Renal Tubular Acidosis, Metabolic Alkalosis
In this episode, Dr Harrison speaks with Dharminder Singh, MD, about the evaluation of renal tubular acidosis (RTA) and how to evaluate metabolic alkalosis. The first patient case presentation is a patient with a distal type 1 RTA, and the second patient case presentation is a patient with a metabolic alkalosis.
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Anil Harrison, MD, is the Associate Program Director of the Internal Medicine Residency Program and the Ambulatory Care Director at Touro University and St Joseph’s Medical Center-Dignity Health (Stockton, CA). Dr Harrison is board certified in India and the United States.
Dharminder Singh, MD, is an internal medicine chief resident at St Joseph’s Medical Center (Stockton, CA).
Moderator: Hello, everyone and welcome to Multidisciplinary Dialogue Clinical Rounds and Case Reviews with your host Dr Anil Harrison, who is the Associate Program Director for the Internal Medicine Residency program and the Ambulatory Care Director at Tour University and St Joseph's Medical Center Dignity Health in Stockton, California. Today, we have two case presentations that Dr Harrison and Dr Dharminder Singh will analyze and provide treatment insights. Dr Singh is an internal medicine chief resident at St Joseph's Medical Center in Stockton, California. In this episode, we'll discuss renal tubular acidosis. The views of the speakers are their own and do not reflect the views of their respective institutions or the views of Consultant 360.
Dr Anil Harrison: Good afternoon, Dharminder.
Dr Dharminder Singh: Good afternoon, Dr Harrison.
Dr Anil Harrison: It's a beautiful day. And today, we're going to continue with a podcast on the evaluation of blood gases. But would you like to hear a pizza joke?
Dr Dharminder Singh: Sure, why not? Let's start with a pizza joke. I'm kind of hungry too.
Dr Anil Harrison: Nah, nevermind. It's too cheesy.
Dr Dharminder Singh: All right. Today, we'll talk about ABG cases, and renal tubular acidosis. And we'll start out with the first question. This is a 50-year-old with a history of kidney stones, arthritis and bipolar disorder on lithium. Presents with fatigue. Patient's sodium is 137. Potassium 3, chloride 115. Bicarb of 10, blood sugar of 100. Serum osmolality is 285, BUN is 15 and creatinine is 0.8. And the blood gases as follows: pH is 7.30, PCO2 35, urine pH 7, and UAG is positive. Any thoughts?
Dr Anil Harrison: Yeah, so Dr Singh, the possibility that are given to us are: is this salicylate toxicity, is this a type 4 renal tubular acidosis, is this a distal type 1 renal tubular acidosis, or is this a proximal renal tubular acidosis? This is how I would go about. The first thing you look at is the pH and the pH is 7.3, which is low, and hence this is acidosis. The second thing you look at is the PCO2. You figure what the PCO2 is doing and it is moving in the same direction as the pH. And therefore, this primarily is a metabolic problem. Then, you take a look at the bicarb and you notice that the bicarb is 10, so we confirm that this is a metabolic acidosis. The next thing, of course, as you know, we calculate the anion gap, which is sodium minus chloride minus bicarbonate. And if you calculate the anion gap in this patient is 10, which is normal.
We could safely call this a normal anion gap metabolic acidosis, and in short NAGMA. The next thing is we need to check for an osmolar gap. The measured serum osmolality is, I think, 285, which is what the lab has measured it as. And if we calculate this patient's serum osmolality, it turns out to be 284. You see that there is no significant osmolar gap. The next thing you look at is the urine anion gap, which is positive, and hence this points towards either a type 1 or a type 4 renal tubular acidosis. But with a serum potassium of 3 and a urine pH of 7, this confirms that the patient has a type 1 renal tubular acidosis. Our patient has a normal anion gap acidosis along with a positive urine anion gap, a urine pH that is alkaline, a low serum potassium and a history of kidney stones, I feel points towards a type 1 renal tubular acidosis.
And I feel that the etiology for the type 1 RTA is possibly the connective tissue disorder that the patient has. The next thing is Dr. Singh, how do we differentiate the three different types of renal tubular acidosis found in adults? In type 1 renal tubular acidosis, the problem is actually in acidifying the urine, and hence the urine pH is either 6 or more than 6. Due to a lack of citrate, kidney stones are more common. The etiologies for a type 1 renal tubular acidosis would be things like: hereditary, amphotericin, collagen vascular disease, or nephrocalcinosis, and even multiple myeloma can do that. In proximal renal tubular acidosis as opposed to the distal renal tubular acidosis, there is no issue as to define the urine. The problem is actually in the reabsorption of bicarbonate, and hence the urine pH is less than 5.5.
There is hypokalemia very similar to type 1 RTA. And the etiologies for a type 2 RTA are, again, hereditary, sulfonamides, carbonic anhydrase inhibitors, or Fanconi syndrome, and even multiple myeloma can do that. In type 4 RTA because of aldosterone deficiency or resistance, the serum potassium is elevated, the urine pH can be variable, and the etiologies are usually things like: hyporeninemic, hypoaldosteronism, hypertension, diabetes, chronic interstitial nephritis, aldosterone resistance, et cetera. This is my take on our patient. Okay, so if you agree Dr. Singh, we can move on to another case if you have one.
Dr Dharminder Singh: Sure. I have this 22 years old with a normal blood pressure. Presents with myalgia, fatigue. Sodium of 138, potassium 2.4, chloride 94, bicarb of 34, BUN of 15, creatinine 1, and calcium of 10.4. Magnesium 1.1 with normal TSH and CK. Urine chloride is more than 15. Urine calcium is low. Serum potassium and magnesium failed to correct with the potassium and magnesium supplement. ABGs as follows: pH of 7.49 and PCO2 of 49.
Dr Anil Harrison: What do you think this patient might have? Could it be Bartter syndrome, could it be surreptitious vomiting, could it be mineralocorticoid excess, could it be Gitelman syndrome, or could it be a surreptitious diuretic use? This is what I look at, is first take a look at the pH. The pH is 7.49, which confirms alkalosis. Then, you take a look at the PCO2 and the PCO2 is moving in the same direction as the pH. Therefore, this is primarily a metabolic problem. And with a bicarb of 34, you could safely call this. This is a case of metabolic alkalosis. With the metabolic alkalosis, the next thing you do is you check the volume status and the blood pressure. And if you see, this patient's blood pressure is normal and the potassium is low, and you tell me that the magnesium failed to correct with supplementation.
The possibilities could be contraction alkalosis, it could be NG suctioning, or vomiting. In these instances, the urine chloride, it would be less than 10. However, if the patient is surreptitiously taking diuretics or has Bartter's or Gitelman syndrome, the urine chloride will be elevated. The next thing is what is the urine chloride? Now, this patient's urine chloride being 15, the patient may be surreptitiously using diuretics or might have Bartter's or Gitelman's. The next thing to do is a urine diuretic screen. And only if that is negative, you proceed to consider Bartter's or Gitelman's because they are not that common. Then, you check the urine calcium, and if the urine calcium is elevated, it is Bartter's syndrome. In our patient, the urine calcium is low. Since the defect in Gitelman's is similar to how thiazide diuretics work, therefore, the urine calcium will be low since calcium is reabsorbed.
Recapping evaluation of metabolic alkalosis, the first thing to do is to assess the volume status and you'd agree if the volume status is low or low normal, you consider things like: contraction alkalosis, vomiting, NG suctioning, diuretics, or Bartter's and Gitelman syndrome. On the other hand, if the volume status is high or high normal, you check the person's blood pressure and potassium. If the blood pressure and potassium are both elevated, it probably represents mineralocorticoid excess. And in that scenario, you check aldosterone and renin levels. If the aldosterone is elevated and the renin is not, and the aldosterone to renin ratio is greater than 20, this represents a primary hyperaldosteronism.
If both renin and aldosterone are elevated, then that is secondary hyperaldosteronism, and the ratio of aldosterone to renin is less than 20. If both renin and aldosterone are normal, it could be that the patient has Cushing syndrome. If both aldosterone and renin are low, this could represent exogenous steroids or liquorice ingestion or Liddle's syndrome. Also, if both blood pressure and potassium are normal, you might want to consider milk-alkali syndrome. Again, if the blood pressure is normal and the potassium is low, consider severe hypokalemia as the etiology. The reason being that the hydrogen ions outside the cell, they get into the cell and potassium comes out, so that is why you get hypokalemia along with metabolic alkalosis.
Dr Dharminder Singh: That sounds pretty good. How about another joke?
Dr Anil Harrison: Okay. What does a clock do when it's hungry? It goes back for seconds.
Dr Dharminder Singh: Well, thank you so much for this session, Dr. Harrison.
Dr Anil Harrison: Thank you so much, Dr. Singh. I hope everybody enjoys it and I hope everybody has watched a previous podcast on evaluation on arterial blood gases, and we have another one coming up very soon. Stay tuned. Have a great day. Bye-bye.
Dr Dharminder Singh: Thank you.