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Assess renal potassium handling in hyper- or hypokalemia
TTKG = (UK/SK) / (UOsm/SOsm)
Requires: Urine Osm > Serum Osm, Urine Na > 25 mEq/L
Some studies question TTKG validity due to urea recycling assumptions. Consider as one piece of clinical picture, not definitive.
TTKG estimates the potassium gradient in the cortical collecting duct, reflecting aldosterone activity and renal K+ secretion capacity.
The formula assumes water reabsorption in the medullary collecting duct. Dilute urine violates this assumption and makes TTKG unreliable.
Use with caution. Diuretics affect urine electrolytes and osmolality. Results may be difficult to interpret. Consider stopping diuretics if safe.
On a normal diet, TTKG is typically 8-9. It should increase to >10 in hyperkalemia (more K+ excretion) and decrease to <3 in hypokalemia (K+ conservation).
Aldosterone increases K+ secretion in the collecting duct. High aldosterone = high TTKG. Low aldosterone = low TTKG.
No. TTKG is one tool among many. Use in conjunction with clinical history, serum/urine electrolytes, aldosterone/renin levels, and medication review.
In unexplained hyperkalemia with low TTKG, always check: ACEi/ARBs, NSAIDs, K+-sparing diuretics, TMP-SMX, heparin, and aldosterone/renin levels.