potassium, aldosterone, and hypertension: how physiology...
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Potassium, Aldosterone, and Hypertension: How Physiology
Determines TreatmentJamie Johnston, MD
University of PittsburghSchool of Medicine
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No Disclosures
Acknowledgements: Evan Ray, MD, PhD
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Objectives
Identify patients that should be evaluated for primary aldosteronism
Recall evaluation for primary aldosteronism Describe effect of anti-hypertensive medications on
potassium Describe benefits of potassium
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Hypertension: How common in the US?
One in three adults Americans have hypertension(Hypertension. 2004;44:398–404)
76.4 million Americans age 20 or older have HTN NHANES [2005-2008]. NCHS and NHBLI
Primary hypertension – 85%
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Hypertension U.S. Prevalence (National Health and Nutrition Examination Survey 2011-2012)
https://www.cdc.gov/nchs/images/databriefs/101-150/db133_fig1.png)
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Aldosterone
Release stimulated by Volume depletion Hyperkalemia
Distal nephron Collecting duct Distal Tubule
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Examples of Identifiable Causes of Hypertension
Renovascular diseaseRenal parenchymal
disease Polycystic kidneysAortic coarctationSleep apnea
Pheochromocytoma Primary aldosteronism**Cushing syndromeHyperparathyroidismHypo/hyperthyroidism Exogenous causes
DrugsBCPsES agents
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Primary Hyperaldosteronism
Most common secondary form of hypertension Prevalence 5 – 13% of all hypertension Higher Risks than Primary hypertension
More cardiovascular events Increased prevalence of metabolic syndrome Increased LVH Increased albuminuria
Young WF, Clinical Endocrinology (2007) 66, 607–618
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Case Presentation23 year old woman referred to Hypertension Clinic for difficult-to-treat hypertension. History of present illnessDiagnosed at 16 years of ageAge 24, presented with headache, chest painBlood pressure 200/114K 2.8Discharged on atenolol, irbesartan, potassium
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Case Presentation Past Medical History1st period age 13, irregular periodsChronic sinusitisOverweight
Meds: Metoprolol, irbesartan, ASA, Ethinyl estradiol/desogestrel OCP Social History: Denied tobacco, alcohol, illicit drugs or natural black licoriceLittle exercise
Family History: father, grandfather with hypertension
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Case Presentation Vital signs:
• Wt 196, Height 68.5 inches, BMI 29.4 kg/m2
• BP 160/104 RUE, 154/100 LUE Physical exam:
• Appears comfortable• Optic fundus - AV nicking• Heart regular, 1/6 SEM entire precordium
PMI 6th ICS
Labs: Na 142, K 3.0, Cl 107, CO2 24, sCr 0.7
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Primary Hyperaldosteronism
Stowasser, et al. J Hypertens. 2003;21:2149-2157.
Normal• Aldo upright 4-31• Upright plasma renin activity 0.5 – 3.3
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Refractory Hypertension
Aldo-renin ratio (ARR)
<25 >50 & aldo > 10 ng/dlARR 25-50
Confirmatory Testing
Start Mineralocorticoid receptor blocker
Primary aldosteronism unlikely
+-Surgical Candidate?
Adapted from Johnson et al. Comprehensive Clinical Nephrology, 5th ed. 2015
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Confirmatory TestingTest Method Evaluation Limitations
Oral NaCl load >200 mmol/day for 3 d24 hour urine aldo
Urine aldo< 10 ug/d (-)>12 ug/d (+)
Severe htn, CKD, CHF, hypokalemia
Saline Infusion Test
2 L NS over 4 hourAM
recumbent
Plasma aldo< 5 ng/dl unlikely>10 ng/dl likely
Severe htn, CKD, CHF, hypokalemia
Fludrocortisone suppression
0.1 q 6 for 4 days +high salt
Plasma Aldo > 4 ng/dlPRA > 1 ng/ml/h
hospitalization
Captopril challenge
25-50 mg labs immediately before and 1-2 hrpost
Plasma aldodecreases by >30%
Greater false positive and negative rate than first 3
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Surgical Candidate?Yes No
Optimize Mineralocorticoid receptor blockerAdrenal Imaging CT Scan -
Continue Mineralocorticoid receptor blockerAdrenal Vein Aldo Sampling
Optimize Mineralocorticoid receptor blocker
Good BP response?
Yes
No
Unilateral Bilateral
+
Laparoscopicadrenalectomy
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What causes hypertension?
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Na+ Balance and Blood Pressure
Na+ balance: Na+in – Na+
out
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Sodium Consumption and HTN
Mente et al. 2014 NEJM (PURE Study – Prospective Urban Rural Epidemiology)
mmHg/g Na+ excreted
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What about potassium?
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Potassium – Basic Facts 98-99% of K is in the cells Extracellular fluid - 2% of total body K, 70 mmol Necessary for
Nerve conduction Cell volume regulation Electrolyte transport
Hypo or hyperkalemia occurs in 30% of hospitalized patients*.
*Shemer Isr J Med Sci 1983, Paice Postgrad Med J 1986
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Exchange of K+ for Na+ in Westernized diet
Pierre Meneton et al. (2004) Am J Physiol Renal Physiol
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And we give drugs that affect potassium
Diuretics – decrease potassium
RAAS agents – increase potassium
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Blood pressure and Plasma K
C, Beretta-Piccoli et al Clinical Science (London) (1982) 63,257-270
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Blood pressure, sodium and potassium excretion
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All-Cause Mortality and Serum K Levels in Patients with CKD
Non-Dialysis CKD1 Peritoneal Dialysis2
Multivariable adjusted log hazards (solid line) and 95% confidence intervals (dashed lines) of all-cause predialysis mortality associated with serum potassium levels in the
entire study population (n=1,227).
Association of serum potassium, used as a time-varying covariate, with mortality in patients undergoing peritoneal dialysis
(n=10,454). Dashed lines represent 95% confidence intervals.
1) Hayes J, et al. Nephron Clin Pract. 2012;120:c8-c16.2) Torlén K, et al. Clin J Am Soc Nephrol. 2012;7:1272-1284.
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Potassium Supplementation and Blood Pressure
Siani et al. (1987) 37 hypertensive
subjects, randomized Intervention:
48 mEq KCl or placebo daily
15 weeks Outcomes
Blood pressure
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Does K+ reduce the need for anti-hypertensives?
Trial: 57 persons with well-controlled HTN Intervention:
Randomized to high or normal K+ diet Nutritional counseling to increase K+
3 to 6 rations of fruits or vegetables / day Steamed, not boiled
Calories held constant Subjects seen monthly by a blinded
physician Medications titrated appropriately
1 year
Findings Urinary K + increased 46% No change in urinary Na+
Siani et al. (1991) Ann Int Med
*
*
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Potassium Intake and Blood Pressure
Aburto et al (2013) BMJ22 randomized, controlled trials
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How Does K+ Reduce BP?
Corvol P et al. (1977) Endocrinology
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How Does K+ Reduce BP? 11 male subjects (24-31 yo) Overnight fast Bolus of either 500 cc NSS (control) or 500 cc NSS + 32 mEq KCl
Results Compared to control p
Serum K+ Increased 0.64 ± 0.04 mmol/L < 0.001
Urine K+ Increased 13.8 ± 1.9 mEq < 0.001
Urine Volume Increased 138.6 ± 33.6 mL < 0.01
Urine Na+ Increased 18.6 ± 5.8 mEq < 0.01
Aldosterone Increased 3.6 ± 8.9 ng/dL < 0.01
Barnes et al. (1984) Clinical Science K+ affects aldosterone signaling.
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K+ Loading, Na+ Excretion, and Aldosterone Healthy volunteers 22-26 yo Metabolic ward
Baseline diet 100 mmol K+ / day 100 mmol Na+ / day
Supplement started: Total K+ 400 mEq/day
Electrolytes measured hourly over 8 hours Baseline After 1st K+ load 72 hrs
Discharged home 20 days
Rabelink et al. (1990) Kidney Intl
Conclusions: K+ loading• 400 mEq/day was safe• Increased aldosterone• Increased Na+ excretion
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Hypertension Clinic K+ Recommendations(Matt Muldoon, MD; Kelly Junker, PharmD, Mark Dinga RD)
Patients eGFR ≥ 45 Serum K+ ≤ 4.6 mEq/L Not recently started on
ACEi / ARB K+-sparing diuretic
Dietary recommendations Na+ 2000 mg/day Increase consumption of K+-rich food (DASH Diet)
E.g. un-boiled root vegetables, fruits
For patients who cannot increase K+-rich foods Over-the-counter KCl Powder ($5/month)
Patients ≤ 130 lbs: 1 tsp (75 mEq) Patients > 130 lbs 1½ tsp (125 mEq)
Monitoring of serum K+
Matt Muldoon, MD; Kelly Junker, PharmD, Mark Dinga RD
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Why Does K do this?
Distal nephron Collecting duct Distal Tubule
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RAAS Inhibition and CKD ACEis and ARBs
Hypertension Rx
Rx of CKD, heart failure, and diabetic nephropathy
But impair renal potassium secretion, increasing the risk of hyperkalemia
This can raise a dilemma in treating patients with CKD or other conditions
Kovesdy C. Nat Rev Nephrol. 2014;10:653-662.
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Epstein M, et al. Am J Manag Care. 2015;21(11 Suppl):S212-S220.
Adverse Outcomes or Mortality by Prior RAAS Inhibitor Dose
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In Patients at Risk for Hyperkalemia due to RAAS Inhibition
• Monitor kidney function (eGFR, ACR)• Monitor serum potassium levels• Discontinue drugs that increase hyperkalemia risk, if possible• Prescribe low-potassium diet• Prescribe diuretics (loop diuretics when eGFR <30 mL/min)• Correct metabolic acidosis in patients with CKD• If required, initiate therapy with low-dose ACEi or ARB and monitor• Newer potassium binders may offer a potential option to continue RAAS
inhibition in patients who need these therapies
GFR, glomerular filtration rate; ACR, albumin-to-creatinine ratio; RAAS, Renin-Angiotensin-Aldosterone System
Modified form Palmer B. N Engl J Med. 2004;351:585-592.Makar M, Pun P. Am J Kidney Dis. 2017. [Epub ahead of print]Sterns R, et al. Kidney Int. 2016;89:546-554.Dunn J, et al. Am J Manag Care. 2015;21(15 Suppl):s307-s315.
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