Cases reported "Polyuria"

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1/4. Persistent water diuresis in renal amyloidosis. A case report.

    A 67-year-old male with previous history of osteomyelitis presented with persistent thirst and polyuria. His urine remained hyposmolar to plasma after overnight fasting and administration of pitressin. biopsy and postmortem examination revealed renal amyloidosis with involvement of many glomeruli and smaller vessels. Amyloid was also found in the medulla, particularly around the collecting tubules. It is suggested that amyloid interfered directly with diffusion of water through the walls of the collecting tubules.
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2/4. Obstructive polyuric renal failure following renal transplantation.

    In a previously nephrectomized patient with a well functioning renal allograft, acute renal failure with massive polyuria and hypertension developed. Relief of a periureteric obstruction resulted in rapid correction of all three. Pathogenesis of hypotonic polyuria is thought to be a defect in the collecting duct permeability to water, stimulating nephrogenic diabetes insipidus. Normal urinary dilution and acidification suggest intact function of the ascending loop of henle and distal convoluted tubules. The quick reversal of polyuria and renal failure after obtaining relief of the obstruction suggest that both the decrease in the glomerular filtration rate and tubular dysfunctions are due to functional changes in the nephron rather than to organic damage, a possibility also borne out by the findings in a renal biopsy specimen showing normal glomeruli and intact tubular epithelial cells. Ureteric obstruction should be considered in any patient with renal failure and polyuria; it may be a correctable cause of hypertension.
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3/4. Mechanism of inappropriate polyuria in septic patients.

    Inappropriate polyuria leading to hypovolemia and hypotension occurs frequently in severely septic patients. It's etiology was studied in three patients with polyuria and systolic hypotension. glomerular filtration rate and renal blood flow were measured by the standard renal clearance techniques. Renal blood flow distribution to the outer cortex, inner cortex-outer medulla, and the inner medulla were measured by radioactive xenon. The glomerular filtration rate, renal blood flow, and renal blood flow distribution were normal. polyuria does not result from a maldistribution of renal blood flow. Antidiuretic hormone did not alter the polyuric syndrome. These data suggest that sepsis produces a blockade at either the distal tubule or the collecting duct, thereby preventing salt and water conservation. This blockade may be due to either a toxin or a toxic metabolic breakdown product of sepsis.
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4/4. An extreme example of the neonatal form of Bartter's syndrome.

    A male infant is described who had polyuria over the 4 months of his life with urine volumes exceeding 1,000 ml/kg per day, severe serum electrolyte losses, metabolic alkalosis and increased plasma renin activity (56 ng/ml per hour). He had a normal blood pressure and glomerular filtration rate when fluid replete. The urine flow rate was about 25% of the glomerular filtration rate. Renal histology showed hyperplasia of the juxtaglomerular apparatus and abnormalities of the proximal tubules. The features of this case suggest an extreme form of Bartter's syndrome presenting from the first days of life.
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