Acute respiratory failure is an important risk factor for mortality in patients with acute pesticide poisoning. Therefore, it is necessary to investigate the risk factors to predict respiratory failure in these patients. This study retrospectively investigated the clinical features of respiratory failure among patients with acute pesticide poisoning requiring mechanical ventilation. This study included patients who were admitted with intentional poisoning by pesticide ingestion from January 2017 to December 2019. Paraquat intoxication was excluded. Among 469 patients with acute pesticide poisoning, 398 patients were enrolled in this study. The respiratory failure rate was 30.4%. The rate of respiratory failure according to the type of pesticide was carbamate (75.0%), organophosphate (52.6%), glufosinate (52.1%), glyphosate (23%), pyrethroid (8.9%), and others (17%). The mortality was 25.6% in the respiratory failure group. The risk factors for respiratory failure were old age, low body mass index, and ingestion of more than 300 mL. In conclusion, respiratory failure is a risk factor for mortality in pesticide poisoning. Old age, low body mass index, and ingestion of more than 300 mL are the risk factors for predicting respiratory failure.

Acute respiratory failure is an important risk factor for mortality in patients with acute pesticide poisoning. Therefore, it is necessary to investigate the risk factors to predict respiratory failure in these patients. This study retrospectively investigated the clinical features of respiratory failure among patients with acute pesticide poisoning requiring mechanical ventilation. This study included patients who were admitted with intentional poisoning by pesticide ingestion from January 2017 to December 2019. Paraquat intoxication was excluded. Among 469 patients with acute pesticide poisoning, 398 patients were enrolled in this study. The respiratory failure rate was 30.4%. The rate of respiratory failure according to the type of pesticide was carbamate (75.0%), organophosphate (52.6%), glufosinate (52.1%), glyphosate (23%), pyrethroid (8.9%), and others (17%). The mortality was 25.6% in the respiratory failure group. The risk factors for respiratory failure were old age, low body mass index, and ingestion of more than 300 mL. In conclusion, respiratory failure is a risk factor for mortality in pesticide poisoning. Old age, low body mass index, and ingestion of more than 300 mL are the risk factors for predicting respiratory failure.

To determine the relationship between the oral ingestion volume of xylene and methyl hippuric acid (MHA) in urine, we measured MHA in 11 patients whose ingested xylene volume was identified. The best-fit equation between urine MHA and ingested amount of xylene was as follows: y (ingested amount of xylene, mL/kg) = −0.052x² + 0.756x (x = MHA in urine in g/g creatinine). From this equation, we estimated the ingested xylene volume in 194 patients who had ingested pesticide of which the formulation was not available. Our results demonstrated that oxadiazole, dinitroaniline, chloroacetamide, organophosphate, and pyrethroid were xylene-containing pesticide classes, while the paraquat, glyphosate, glufosinate, synthetic auxin, fungicide, neonicotinoid, and carbamate classes were xylene-free pesticides. Sub-group univariate analysis showed a significant association between MHA levels in urine and ventilator necessity in the pyrethroid group. However, this association was not observed in the organophosphate group. Our results suggest that MHA in urine is a surrogate marker for xylene ingestion, and high urine MHA levels may be a risk factor for poor clinical outcome with some pesticide poisoning.
Biomarkers ; Eating ; Humans ; Indoleacetic Acids ; Paraquat ; Pesticides ; Poisoning* ; Respiratory Insufficiency ; Risk Factors ; Ventilators, Mechanical ; Xylenes*

BACKGROUND: Several studies have suggested that proton pump inhibitor (PPI) use is associated with adverse renal outcomes, but obvious evidence for this association is lacking. We investigated the association between PPI use and adverse renal outcomes in patients who had undergone percutaneous coronary intervention. METHODS: Of the 1,284 patients hospitalized for percutaneous coronary intervention between January 2007 and May 2012, 934 patients with baseline estimated glomerular filtration rate greater than 60 mL/min/1.73 m2 were enrolled. Multivariable Cox models were used to examine whether PPI use was associated with acute and chronic adverse renal outcomes. RESULTS: In adjusted time-dependent Cox models, PPI use was associated with acute kidney injury (hazard ratio [HR], 1.46; 95% confidence interval [95% CI], 1.05–2.02), especially in patients aged 65 years or younger (HR, 2.08; 95% CI, 1.09 3.96) or in patients with diabetes (HR, 2.00; 95% CI, 1.23–3.25). In multivariable Cox models, the association between duration of PPI use and chronic kidney disease development was not statistically significant (HR of heavy users, 1.50; 95% CI, 0.61–3.67), but a longer duration of PPI use was associated with mild renal progression in patients younger than 65 years (HR of heavy users, 2.24; 95% CI, 1.09–4.60). CONCLUSION: Our results suggest that PPI use increases the risk of AKI development, and that PPI use is more significantly associated with acute and chronic renal injuries in younger patients.
Acute Kidney Injury ; Coronary Artery Disease* ; Coronary Vessels* ; Glomerular Filtration Rate ; Humans ; Kidney Failure, Chronic ; Percutaneous Coronary Intervention ; Proportional Hazards Models ; Proton Pump Inhibitors ; Proton Pumps* ; Protons* ; Renal Insufficiency, Chronic ; Risk Factors

Hypermagnesemia is a rare condition that is usually iatrogenic in patients with elderly or renal failure. Severe hypermagnesemia is uncommon in patients with a normal renal function. Symptoms due to hypermagnesemia can range from mild symptoms, such as nausea, to severe symptoms, such as cardiac and respiratory arrest. This paper describes a case of a 49-year-old woman who ingested a magnesium-containing fertilizer with normal renal function. Cardiac arrest occurred eight hours after poisoning.Electrocardiography changed from a narrow QRS to a wide QRS and then to a complete atrioventricular block. Her hemodynamic state was unstable. Continuous renal replacement therapy was performed to remove magnesium from the blood, with the subsequent resolution of arrhythmia and hemodynamic stabilization. This paper reviews the pathophysiologic effects of magnesium on the cardiovascular system, clinical manifestation, and treatment of hypermagnesemia.

Hypermagnesemia is a rare condition that is usually iatrogenic in patients with elderly or renal failure. Severe hypermagnesemia is uncommon in patients with a normal renal function. Symptoms due to hypermagnesemia can range from mild symptoms, such as nausea, to severe symptoms, such as cardiac and respiratory arrest. This paper describes a case of a 49-year-old woman who ingested a magnesium-containing fertilizer with normal renal function. Cardiac arrest occurred eight hours after poisoning.Electrocardiography changed from a narrow QRS to a wide QRS and then to a complete atrioventricular block. Her hemodynamic state was unstable. Continuous renal replacement therapy was performed to remove magnesium from the blood, with the subsequent resolution of arrhythmia and hemodynamic stabilization. This paper reviews the pathophysiologic effects of magnesium on the cardiovascular system, clinical manifestation, and treatment of hypermagnesemia.

BACKGROUND/AIMS: Most pesticide formulations contain both chief and additive ingredients. But, the additives may not have been tested as thoroughly as the chief ingredients. The surfactant, nonyl phenoxypolyethoxylethanol (NP40), is an additive frequently present in pesticide formulations. We investigated the effects of NP40 and other constituents of a validamycin pesticide formulation on cell viability and on the expression of genes involved in cell damage pathways. METHODS: The effects of validamycin pesticide ingredients on cell viability and of NP40 on the mRNA expression of 80 genes involved in nine key cellular pathways were examined in the human neuroblastoma SK-N-SH cell line. RESULTS: The chemicals present in the validamycin pesticide formulation were cytotoxic to SK-N-SH cells and NP40 showed the greatest cytotoxicity. A range of gene expression changes were identified, with both up- and down-regulation of genes within the same pathway. However, all genes tested in the necrosis signaling pathway were down-regulated and all genes tested in the cell cycle checkpoint/arrest pathway were up-regulated. The median fold-change in gene expression was significantly higher in the cell cycle checkpoint/arrest pathway than in the hypoxia pathway category (p = 0.0064). The 70 kDa heat shock protein 4 gene, within the heat shock protein/unfolded protein response category, showed the highest individual increase in expression (26.1-fold). CONCLUSIONS: NP40 appeared to be particularly harmful, inducing gene expression changes that indicated genotoxicity, activation of the cell death (necrosis signaling) pathway, and induction of the 70 kDa heat shock protein 4 gene.
Aged ; Cell Cycle Checkpoints/drug effects/genetics ; Cell Line, Tumor ; Cell Survival/drug effects ; Dose-Response Relationship, Drug ; Female ; Gene Expression Regulation/drug effects ; Genes, cdc ; HSP110 Heat-Shock Proteins/genetics/metabolism ; Humans ; Inositol/*analogs & derivatives/chemistry/poisoning ; Necrosis ; Neurons/*drug effects/metabolism/pathology ; Nonoxynol/chemistry/*toxicity ; Pesticides/chemistry/*poisoning ; RNA, Messenger/metabolism ; Signal Transduction/drug effects ; Surface-Active Agents/chemistry/*toxicity

Pesticide formulation includes solvents (methanol and xylene) and antifreeze (ethylene glycol) whose metabolites are anions such as formic acid, hippuric acid, and oxalate. However, the effect of the anion gap on clinical outcome in acute pesticide intoxication requires clarification. In this prospective study, we compared the anion gap and other parameters between surviving versus deceased patients with acute pesticide intoxication. The following parameters were assessed in 1,058 patients with acute pesticide intoxication: blood chemistry (blood urea nitrogen, creatinine, glucose, lactic acid, liver enzymes, albumin, globulin, and urate), urinalysis (ketone bodies), arterial blood gas analysis, electrolytes (Na+, K+, Cl- HCO3 -, Ca++), pesticide field of use, class, and ingestion amount, clinical outcome (death rate, length of hospital stay, length of intensive care unit stay, and seriousness of toxic symptoms), and the calculated anion gap. Among the 481 patients with a high anion gap, 52.2% had a blood pH in the physiologic range, 35.8% had metabolic acidosis, and 12.1% had acidemia. Age, anion gap, pesticide field of use, pesticide class, seriousness of symptoms (all P < 0.001), and time lag after ingestion (P = 0.048) were significant risk factors for death in univariate analyses. Among these, age, anion gap, and pesticide class were significant risk factors for death in a multiple logistic regression analysis (P < 0.001). In conclusions, high anion gap is a significant risk factor for death, regardless of the accompanying acid-base balance status in patients with acute pesticide intoxication.
Acid-Base Equilibrium ; Acidosis/etiology ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Anions/*chemistry/metabolism ; Biomarkers/*chemistry/metabolism ; Blood Gas Analysis ; Chemically-Induced Disorders/mortality/pathology ; Electrolytes/analysis ; Female ; Humans ; Intensive Care Units ; Logistic Models ; Male ; Middle Aged ; Odds Ratio ; Pesticides/*poisoning ; Prospective Studies ; Risk Factors ; Survival Analysis ; Urinalysis ; Young Adult

Purpose: This study aimed to compare the brain perfusion status of patients with chronic kidney disease to a normal control group to identify any significant differences. Materials and Methods: The perfusion state of the brain was measured by MRI using the arterial spin labeling technique in 36 patients undergoing hemodialysis due to chronic kidney disease and 36 normal controls. Images were then analyzed in a voxel-wise manner to detect brain areas showing significant perfusion differences between the two groups. Results: Patients with chronic kidney disease showed increased perfusion in the form of large clusters across the right fronto-parieto-temporal lobe and the left parieto-occipital lobe. In addition, perfusion increased in the bilateral thalami, midbrain, pons, and cerebellum (p < 0.01, familywise error corrected). Conclusion Brain perfusion appears to increase in patients with chronic kidney disease compared to normal controls. Uremic toxicity is thought to be the cause of this increase as it can cause damage to the microscopic blood vessels and their surrounding structures.

Background: Proteinuria is a significant risk factor for progression of IgA nephropathy (IgAN) and has a positive correlation with severity of foot process effacement (FPE). We evaluated the relationship of FPE with proteinuria and histologic characteristics, including the Oxford classification. Methods: Patients who underwent renal biopsy and were diagnosed with IgAN at a single center were retrospectively reviewed. Patients aged less than 18 years and those with the possibility of secondary causes were excluded from the study. Subsequently, we evaluated the association between degree of proteinuria, severity of FPE, and histologic characteristics, including the Oxford classification and other immunofluorescence stains. Results: A total of 805 cases of renal biopsy was performed at our institution, and 327 patients were diagnosed with IgAN. Among them, 82 patients were excluded. Severity of FPE had an impact on the degree of proteinuria. Notably, the group with diffuse FPE had more than about 1.3 g/day of urine protein compared to those with rare FPE. Among the histologic characteristics, M1 score and immune deposition of IgG affected severity of FPE (hazard ratios [95% confidence interval], 1.90 [1.10 to 3.26], and 3.77 [1.66 to 8.54], respectively). Conclusion Severity of FPE had an impact on the degree of proteinuria and may be associated with the pathogenesis of IgAN.