Figure 325

Approach to hyperkalemia: hyporeninemic hypoaldosteronism. Hyporeninemic hypoal-dosteronism accounts for the majority of cases of unexplained hyperkalemia in patients with reduced glomerular filtration rate (GFR) whose level of renal insufficiency is not what would be expected to cause hyperkalemia. Interstitial renal disease is a feature of most of the diseases listed. The transtubular potassium gradient (see Fig. 3-26) can be used to distinguish between primary tubule defects and hyporeninemic hypoaldostero-nism. Although the transtubular potassium gradient should be low in both disorders, exogenous mineralocorticoid would normalize transtubular potassium gradient in hyporeninemic hypoaldosteronism.

Physiologic basis of the transtubular potassium concentration gradient (TTKG). Secretion of potassium in the cortical collecting duct and outer medullary collecting duct accounts for the vast majority of potassium excreted in the urine. Potassium secretion in these segments is influenced mainly by aldosterone, plasma potassium concentrations, and the anion composition of the fluid in the lumen. Use of the TTKG assumes that negligible amounts of potassium are secreted or reabsorbed distal to these sites. The final urinary potassium concentration then depends on water reabsorption in the medullary collecting ducts, which results in a rise in the final urinary potassium concentration without addition of significant amounts of potassium to the urine. The TTKG is calculated as follows:

The ratio of (U/P)osm allows for "correction" of the final urinary potassium concentration for the amount of water reabsorbed in the medullary collecting duct. In effect, the TTKG is an index of the gradient of potassium achieved at potassium secretory sites, independent of urine flow rate. The urine must at least be iso-osmolal with respect to serum if the TTKG is to be meaningful [20].

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