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.

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

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

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.

Microscopic polyangiitis (MPA) is a systemic small vessel vasculitis with few or no immune deposits and no granulomatous inflammation. Peripheral neuropathy occurs in approximately 20%–30% of patients with MPA. We report a case of a 66-year-old woman who presented with paresthesia and motor weakness of the extremities and rapidly progressive glomerulonephritis. She was later diagnosed with MPA based on the findings of positive perinuclear antineutrophil cytoplasmic antibody along with findings on kidney biopsy. Nerve conduction study showed symmetric sensorimotor polyneuropathy. We followed the patient for 3 years, and she showed good functional outcome after immune-modulating therapy although Five-Factor Score more than 2 at diagnosis.
Aged ; Antibodies, Antineutrophil Cytoplasmic ; Biopsy ; Diagnosis ; Extremities ; Female ; Follow-Up Studies* ; Glomerulonephritis ; Humans ; Inflammation ; Kidney ; Microscopic Polyangiitis* ; Neural Conduction ; Paresthesia ; Peripheral Nervous System Diseases* ; Polyneuropathies ; Vasculitis

We investigated whether glyphosate influences the cellular toxicity of the surfactants TN-20 and LN-10 on the mouse fibroblast-like cells, alveolar epithelial cells, and a heart cell line. The cytotoxicity of TN-20 and LN-10 (0.4-100 microM), in the presence or absence of glyphosate was determined by assessing membrane integrity. TN-20 toxicity was significantly lower in the presence of 50 microM glyphosate for the fibroblast-like cell (6.25 microM; 3.9% +/- 3.4% vs -4.8% +/- 0.7%), for the alveolar cells (0.78 microM; 5.7% +/- 0.9% vs 0.1% +/- 0.6%), and for the heart cell line (25.0 microM; 7.9% +/- 3.0% vs 19.4% +/- 0.7%) compared to that of TN-20 alone. The cellular toxicity of LN-10 towards the fibroblast-like cells was found to be increased in the presence of 50 microM glyphosate when LN-10 concentrations of 50 microM (31.3% +/- 3.9% vs 19.2% +/- 0.9%) and 100 microM (62.1% +/- 3.4% vs 39.0% +/- 0.7%) were compared to that of LN-10 alone. These results suggest that the mixture toxicity may be a factor in glyphosate-surfactant toxicity in patients with acute glyphosate herbicide intoxication.
Animals ; Cell Line ; Cell Survival/drug effects ; Glycine/*analogs & derivatives/chemistry/toxicity ; Herbicides/chemistry/*toxicity ; Mice ; Polyethylene Glycols/*chemistry ; Surface-Active Agents/*chemistry

Precise measurement of postvoid residual (PVR) urine volume is a key factor in assessing patients with voiding dysfunction, including those with lower urinary tract problems. The safe and noninvasive ultrasound bladder scan is the preferred mode to measure PVR volume. However, this procedure has a false-positive rate up to 9%, in the presence of ovarian cysts, renal cysts, ascites, or uterine myoma with cystic degeneration. Until now, cystic lesions are known to cause false positivity in ultrasound bladder scanner. However, we encountered falsely-elevated PVR in two cases of non-cystic uterine myomas. We present these cases with detailed radiologic images and volume measurement data.
Ascites ; Female ; Humans ; Leiomyoma* ; Myoma ; Ovarian Cysts ; Ultrasonography ; Urinary Bladder ; Urinary Tract

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