Comments on: Another hyperkalemia – my explanation

By: Pro Nephros

Pro Nephros — Tue, 21 Apr 2009 17:51:59 +0000

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.

By: Pro Nephros

Pro Nephros — Tue, 21 Apr 2009 04:05:16 +0000

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.

By: Dave Hammon

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