Acid-Base Disorders 3

Renal tubular acidosis. How do we recognize renal tubular acidosis? Number one, what I said before; first have a blood pH. You’ve got to have acidosis. I can’t tell you how often I have been consulted by some of you out there who will remain anonymous, in the audience, who say, “Low CO2, low bicarbonate, we obviously have an acidosis. Please evaluate the acidosis for us.” And it turns out, of course, that it’s a compensation because the blood pH, when we got it, was 7.6. So number one, be sure you know the acid-base status. Start stepwise. Start with your first step which is; know the primary disorder. Then these patients are hyperchloremic. They have a normal anion gap. Not a high anion gap. They have a relatively low serum K for the degree of acidosis, and this is true of type I and type II RTA’s. And they have an inappropriately high urinary pH. If you have all of these, you more than likely have an RTA. So these are the characteristics. This right here is something to look at. If you don’t look at anything else in RTA, look at this. Because this is the link, this is the association that will allow you to get it through the test.

Now there are different types. We nephrologists have an incredible amount of imagination and wit, so we of course call them type I and type II, with our great creativity. Type I is called distal RTA. It is caused by a problem in the distal tubule with the inability to decrease the urine pH to 5.5 during acidosis. Because the kidney can’t push out hydrogen ions out of the body. There is one of a number of molecular defects that cause the kidney to be unable to kick out hydrogen ions. You eat 3 milliequivalents per kilo of hydrogen ion per day in your phosphates and your sulfates and the things that you eat. You can’t get rid of them in RTA. Thus, you become a big walking hydrogen ion. The associated problems with type I – this is an important association – nephrocalcinosis. Another; we’ve said before, hypokalemia and low urinary citrate. Remember the two types of acidosis that give you low potassium, DKA – because you are peeing out all that K – and RTA. RTA, relative hypokalemia. It turns out that you get a secondary hyperaldosteronism and that’s why you get hypokalemia. What’s important to remember is low acidosis, low K; low or normal K – even a normal-ish K – you’ve got to really think about it because the K should be high when you are very acidotic. Think DKA or RTA.

How do you evaluate these patients? They have a hyperchloremic metabolic acidosis and they have a positive urinary anion gap. That’s because these patients don’t make very much ammonia. The urine – a lot of the positives that are over here to balance out the chlorides, etc. – is ammonia and usually the sodium plus potassium minus chloride normally is a negative number. But in distal RTA the sodium plus the potassium minus the chloride is a positive number in distal RTA. We’ll get to proximal RTA in a minute. And in normals, it’s a negative number. The urine pH, for the sake of this discussion here, is always greater than 5.5. There are situations where it may be below that but not in a million years will they ask you. So for the situation that we are talking about here, with regard to 98% of RTA’s, urine pH always greater than 5.5. You can bicarbonate load these patients and do a study called a urine PCO2 minus blood PCO2 and the values are given here. This is a question for pediatric nephrology Boards. Not for general peds Boards. You won’t get asked it.

The types; it is associated with many many things, and I’ve listed a number of them here. Genetically transmitted disease, autoimmune diseases and disorders associated with nephrocalcinosis. If you hear nephrocalcinosis and acidosis, think type I RTA, and there are a couple of situations here. Drugs that have tubular toxicity; we talked about hypokalemia with cisplatin and amphotericin. Amphotericin will also give you a situation of RTA. Amphotericin also gives you renal failure in very sick patients, but in patients that are not so sick and we are using lower doses of amphotericin, there is a tubular toxicity, and that’s amphotericin-B I’m talking about. Others include pyelonephritis obstruction and kidney transplant.

Leave a Reply

Your email address will not be published. Required fields are marked *