Medline ® Abstracts for References 91-93
of 'Causes and evaluation of hyperkalemia in adults'
New clinical approach to evaluate disorders of potassium excretion.
West ML, Marsden PA, Richardson RM, Zettle RM, Halperin ML
Miner Electrolyte Metab. 1986;12(4):234.
A new clinical approach to patients with disorders of potassium excretion is reported. This approach uses a urinary index, the ratio of potassium concentrations in the urine to vein after adjusting the urine potassium concentration for medullary water abstraction. This index provides a semiquantitative assessment of the apparent transtubular potassium concentration gradient (TTKG) in the major distal nephron segment where potassium is secreted. Three clinical situations are presented where the use of this index provided a better indication of the renal action of mineralocorticoids than did the traditional approach; in each case, the presence of mineralocorticoids was known as drugs with this action were administered. We emphasize that use of this index is restricted to situations where the urine is not hypotonic and distal nephron sodium delivery is not limiting for potassium secretion (greater than 25 mM, twice the sodium concentration required for maximum potassium transport at this nephron site).
The transtubular potassium concentration in patients with hypokalemia and hyperkalemia.
Ethier JH, Kamel KS, Magner PO, Lemann J Jr, Halperin ML
Am J Kidney Dis. 1990;15(4):309.
It is advantageous to make an independent assessment of the potassium (K) secretory process and the luminal flow rate in the renal cortex to evaluate K handling by the kidney during hypokalemia or hyperkalemia. The transtubular potassium concentration gradient (TTKG) is a semiquantitative index of the activity of the K secretory process. The purpose of this study was to define expected values for the TTKG in normal subjects with hypokalemia or following an acute K load. During hypokalemia of non-renal origin, the TTKG was 0.9 +/- 0.2; in contrast, the TTKG was significantly higher during the hypokalemia of hyperaldosteronism, 6.7 +/- 1.3. The TTKG was 11.8 +/- 3.6, 2 hours after normokalemic subjects received 0.2 mg 9 alpha-fludrocortisone (9 alpha-F). To obtain expected values during hyperkalemia, normal subjects ingested 50 mmol potassium chloride; 2 hours later, the TTKG was 13.1 +/- 3.8. Therefore, the expected value for the TTKG must be interpreted relative to the concentration of K in the plasma. Circumstances were also defined where the TTKG is low despite hyperaldosteronism, namely, during a water diuresis and pre-existing hypokalemia.
Renal Division, St. Michael's Hospital, University of Toronto, Canada.
The utility of the transtubular potassium gradient in the evaluation of hyperkalemia.
Choi MJ, Ziyadeh FN
J Am Soc Nephrol. 2008 Mar;19(3):424-6. Epub 2008 Jan 23.
The transtubular potassium gradient (TTKG) is used to gauge renal potassium secretion by the cortical collecting duct, indirectly assessing mineralocorticoid bioactivity in patients who have hypo- or hyperkalemia. TTKG values<6 indicate an inappropriate renal response to hyperkalemia, whereas values>2 during hypokalemia point to renal loss. Hypokalemia is not addressed here. Studies supporting the usefulness of the TTKG in hyperkalemia are limited to case series. This calculation may be most useful in distinguishing hyperkalemic patients who have mineralocorticoid deficiency versus resistance by observing a change in TTKG values after physiologic or pharmacologic doses of mineralocorticoids.
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.