J Clin Hypertens. 2018;20:611–612. wileyonlinelibrary.com/journal/jch
©2018 Wiley Periodicals, Inc.
LETTER TO THE EDITOR
Dietary potassium and cardiovascular profile. Results from the
modification of diet in renal disease dataset
We have recently reported that dietary potassium correlates neg-
atively with body mass index (BMI) and proteinuria.
high potassium diets have a protective effect against the devel-
opment of vascular damage induced by salt loading.
In an effort
to dissect the possible mechanisms of the benefits of dietary po-
tassium, we studied the relationship between daily potassium in-
take and several markers of interest to cardiovascular disease and
We performed analysis on the baseline data of the National
Institute of Health- funded Modification of Diet in Renal Disease
(MDRD) study. We performed bivariate correlation (Pearson) be-
tween dietary potassium (food only) intake and BUN- to- creatinine
ratio (BUN:Cr), serum calcium (mg/dL), hematocrit (%), hemo-
globin A1C (%), serum uric acid (mg/dL), and stroke volume (SV)
estimated according to a validated equation using noninvasive
Our results revealed a significant positive correla-
tion between daily potassium intake and BUN:Cr, hematocrit, and
serum calcium and significant negative correlation with SV, serum
uric acid, and hemoglobin A1C. The descriptive statistics of the
variables studied, and bivariate correlations with dietary potas-
sium are shown in Table.
The statistical associations of dietary potassium intake with SV,
BUN:Cr, serum calcium, and HCT are similar to those of thiazide di-
uretics. These similarities can be explained by the effect of orally in-
gested potassium on an ill- defined gastrointestinal sensor that leads
through a feed- forward mechanism to dephosphorylation of the
sodium- chloride cotransporter in the distal convoluted tubules. This
effect is equivalent to the effect of thiazide diuretics and explains the
antihypertensive property of dietary potassium.
On the other hand,
effects of dietary potassium on uric acid and hemoglobin A1C are
opposite to what is expected from thiazide diuretics. Production of
uric acid, the end product of xanthine metabolism in humans, yields
an equimolar amount of superoxide. Experimentally, a high- potassium
diet was shown to have a potent protective effect on left ventricular
active relaxation independent of blood pressure, partly through the
inhibition of cardiac NADPH oxidase activity.
In another study, the
antihypertensive effect of dietary potassium was accompanied by
sympathetic nerve inhibition in salt- sensitive hypertension, a marker
of insulin resistance.
Renalase, a monoamine oxidase in the blood that
is primarily secreted by the kidneys can metabolize catecholamines
and regulate sympathetic activity. Renalase mRNA and protein levels
increased along with decreased catecholamine levels in plasma and led
to a decrease in blood pressure in salt- sensitive rats treated with high
salt/potassium intake, compared with that of the high salt intake salt-
sensitive control rats.
Moreover, reactive oxygen species are a critical
mediator of the Na- K- ATPase pump signaling, and their generation can
be attenuated by potassium transit into the cells.
Taking into consid-
eration the type of the dataset analyzed and the cross- sectional nature
of the analysis, our results cannot be expanded beyond a correlation,
but when taken together with other existing evidence from animal and
human experiments, it is reasonable to conclude that the protective
effects of a high potassium diet can be explained by its antihyperten-
sive and antioxidant properties.
The MDRD study was conducted by the MDRD Investigators and sup-
ported by the National Institute of Diabetes and Digestive and Kidney
Diseases (NIDDK). The data from the MDRD reported here were sup-
plied by the NIDDK Central Repositories. This manuscript was not pre-
pared in collaboration with Investigators of the MDRD study and does
not necessarily reflect the opinions or views of the MDRD study, the
NIDDK Central Repositories, or the NIDDK.
TABLE Descriptive statistics and correlations
Variables N Minimum Maximum Mean Std. deviation
with dietary K P
Diet potassium, food only (meq/24 h) 5338 9.3 139.6 37.4 13.1
Stroke volume 2854 15.3 101.4 41.2 9.2 −0.038 .04
BUN/Cr 2846 5.8 61.3 15.2 4.5 0.131 <.001
Serum uric acid (mg/dL) 1106 1.7 17.4 7.6 1.7 −0.074 .01
Calcium (mg/dL) 2827 5.9 11.9 9.1 0.5 0.052 .006
Hematocrit (%) 2777 19.0 60.0 39.0 5.6 0.074 <.001
Hemoglobin A1c (%) 1093 3.8 15.0 5.7 0.9 −0.069 .02