Back again for my 2nd #tweetorial on urine electrolytes. Next up is urine chloride (UCl).
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In my (limited) clinical experience, UCl is ordered/utilized/discussed far less compared to its buddy ion UNa. Should it be this way? Lets explore.
First, a question. When do you order UCl?
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I imagine many would say to evaluate unexplained metabolic alkalosis given the classic teaching of chloride-responsive vs chloride-resistant metabolic alkalosis. However, I’m still waiting for one of these enigmatic cases.
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Others may order it to calculate the urine anion gap (UAG) in evaluation of an unexplained NAGMA. While RTAs are under recognized, they are still uncommon disorders.
NOTE: for great teaching on RTAs & the UAG, see the #tweetorials by @justinberk & @amyaimei(links at the end)
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So what’s left? Lets take a step back.
One of the guiding principles of human physiology is the maintenance of electroneutrality. In regards to the ECF compartment, which two ions are the most abundant?
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Na & Cl! Given this, shouldn’t our applications (and nuances/caveats) for UNa apply to UCl as well?
Yes, they do! In fact, using them together can improve clinical utility. Back to #Aragorn to illustrate:
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Aragorn stops at The Shire to picnic w/ his hobbit friends. While Sam is a skilled gardener, his potato salad leaves much to be desired. Unfortunately, a severe vomiting illness quickly spreads through the picnickers & even the mighty Aragorn cannot escape.
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~1 day later and 5lbs lighter, his symptoms begin to lighten. At this time, what would we expect his volume/total body salt status to be?
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We’d expect it to be low, given his volume loss from vomiting. As such, what do we expect his [UNa] to be?
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We’d expect it to be low…but it returns at 42mEq/L. Why might that be?
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Bicarbonaturia! Vomiting leads to a met alkalosis that drives compensatory urinary bicarb excretion. This excess bicarb binds Na, leading to the higher than expected [UNa] value. This also helps to maintain the all-important electroneutrality!
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This is where UCl comes in. In a state of volume depletion, what would we expect [UCl] to be?
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We’d expect it to be low, indicating an appropriate response by the kidney to a low volume state.
NOTE: Like [UNa], some sources use [UCl]<15mEq/L as the cut off for an appropriate response to a prerenal state.
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Lets draw some conclusions w/ the info thus far:
-Using [UNa] & [UCl] together can improve diagnostic accuracy of volume status over either in isolation.
-A value of <20mEq/L for either is indicative of a salt-retaining state (i.e. ⬇️effective arterial blood volume=EABV).
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With the principles above, lets discuss the expected clinical scenarios for the 4 possible UNa, UCl combinations.
When would we expect to see a low UNa & UCl?
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We’d expect to see this combination in states of decreased EABV. This could occur w/ hypovolemia, such as from lack of PO intake, or in Na-avid states such as CHF, cirrhosis, and CKD.
When would we see a low UNa & high UCl?
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We’d expect to see this combo in states of ⬇️ EABV. This could occur w/ hypovolemia 2/2 diarrhea, where the resulting metabolic acidosis (&hypoK) leads to ⬆️NH4 excretion w/ consequent ⬆️ Cl excretion to maintain electoneutrality.
When would we see a high UNa & low UCl?
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Again, we’d expect to see this combo in states of ⬇️EABV. Think back to Aragorn:vomiting leading to metabolic alkalosis and bicarbonaturia is a classic scenario. Another non-reabsorbable anion effect(ex. ketoanion, drugs such as piperacillin) could also explain this scenario.
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Beyond history, urine pH can be used to help to determine the identity of this anion. See the pic below for further explanation.
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PEARL: Accuracy ranges widely w/ dipstick pH measurements w/ a margin of error as high +/- 1 pH unit. As such, if you wish to use urine pH to help w/ clinical interpretation, a separate urine pH test, measured via a pH electrode, should be ordered.
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Finally, when would we see a high UNa & UCl?
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This is a little tougher. We could see this combination in states of⬇️EABV. This includes tubular dysfunction, such as w/ diuretic use or tubulopathies (ex. Bartter & Gitelman syndromes).
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However, this could also be seen in states of⬆️EABV, such as may occur w/ excess IVF administration or in states of mineralocorticoid excess (ex. Conn syndrome).
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Additionally, an AGMA – w/ excretion of Na salts of the excess acid & NH4Cl to attempt to offset the extra-renal acidemia – could lead to this combination as well.
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A lot of information, so lets summarize w/ a graphic (see below).
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One last point. What electrolyte disturbance is often seen w/ volume depletion and subsequent RAAS activation?
Hypokalemia! As you might have guessed, UCl & UNa have been found to helpful in the assessment of chronic, normotensive hypokalemia.
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Interestingly, in this study (ncbi.nlm.nih.gov/pubmed/28213045), it outperformed UK, TTKG, & UK/UCr in the diagnosis of extrarenal causes of hypokalemia, in particular anorexia/bulimia & laxative abuse.
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Fin. Take Aways summarized in pic below.
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-While I don’t think this #tweetorial will increase my frequency of testing for UNa or UCl, I do think I will no longer order one without the other.
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I’ll think to use UNa & UCl for the following scenarios:
-assessment of dysnatremias
-unexplained acid-base disturbances– including metabolic alkalosis, NAGMA
-challenging volume status assessment
-diuretic response
-unexplained chronic, normotensive hypokalemia
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When do you use UCl #medtwitter, #nephtwitter?
@kidneyboy @NephroGuy @rabihmgeha @doc_connors @KylieAdamek @GlassockJ @NephRodby @medrants @NephroMD @drlessing @edgarvlermamd @RenalFellowNtwk @stuartlinas @JohnRMontford @sargsyanz @ABRezMed @KourtneyKing
References:
DOI: 10.2215/CJN.10330818
DOI: 10.1152/ajprenal.00130.2018
DOI: 10.1016/j.amjmed.2017.01.023
DOI: 10.1681/ASN.2010121289
PMID: 7077808
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