Collecting Duct (CD): Other Renal Tubular Acidoses

by Carlo Raj, MD

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    00:00 Important renal tubular acidoses that you want to know further and really this kind summarizes the two that you need to know down the collecting duct. So lets keep it simple.

    00:11 You need to know about one, two and four. Remember two? You do. How many lines you need to form an X? One. Two. What part of the nephron requires an X? Proximal convoluted tubule, Are we clear now? What was my problem with proximal convoluted tubule RTA type II? There might have been an issue with your carbonic anhydrase. Remember that discussion that we had quite extensively. Let us now jump over and skip down to the distal convoluted tubule, please. In the distal convoluted tubule, we will first take a look at type I. Now it can be in the collecting duct distal region. Do not get hung up for the exact location.

    00:56 That is going to be at this point not the best use of your time. The best use of your time at this point is that you know that you are not in the proximal convoluted tubule.

    01:06 So what is going with type I? Now the details as far as how this occurs is a little theoretical, but all we know for sure is this first bullet point for type I RTA, distal.

    01:22 Impaired excretion of hydrogen. When you say renal tubular acidosis couple of things automatically come to mind. That acidosis is referring to your pH in your blood, blood, blood. Not your urine. And your blood being decreased. Number 1. How did this occur? In the distal convoluted tubule, you would not able to properly get rid of your hydrogen, hydrogen, hydrogen, therefore, remains within the blood. What happens to your pH? Drops. Next, as I said unclear in terms of its etiology, hydrogen remains back in your blood results in severe non-anion gap, metabolic acidosis. What does that mean to you? Let sync together. When you do metabolic acidosis, you are going to do anion gap. Always. So metabolic acidosis anion gap that should be next step in terms of diagnosis. What is anion gap mean to you? It is your cations minus the anions. The cation is the sodium. The anions are your chloride and bicarb. When you do that formula, you end up getting a normal anion gap between 8 and 12 clinically we call this a non-anion gap. Okay. Severe though severe.

    02:37 Now the causes include the following. These are things which you are looking for underlying with type I, maybe it's do re mi fa so la. What am I talking about? What is this? This is ro and you have heard of la. In other words Ssa and Ssb. Really. Remember clinical practice all jokes aside. Clinical practice Ssa and Ssb is huge for you to diagnose Sjogren. Ssa is going to ro. Ssb is going to la. Okay. If you want, you may want to use lab, la is Ssb.

    03:22 Ro is Ssa. What is my diagnosis? Autoimmune disease called Sjogren. Type I RTA. Tell me about Sjogren. No tears. Xerophthalmia. The lacrimal gland has been knocked out. Autoimmune disease.

    03:41 What about your mouth? No saliva. You can’t protect the teeth maybe dental caries causes xerostomia. Sjogren. Number 1. Distinguishing feature dryness. Autoimmune diseases, Sjogren, children, hereditary transport defect, of what? Hydrogen. That is type I. So type II proximal convoluted tubule.

    04:04 You cannot reabsorb bicarb. Welcome to RTA type II. RTA type I distal...

    04:10 hydrogen, is it going to be type IV? Type IV renal tubular acidosis, hypoaldosteronism.

    04:19 If you don't have sufficient amount of aldosterone, hence the time that we have spent on truly understanding aldosterone and at some point maybe even got bored, which is a good thing, which means that you know aldosterone in and out. So based on that you tell me what just happened.

    04:37 If for whatever reason aldosterone is not present or inadequately present, then your sodium is not being properly reabsorbed. Look for decreased sodium. Okay fine. Next what about potassium? You can't properly get rid of this so it may result in hyperkalemia. Okay fine.

    04:52 I understand the electrolytes Dr.Raj get to the point. Renal tubular acidosis. This is the only one in which you would have hyperkalemia and you can’t get rid of the hydrogen. What happens to your pH, please? Here you go. Acidosis. So type IV renal tubular acidosis is a simple as understanding that there is either aldosterone inadequacy or there is resistance to that aldosterone resulting in acidosis with prominent hyperkalemia. Did we see such a thing with type II RTA? No, we did not see hyperkalemia in type II. What about type I? We did not see hyperkalemia in type I. In type I the hydrogen for unclear etiology know that, you are not able to properly secrete your hydrogen. In type II, one more time maybe it's issues with your carbonic anhydrase and just to be technical in the proximal convoluted tubule with type II may be you are not able to get rid of that hydrogen. So therefore resulting in RTA I, II and IV. This would be a good time for you to review all of the three major renal tubular acidoses, metabolic acidosis non-anion gap type of issues. What about type III, Dr. Raj? Let it go. Please, can you do that for me? TypeI, II and IV is what you pay attention to. Period.

    06:24 Medical findings of Addison's. You will find this to be interesting. In Addison's disease, lets stop here. What does that mean? I want to take the ADD in Addison's, what does that spell? Add. So you are adding hormones to this disease. There you have it. So what ends up happening primarily is that the adrenal gland is primarily destroyed so that adrenal gland is gone. It is destroyed. What do you need to do? You need to add hormones. Is that clear? So what is this called when adrenal gland is dead and you don't have, number 1: aldosterone.

    07:07 Number 2: it's a fasciculata. Cortisol, you don't have that either. And those are two that you want to pay attention to, because that will then give you a diagnosis of Addison's for right now since we are doing nephrology lets stick with the aldosterone, shall we? Thank you.

    07:26 So this is primary adrenal insufficiency aka Addison's. Okay. If you don't have your glomerulosa working properly, you don't have aldosterone, can you then walk me through and may result in what kind of renal tubular acidosis? Type IV, good. Hyponatremia, hypokalemia. You get that.

    07:44 I am not going to cover that again. We have done that plenty. Due to inhibition of sodium reabsorption and potassium excretion, hypertonic loss of sodium in the urine. It is a salt wasting disease. Salt wasting disease, what kind of question are going to get here in physio? Walk you through this. You are losing fluid. What happens to ECF? You are losing fluid.

    08:09 What is the first compartment that you always pay attention to? Work with me here. Look at me. What is the first compartment you pay attention to? It is always a plasma compartment.

    08:19 Where is the plasma compartment in the ECF? Are we good? You are losing fluid. Plasma compartment contracts. ECF compartment contracts. Stop there. In Addison's disease, you are losing a lot of, look at what that says. Hypertonic loss of sodium. So you are losing fluid, granted but you are losing a lot of solutes. So ECF osmolarity decreases. ECF volume decreases.

    08:52 Number 3, If your ECF osmolarity decreases, where are you going to go? Into the ICF. Are we clear? If you go into the ICF, what happens to ICF volume? Expansion, good. If water goes into the ICF, what happens to ICF osmolarity? Decreases. Do you see how simple this is when you understand the physio, you can bring in the clinical application? You don't have to sit there and memorize. But if you go through that order every single time, you are in good shape.

    09:24 ECF volume, ECF osmolarity, ICF volume, ICF osmolarity in that order . Next, retention of hydrogen. What does it cause? RTA type IV.

    About the Lecture

    The lecture Collecting Duct (CD): Other Renal Tubular Acidoses by Carlo Raj, MD is from the course Diseases of the Nephron.

    Included Quiz Questions

    1. Anion gap metabolic acidosis
    2. Xeropthalmia
    3. Type 1 renal tubular acidosis
    4. SSA and SSB antibodies
    5. Non-anion gap metabolic acidosis
    1. Hypoaldosteronism
    2. Proximal renal tubular acidosis
    3. Distal renal tubular acidosis
    4. Type III renal tubular acidosis
    5. Hyperaldosteronism
    1. Distal convoluted tubular location and an anion gap of 10
    2. Distal convoluted tubular location and an anion gap of 20
    3. Proximal convoluted tubular location and an anion gap of 10
    4. Proximal convoluted tubular location and an anion gap of 20
    1. Increased ECF osmolarity
    2. Decreased ECF osmolarity
    3. Decreased ECF volume
    4. Increased ICF volume
    5. Decreased ICF osmolarity
    1. Increased urinary sodium
    2. Increased urinary potassium
    3. Metabolic alkalosis
    4. Hypokalemia
    5. Hypernatremia
    1. Impaired excretion of H⁺
    2. Deficiency of aldosterone
    3. Impaired bicarbonate production
    4. Impaired bicarbonate reabsorption
    5. Resistance to aldosterone

    Author of lecture Collecting Duct (CD): Other Renal Tubular Acidoses

     Carlo Raj, MD

    Carlo Raj, MD

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