1.Renal Vein Thrombosis in Obese Patient.
Min Jeong SON ; Ha Jeong LEE ; Kook Hwan OH ; Kwon Wook JOO ; Sunhngwon KIM
Korean Journal of Nephrology 2009;28(5):501-504
Renal vein thrombosis (RVT) is mostly related with other causes. The underlying conditions of RVT were nephrotic syndrome, trauma, cancer, anatomical anomalies, and other hypercoagulable status. Especially hypercoagulable status was rarely caused by obesity. We diagnosed renal vein thrombosis from an obese patient with hypertriglyceridemia. A male patient visited the Seoul National University Hospital for evaluating the reason of his flank pain. The pain started from two weeks ago, He had regarded flank pain as his obesity status (his weight was 84 kg and Body mass index was 29.41 kg/m2). So he had lost his weight by over-sweating one day before. At initial examination, his blood pressure was 128/75 mmHg, pulse rate was 72/min, respiration rate was 20/min and body temperature was 36.2degrees C. Blood chemistries revealed total cholesterol 218 mg/dL, Blood urea nitrogen/creatinine 12/1.3 mg/dL Urinalysis showed specific gravity 1.015, pH 5.5, protein 2+, blood 2+, RBC/WBC 1-4/<1 HPF on microscopic examination. Twenty-four hour collection of the urine showed protein 329 mg/day, creatinine clearance 90 mL/min. Renal vein thrombosis was visualized on the renal computed tomography and pulmonary embolism on the lung scan. Then, anticoagulant therapy was started after coagulation related tests. However, no abnormality of coagulation tests was detected. The evidence of malignancy was not detected either. After anticoagulation therapy, the pain was subsided. The only underlying cause for his hypercoagulability was considered obese status. Unfortunately we had not checked the triglyceride, initially. So we could not prioritize the reason of renal vein thrombosis into hypertriyglyceridemia. We considered that his obese status and subsequent hypertriyglyceridemia might be one of the causes of renal vein thrombosis.
Blood Pressure
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Body Mass Index
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Body Temperature
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Cholesterol
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Creatinine
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Flank Pain
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Heart Rate
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Humans
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Hydrogen-Ion Concentration
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Hypertriglyceridemia
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Lung
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Male
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Nephrotic Syndrome
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Obesity
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Pulmonary Embolism
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Renal Veins
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Respiratory Rate
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Specific Gravity
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Thrombophilia
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Thrombosis
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Urea
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Urinalysis
2.2 Cases of Severe Hyperchloremic Metabolic Acidosis after Orthotopic Neobladder Replacement and Augmentation Enterocystoplasty.
Hankyu LEE ; Hui Kyuoung SUN ; Dong Ki KIM ; Kook Hwan OH ; Yon Su KIM ; Curie AHN ; Jin Suk HAN ; Sunhngwon KIM ; Cheol KWAK ; Seungjune OH ; Kwon Wook JOO
Korean Journal of Nephrology 2010;29(5):600-605
The use of intestinal segments in the reconstruction and plasty of urinary bladder for malignant or nonmalignant conditions is widely accepted. Metabolic derangements including hyperchloremic metabolic acidosis and malabsorption of lipid may occur after surgery. Main pathophysiology of hyperchloremic metabolic acidosis is the exchange of urinary chloride with luminal bicarbonate and duration of urine in contact with the intestinal mucosa can affect the severity of metabolic acidosis. We experienced two cases of severe hyperchloremic metabolic acidosis which developed in patients with chronic kidney disease, urinary tract infection and orthotopic neobladder or augmentation enterocystoplasty for the treatment of bladder cancer and neurogenic bladder, respectively.
Acidosis
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Humans
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Intestinal Mucosa
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Phenobarbital
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Renal Insufficiency, Chronic
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Urinary Bladder
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Urinary Bladder Neoplasms
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Urinary Bladder, Neurogenic
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Urinary Diversion
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Urinary Tract Infections