Gastrointestinal and renal excretion of potassium in African–Americans and White Americans

Rosa, Robert M.; Jesus, Ernest De; Sperling, Kevin; Suh, Annie; Gmurczyk, Aleksandra; Myrie, Kevin A.; Rosner, Karol; Lerma, Edgar V.; Yu, William; Breuer, Richard I.; Young, James B.

doi:10.1097/hjh.0b013e32835a27b3

Cited by 5 publications

(5 citation statements)

References 36 publications

(46 reference statements)

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“…This is probably due to the lack of supervision of the diet when participants had their meals off-site, one of the pitfalls of these types of studies. Cumulative K ϩ gastrointestinal excretion was also not different after 9 days of controlled intake, and this result was accompanied by lower rates of excretion in African Americans (594). Because the proximal tubule and thick ascending limb reabsorb 85% of the filtered K ϩ and only the thick ascending limb reabsorbs it actively, differences in K ϩ excretion before individuals reach balance could be due to a defect increasing the activity of the thick ascending limb.…”

Section: A Racial Differencesmentioning

confidence: 84%

Thick Ascending Limb Sodium Transport in the Pathogenesis of Hypertension

Gonzalez‐Vicente

Sáez

Monzón

et al. 2019

Physiological Reviews

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The thick ascending limb plays a key role in maintaining water and electrolyte balance. The importance of this segment in regulating blood pressure is evidenced by the effect of loop diuretics or local genetic defects on this parameter. Hormones and factors produced by thick ascending limbs have both autocrine and paracrine effects, which can extend prohypertensive signaling to other structures of the nephron. In this review, we discuss the role of the thick ascending limb in the development of hypertension, not as a sole participant, but one that works within the rich biological context of the renal medulla. We first provide an overview of the basic physiology of the segment and the anatomical considerations necessary to understand its relationship with other renal structures. We explore the physiopathological changes in thick ascending limbs occurring in both genetic and induced animal models of hypertension. We then discuss the racial differences and genetic defects that affect blood pressure in humans through changes in thick ascending limb transport rates. Throughout the text, we scrutinize methodologies and discuss the limitations of research techniques that, when overlooked, can lead investigators to make erroneous conclusions. Thus, in addition to advancing an understanding of the basic mechanisms of physiology, the ultimate goal of this work is to understand our research tools, to make better use of them, and to contextualize research data. Future advances in renal hypertension research will require not only collection of new experimental data, but also integration of our current knowledge.

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Section: A Racial Differencesmentioning

confidence: 84%

Thick Ascending Limb Sodium Transport in the Pathogenesis of Hypertension

Gonzalez‐Vicente

Sáez

Monzón

et al. 2019

Physiological Reviews

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“…Potassium as a supplemental salt was retained the most efficiently, reflecting higher net absorption efficiency. Of the seven trials examined by the 2019 DRI committee, potassium intake level of approximately 56 mmol/d or 2200 mg/d or greater resulted in a positive balance [ 20 , 21 , 22 , 23 , 24 , 42 ] levels of 54 mmol/d or 21 mg/d or less resulted in a negative balance [ 22 , 24 ], and one study reported neutral balance at an intake of 52 mmol/d or 2034 mg/d [ 43 ]. Our study evaluated potassium intake levels above 59 mmol/d or 2300 mg/d and resulted in positive potassium balance in all phases.…”

Section: Discussionmentioning

confidence: 99%

“…Only seven studies with assessment of complete intake, urinary, and fecal losses were available to the DRI committee. These studies showed an increase in urinary potassium with increasing intake (primary mode of excretion) [ 20 ], fecal losses averaging approximately 10.7 mmol/d (420 mg/d)) at intakes ranging from 59 to 100 mg/d (2300 to 3900 mg/d) [ 21 , 22 , 23 ], as well as variable losses due to sweat [ 24 , 25 , 26 , 27 , 28 ]. Given the limited number and overall heterogeneity in study design and findings, the committee concluded that there was insufficient evidence to establish potassium intake recommendations.…”

Section: Introductionmentioning

confidence: 99%

Short-Term RCT of Increased Dietary Potassium from Potato or Potassium Gluconate: Effect on Blood Pressure, Microcirculation, and Potassium and Sodium Retention in Pre-Hypertensive-to-Hypertensive Adults

2021

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Increased potassium intake has been linked to improvements in cardiovascular and other health outcomes. We assessed increasing potassium intake through food or supplements as part of a controlled diet on blood pressure (BP), microcirculation (endothelial function), and potassium and sodium retention in thirty pre-hypertensive-to-hypertensive men and women. Participants were randomly assigned to a sequence of four 17 day dietary potassium treatments: a basal diet (control) of 60 mmol/d and three phases of 85 mmol/d added as potatoes, French fries, or a potassium gluconate supplement. Blood pressure was measured by manual auscultation, cutaneous microvascular and endothelial function by thermal hyperemia, utilizing laser Doppler flowmetry, and mineral retention by metabolic balance. There were no significant differences among treatments for end-of-treatment BP, change in BP over time, or endothelial function using a mixed-model ANOVA. However, there was a greater change in systolic blood pressure (SBP) over time by feeding baked/boiled potatoes compared with control (−6.0 mmHg vs. −2.6 mmHg; p = 0.011) using contrast analysis. Potassium retention was highest with supplements. Individuals with a higher cardiometabolic risk may benefit by increasing potassium intake. This trial was registered at ClinicalTrials.gov as NCT02697708.

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“…With a supplementation of 40 mmol KCl per day (the amount of potassium in approximately four bananas) the average urine potassium excretion increased from 72 to 107 mmol/day. This translates to a dietary intake of approximately 120 mmol/day when considering approximately 10% fecal potassium loss 40 and is therefore at the higher end of the current dietary reference values (90-120 mmol/day). 14,15 Potassium supplementation was associated with a rise in the plasma potassium concentration of on average 0.4 mmol/L.…”

Section: Discussionmentioning

confidence: 99%

Effects of Short-Term Potassium Chloride Supplementation in Patients with CKD

Gritter

Wouda

Yeung

et al. 2022

JASN

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BackgroundObservational studies suggest that adequate dietary potassium intake (90–120 mmol/day) may be renoprotective, but the effects of increasing dietary potassium and the risk of hyperkalemia are unknown.MethodsThis is a prespecified analysis of the run-in phase of a clinical trial in which 191 patients (age 68±11 years, 74% males, 86% European ancestry, eGFR 31±9 ml/min per 1.73 m2, 83% renin-angiotensin system inhibitors, 38% diabetes) were treated with 40 mmol potassium chloride (KCl) per day for 2 weeks.ResultsKCl supplementation significantly increased urinary potassium excretion (72±24 to 107±29 mmol/day), plasma potassium (4.3±0.5 to 4.7±0.6 mmol/L), and plasma aldosterone (281 [198–431] to 351 [241–494] ng/L), but had no significant effect on urinary sodium excretion, plasma renin, BP, eGFR, or albuminuria. Furthermore, KCl supplementation increased plasma chloride (104±3 to 105±4 mmol/L) and reduced plasma bicarbonate (24.5±3.4 to 23.7±3.5 mmol/L) and urine pH (all P<0.001), but did not change urinary ammonium excretion. In total, 21 participants (11%) developed hyperkalemia (plasma potassium 5.9±0.4 mmol/L). They were older and had higher baseline plasma potassium.ConclusionsIn patients with CKD stage G3b–4, increasing dietary potassium intake to recommended levels with potassium chloride supplementation raises plasma potassium by 0.4 mmol/L. This may result in hyperkalemia in older patients or those with higher baseline plasma potassium. Longer-term studies should address whether cardiorenal protection outweighs the risk of hyperkalemia.Clinical trial number:NCT03253172

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Gastrointestinal and renal excretion of potassium in African–Americans and White Americans

Abstract: The racial difference in urinary K(+) handling manifested by decreased excretion of K(+) in African-Americans cannot be attributed to an increase in net gastrointestinal excretion of this cation.

Cited by 5 publications

References 36 publications

Thick Ascending Limb Sodium Transport in the Pathogenesis of Hypertension

Thick Ascending Limb Sodium Transport in the Pathogenesis of Hypertension

Short-Term RCT of Increased Dietary Potassium from Potato or Potassium Gluconate: Effect on Blood Pressure, Microcirculation, and Potassium and Sodium Retention in Pre-Hypertensive-to-Hypertensive Adults

Effects of Short-Term Potassium Chloride Supplementation in Patients with CKD

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