scholarly journals Dietary potassium and the kidney: lifesaving physiology

2020 ◽  
Vol 13 (6) ◽  
pp. 952-968
Author(s):  
Kuang-Yu Wei ◽  
Martin Gritter ◽  
Liffert Vogt ◽  
Martin H de Borst ◽  
Joris I Rotmans ◽  
...  
Keyword(s):  
Clinical Medicine ◽  
Collecting Duct ◽  
Epidemiological Studies ◽  
High Sodium ◽  
Potassium Intake ◽  
Dietary Potassium ◽  
Urinary Potassium ◽  
Low Potassium ◽  
Independent Effects ◽  
Potassium Binders

Abstract Potassium often has a negative connotation in Nephrology as patients with chronic kidney disease (CKD) are prone to develop hyperkalaemia. Approaches to the management of chronic hyperkalaemia include a low potassium diet or potassium binders. Yet, emerging data indicate that dietary potassium may be beneficial for patients with CKD. Epidemiological studies have shown that a higher urinary potassium excretion (as proxy for higher dietary potassium intake) is associated with lower blood pressure (BP) and lower cardiovascular risk, as well as better kidney outcomes. Considering that the composition of our current diet is characterized by a high sodium and low potassium content, increasing dietary potassium may be equally important as reducing sodium. Recent studies have revealed that dietary potassium modulates the activity of the thiazide-sensitive sodium-chloride cotransporter in the distal convoluted tubule (DCT). The DCT acts as a potassium sensor to control the delivery of sodium to the collecting duct, the potassium-secreting portion of the kidney. Physiologically, this allows immediate kaliuresis after a potassium load, and conservation of potassium during potassium deficiency. Clinically, it provides a novel explanation for the inverse relationship between dietary potassium and BP. Moreover, increasing dietary potassium intake can exert BP-independent effects on the kidney by relieving the deleterious effects of a low potassium diet (inflammation, oxidative stress and fibrosis). The aim of this comprehensive review is to link physiology with clinical medicine by proposing that the same mechanisms that allow us to excrete an acute potassium load also protect us from hypertension, cardiovascular disease and CKD.

Abstract P184: Effects of Sodium and Potassium Supplementation on Blood Pressure and Arterial Stiffness in Untreated (Pre)Hypertensives on a Low-Sodium, Low-Potassium Diet

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Lieke Gijsbers ◽  
James Dower ◽  
Marco Mensink ◽  
Johanna M Geleijnse
Keyword(s):  
Blood Pressure ◽  
Arterial Stiffness ◽  
Random Order ◽  
Potassium Intake ◽  
Low Sodium ◽  
Potassium Supplementation ◽  
Urinary Potassium ◽  
Low Potassium ◽  
Sodium And Potassium ◽  
Sodium Supplementation

Introduction: We performed a 12-week randomized placebo-controlled crossover study to examine the effects of sodium and potassium supplementation on blood pressure (BP) and arterial stiffness in untreated (pre)hypertensive individuals on a low-sodium, low-potassium diet. Methods: During the study, subjects were on a fully controlled diet that provided on average 2.4 g/d of sodium (equals 6 g/d of salt) and 2.2 g/d of potassium. After a 1-week run-in period, 37 subjects received capsules with supplemental sodium (3 g/d, equals 7.5 g/d of salt), supplemental potassium (3 g/d), or placebo, for four weeks each (not separated by wash-out), in random order. Fasting office BP, 24-h ambulatory BP, and measures of arterial stiffness (SphygmoCor®) were assessed at baseline and after each treatment. Results: Subjects had a mean pre-treatment BP of 145/81 mmHg and 68% (25 of 37) had systolic BP (SBP) ≥140 mmHg. In 36 subjects who completed the study, sodium supplementation increased urinary sodium by 97.6 mmol/24h (2.2 g/d) and potassium supplementation increased urinary potassium by 62.9 mmol/24h (2.5 g/d), compared to placebo (Table). Sodium supplementation significantly increased office BP by 7.5/3.3 mmHg, 24-h BP by 7.0/2.1 mmHg and central BP by 8.5/3.6 mmHg. Potassium supplementation significantly reduced 24-h BP by 4.0/1.7 mmHg. Measures of arterial stiffness did not change. Conclusion: Increasing the intake of sodium has a strong adverse effect on BP in untreated (pre)hypertensive individuals. Increased potassium intake, however, lowers BP even when people are on a reduced sodium diet. Short-term changes in sodium and potassium intake have little effect on arterial stiffness. Trial registration: ClinicalTrials.gov Identifier: NCT01575041

High sodium and low potassium intake in patients with Type 2 diabetes

2010 ◽  
Vol 27 (12) ◽  
pp. 1401-1408 ◽  
Author(s):  
E. I. Ekinci ◽  
K. Y. Cheong ◽  
M. Dobson ◽  
E. Premaratne ◽  
S. Finch ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
High Sodium ◽  
Potassium Intake ◽  
Low Potassium

scholarly journals High Sodium and Low Potassium Intake among Italian Children: Relationship with Age, Body Mass and Blood Pressure

PLoS ONE ◽  
2015 ◽  
Vol 10 (4) ◽  
pp. e0121183 ◽  
Author(s):  
Angelo Campanozzi ◽  
Sonia Avallone ◽  
Antonio Barbato ◽  
Roberto Iacone ◽  
Ornella Russo ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Mass ◽  
High Sodium ◽  
Potassium Intake ◽  
Low Potassium ◽  
Italian Children

SOME EFFECTS OF DIETARY POTASSIUM UPON DIGESTIBILITY, SERUM ELECTROLYTES AND UTILIZATION OF POTASSIUM, SODIUM, NITROGEN AND WATER IN HEIFERS

1967 ◽  
Vol 47 (1) ◽  
pp. 39-46 ◽  
Author(s):  
V. V. E. St. Omer ◽  
W. K. Roberts
Keyword(s):  
Urine Volume ◽  
Ammonia Excretion ◽  
Nutrient Utilization ◽  
Fecal Excretion ◽  
Sodium Balance ◽  
Potassium Excretion ◽  
High Potassium ◽  
Dietary Potassium ◽  
Urinary Potassium ◽  
Low Potassium

Balance studies were conducted with heifers weighing between 210–258 kg to determine effects of different dietary potassium levels, 156.6 (low), 439.4 (medium) and 1,086.8 (high) meq upon nutrient utilization. The low potassium ration produced an average negative potassium balance of 25.2 meq daily, while the other rations produced positive potassium balances. Urinary potassium excretion was markedly affected by potassium level while fecal potassium excretion was much less affected: in general, the higher the potassium intake, the higher the urinary and fecal potassium excretions. All heifers were in positive sodium balance and dietary level of potassium did not significantly influence either urinary or fecal excretion of sodium. Nitrogen balance was not significantly affected by treatment, but urinary ammonia excretion was significantly (P < 0.01) higher when the low potassium ration was fed. Water consumption and urine volume were significantly (P < 0.01) higher for the heifers fed high potassium, but water balance was not affected. Apparent digestibilities of energy, dry matter, nitrogen, crude fiber and ether extract were not significantly affected by treatment.Serum potassium levels were lower (P < 0.05) and phosphorus higher (P < 0.05) in heifers receiving the low than in heifers receiving the high level of potassium. Serum concentrations of sodium, chloride, calcium and magnesium were not significantly affected by dietary potassium.From the data, the potassium requirement for maintenance of the heifers was estimated to be 133 meq potassium daily per 100 kg body weight.

scholarly journals Deletion of Kir5.1 Impairs Renal Ability to Excrete Potassium during Increased Dietary Potassium Intake

2019 ◽  
Vol 30 (8) ◽  
pp. 1425-1438 ◽  
Author(s):  
Peng Wu ◽  
Zhong-Xiuzi Gao ◽  
Dan-Dan Zhang ◽  
Xiao-Tong Su ◽  
Wen-Hui Wang ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Potassium Channel ◽  
Basolateral Membrane ◽  
Potassium Conductance ◽  
Plasma Potassium ◽  
Wild Type ◽  
High Potassium ◽  
Potassium Intake ◽  
Dietary Potassium ◽  
Low Potassium

BackgroundThe basolateral potassium channel in the distal convoluted tubule (DCT), comprising the inwardly rectifying potassium channel Kir4.1/Kir5.1 heterotetramer, plays a key role in mediating the effect of dietary potassium intake on the thiazide-sensitive NaCl cotransporter (NCC). The role of Kir5.1 (encoded by Kcnj16) in mediating effects of dietary potassium intake on the NCC and renal potassium excretion is unknown.MethodsWe used electrophysiology, renal clearance, and immunoblotting to study Kir4.1 in the DCT and NCC in Kir5.1 knockout (Kcnj16−/−) and wild-type (Kcnj16+/+) mice fed with normal, high, or low potassium diets.ResultsWe detected a 40-pS and 20-pS potassium channel in the basolateral membrane of the DCT in wild-type and knockout mice, respectively. Compared with wild-type, Kcnj16−/− mice fed a normal potassium diet had higher basolateral potassium conductance, a more negative DCT membrane potential, higher expression of phosphorylated NCC (pNCC) and total NCC (tNCC), and augmented thiazide-induced natriuresis. Neither high- nor low-potassium diets affected the basolateral DCT’s potassium conductance and membrane potential in Kcnj16−/− mice. Although high potassium reduced and low potassium increased the expression of pNCC and tNCC in wild-type mice, these effects were absent in Kcnj16−/− mice. High potassium intake inhibited and low intake augmented thiazide-induced natriuresis in wild-type but not in Kcnj16−/− mice. Compared with wild-type, Kcnj16−/− mice with normal potassium intake had slightly lower plasma potassium but were more hyperkalemic with prolonged high potassium intake and more hypokalemic during potassium restriction.ConclusionsKir5.1 is essential for dietary potassium’s effect on NCC and for maintaining potassium homeostasis.

scholarly journals HIGH SODIUM, LOW POTASSIUM INTAKE AND CHANGES OF BLOOD PRESSURE CATEGORY DURING 7.5 YEARS FOLLOW-UP PERIOD

2019 ◽  
Vol 37 ◽  
pp. e187
Author(s):  
B. Krtalic ◽  
B. Milicic ◽  
L. Gellineo ◽  
T. Knezevic ◽  
A. Jelakovic ◽  
...  
Keyword(s):  
Blood Pressure ◽  
High Sodium ◽  
Potassium Intake ◽  
Low Potassium

Influence of age, sex and potassium excretion on urinary prostaglandins in children

1985 ◽  
Vol 68 (5) ◽  
pp. 601-604 ◽  
Author(s):  
A. Barden ◽  
L. J. Beilin ◽  
R. Vandongen ◽  
I. Rouse
Keyword(s):  
Urinary Excretion ◽  
Significant Influence ◽  
Healthy Children ◽  
Potassium Excretion ◽  
Regression Analyses ◽  
Water Diuresis ◽  
Potassium Intake ◽  
Dietary Potassium ◽  
Urinary Potassium ◽  
Age And Sex

1. Measurement of urinary 6-ketoprostaglandin (PG) F1α and PGE2 excretion in 83 healthy children, aged 5-15 years, revealed that supervised 4 h urine collections under mild water diuresis provided more consistent results than overnight 12 h urine collections. 2. Males had higher urinary excretion of 6-keto-PGF1α but not of PGE2 compared with females. 3. Urinary potassium was related to 6-keto-PGF1α in both 4 and 12 h urine collections and urinary sodium to 6-keto-PGFα in 4 h collections only. 4. In the sexes combined multiple regression analyses revealed age as the only significant influence on prostanoid excretion (P = 0.001). 5. Thus age and sex and dietary potassium intake need to be considered in studies of urinary prostanoids in children.

High potassium intake selectively increases urinary PGF2 alpha excretion in the rat

1985 ◽  
Vol 248 (3) ◽  
pp. F382-F388 ◽  
Author(s):  
A. Nasjletti ◽  
A. Erman ◽  
L. M. Cagen ◽  
D. P. Brooks ◽  
J. T. Crofton ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Reductase Activity ◽  
Control Period ◽  
Plasma Renin ◽  
Experimental Period ◽  
Plasma Potassium ◽  
High Potassium ◽  
Potassium Intake ◽  
Dietary Potassium ◽  
Low Potassium

This study was designed to investigate relationships between dietary potassium and the renal prostaglandin system in rats. The potassium content of the diet was 0.162 mmol/g during the control period and 0.004, 0.162, 1.351, or 2.702 mmol/g during the experimental period. Relative to control data in rats fed a 0.162 mmol/g potassium diet, the urinary excretion of 6-keto-PGF1 alpha was not affected by high potassium intake but increased (P less than 0.05) by 25% in rats fed a low potassium diet for 13 days and was associated with reduction of plasma potassium and with elevation of both plasma renin and net release of 6-keto-PGF1 alpha from renal inner medulla slices incubated in Krebs solution. The excretion of PGF2 alpha was not affected by low potassium intake but increased (P less than 0.05) by about twofold in rats fed a potassium-rich diet (1.351 and 2.702 mmol/g) for 13 days and was associated with elevation of plasma potassium concentration, renal prostaglandin 9-keto-reductase activity, and urinary excretion of kallikrein and vasopressin. The urinary excretion of PGE2 was not altered in rats fed either low or high potassium diets. Altogether, these results indicate selective influence of dietary potassium on the urinary excretion of prostaglandins in the rat.

Dietary Potassium Intake and Mortality in a Prospective Hemodialysis Cohort

2020 ◽  
Author(s):  
Yoko Narasaki ◽  
Yusuke Okuda ◽  
Sara S. Kalantar ◽  
Amy S. You ◽  
Alejandra Novoa ◽  
...  
Keyword(s):  
Potassium Intake ◽  
Dietary Potassium
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