Potassium Board Review – New Wash U Nephrology Web Episode

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Hypokalemia, hypertension, and metabolic alkalosis – this clinical triad can be seen in a variety of interesting disorders that unfortunately are much more common during in-training or board certification exams than in clinical practice.  That doesn’t mean you should cram for them the night before the exam!  Understanding the way these diseases affect potassium handling in the kidney can help learners of all levels acquire a better understanding of normal renal physiology.

This month’s nephrology web episode from Washington University in St. Louis focuses on 4 board-style questions related to potassium disorders, and we hope you find it helpful.  The full episode can be viewed below:


  1. Thanks for your response – I agree with both of your comments. The hypocalciuria in thiazides has always been tough for me to rationalize to fellows and is likely a combination of both mechanisms. Likewise I agree with your point on TTKG, but inevitably it gets ordered for academic purposes and despite not being that helpful clinically, it does make for a nice discussion on it's historic value and physiologic principle.

  2. Nice post. I have 2 comments. Firstly, with regards to the mechanism of hypocalciuria associated with thiazide diuretics, recent data indicates that is actually the proximal tubule (not the distal tubule) that is responsible for this. Apparently, the volume contraction state associated with thiazide use increases calcium reabsorption in the proximal tubule.(http://www.ncbi.nlm.nih.gov/pubmed/15902302). Secondly, TTKG should not be used anymore to provide a semi-quantitative reflection of the driving force to secrete K+ in the CCD. Halperin group developed this parameter with the assumption that there is no significant reabsorption of osmoles beyond the CCD. However, with the discovery of significant urea recycling in the medullary CD, TTKG loses its value.(http://www.ncbi.nlm.nih.gov/pubmed?term=21788894)

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