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Hypoaldosteronism

by Carlo Raj, MD
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    00:01 If that was hyperaldosteronism, we will then move on to hypoaldosteronism.

    00:06 You do the same thing, quickly tell me.

    00:08 Serum levels decreased, potassium levels elevated, hydrogen is increased, thus Ph is decreased.

    00:13 Can you do it that quickly? Yes, you can.

    00:15 Listen to me again, you will get it.

    00:18 Results in… results from type 4 renal tubular acidosis or could result in.

    00:23 What do you mean? I just told you, if you didn’t have enough aldosterone, your hydrogen concentration increases in your plasma, what happens to your Ph? Oh, renal tubular acidosis.

    00:36 When you say renal tubular acidosis, what is that acidosis actually referring to? Not in the urine, right, it is in the plasma.

    00:44 Type 4, type 4, type 4.

    00:46 Remember, RTA, you want to know 1, 2, and 4.

    00:55 However, the biggest difference between this type of RTA and any other, if you don’t have aldosterone, take your time, aldosterone and potassium.

    01:03 If you don’t have aldosterone, you are not getting rid of potassium, you are retaining it resulting in hyperkalemia.

    01:11 Hmm, that is dangerous, that hyperkalemia is dangerous, especially for the heart.

    01:15 You are then causing, as you remember, depolarization of your resting membrane potential and that is not a good thing, is it? Hypoaldosteronism hyporeninemic, how is this occurring? Common in chronic kidney disease, so if the kidney starts decreasing in function then you know that you don’t have enough renin.

    01:38 If you don’t have enough renin then what then happens to your aldosterone level? Decreases.

    01:43 This is called hyporeninemic hypoaldosteronism.

    01:47 Say that three times fast.

    01:49 Language, language, language, apart from may be a little bit of memorization, but really understand what this is saying.

    01:57 Also seen with NSAIDs, cyclosporin and HIV, you could potentially have hyporeninemic hypoaldosteronism.

    02:06 Hyperreninemic hypoaldosteronism, how is this even possible? What if you give an ACE inhibitor? If you give an ACE inhibitor, you have inhibited the conversion of angiotensin 1 into angiotensin 2.

    02:23 Stop there.

    02:24 So, if you don’t even have angiotensin 2, how in the world are you going to stimulate that enzyme called aldosterone synthase? You can’t, resulting in… what is my topic? Good, hypoaldosteronism, but if you block that enzyme, all substrates proximally will increase.

    02:43 You put a block such an… such as an ACE inhibitor, a pril drug, renin increases, hyperreninemic hypoaldosteronism.

    02:52 Heparin, primary adrenal insufficiency in Addison’s disease.

    02:57 In Addison’s disease, how much of your cortex is destroyed? All of it.

    03:03 From henceforth, if you want to think of Addison’s primary adrenal insufficiency, you need to add hormones to your patient because all hormones are deficient, that’s Addison’s.

    03:16 And now, it’s getting really interesting.

    03:21 Conn syndrome, Cushing, Addison’s, students get this confused all the time.

    03:28 Keep replaying this, replaying this, replaying this so that this is firmly etched in your head.

    03:34 You must know the difference between Conn, Cushing and Addison.

    03:38 In Addison, a.k.a. primary adrenal insufficiency, entire cortex is dead, aldosterone is decreased, what is my feedback for aldosterone? Renin, I told you clinically, that is what you are paying attention to, hyperreninemic hypoaldosteronism.

    03:55 Potassium sparing drugs, congenital adrenal hyperplasia, what is this one? The most important enzyme deficiency in congenital isolated hyperplasia 21 beta hydroxylase.

    04:07 If that is deficient, no mineralocorticoid, hypoaldosteronism hyperreninemic.

    04:14 Are we-Are we clear now, hmm? You should be able to go through each one of these differentials and understand why your patient has hypoaldosteronism and what kind of concentration of renin do you actually find.

    04:29 Hypoaldosteronism, transtubular potassium gradient less than 7 in a hyperkalemic patient is suggestive of hypoaldosteronism.

    04:38 If you want to memorize the value, please do so, but you already know that if you don’t have aldosterone that your potassium levels in fact will be elevated.

    04:46 Urine potassium, this is the actual formula for what is known as a transtubular potassium gradient.

    04:55 Keep it in mind, clinically becomes important.

    04:58 After patient upright for 3 hours, check for plasma renin activity, serum aldosterone and serum cortisol, after your patient upright for 3 hours and see as to whether or not you… what kind of levels do you find of your plasma renin, what about your aldosterone and so on and so forth.

    05:17 PRA and aldosterone will be low in hyperreninemic hypoaldosteronism, straightforward.

    05:22 Give me an example there, please.

    05:25 If you are hyperreninemic, it means that maybe you have chronic kidney injury, no rennin.

    05:32 Plasma renin activity will be high in adrenal insufficiency, AI stands for adrenal insufficiency.

    05:39 That is your Addison’s.

    05:43 Topic hypoaldosteronism, no aldosterone, plasma renin activity increased whereas serum aldosterone and cortisol will be low, right, in Addison’s insufficiency or adrenal insufficiency.

    05:56 Tell me about this area in the-in the… in Addison’s, tell me about this area around the mouth.

    06:01 Hyperpigmented.

    06:02 Good.

    06:03 Mineralocorticoid replacement will address the hyperkalemia, but is not-not advisable for many patients with hyperreninemic hypoaldosteronism due to potential for worsening of hypertension and fluid overload.

    06:17 Keep that in mind.

    06:19 So, if you have fluid overload and you are thinking about giving them mineralocorticoid, aren’t you making matters worse? If you have a patient with CHF or if you have a patient that is in a state of increased volume and then you give aldosterone, you are making things worse.

    06:37 In this setting, low potassium diet and if needed, a loop or thiazide diuretic would be much, much, much more advisable to control the hyperkalemia.

    06:47 Spend a minute here on this paragraph so that you understand how, what your next step in management would be, if your patient is suffering from hyporeninemic hypoaldosteronism.

    06:59 That is your primary focus in this paragraph.

    07:01 And your focus here will be more symptoms, try to get rid of the fluid through proper management.


    About the Lecture

    The lecture Hypoaldosteronism by Carlo Raj, MD is from the course Adrenal Gland Disorders.


    Included Quiz Questions

    1. Hypercalcemia
    2. Hyperkalemia
    3. Metabolic acidosis
    4. Suppression of ammonia excretion
    5. Hyponatremia
    1. ACE inhibitor therapy
    2. Chronic kidney disease
    3. Chronic diabetes
    4. Cyclosporin and NSAID use
    5. HIV
    1. TTPK
    2. FF/GFR
    3. Urine osmolarity/serum osmolarity
    4. Cockcroft-Gault equation
    5. Urine K/Serum K
    1. Hyporeninemic hypoaldosteronism
    2. Hypereninemia hypoaldosteronism
    3. Congenital isolated hypoaldosteronism
    4. Congenital adrenal hyperplasia
    5. Primary adrenal insufficiency

    Author of lecture Hypoaldosteronism

     Carlo Raj, MD

    Carlo Raj, MD


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