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the nephron is the filtering unit of the kidney where urine is made. each nephron consists of
think of the nephron as a big factory with an assembly line coming into it (the renal artery). what the factory workers (nephrons) at the separating room (glomerulus) do is separate the blood cells from the serum of the blood and send the serum (filtrate) on for processing (renal tubule) where it is acted upon by eager cells looking to retrieve back some of what they lost (fluids and electrolytes) at the separating room (peritubular capillaries) so they can continue on their way out the back door of the factory and get the heck out of dodge (the renal vein)!
as gfr decreases, plasma creatinine levels increase proportionately without regulatory adjustment. as sodium delivery to the nephron increases, less is reabsorbed, and sodium deficits and volume depletion follow. the kidney becomes incapable of concentrating and diluting urine. when gfr decreases by 30% to 40% (meaning 30-40% of the blood serum is no longer being separated out and sent onward for processing in the renal tubules), progressive metabolic acidosis ensues and tubular secretion of potassium increases. total-body potassium levels may increase to life-threatening levels requiring dialysis.
i've answered several previous questions about renal pathophysiology. i've listed the threads. this stuff is not initially easy to understand with one reading. even i have to sit down and cogitate on it for a while and i worked on a renal unit!
marlonAAPN
13 Posts
why those patient having Acute glomerulonephritis can lead to hyperkalemia?.
thnx.:redbeathe