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polyuria/infarction

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Polyuria polydipsia syndrome showing a renal infarction.

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Clean intermittent catheterization is a well-known procedure of urinary drainage for patients who are unable to empty the bladder sufficiently. However, some patients with bladder dysfunction and nocturnal polyuria fail to obtain the benefits of intermittent catheterization and have annoying
Diabetes mellitus is associated with acute and chronic complications that cause major morbidity and significant mortality. We report a 69-year-old man with unknown diabetes, presenting vague epigastric discomfort, polyuria, polydipsia, fatigue, anorexia, weight loss over 1 week and severe chest pain
Arteriosclerotic and nonarteriosclerotic rats were treated with carbon tetrachloride (CCL4) to induce cirrhosis of the liver. Massive myocardial infarction was then induced in intact and CCL4-treated animals. During acute necrosis (Days 1 thru 3), animals were killed at 4, 8, 12 and 24 h on Days 1

Polyuria and refractory hypernatremia after cardiopulmonary arrest.

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A patient exhibited brain damage, polyuria, and refractory hypernatremia after myocardial infarction and cardiopulmonary arrest. Serum vasopressin levels were relatively fixed and inappropriately low for the elevated serum osmolality. Hypernatremia persisted despite administration of vasopressin;
A 59-year-old man visited Kyoto University Hospital because of general malaise, polyuria, and polydipsia. The diagnosis of primary hyperparathyroidism was made based on hypercalcemia and an elevated circulating PTH level. A nodule was palpable in the left anterior neck. Two weeks later, the serum
BACKGROUND Cerebral salt-wasting syndrome is a condition featuring hyponatremia and dehydration caused by head injury, operation on the brain, subarachnoid hemorrhage, brain tumor and so on. However, there are a few reports of cerebral salt-wasting syndrome caused by cerebral infarction. We describe
OBJECTIVE To investigate the method for establishing animal model of integrative medical disease/ syndrome and its evaluation. METHODS Rat myocardial (heart failure) model was established by anterio-descending coronary arterial ligation, and treated by nitric oxide synthase inhibitor 9-12 weeks
The aim of this study was to determine the efficacy of intranasal desmopressin in the treatment of nocturnal polyuria in men with benign prostatic hyperplasia (BPH). Twelve men with BPH were treated with intranasal desmopressin at bedtime for nocturnal polyuria. All patients underwent

[A 71-year-old man with Cushing reflex].

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BACKGROUND The Cushing reflex in comatose intensive care patients usually indicates that intracranial perfusion is about to be abolished. METHODS A 71-year-old man suffered an attack during which he became comatose. After 14 hours he developed polyuria, dilated fixed pupils and Cushing reflex. The
After elective hospitalization, eleven healthy young women developed symptomatic hyponatremia that was rapidly followed by polyuria, hypernatremia, hyperglycemia, and death. The patients were 30 +/- 2 years old (+/- SE) with initial serum sodium of 140 +/- 1 mmol/L. They all awoke from analgesia
Copeptin, arginine vasopressin (AVP)-associated 39 aminoacid glycopeptide, is a C-terminal part of pro-AVP. AVP acts through V1a, V1b, and V2 receptors. The effect on V1a receptors is connected with arterial vasoconstriction, on V2 with antidiuretic action, and on V1b with the secretion of ACTH,
A 73-year-old woman was admitted with dry mouth, polyposia, polyuria, hyperglycemia (611 mg/dl) and positive urine ketone bodies. Blood glucose levels decreased gradually after initiation of insulin injections. The patient was discharged, but developed involuntary movement of the right extremities
An 18-month-old neutered male domestic shorthair cat was referred with a history of pyrexia, polyuria and polydypsia, and transient episodes of bilateral hindlimb paralysis. Cardiac evaluation revealed severe systemic hypertension and severe concentric hypertrophy of the left ventricle. One month
A 56-year-old woman was hospitalized with a right hemiplegia and aphasia evoking a cerebral infarction. In fact the neurologic deficits were of post-ictal origin, secondary to a partial epilepsy which began a few weeks before, at the same time as a polyuria-polydipsia syndrome revealing diabetes
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