in Type 2 RTA, the distal mechanism by which potassium is secreted in exchange for Na reabsorption is not "hyperactive". The mechanism is functioning in its normal capacity because the distal nephron is able to secrete H+ in exchange for Na reabsorption. This is one explanation for why you don't always see hypokalemia in type 2 RTA.
In type 1 RTA, there is an inability to secrete H+ into the urine. Normally, this secretion of H+ is accompanied by a reabsorption of Na+ from the urine back into the body. The reabsorption of Na+ is the main driving force for the secretion of the H+. Since this mechanism is malfunctioned, Na+ is subsequently reabsorbed at the expense of secreting K+. Thus, in type 1 RTA (distal), there is hypokalemia as Na+ reabsorption is facilitated by K+ secretion.
Thanks for this concise explanation! But it leaves me with a conundrum, which I'm afraid is related but slightly off-topic.. Systemic metabolic acidosis is known cause a decrease in sodium and water reabsorption in the kidney, resulting in an increase in urine volume. One example would be the attendant water loss from fasting-induced ketoacidosis. According to the mechanisms described here and in most textbooks, the opposite should occur, i.e., as H+ is excreted and HCO3- is reabsorbed, more Na+ (along with water) would be reabsorbed, resulting in decreased urine volume.
cool.I thought "somehow" osmotic overload of H+ was causing K+ secretion although acidosis causes the Na/K ATPase pump( on basolateral membrane) to malfunction and is actually supposed to causes hyperkalemia.Thanks now hypokalemia and acidosis are more cohesive with each other in RTA 1 but what about RTA 2?
I am sorry but I am looking through Guyton and other books of physiology.The only pumps for H+ secretion at the distal tubule are H+ ATPase pump and H/K ATPase pump in the alpha intercalated cells of the distal tubules These are the pumps that are dysfunctional in dRTA.No mention of Na/H pump ???
Problem is that you cannot use the urine anion gap reliably at pH urine > 6.5!? But if serum pH is acidic on blood gas, is that rule obviated as it exists to exclude situations where HCO3 is being excreted?
So, so, so helpful! Thank you!
in Type 2 RTA, the distal mechanism by which potassium is secreted in exchange for Na reabsorption is not "hyperactive". The mechanism is functioning in its normal capacity because the distal nephron is able to secrete H+ in exchange for Na reabsorption. This is one explanation for why you don't always see hypokalemia in type 2 RTA.
Nephrology On-Demand “distal nephron is able to secrete H+ in type 2RTA ?”
In type 1 RTA, there is an inability to secrete H+ into the urine. Normally, this secretion of H+ is accompanied by a reabsorption of Na+ from the urine back into the body. The reabsorption of Na+ is the main driving force for the secretion of the H+. Since this mechanism is malfunctioned, Na+ is subsequently reabsorbed at the expense of secreting K+. Thus, in type 1 RTA (distal), there is hypokalemia as Na+ reabsorption is facilitated by K+ secretion.
I think the explanation is perfect.The person knows exactly what he is talking about.However can you please explain hypokalemia in type 1 n 2
soo good
and that explains how if H+ is not secreted through H/K ATPase pump then K+ can also be not reabsorbed at this site leading to hypokalemia
Thanks for this concise explanation! But it leaves me with a conundrum, which I'm afraid is related but slightly off-topic.. Systemic metabolic acidosis is known cause a decrease in sodium and water reabsorption in the kidney, resulting in an increase in urine volume. One example would be the attendant water loss from fasting-induced ketoacidosis. According to the mechanisms described here and in most textbooks, the opposite should occur, i.e., as H+ is excreted and HCO3- is reabsorbed, more Na+ (along with water) would be reabsorbed, resulting in decreased urine volume.
cool.I thought "somehow" osmotic overload of H+ was causing K+ secretion although acidosis causes the Na/K ATPase pump( on basolateral membrane) to malfunction and is actually supposed to causes hyperkalemia.Thanks now hypokalemia and acidosis are more cohesive with each other in RTA 1 but what about RTA 2?
I am sorry but I am looking through Guyton and other books of physiology.The only pumps for H+ secretion at the distal tubule are H+ ATPase pump and H/K ATPase pump in the alpha intercalated cells of the distal tubules These are the pumps that are dysfunctional in dRTA.No mention of Na/H pump ???
Problem is that you cannot use the urine anion gap reliably at pH urine > 6.5!? But if serum pH is acidic on blood gas, is that rule obviated as it exists to exclude situations where HCO3 is being excreted?
I thought the PCT only reabsorbs water. Isnt that so?
PCT reabsorbs both sodium and water. There are Na+ H+ channels present on the PCT