SIRI were the independent predictors of CIN. SIRI had a higher odds ratio compared to NLR. CONCLUSION: SIRI had greater diagnostic power than NLR and MLR and it can easily be used by physicians for the identification of high-risk patients for the occurrence of CIN.

Use of non-steroidal anti-inflammatory drugs in renal transplant patients: A retrospective study.

BACKGROUND: Renal transplants are often prescribed non-steroidal anti-inflammatory drugs (NSAIDs) for analgesic purposes. OBJECTIVE: Considering the dearth of data, we carried out the present study to evaluate the use of various NSAIDs and the incidence of acute kidney injury (AKI) in transplant patients. METHODS: A retrospective study amongst renal transplant patients prescribed at least one dose of NSAID was carried between January and December 2020 at the Department of Nephrology, Salmaniya Medical Complex, Kingdom of Bahrain. The patients' demographic details, serum creatinine values, and drug-related details were obtained. The Kidney Disease Improving Global Outcomes (KDIGO) criteria were used for defining AKI. RESULTS: Eighty-seven patients were included. Forty-three patients were prescribed diclofenac, 60 received ibuprofen, six received indomethacin, 10 were administered mefenamic acid, and 11 received naproxen. Due to multiple courses of NSAID prescription, a total of 70 prescriptions were identified for diclofenac, 80 for ibuprofen, six for indomethacin, 11 for mefenamic acid, and 16 for naproxen. No significant differences were observed in the absolute (p = 0.08) and percent changes in serum creatinine (p = 0.1) between the NSAIDs. Twenty-eight (15.2%) courses of NSAID therapy met the KDIGO criteria for AKI. Age (OR: 1.1, 95% CI: 1.007, 1.2; p = 0.02), concomitant everolimus (OR: 483, 95% CI: 4.3, 54407; p = 0.01), and mycophenolate + cyclosporine + azathioprine (OR: 63.4E+006, 95% CI: 203.2157 to 19.8E+012; p = 0.005) administration were observed with significant risk of NSAID-induced AKI. CONCLUSION: We observed possible NSAID-induced AKI to an extent of around 15.2% in our renal transplant patients. No significant differences were observed in the incidence of AKI between various NSAIDs and none of them had either graft failure or death.

Alpha-Mangostin ameliorates acute kidney injury via modifying levels of circulating TNF-α and IL-6 in glycerol-induced rhabdomyolysis animal model.

Alpha mangostin (AM), isolated from G. mangostana, showed beneficial effects in several disorders due to its antioxidant and anti-inflammatory properties. Acute kidney injury (AKI) due to different etiologies can develop into severe complications, resulting in high mortality rates. In this work, AM is tested for its ability to alleviate AKI in glycerol-induced AKI rat model, where 30 Male Sprague-Dawley rats were assigned to a healthy group, glycerol-treated group and AM-treated group. Glycerol- and AM groups received a single dose of glycerol (per IM, 50% glycerol in saline, 8 ml/kg), whereas control group was injected with saline. AM treatment (a single daily dose, per IP, 175mg/kg) was accomplished for three days. Animals were executed to collect blood samples and kidney tissue for biochemical and histological examination. It was found that glycerol induced increase in serum creatinine, blood urea nitrogen (BUN), lipid peroxidation, serum magnesium, TNF-α and IL-6. It also induced renal edema and hypocalcemia along with histopathological renal damage. AM treatment improved renal histological features and alleviated increase in serum creatinine, BUN, serum magnesium, TNF-α and IL-6 levels, as well as renal edema and lipid peroxidation but did not affect serum calcium levels. This suggests AM as a potential therapeutic agent for treating AKI mainly via its antioxidant and anti-inflammatory properties.

A new marker for the prediction of contrast induced-acute kidney injury following primary percutaneous coronary intervention: logarithm of haemoglobin-albumin product.

BACKGROUND: Contrast-induced acute kidney injury (CI-AKI) is a disorder that adversely affects the prognosis of STEMI. The study aimed to assess the predictive value of a new marker, logarithm of haemoglobin and albumin product (LHAP) on the risk of CI-AKI development after primary percutaneous coronary intervention (p-pci). METHOD: We retrospectively enrolled 3057 patients with ST-elevation acute myocardial infarction who were treated with p-PCI. The primary outcome was CI-AKI, defined as >25% or >0.5 mg/dl increase of baseline creatinine values during post-procedural 48 h. RESULTS: First, a baseline model was produced to determine the predictors of CI-AKI, then haemoglobin, albumin and LHAP were included in the base model and the performances of all models were compared. The predictive accuracy (Likelihood ratio χ2 and R2) and discrimination (ROC-AUC) of the model including LHAP were significantly higher than that of models including both albumin and Hgb. LHAP best cut-off value for the development of CI-AKI was 9.26 (sensitivity 68% and specificity 66%). CONCLUSION: LHAP values were the most important predictor of CI-AKI, followed by creatinine value and Killip class. LHAP values are significantly associated with CI-AKI after p-PCI.

SSRI/SNRI -induced Hyponatremia: A Case Series of 26 Patients in a Single Institution from 2018 to 2020.

Antidepressant medications are widely used by patients with depression or a depressive disorder. In spite of a generally favorable safety profile of selective serotonin reuptake inhibitors or serotonin - norepinephrine reuptake inhibitors (SSRI/SNRI), several cases of a possible connection between SSRI/SNRI and hyponatremia have been reported. To describe the clinical characteristics of patients with hyponatremia after SSRI/SNRI exposure, and to examine the association between SSRI/SNRI exposure and the presence of hyponatremia in a Chinese population. A retrospective single-center case series study. We performed a retrospective evaluation of inpatients with SSRI/SNRI-induced hyponatremia from a single institution in China between 2018 and 2020. Clinical data were obtained through review of medical records. Patients who met the initial inclusion criteria but did not develop hyponatremia acted as controls. The study was approved by the Clinical Research Ethics Board of Beijing Hospital (Beijing, P.R. China). We identified 26 patients with SSRI/SNRI-induced hyponatremia. The incidence rate of hyponatremia was 1.34% (26/1937) in the study population. The mean age at diagnosis was 72.58 (±12.84) years, with a male: female ratio of 1:1.42. The duration between SSRI/SNRI exposure and the onset of hyponatremia was 7.65 (±4.88) days. The minimum serum sodium level was 2328.23 (±107.25) mg/dL in the study group. Seventeen patients (65.38%) received sodium supplements. Four patients (15.38%) switched to another antidepressant. Fifteen patients (57.69%) recovered by the time of discharge. There were significant differences in serum potassium, serum magnesium and serum creatinine level between the two groups (p < 0.05). The rate of use of sertraline was significantly higher in the study group compared with the control group (p < 0.05). This pattern was not found in other SSRI/SNRI (p > 0.05). The results of our study show that SSRI/SNRI exposure, in addition to hyponatremia, may also affect the level of serum potassium, serum magnesium and serum creatinine. A history of hyponatremia and exposure to SSRI/SNRI may be potential risk factors for the development of hyponatremia. Future prospective studies are needed to validate these findings.

Chronic kidney disease promotes cerebral microhemorrhage formation.

BACKGROUND: Chronic kidney disease (CKD) is increasingly recognized as a stroke risk factor, but its exact relationship with cerebrovascular disease is not well-understood. We investigated the development of cerebral small vessel disease using in vivo and in vitro models of CKD. METHODS: CKD was produced in aged C57BL/6J mice using an adenine-induced tubulointerstitial nephritis model. We analyzed brain histology using Prussian blue staining to examine formation of cerebral microhemorrhage (CMH), the hemorrhagic component of small vessel disease and the neuropathological substrate of MRI-demonstrable cerebral microbleeds. In cell culture studies, we examined effects of serum from healthy or CKD patients and gut-derived uremic toxins on brain microvascular endothelial barrier. RESULTS: CKD was induced in aged C57BL/6J mice with significant increases in both serum creatinine and cystatin C levels (p < 0.0001) without elevation of systolic or diastolic blood pressure. CMH was significantly increased and positively correlated with serum creatinine level (Spearman r = 0.37, p < 0.01). Moreover, CKD significantly increased Iba-1-positive immunoreactivity by 51% (p < 0.001), induced a phenotypic switch from resting to activated microglia, and enhanced fibrinogen extravasation across the blood-brain barrier (BBB) by 34% (p < 0.05). On analysis stratified by sex, the increase in CMH number was more pronounced in male mice and this correlated with greater creatinine elevation in male compared with female mice. Microglial depletion with PLX3397 diet significantly decreased CMH formation in CKD mice without affecting serum creatinine levels. Incubation of CKD serum significantly reduced transendothelial electrical resistance (TEER) (p < 0.01) and increased sodium fluorescein permeability (p < 0.05) across the endothelial monolayer. Uremic toxins (i.e., indoxyl sulfate, p-cresyl sulfate, and trimethylamine-N-oxide) in combination with urea and lipopolysaccharide induced a marked drop in TEER compared with the control group (p < 0.0001). CONCLUSIONS: CKD promotes the development of CMH in aged mice independent of blood pressure but directly proportional to the degree of renal impairment. These effects of CKD are likely mediated in part by microglia and are associated with BBB impairment. The latter is likely related to gut-derived bacteria-dependent toxins classically associated with CKD. Overall, these findings demonstrate an important role of CKD in the development of cerebral small vessel disease.

Predictive value of hemoglobin-to-red blood cell distribution width ratio for contrast-induced nephropathy after emergency percutaneous coronary intervention.

BACKGROUND: Although the relationship of either hemoglobin or red blood cell distribution width (RDW) with contrast-induced nephropathy (CIN) has been reported individually. To date, no studies have evaluated the predictive value of hemoglobin-to-red blood cell distribution width ratio (HRR) for CIN. METHODS: A total of 1658 elderly patients with ST-segment elevation myocardial infarction (STEMI) undergoing emergency percutaneous coronary intervention (PCI) were retrospectively screened. Preoperative complete blood count was collected and the HRR was calculated as the ratio of hemoglobin to RDW. CIN was defined as an absolute ≥0.5 mg/dL (44.2 µmol/L) or a relative ≥25% increase in creatinine level at 72 h after contrast administration. Univariate and multivariate regression analysis were conducted to determine the effective predictors for CIN. The ROC curve analysis was plotted to determine the optimal cutoff value for HRR in predicting CIN. RESULTS: The overall incidence of CIN was 8.38%. The HRR was significantly lower in the CIN group compared with the non-CIN group (0.87 ± 0.15 vs 1.24 ± 0.23, p < 0.001). After multivariate regression analysis was performed, HRR was noted to be an effective predictor for the development of CIN (OR 1.617, 95% CI 1.439-2.706, p = 0.014), along with age, creatinine, eGFR, hs-CRP and contrast volume. An optimal cutoff value of 0.94 or lower for HRR was identified with 82.4% sensitivity and 63.5% specificity to predict CIN. CONCLUSION: Lower HRR on admission was an effective predictor for CIN in elderly patients with STEMI undergoing emergency PCI. HRR may be a convenient, economical and reliable biomarker for risk stratification.

Immune checkpoint inhibitor induced myocarditis, myasthenia gravis, and myositis: A single-center case series.

BACKGROUND: Immune checkpoint inhibitors can result in overlap syndrome comprised of myasthenia gravis, myositis and myocarditis. However, the mortality predictors have not been clearly delineated. METHODS: We examined the characteristics of 11 patients diagnosed with overlap syndrome at Cleveland Clinic. All the available clinical, diagnostic, biochemical and disease specific factors were examined. Clinical predictors of increased mortality were using student t-test for parametric data and Wilcoxon-signed rank testing for nonparametric data. RESULTS: Seven patients out of eleven patients were alive during the analysis. Our study did confirm that troponins were indicator of early demise. However, study showed that elevated creatinine, BUN, and decreased hemoglobin were also observed in patients who met early demise. Unlike previously published studies, elevated NT Pro-BNP and reduced left ventricular ejection fraction were not a seen in this study. However, there were higher incidence of electrical abnormalities in deceased patients when compared to alive. CONCLUSION: Our study is first to examine various clinical parameters of overlap syndrome that might be predictive of mortality. This study confirms troponin as possible predictor and adds elevated creatinine, BUN and reduced hemoglobin as possible early biomarkers in deceased patients. The analysis showed that reduced LVEF was not a seen in deceased patients.

A retrospective analysis to estimate trough concentrations of teicoplanin in patients with suspected or documented Gram-positive infections

Abstract Teicoplanin is a glycopeptide antibiotic commonly used to treat Gram-positive bacterial infections in the clinic. The aim of this study was to provide a therapeutic reference for the clinical application and dosage regimen adjustment of teicoplanin by identifying factors associated with its plasma trough concentration (Ctrough). A retrospective study was performed on patients with suspected or documented Gram-positive infections who were hospitalized from November 2017 to January 2020 and treated with teicoplanin while undergoing routine therapeutic drug monitoring (TDM). A total of 112 Ctrough trough measurements were obtained from 72 patients were included in this study. SPSS software was used for correlation analysis and receiver operator characteristic curve (ROC) analysis. The Ctrough for teicoplanin showed statistically significant relationships (P<0.05) with PLT, Scr, CLcr, eGFR, BUN and Cys-C. ROC curve analysis revealed that CLcr and eGFR were more sensitive and specific for Ctrough compared to the other factors. These findings should be considered in the clinical application of teicoplanin and for its dosage adjustment.

Exosomes from adipose-derived stem cells inhibit inflammation and oxidative stress in LPS-acute kidney injury.

Acute renal damage presents a significant danger to kidney health. Previous research has found that acute kidney injury shows high levels of oxidative stress and inflammation caused by sepsis. Although mesenchymal stem cells (MSCs) can repair acute kidney injury. However, involvement of MSCs exosomes generated from adipose tissue and bone marrow in lipopolysaccharide-induced acute kidney damage is not clear. LPS (7.5 mg/kg) intraperitoneal injection was used to produce AKI, and 30 min before the LPS administration, adipose-derived MSCs (ADSCs) exosomes (1 × 105 and 5 × 105) and bone marrow-derived MSCs(BMSCs) exosomes (1 × 105 and 5 × 105) were delivered individually. The function of the rat kidney was explored. Inflammation, oxidative stress, and autophagy levels were further investigated. Both adipose-derived and bone marrow-derived MSCs can enhance renal function and structural damage, such as BUN, Creatinine, and cystatin C levels, as well as tubular damage scores. These findings indicate that both adipose-derived MSCs exosomes and bone marrow-derived MSCs exosomes decrease oxidative stress and inflammation, as well as make a substantial influence on kidney tissue in autophagy levels. Furthermore, compared to bone marrow-derived MSCs exosomes, adipose-derived MSCs exosomes improved kidney function and structure more significantly. We discovered that adipose-derived MSCs exosomes protect against LPS-induced AKI by inhibiting oxidative stress and inflammation.

Ruscogenin Prevents Folic Acid-Induced Acute Kidney Damage by Inhibiting Rev-erbα/ß-Mediated Ferroptosis.

To investigate the pharmacodynamic effects of ruscogenin on acute kidney injury and the Rev-erbα/ß regulation of ferroptosis intervention mechanism. The C57BL-6 mice were induced acute kidney injury with folic acid. Plasma, urine, and kidney samples were collected after intraperitoneal injection of ruscogenin (0.01, 0.1, and 1 mg/kg). We measured mouse kidney function indicators, including creatinine (CRE), blood urea nitrogen (BUN), N-acetyl-ß-D-glucosidase (NAG), albumin, albumin and creatinine rate (ACR), renal index, and renal injury molecule-1 expression. Meanwhile, we detected the levels of ferroptosis indicators malondialdehyde (MDA), carbonylated proteins, iron ions, glutathione peroxidase 4 (GPX-4), and glutathione (GSH). The expression of solute carrier family 7 member 11 (Slc7a11), heme oxygenase-1 (HO-1), and Rev-erbα/ß were detected by the Western blot and quantitative reverse transcription polymerase chain reaction (qRT-PCR), respectively. Ruscogenin (1 mg/kg) significantly reduced the index of folic acid-induced acute kidney injury and alleviated acute kidney injury. In kidney tissues, ruscogenin inhibited folic acid-induced Rev-erbα/ß expression, restored HO-1 and SLC7A11 expression to normal levels, and alleviated ferroptosis. Ruscogenin ameliorates acute kidney injury via suppressing ferroptosis in kidney tissues through modulation of the Rev-erbα/ß-SLC7A11/HO-1 pathway.

New perspectives on contrast-induced nephropathy during coronary interventions.

Tweetable abstract To reduce contrast-induced nephropathy as a complication of percutaneous coronary intervention, several thresholds have been proposed, including maximum contrast dose, contrast volume/estimated glomerular filtration rate, revised maximal contrast dose and zero-contrast percutaneous coronary intervention in select patients.

To reduce contrast-induced nephropathy as a complication of percutaneous coronary intervention, several thresholds have been proposed, including maximum contrast dose, contrast volume/estimated glomerular filtration rate, revised maximal contrast dose and zero-contrast percutaneous coronary intervention in select patients.

The Effect of Intravenous Mannitol Combined With Normal Saline in Preventing Cisplatin-Induced Nephrotoxicity: A Randomized, Double-Blind, Placebo-Controlled Trial.

PURPOSE: Nephrotoxicity is a major dose-limiting toxicity among patients with cancer who were treated with cisplatin. Although no standard approach is available to prevent cisplatin-induced nephrotoxicity, administering intravenous isotonic saline is recommended. Additionally, mannitol combined with hydration has been evaluated, but none of them have been established. Our study aimed to determine the efficacy of mannitol combined hydration to prevent cisplatin-induced nephrotoxicity. PATIENTS AND METHODS: This study was a phase II, randomized, placebo-controlled design. All patients with solid cancers who were treated with cisplatin (n = 48) were randomly assigned to receive either placebo (n = 25) or 20 g of mannitol (n = 23) after completing 2 L of prehydration and receiving cisplatin. Serum creatinine, blood urea nitrogen, electrolyte, and glomerular filtration rate (GFR) were measured at baseline and days 2 and 7. Moreover, GFR was calculated based on the 24-hour urine creatinine clearance rate to assess renal function at baseline and 48 hours after receiving cisplatin. Severity of nausea and vomiting was evaluated using Common Terminology Criteria for Adverse Events. RESULTS: No difference was found regarding baseline characteristics between the two groups. Seven of 23 patients (37.4%) in the mannitol group and 10 of 25 patients (40%) in the placebo group increased serum creatinine level ≥ 0.3 mg/dL at 48 hours after intervention (P value = .48). Patients receiving mannitol exhibited significantly lower incidence of 24-hour urine GFR below 60 mL/min/1.73 m than those in the placebo group (13.6% v 48.0% in the placebo group; P value = .012). Univariate analysis showed the greatest benefit for administering mannitol among patients receiving cisplatin > 80 mg/m2, or patients receiving concomitant radiation. CONCLUSION: Mannitol combined with hydration significantly prevented cisplatin-induced nephrotoxicity. Additionally, mannitol should be particularly considered among patients with cancer, treated with cisplatin > 80 mg/m2, or patients receiving concomitant radiation.

Iopromide and Iodixanol in the Development of Postoperative Contrast Nephropathy in Patients with Renal Insufficiency: A Meta-Analysis.

In order to compare the effects of iopromide and isoxazole on postoperative contrast-induced nephropathy in patients with renal insufficiency, the paper searches for randomized controlled trials and retrospective cohort studies comparing the effects of iopromide and iodixanol on renal function in patients with renal insufficiency after surgery. The data are extracted from eligible studies. We tried to assess the incidence of contrast-agent nephropathy, preoperative and postoperative serum creatinine indicators, and mortality. This paper includes 8 studies with a total of 1243 patients. The incidence of contrast-induced nephropathy in the iopromide group is higher than that in the iodixanol group, and there is no significant difference between the two groups in postoperative mortality and preoperative serum creatinine expression. Sensitivity analysis and funnel chart show that our research is robust and has low publication bias. Our research shows that in patients with renal insufficiency, the incidence of contrast-medium nephropathy in the iopromide group is higher than that in the iodixanol group. Iodixanol is safer and has less effect on patients' serum creatinine levels.

Impact of 719Trp>Arg Polymorphism of KIF 6 Gene on Contrast Induced Nephropathy in Patients Undergoing Coronary Angiography or Percutaneous Coronary Intervention.

Background: The identification of preventive strategies, such as statin therapy, is crucial for the management of contrast-induced nephropathy (CIN). Several studies showed the association between KIF6 polymorphism (replacement of Trp719 with Arg) and an increased cardiovascular risk, while others showed a correlation between 'pleiotropic' effects of statins and a reduction in cardiovascular events in the population with the risk allele due to the documented modulation of response to statin by KIF6 polymorphism. Aim of this study is to assess the impact of KIF6 polymorphism on the development of CIN. Methods: We analysed 1253 consecutive patients undergoing coronary angiography/PCI. Serum creatinine was collected at baseline, 24 and 48 hours after contrast exposure. We identified the different allelic patterns and assessed the incidence of CIN (absolute increase of 0.5mg/dL or relative >25% in creatinine at 24 and 48h). Results: KIF6 Arg mutation was found in 669 patients (heterozygotes n = 525, homozygotes n = 144). The total prevalence of CIN was 12.5% and we did not find any association between KIF6 polymorphism and CIN development (11.3%, 13.7%, 13.2% p = 0.30). At subgroups analysis among statin 'naïve' patients we found a higher prevalence of CIN in homozygous patients as compared to wild-type (20.7% vs 11.3%, p = 0.05), while opposite results were observed among patients with statin therapy (8.6% vs 13.2%, p = 0.28). Conclusion: KIF6 homozygous Arg was associated with a significant increase in the risk of CIN only among statin naive patients. Future studies are needed to evaluate the beneficial effects of statin especially in this subset of patients.

Artificial Intelligence Algorithm-Based Computed Tomography Image in Assessment of Acute Renal Insufficiency of Patients Undergoing Percutaneous Coronary Intervention.

This study was aimed to analyze the changes in renal function of patients undergoing percutaneous coronary intervention (PCI) surgery and the characteristics of their computed tomography (CT) image based on artificial intelligence algorithms. In this study, 104 patients with coronary atherosclerotic heart disease (CAHD) were treated as the research objects. They were divided into an experimental group (patients who underwent CAG and PCI within 1 week after enhanced coronary CT (ECCT)) and the control group (patients who underwent CAG and PCI within 1-3 weeks after ECCT). Renal imaging scans of patients were performed by CT based on discrete inseparable shear transform (DNST) optimized algorithm, which was named as O-DNST. The results showed that the serum creatinine (Scr), blood urea nitrogen (BUN), and urine protein (UP) levels of patients in the experimental group were significantly higher than those of the control group 24-72 hours after surgery, while the levels of endogenous creatinine clearance (Ccr) and estimated glomerular filtration rate (eGFR) were significantly lower than those of the control group (P < 0.05). The levels of ß2 microglobulin (ß2-MG), C-reactive protein (CRP), interleukin 6 (IL-6), and tumor necrosis factor (TNF-α) in the experimental group were significantly higher than those in the control group 24-72 hours after surgery (P < 0.05). The incidence of contrast-induced nephropathy (CIN) in the experimental group (15.38%) was significantly higher than that in the control group (5.8%), and the difference was statistically significant (P < 0.05). The results showed that repeated application of contrast agent in a short period of time can promote the increase of serum inflammation levels in PCI patients, which may be a risk factor for CIN in PCI patients.

Efficacy of brain natriuretic peptide vs. nicorandil in preventing contrast-induced nephropathy: a network meta-analysis.

This study aimed to conduct a network meta-analysis (NMA) to compare the efficacy of brain natriuretic peptide (BNP) vs nicorandil for preventing contrast-induced nephropathy (CIN). Databases of Pubmed, Cochrane, Embase, Web of Science were searched by keywords for eligible studies of randomized controlled trials investigating different agents (BNP, nicorandil, nitroglycerin, intravenous saline) for preventing CIN. The outcomes included a change in serum creatinine level at 48 h and the incidence of CIN after percutaneous coronary intervention (PCI) or coronary angiography (CAG). A total of 13 studies with 3,462 patients were included. Compared with intravenous saline alone, except for nitroglycerin (odds ratio [OR]: 1.02, 95% CI [0.36-2.88]), the other drugs significantly reduced the CIN incidence with OR of 0.35 (95% CI [0.24-0.51]) for BNP, 0.52 (0.29, 0.94) for usual-dose nicorandil, 0.28 (0.19, 0.43) for double-dose nicorandil. BNP and double-dose nicorandil significantly decreased the change of serum creatinine (SCr) levels with mean difference (MD) of -6.98, (-10.01, -3.95) for BNP, -8.78, (-11.63, -5.93) for double-dose nicorandil. No significant differences were observed in the change of SCr levels for nitroglycerin (-4.97, [-11.46, 1.52]) and usual-dose nicorandil (-2.32, [-5.52, 0.89]) compared with intravenous saline alone. For double-dose nicorandil, the CIN incidence and the change of SCr level in group of 4-5 days treatment course were more than group of less than or equal to 24 h treatment course (OR of 1.48, [0.63-3.46] and MD of 2.48, [-1.96, 6.91]). In conclusion, BNP and double-dose nicorandil can have effects on preventing the incidence of CIN and double-dose nicorandil performed better than BNP. In double-dose nicorandil groups, a course of less than or equal to 24 h before and after procedure performed with better efficacy than a course of 4-5 days.

ORIGANUM MAJORANA ATTENUATES CIPROFLOXACIN-INDUCED NEPHROPATHY IN RATS.

OBJECTIVE: The aim: The researchers wanted to discover if Origanum majorana (O. M.) has any renoprotective qualities in a CIN rat model. PATIENTS AND METHODS: Materials and methods: Control, ciprofloxacin (ciprofloxacin-induced CIN), two O. majorana groups (rats treated with O. majorana 30 mg and 45 mg), and two ciprofloxacin Plus O. majorana groups (n = 8) were randomly assigned to rats (CIN rats treated with O. majorana at 30 mg and 45 mg). Renal function tests were performed, as well as histological investigation. RESULTS: Results: The levels of serum blood urea nitrogen (BUN) and creatinine increased after ciprofloxacin treatment. The serum BUN and creatinine levels in the ciprofloxacin + O. majorana groups were lower as well as in O. majorana groups, however, kidney damage was higher in the ciprofloxacin group and reduced tissue damage in combination groups and O. majorana groups rats. CONCLUSION: Conclusions: O. majorana decreases experimental CIN in vivo. This effect is thought to activate the antioxidant defenses pathway.