tag:blogger.com,1999:blog-4230162007222918868.post1015508014982993185..comments2023-09-19T05:50:03.130-04:00Comments on Renal Fellow Network: The urine's the thing...Gearoid McMahonhttp://www.blogger.com/profile/08049723797363526138noreply@blogger.comBlogger1125tag:blogger.com,1999:blog-4230162007222918868.post-11795076410494158102010-05-01T23:26:49.053-04:002010-05-01T23:26:49.053-04:00Here is a little more detailed explanation incorpo...Here is a little more detailed explanation incorporated into the original post for those wanting it, courtesy of Dr. Julian Seifter......<br /><br />Initially, as blood bicarbonate is raised due to gastric acid loss, the bicarbonate spills into the urine, accompanied by sodium and potassium. The urine is alkaline, K losses gradually increase due to the bicarbonaturia, and sodium losses contribute to the volume depletion while the high Na concentration of urine belies the ECF depletion. Metabolic alkalosis induced by gastric loss is associated with extracellular volume depletion and a fall in GFR. In this setting, increased AII and secondary hyperaldosteronism ensue, leading to sodium retention and further potassium wasting,. The GI losses are also associated with chloride depletion and hypochloremia. Chloride reabsorption in the setting of gastric Cl losses results in low urinary Cl concentrations. Sodium reabsorption through the epithelial Na channels in the principal cells of the collecting segments and cortical collecting duct, create a greater lumen-negativity that enhances K secretion and H+ secretion. The result is maintainence of alkalosis, steady increases in bicarbonate reabsorption and continued urinary K losses. Ultimately, due to enhanced Na and HCO3 reabsorption in the proximal and distal nephron (due to hypokalemia, hypovolemia and aldosterone, meatbolic alkalosis persists while all filtered bicarbonate is reabsorbed. The steady state is reached and urinary Na is appropriately low, and urinary pH is acid, a condition known as paradoxical aciduria in metabolic alkalemia. Such alkaloses are termed saline responsive, as administration of saline leads to correction of hypovolemia and therefore removes the stimulus to proximal NaHCO3 reabsorption and aldosterone, while at the same time chloride replenishment allows for the excretion of bicarbonate, leading to an appropriately alkaline urine and rapid correction of the electrolyte abnormalities as long as the K deficit is corrected with Cl salts.Ernest Mandelhttps://www.blogger.com/profile/06718621055634863757noreply@blogger.com