This transtubular potassium gradient (TTKG) calculator is based on the kidney index helping in the differential diagnosis of hyperkalemia and hypokalemia. You can find more information on the TTKG index results and the variables involved in the text placed under the form.
How does this transtubular potassium gradient (TTKG) calculator work?
This is a health tool that offers information regarding the conservation of potassium in the collecting ducts of the kidney. The transtubular potassium gradient TTKG calculator is used in the differential diagnosis of hyperkalemia and hypokalemia. It basically analyses the ratio of potassium located in the lumen of the kidney cortical collecting ducts (CCD) compared to that of potassium in the peritubular capillaries.
The variables used in the formula are provided in the following lines:
■ Urine K measured in mEq/L – helps establish the pathophysiologic mechanism behind the K hyper or hypo levels. Usually clinically assessed as spot urine test. Low urine K (<20 mEq/L) indicates gastrointestinal loss while high urine K (>40 mEq/L) is consistent with some form of renal loss.
■ Plasma osmolality measured in mOsm/kg – the urine to plasma ratio is used to account and adjust for the water reabsorbing that occurs in the medullary part.
■ Plasma K measured in mEq/L – the urine to plasma K ratio measures the gradient for K secretion.
■ Urine osmolality measured in mOsm/kg – indicative of whether the urine potassium sample is relevant, values above 700 mOsm/kg might suggest kidneys excrete too much K, if urine osmolarity doesn’t show a properly concentrated urine, this might indicate renal loss.
TTKG = (Urine K x Plasma osm) / (Plasma K x Urine osm)
In theory, there are some restrictions to the above formula and that should be used only when urine osmolarity is above 300 mOsm/kg and urine sodium is above 25 mEq/L because it doesn’t exclude the occurrence of a possible potassium wasting syndrome.
For the clarity of the following explanations, should be mentioned that hypokalemia with serum potassium low levels is defined at 3.5 mEq/L and is most commonly met due to K losses caused by diuretics or gastrointestinal disease.
TTKG index interpretation
The TTKG also aims at revealing whether the kidneys are adjusting to the potassium processes that are happening in the collecting tube.
The normal value range falls between 8 and 9 in healthy patients with a normal diet. However, in case there is a high potassium intake in the diet, more K will be excreted and the transtubular potassium gradient will reach values above 10 (was also found to rise up until 11) and the same but opposite happens with low levels and low intake. These need to be discriminated against high levels caused by hyperkalemia and low levels due to hypokalemia.
On the other side, high TTKGs accompanied by overall hypokalemia can be a sign of hyperaldosteroinism or Liddle’s syndrome.
There is also the situation where there is a low TTKG, below 7 that is still followed by high potassium levels, indicative of hyperkalemia. In this case, especially if this is accompanied by low plasma sodium and high urine Na, we are talking about the likeliness of mineralocorticoid deficiency.
TTKGs under 3 are consistent with potassium depletion or hypokalemia only if the regulatory mechanisms of the body are in place and there is a reduced urinary excretion of K. Low TTKGs accompanied by hyperkalemia suggests a type IV renal tubular acidosis.
The utility of the index in diagnosis has been especially put to question in patients with hyperkalemia due to medication and in renal transplant patients with high K levels.
There was discovered a positive correlation between the mineralocorticoid activity and the tubular gradient index but the underlying mechanisms and whether the index can be used in this assessment as well is still to be researched.
1) Ethier JH, Kamel KS, Magner PO, Lemann J Jr, Halperin ML. (1990) . Am J Kidney Dis; 15(4):309-15.
2) Choi MJ, Ziyadeh FN. (2008) . J Am Soc Nephrol; 19(3):424-6.
3) Joo KW, Chang SH, Lee JG, Na KY, Kim YS, Ahn C, Han JS, Kim S, Lee JS. (2000) . J Nephrol; 13(2):120-5.04 Nov, 2015 | 0 comments