Investigation of the Protective Effects of Magnesium on Bupivacaine-Induced Toxicity at the Level of Colon Cell Culture.

The primary objective of this in vitro study was to prevent the risk of toxicity associated with bupivacaine, widely used in clinical practice, by using magnesium (Mg), a readily available and cost-effective element, as an adjuvant. We hypothesized that Mg might exhibit a protective effect against cytotoxicity in a colon cell culture model under conditions of bupivacaine-induced LAST. Our secondary aim was to investigate its effect on genotoxicity, apoptosis, and iROS. CCD-18Co cells were used in our study. Control group (group C), Bupivacaine group (group B), Magnesium group (group M), and Bupivacaine+Mg group (group BM) were created. The viability of CCD-18Co cells incubated for 24 h in group C was determined to be 100%. These cells were evenly divided, and bupivacaine was administered to group B at concentrations of 5 to 300 µM. In group M, doses of Mg at 0.625 to 320 mEq were added. It was determined that the maximum viability was observed at a Mg dose of 40 mEq (p < 0.05). In group BM, bupivacaine was administered at the same concentrations in combination with Mg (40 mEq), and cell viability was measured. DNA damage, apoptosis, and iROS were assessed at concentrations of bupivacaine by administering 40 mEq Mg. In group B, viability decreased dose-dependently in CCD-18Co (p < 0.05, p < 0.01, p < 0.001). In group BM, the viability decreased in cells at increasing concentrations compared to group C (p < 0.05, p < 0.01, p < 0.001), but the viability was affected positively compared to group B (p < 0.05). In group B, DNA damage increased (p < 0.05, p < 0.001). In group BM, DNA damage increased (p < 0.05, p < 0.001). However, in group BM, DNA damage levels were reduced compared to group B (p < 0.05, p < 0.01). In group B, apoptosis increased (p < 0.05, p < 0.001); in group BM, apoptosis increased (p < 0.001) compared to group C. However, in group BM, apoptosis decreased compared to group B (p< 0.05). iROS increased in group B (p < 0.05, p < 0.01, p < 0.01) and group BM (p < 0.05, p < 0.01, p < 0.001) compared to the group C. However, in group BM, iROS decreased in comparison to group B (p < 0.05). In conclusion, Mg exhibits a protective effect against bupivacaine-induced toxicity.

A Comparison of the Effects of Dexamethasone and Methylprednisolone, Used on Level-3 Intensive Care COVID-19 Patients, on Mortality: A Multi-Center Retrospective Study.

BACKGROUND: Coronavirus disease 2019 (COVID-19) is often a mild disease, usually manifesting with respiratory complaints, and is sometimes mortal due to multiple organ failure. Hyperinflammation is a known COVID-19 component and is associated with organ dysfunction, disease severity and mortality. Controlling hyperinflammatory response is crucial in determining treatment direction. An important agent in providing this control is corticosteroids. This study aimed to determine whether dexamethasone and methylprednisolone, doses, administration time and duration in COVID-19 treatment are associated with improved treatment outcomes. METHODS: This retrospective multicenter study was conducted with participation of 6 healthcare centers which collected data by retrospectively examining files of 1,340 patients admitted to intensive care unit due to COVID-19 between March 2020 and September 2021, diagnosed with polymerase chain reaction (+) and/or clinically and radiologically. RESULTS: Mortality in the pulse methylprednisolone group was statistically significantly higher than that in the other 3 groups. Mortality was higher in older patients with comorbidities such as hypertension, diabetes mellitus, chronic kidney failure, coronary artery disease, and dementia. Pulse and mini-pulse steroid doses were less effective than standard methylprednisolone and dexamethasone doses, pulse steroid doses being associated with high mortality. Standard-dose methylprednisolone and dexamethasone led to similar effects, but standard dose methylprednisolone was more effective in severe patients who required mechanical ventilation (MV). Infection development was related to steroid treatment duration, not cumulative steroid dose. CONCLUSION: Corticosteroids are shown to be beneficial in critical COVID-19, but the role of early corticosteroids in mild COVID-19 patients remains unclear. The anti-inflammatory effects of corticosteroids may have a positive effect by reducing mortality in severe COVID-19 patients. Although dexamethasone was first used for this purpose, methylprednisolone was found to be as effective at standard doses. Methylprednisolone administered at standard doses was associated with greater PaO2/FiO2 ratios than dexamethasone, especially in the severe group requiring MV. High dose pulse steroid doses are closely associated with mortality and standard methylprednisolone dose is recommended.

A standard hemodialysis prescription to prevent osmotic demyelination in hyponatremic patients requiring dialysis.

INTRODUCTION: We aimed to investigate the effect of a standard hemodialysis prescription in hyponatremic patients requiring hemodialysis on the development of osmotic demyelination syndrome. METHODS: Ninety-nine patients who were treated with hemodialysis for the first time and had a pre-dialysis sodium value of ≤125 meq/L included in the study. Standard hemodialysis treatment was applied to all patients. Biochemical data before, immediately after and 24 h after hemodialysis were recorded retrospectively. All patients followed up for 2 weeks and magnetic resonance imaging was performed in patients with neurological symptoms. RESULTS: Eight patients had a sodium increase of more than 12 meq/L at 24-h after hemodialysis. Although hyponatremia was corrected rapidly with hemodialysis, none of the 99 azotemic patients developed osmotic demyelination syndrome. CONCLUSION: We did not observe osmotic demyelination syndrome in hyponatremic patients with azotemia treated with standard protocol hemodialysis. However, caution should still be exercised in high-risk patients for osmotic demyelination.

Evaluation of renal fibrosis in various causes of glomerulonephritis by MR elastography: a clinicopathologic comparative analysis.

BACKGROUND: Renal parenchymal fibrosis is the most important determinant of kidney disease progression and it is determined via biopsy. The aim of this study is to evaluate the renal stiffness noninvasively by magnetic resonance elastography (MRE) and to compare it with clinicopathologic parameters in glomerulonephritis and AA amyloidosis patients. METHODS: Thirty-four patients with glomerular filtration rate (GFR) over 20 ml/min/1.73m2 had non-contrast MRE prospectively. Kidney stiffness values were obtained from whole kidney, cortex, and medulla. Values were correlated with GFR, albuminuria, proteinuria, and degree of fibrosis that are assessed via renal biopsy. Patients were grouped clinicopathologically to assess the relation between stiffness and chronicity. RESULTS: Mean whole kidney, cortex, and medulla stiffnesses were 3.78 (± 1.26), 3.63 (± 1.25), and 4.77 (± 2.03) kPa, respectively. Mean global glomerulosclerosis was 22% (± 18%) and median segmental glomerulosclerosis was 4% (min-max: 0%-100%). Extent of tubulointerstitial fibrosis was less than 25% in 26 of the patients (76.5%), 25%-50% in 6 of the patients (17.6%), and higher than 50% in 2 of the patients (5.9%). Fourteen patients were defined to have chronic renal parenchymal injury. MRE-derived stiffness values correlated negatively with parameters of fibrosis. Lower stiffness values were observed in patients with chronic renal injury compared to those without (P < 0.05 for whole kidney and medulla MRE-derived stiffness). CONCLUSION: MRE-derived stiffness values were lower in patients with chronic injury. Stiffness decreases as glomerulosclerosis and tubulointerstitial fibrosis progresses in patients with primary glomerulonephritis and AA amyloidosis. With future studies, there may be a role for MRE to assess renal function in concert with conventional markers.

Efficacy and Safety of Switching to Azathioprine for Mycophenolate-Induced Diarrhea in Renal Transplant Recipients.

BACKGROUND: Diarrhea is a common adverse effect of mycophenolate treatment in renal transplant recipients. In patients with mycophenolate-induced diarrhea, one option is to switch to mycophenolate to azathioprine. In this study, we aimed to define the safety and efficacy of switching from mycophenolate to azathioprine for mycophenolate-related diarrhea in renal transplant recipients. METHODS: A total of 177 patients, 59 of whom were switched to azathioprine because of diarrhea and 118 of whom comprised a matched control group without diarrhea and continued mycophenolate treatment participated in this study. We analyzed the effect of switching to azathioprine from mycophenolate on amelioration of diarrhea and graft survival. RESULTS: We observed that 89.8% of patients who switched to azathioprine because of diarrhea had improved diarrhea complaints. Patients switched to azathioprine because of diarrhea had lower glomerular filtration rates (P < .001) and higher proteinuria (P < .001) compared with the control group before the switch. Patients switched to azathioprine compared with a subgroup of 59 control patients were matched to patients switched to azathioprine in terms of baseline renal function and proteinuria in addition to demographic parameters had higher 10-year graft loss compared with patients who continued mycophenolate (P = .03). Particularly in patients with a glomerular filtration rate <30 mL/min at the time of conversion, the risk of early graft loss was high. CONCLUSIONS: Although switching from mycophenolate to azathioprine was an effective approach to improve diarrhea, this approach is associated with increased risk of graft loss.