Data reported recently suggest that acute kidney injury (AKI) is a systemic disease that adversely affects the function of other organs-including the heart, lung, liver, brain and immune system-which is related to the high mortality rate of affected patients. Kidney and lung function are closely related in both health and disease. Data support deleterious bidirectional crosstalk between the lung and kidney. AKI is a common complication in patients with acute respiratory distress syndrome, and has been reported to exert adverse effects on the lungs. Mortality rates for AKI combined with acute lung injury (ALI) can be up to 80% in critically ill patients. Although AKI-associated ALI presents clinically as increased pulmonary edema, the mechanism of AKI-associated ALI extends beyond simple volume overload. Data from animal studies suggest that AKI-induced pulmonary edema is related to both cardiogenic edema (due to elevated hydrostatic pressure) and non-cardiogenic edema (due to pulmonary endothelial and epithelial cell injury caused by inflammation, oxidative stress, and apoptosis). ALI with mechanical ventilation causes a decline in renal hemodynamic function and apoptosis. Elucidation of the mechanisms of kidney-lung crosstalk would facilitate development of effective therapies and reduce the mortality rate of AKI combined with respiratory failure.
Acute Kidney Injury ; Acute Lung Injury ; Animals ; Apoptosis ; Brain ; Critical Illness ; Edema ; Epithelial Cells ; Heart ; Hemodynamics ; Humans ; Inflammation ; Kidney* ; Liver ; Lung* ; Mortality ; Oxidative Stress ; Pulmonary Edema ; Respiration, Artificial ; Respiratory Distress Syndrome, Adult ; Respiratory Insufficiency

Chronic kidney disease (CKD) leads to cognitive impairment and emotional changes. However, the precise mechanism underlying the crosstalk between the kidneys and the nervous system is not fully understood. Inflammation and cerebrovascular disease can influence the development of depression in CKD. CKD is one of the strongest risk factors for cognitive impairment. Moreover, cognitive impairment occurs in CKD as patients experience the dysregulation of several brain functional domains due to damage caused to multiple cortical regions and to subcortical modulatory neurons. The differences in structural brain changes between CKD and non-CKD dementia may be attributable to the different mechanisms that occur in CKD. The kidney and brain have similar anatomical vascular systems, which may be susceptible to traditional risk factors. Vascular factors are assumed to be involved in the development of cognitive impairment in patients with CKD. Vascular injury induces white matter lesions, silent infarction, and microbleeds. Uremic toxins may also be directly related to cognitive impairment in CKD. Many uremic toxins, such as indoxyl sulfate, are likely to have an impact on the central nervous system. Further studies are required to identify therapeutic targets to prevent changes in the brain in patients with CKD.

In this article, Table 1's data was given incorrectly. Metodopramide should be corrected as Metoclopramide.

Soft-tissue sarcomas account for 1% of all solid tumors. Of these, less than 15% will occur in the retroperitoneum. Late diagnosis and large tumor size make retroperitoneal sarcomas difficult to resect. Resection with wide margins in all directions is rarely possible owing to proximity to vital structures. Radiation therapy is limited in dosage and, as with chemotherapy, has only been successful in a limited number of cases. These problems result in a poor prognosis. A series of patients with retroperitoneal sarcoma was reviewed with a focus on issues of surgical management and prognostic factors. A retrospective analysis of 12 patients with retroperitoneal sarcomas who had undergone operations at the Department of Surgery, Inje University Paik Hospital, Seoul, from 1980 through 1996 was performed. The mean age of the 10 adult patients was 51 years; the male-to-female ratio was 2:1. Eighty-three percent of the patients presented with an abdominal mass. The mean diameter of the tumors was 18.3 cm. Leimyosarcomas(33%) and liposarcomas(25%) comprised the majority of the histologic types. The tumor grades were I, II, and III in 3 cases each. Resection of the tumor was possible in 75%(9/12) of the cases, although 17% of the resections were incomplete. Resection of adjacent organs was required in 66% of the cases. The resectability rose from 60% in 80s to 86% in 90s, with no statistical significance, possibly due to the small number of cases in this series. There was no postoperative morbidity or mortality. Actuarial 1-, 3-, and 5-year survival rates after resection were 75%, 60%, and 30%, respectively. Four of the 7(57%) patients who underwent complete resections had recurrence 3 to 33 months after surgery; this was notable for grade II or III tumors only. Two patients with grade I tumors are alive 65 and 102 months respectively after complete resection and show no evidence of the disease. One patient who underwent an incomplete resection of the tumor died 50 months after the operation. Only the tumor grade was a significant prognostic factor(p=0.0207). In conclusion, a wide en-bloc resection of a retroperitoneal sarcoma with a clear margin in all directions is a prerequisite for long-term survival. Aggressive follow-up for the first 3 years after a complete resection of a high-grade tumor is justified.
Adult ; Delayed Diagnosis ; Drug Therapy ; Follow-Up Studies ; Humans ; Mortality ; Prognosis ; Recurrence ; Retrospective Studies ; Sarcoma* ; Seoul ; Survival Rate

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.

The mortality rate of acute paraquat (PQ) poisoning depends on the PQ concentration in the blood. It has been shown that the kidneys eliminate PQ effectively. However, early renal function deterioration is frequently observed in acute PQ intoxication. This study is designed to compare the efficacy of PQ elimination with hemoperfusion (HP) and kidneys, taking into account the functional deterioration of the kidneys. The amount of renal and HP excretion of PQ were measured during the procedure of HP in patients with acute PQ intoxication. The PQ clearance and the actual amount of PQ elimination by the HP cartridge during the HP procedure were 111+/-11 mL/min (range; 13.2-162.2 mL/min) and 251.4+/-506.3 mg (range; 4.6- 1,655.7) each. While, the renal clearance and actual amount of renal elimination of PQ was 79.8+/-56.0 mL/min (range; 9.7-177.0) and 75.4+/-73.6 mg (range; 4.9- 245.8). As the creatinine clearance decreased, the PQ elimination by HP was as effective as or more effective than the renal elimination. In conclusion, early HP must be provided for life saving treatment in patients with acute PQ intoxication.
Adult ; Aged ; Creatinine/blood ; Emergency Medicine/methods ; Female ; Hemoperfusion/*methods ; Herbicides/*poisoning ; Humans ; Kidney/drug effects/physiology ; Male ; Middle Aged ; Overdose/therapy ; Paraquat/*poisoning ; Renal Dialysis/*methods ; Suicide

BACKGROUND/AIMS: Based on preliminary in vitro data from a previous study, we proposed that 50 mg/kg glutathione (GSH) would be adequate for suppressing reactive oxygen species in patients with acute paraquat (PQ) intoxication. METHODS: Serum levels of reactive oxygen metabolites (ROM) were measured before and after the administration of 50 mg/kg GSH to each of five patients with acute PQ intoxication. RESULTS: In one patient, extremely high pretreatment ROM levels began to decrease prior to GSH administration. However, in the remaining four cases, ROM levels did not change significantly prior to GSH administration. ROM levels decreased significantly after GSH administration in all cases. In two cases, ROM levels decreased below that observed in the general population; one of these patients died after a cardiac arrest at 3 hours after PQ ingestion, while the other represented the sole survivor of PQ intoxication observed in this study. In the survivor, ROM levels decreased during the first 8 hours of GSH treatment, and finally dropped below the mean ROM level observed in the general population. CONCLUSIONS: Treatment with 50 mg/kg GSH significantly suppressed serum ROM levels in PQ-intoxicated patients. However, this dose was not sufficient to suppress ROM levels when the PQ concentration was extremely high.
Adult ; Aged ; Antioxidants/administration & dosage ; Case-Control Studies ; Fatal Outcome ; Glutathione/*administration & dosage ; Herbicides/administration & dosage/poisoning ; Humans ; Male ; Middle Aged ; Paraquat/administration & dosage/*poisoning ; Pilot Projects ; Reactive Oxygen Species/*blood ; Time Factors ; Treatment Outcome

Although glufosinate ammonium herbicides are considered safe when used properly, ingestion of the undiluted form can cause grave outcomes. Recently, we treated a 34-yr-old man who ingested glufosinate ammonium herbicide. In the course of treatment, the patient developed apnea, mental deterioration, and sixth cranial nerve palsy; he has since been discharged with full recovery after intensive care. This case report describes the clinical features of glufosinate intoxication with a focus on sixth cranial nerve palsy. Our observation suggests that neurologic manifestations after ingestion of a "low-grade toxicity herbicide" are variable and more complex than that was previously considered.
Abducens Nerve Diseases/*chemically induced/drug therapy ; Adult ; Aminobutyrates/*poisoning ; Enzyme Inhibitors/poisoning ; Herbicides/*poisoning ; Humans ; Male ; Seizures/chemically induced ; Surface-Active Agents/poisoning ; Unconsciousness/chemically induced

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*