Loops question

[phd89]

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Question 1
FA says-- "Loops abolish hypertonicity of medulla preventing conc. of urine

I thought loops blocked the na/k/cl channel so all these ions would not be reabsorbed by the think ascending limb and stay in the tubule to inc the osmolarity of the tubule can someone explain this?

Question 2
Also In Type 2 Renal Tubular Acidosis there is loss of HCO3 in the urine but still an acidic urine shouldn't it be an alkaline urine since the HCO3 is in it?

 

[withrye]

Question 1
FA says-- "Loops abolish hypertonicity of medulla preventing conc. of urine

I thought loops blocked the na/k/cl channel so all these ions would not be reabsorbed by the think ascending limb and stay in the tubule to inc the osmolarity of the tubule can someone explain this?

Question 2
Also In Type 2 Renal Tubular Acidosis there is loss of HCO3 in the urine but still an acidic urine shouldn't it be an alkaline urine since the HCO3 is in it?

#1: Remember that the reason water leaves the tubule on its way down is that it's surrounded by a hypertonic medullary space. That hypertonic interstitium is created by the NKCC pump in the TAL. If you block the NKCC pump, the water will have little cause to exit in the descending limb, so no concentration occurs. You're still correct in saying that those solutes remain in the fluid once they get to the TAL, but it's more important to remember that you haven't lost any water either.

#2: The acidification of the urine happens largely by the distal intercalated cells. Because these aren't broken, you're still able to pump H+ into the bicarb-rich urine. The effect of this is that the urine can still be acidified, but you end up losing more bicarb than normal, leading to an acidosis in the body.

 

[Phloston]

Question 1
FA says-- "Loops abolish hypertonicity of medulla preventing conc. of urine

I thought loops blocked the na/k/cl channel so all these ions would not be reabsorbed by the think ascending limb and stay in the tubule to inc the osmolarity of the tubule can someone explain this?

The electrolytes reabsorbed by the ascending loop create the drive for the medullary collecting duct to reabsorb free water when vasopressin is present.

The ultimate determinant of whether your urine is dilute or concentrated is your ADH-regulated medullary principal cells. Think about it: in DI, urine is ultra-dilute, even though the rest of the nephron is working just fine.

So if you decrease hypertonicity of the medullary interstitium via the use of loops, free H2O is less likely to be pulled from the lumen of the medullary collecting ducts when ADH is present, thereby demolishing urine concentrating ability.

The vasa recta also contributes to this. There's an ascending and descending limb. The descending limb reabsorbs NaCl while secreting H2O; the ascending limb secretes NaCl while reabsorbing H2O. The descending limb runs along the ascending loop of Henle, so that creates extra driving force for the active symport in the loop. The ascending limb runs closer to the collecting ducts, so it can create additional drive for free H2O reabsorption.

In sickle cell anaemia or diabetes, the vasa recta is damaged. This leads to decreased ability to concentrate the urine because the vasa recta creates a more significant drive for free H2O reabsorption from the medullary collecting duct than it does from the loop, which has active transport. When kidney damage is very severe, however, urine diluting ability is lost as well.

Question 2
Also In Type 2 Renal Tubular Acidosis there is loss of HCO3 in the urine but still an acidic urine shouldn't it be an alkaline urine since the HCO3 is in it?

The loss of HCO3- (an anion) at the PCT necessitates a cation be lost with it (Na+ or K+). This is the equivalent of using acetazolamide. And with acetazolamide-use, you get Na+ losses, which are reclaimed by the cortical principal cells, under the control of aldosterone. However, aldosterone is non-selective in its funtion; in order to increase Na+ reabsorption at the cortical principal cells, H+ must be secreted at the cortical intercalated cells. Therefore, the PCT Na+ losses drive the CCD H+ secretion to an extent that supersedes the PCT HCO3- losses, thereby inducing acidic urine.

RTA-II is associated with Fanconi syndrome, which can lead to osteomalacia/rickets.


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Edit:

Important note: ADH induces medullary CD effects, whereas aldosterone induces cortical CD effects.