Another hyperkalemia – my explanation

17 Apr
2009

To restate – this basic metabolic panel -

Electrolyte panel
Na  138 Cl  115 BUN  35
K 7.3 HCO3  14 creat  1.8
Blood Sugar  154

 Several commenters recognized that this patient has a type IV RTA with a respiratory acidosis.  The cause of the respiratory acidosis was either hypoventilation syndrome or weakness from the hyperkalemia.  His type IV RTA is interesting.

5 months ago his BMP showed

Electrolyte panel
Na  142 Cl  107 BUN 16
K 5.4 HCO3  22 creat  1.1
Blood Sugar  73

 He was appropriately taking enalapril 20 mg b.i.d. for his hypertension.  I suspect that the enalapril contributed to decreased aldosterone, and then the NSAID exacerbated the problem by decreasing renin production.  He also probably had some mild acute renal failure from the NSAID.  His renal function recovered with stopping the NSAID and the enalapril. 

For interest, his urine pH was 5.0 and urine Na 94, K 27, Cl 86.

We do have some evidence that the hypoventilation (and respiratory acidosis) was temporary.  I will rewrite his inital ABG, then give his ABG after potassium is corrected.

ABG
pH 7.18
pCO2 38
pO2 76

then

ABG
pH 7.35
pCO2 30
pO2 78

 Thanks for all the comments – especially from the practicing nephrologists.  I would like their comments on these further data.

 

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3 Responses to Another hyperkalemia – my explanation

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Dave Hammon

April 17th, 2009 at 11:46 am

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Pro Nephros

April 20th, 2009 at 11:05 pm

Umm – no fairsies! We didn’t hear about the enalapril before. You can’t make a diagnosis of Type 4 RTA in someone on enalapril – and, of course, my previous comment about underlying renal disease may not apply. That being said, the correction of respiratory acidosis is prima facie evidence that hyperkalemia was contributing to hypoventilation, presumably through respiratory muscle weakness. Also, the urine pH of 5.0 illustrates a fundamental concept about the impairment of acid excretion in hyperkalemia – that is, unlike classic “Type I” distal RTA, the pH gradient across the collecting duct is usually unimpaired in hyperkalemia. What is lacking is the supply of ammonium ions to carry the bulk of the protons – thus, net acid excretion is low despite the low urine pH, and one sees no urinary anion gap. Finally, the relatively low urine K in the face of severe hyperkalemia and adequate urine Na shows that either aldosterone levels were very low, or that aldosterone’s ability to affect the collecting duct was impaired (presumably the former, since the defect was reversible). As pointed out by Simon Prince previously, the transtubular gradient of potassium (which requires urine osmolality for its calculation) might help nail down this latter point in a more quantitative fashion.

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Pro Nephros

April 21st, 2009 at 12:51 pm

Correction – I just realized I left a proofreading error in the above comment. When renal ammoniagenesis is normal, there is a negative urine “anion gap” – that is, the chloride is usually higher than the sum of sodium and potassioum, due to the unmeasured ammonium chloride in the urine. In hyperkalemia with impaired renal ammoniagenesis, the urine anion gap will generally be positive; i.e. there is no NEGATIVE anion gap.

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