1. Volume 88, Issue 6, Pages 1383-1391 (December 2015)
Evidence for a gastrointestinal–renal kaliuretic signaling axis in humans 
Richard A. Preston, David Afshartous, Rolando Rodco, Alberto B. Alonso, Dyal Garg 
Kidney International 
Volume 88, Issue 6, Pages (December 2015)
DOI: /ki
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2. Figure 1
Serum potassium concentration (mmol/l). Following 35mmol oral potassium (KCl), mean serum potassium concentration increased from baseline 4.52 (95% confidence interval: 4.401, 4.62) to a peak 5.03 (4.81, 5.25; P<0.001)mmol/l at 30min. Following the potassium-deficient meal alone (Meal), serum potassium concentration decreased from baseline 4.54 (4.31, 4.76) to 3.90 (3.78, 4.01; P<0.001)mmol/l at 60min and remained depressed. With 35mmol oral potassium plus potassium-deficient meal (Meal+KCl), serum potassium concentration did not increase at any time point during the 5-h study period.
Kidney International  , DOI: ( /ki )
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3. Figure 2
Potassium excretion (mmol/h). Following KCl alone, mean potassium excretion rapidly increased to a peak 10.0 (8.24, 11.75; P<0.001)mmol/h at 60min then returned toward baseline. With Meal alone, UKV decreased to 1.84 (1.63, 2.04; P=0.002)mmol/h at 120min. With administration of Meal+KCl UKV increased from baseline 2.54 (2.14, 2.94)mmol/h to a peak of 5.14 (3.67, 6.60; P<0.001)mmol/h at 60min and remained elevated.
Kidney International  , DOI: ( /ki )
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4. Figure 3
Cumulative potassium excretion (mmol). Cumulative potassium excretion increased rapidly and reached (36.22, 44.27)mmol following KCl alone. Following Meal+KCl, cumulative potassium excretion reached (22.36, 30.50)mmol. Cumulative excretion following Meal alone reached only (14.41, 18.61)mmol. All pairwise comparisons of cumulative potassium excretion among the three experiments were statistically significant (P<0.001) including the comparison of Meal vs. Meal+KCl.
Kidney International  , DOI: ( /ki )
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5. Figure 4
Plasma aldosterone (ng/dl). In response to KCl alone, mean plasma aldosterone rapidly reached a peak of 32.1 (24.88, 39.32; P<0.001)ng/dl at 30min. Following Meal alone, plasma aldosterone did not increase at any time point throughout the collection period. Following Meal+KCl, plasma aldosterone demonstrated a small increase to 25.85ng/dl at 30min.
Kidney International  , DOI: ( /ki )
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6. Figure 5
Insulin (μIU/ml). Insulin did not increase in response to 35mmol oral KCl alone. This was a consistent finding across study subjects following KCl alone. With Meal alone, insulin increased sharply to 190.4μIU/ml at 30min and reached a peak of (147.3, 338.1; P<0.001)μIU/ml at 90min. Following Meal+KCl, insulin increased to 192.1μIU/ml at 30min and a peak of (134.3, 300.5, P<0.001)μIU/ml at 90min.
Kidney International  , DOI: ( /ki )
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7. Figure 6
Meal + KCL experiment following aldosterone blockade. The Meal+KCl experiment was conducted in 12 additional volunteers following aldosterone blockade with 200mg eplerenone twice on the day prior and 400mg on the day of the Meal+KCl potassium handling experiment. (a) Serum potassium in response to Meal+KCl following eplerenone 400mg. Serum potassium did not increase following Meal+KCl. (b) Potassium excretion in response to Meal+KCl following eplerenone 400mg. Potassium excretion was 2.9 mmol/h (0.393) at baseline and increased to 4.47 (0.66)mmol/h at 60min. (c) Cumulative potassium excretion in response to Meal+KCl following eplerenone. Cumulative potassium in response to Meal+KCl reached 22.6 (1.99)mmol at hour 5 of the collection period.
Kidney International  , DOI: ( /ki )
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8. Figure 7
Urine sodium-to-potassium ratio for subjects receiving and subjects not receiving 400mg eplerenone. The UNa/UK ratio was 2.32 (1.76, 2.89) for subjects receiving eplerenone and 0.65 (0.49, 0.81) for subjects not receiving eplerenone (P<0.001).
Kidney International  , DOI: ( /ki )
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