30-year-old male was admitted with general weakness and drowsy mental status. He had eaten only 3-4 spoons of brown rice and fresh vegetable without salt for 3 months to treat his tic disorder, and he had been in bedridden state. He has had weight loss of 14 kg in the last 3 months. We report a patient with orthorexia nervosa who developed hyponatremia, metabolic acidosis, subcutaneous emphysema, mediastinal emphysema, pneumothorax, and pancytopenia and we will review the literature. Also, we mention to prevent refeeding syndrome, and to start and maintain feeding in malnourished patients.

This is a case of a sudden cardio-pulmonary arrest in a 29 year-old female, which occurred immediately after a large bolus infusion of propofol (100 mg) intravenously during dilatation and curettage. The arrest suddenly occurred, and the patient was eventually transferred to our emergency room (ER) on cardiopulmonary resuscitation. At that time, severe hyperkalemia up to 9.1 mEq/ L and ventricular fibrillation were noted. Resuscitation in ER worked successfully with conversion of electrocardiograph to sinus rhythm, but this patient expired unfortunately. On view of this acute event immediately after the bolus injection of propofol accompanied without other identified causes, severe hyperkalemia induced by propofol was strongly assumed to be the cause of death. To our understanding with the literature survey, propofol as a cause of hyperkalemia has not been well described yet. Through this case, the relationship as a cause and an effect between propofol and hyperkalemia is suggested.

Bupropion is widely used for the treatment of depressive disorder and smoking cessation. Hyponatremia, including a syndrome of inappropriate secretion of antidiuretic hormone (SIADH), is not rare complication of treatment with antipsychotic drugs. We report a 60-year-old man who experienced severe hyponatremia after a treatment with bupropion for depressive disorder for the first time in the Korea.

This study aimed to investigate the influence of different peritoneal dialysis regimens on blood pressure control, the diurnal pattern of blood pressure and left ventricular hypertrophy in patients on peritoneal dialysis. Forty-four patients undergoing peritoneal dialysis were enrolled into the study. Patients were treated with different regimens of peritoneal dialysis: 26 patients on continuous ambulatory peritoneal dialysis (CAPD) and 18 patients on automated peritoneal dialysis (APD). All patients performed 24-hour ambulatory blood pressure monitoring (ABPM) and echocardiography. Echocardiography was performed for measurement of cardiac parameters and calculation of left ventricular mass index (LVMI). There were no significant differences in average of systolic and diastolic blood pressure during 24-hour, daytime, and nighttime between CAPD and APD groups. There were no significant differences in diurnal variation of blood pressure, systolic and diastolic blood pressure load, and LVMI between CAPD and APD groups. LVMI was associated with 24 hour systolic blood pressure load (r = 0.311, P

Cyclophosphamide is clinically useful in treating malignancy and rheumatologic disease, but has limitations in that it induces hyponatremia. The mechanisms by which cyclophosphamide induces water retention in the kidney have yet to be identified. This study was undertaken to test the hypothesis that cyclophosphamide may produce water retention via the proximal nephron, where aquaporin-1 (AQP1) and aquaporin-7 (AQP7) water channels participate in water absorption. To test this hypothesis, we gave a single dose of intraperitoneal cyclophosphamide to male Sprague-Dawley rats and treated rabbit proximal tubule cells (PTCs) with 4-hydroperoxycyclophosphamide (4-HC), an active metabolite of cyclophosphamide. In the short-term 3-day rat study, AQP1 protein expression was significantly increased in the whole kidney homogenates by cyclophosphamide administration at 48 (614 ± 194%, P

Mineral metabolism abnormalities, such as low 1,25-dihydroxyvitamin D (1,25(OH)2D) and elevated parathyroid hormone (PTH), are common at even higher glomerular filtration rate than previously described. Levels of 25-hydroxyvitamin D (25(OH)D) show an inverse correlation with those of intact PTH and phosphorus. Studies of the general population found much higher allcause and cardiovascular (CV) mortality for patients with lower levels of vitamin D; this finding suggests that low 25(OH)D level is a risk factor and predictive of CV events in patients without chronic kidney disease (CKD). 25(OH)D/1,25(OH)2D becomes deficient with progression of CKD. Additionally, studies of dialysis patients have found an association of vitamin D deficiency with increased mortality. Restoration of the physiology of vitamin D receptor activation should be essential therapy for CKD patients.