Bastyr Center for Natural Health



Bastyr Center for Natural Health

Clinic Shift of Eric Yarnell, ND

Last updated 8 Sept 2015

Hypertension Policies and Procedures

FOC Information to Obtain

1. When did the hypertension begin?

2. How was the hypertension diagnosed? (And was it by the clinical standard, of three consecutive elevated readings?)

3. Have there been any complications of the hypertension? (retinopathy, proteinuria, renal failure, TIA, stroke)

4. Is the hypertension symptomatic? (headache, pounding heart)

5. What treatments, natural or otherwise, have been and are being used? Are they effective?

6. Does the patient have a home BP cuff? Has it been checked against any other device for accuracy? Do they use it? How often? Do they record and track the results?

7. Is there a family history of hypertension or strokes?

Plasma Renin Activity and Aldosterone Assessment

Patients should have a fasting morning plasma renin activity test along with a serum aldosterone to help determine the cause of their hypertension if it is not known. If they are taking an ACEI, ARB, or beta-blocker, they must first be switched to a different drug class (preferably reserpine or a CCB) for 6 wk before a valid test can be determined.

Low-Renin hypertension: PRA 0.65 ng/ml/hr (~50% of patients), vasoconstrictive

High-Renin hypertension: PRA >3.7 ng/ml/hr (~20% of patients), vasoconstrictive

| |Volume Hypertension |Renin Hypertension (“Dry,” Vasoconstrictive, or Inflammatory |

| |(“Wet” or Low-Renin Hypertension, Aldosteronism, |Hypertension) |

| |Aldosterone dominance) | |

|PRA |0.65 ng/ml/hr |

|Direct Renin |5 mU/ml |

|(less accurate) | | |

|Main etiology |Sodium-volume, r/o adrenal adenoma and |Renin-angiotensin-induced vasoconstriction/inflammation |

| |hyperaldosteronism* |r/o bilateral renal arterial stenosis (Kotliar 2010) |

| |r/o unilateral renal artery stenosis (Kotliar | |

| |2010) | |

|Frequency |33% of patients |67% of patients |

| |More common in elderly, blacks and Hispanics | |

|Complications |Uncommon, not related to severity of BP |Frequent, severe, out of proportion to BP |

* Elevated morning (0800-1000) plasma aldosterone concentration to PRA ratio is main clue, followed by oral salt challenge followed by urine aldosterone concentration.

Treatment Based on Plasma Renin Activity

| |Volume Hypertension |Renin Hypertension (“Dry,” Vasoconstrictive, or Inflammatory |

| |(“Wet” or Low-Renin Hypertension, Aldosteronism, |Hypertension) |

| |Aldosterone dominance) | |

|Diet indicated |Low salt |Anti-inflammatory |

|Herbs indicated |Diuretics (Urtica leaf, Taraxacum leaf, Solidago,|ACEi (Allium, Crataegus, Salvia miltiorrrhiza, Ganoderma, Olea,|

| |Apium, etc.) |etc.) |

| | |Rauvolfia serpentaria |

| | |Inflammation modulators |

|Drugs indicated (bold = |thiazide diuretic |ACEi |

|first-line therapy) |aldosterone inhibitor* |ARB |

| |calcium channel blocker |beta blocker (reduce renin secretion) |

| |alpha blocker** |reserpine |

|Drugs contraindicated |Glycyrrhiza |diuretics |

* Spironolactone, eplerenone (the latter a mineralocorticoid receptor antagonist). These are potassium-sparing agents

** Not recommended, as studies show these drugs increase mortality long-term.

Treatment of Essential Hypertension

Volume Hypertension

1. Rule out renal artery stenosis (Kotliar, et al. 2010)

2. Salt restriction

Salt restriction does not cause rapid changes in blood pressure because renin synthesis goes up in response to salt restriction, leading to sodium retention by the kidneys and vasoconstriction (via angiotensins), which maintains blood volume and blood pressure.

Restricting dietary salt is helpful only in those patients who are salt sensitive or with low-renin hypertension, ie with PRA 20 ng/dl/ng/ml/h or >555 pmol/L/ng/ml/h), hypokalemia, minimal cardiovascular, retinal or renal complications

Note: most common cause of secondary hypertension (and overall surprisingly common, perhaps as much as 10% of people with isolated hypertension)

Mechanism: benign adrenal tumors secretes excess aldosterone => high filtered sodium load =>

1) increased water retention by kidneys => increased blood volume => hypertension

2) suppresses renin synthesis => no feedback inhibition of tumor

1. Refer the patient for confirmation testing (imaging to detect large adrenal tumors or hypertrophied adrenals), subtyping, and assessment for appropriateness of surgery.

2. Patients should eat a low-sodium diet.

3. Patients should exercise regularly.

4. Patients should maintain a healthy body weight.

5. Patients should avoid tobacco products.

6. Patients with small or non-observable adenomas should be treated with mineralocorticoid blockers (typically spironolactone 12.5-25 mg qd, raised to 400 mg qd until normokalemia is achieved, then slowly dropped to 25-50 mg qd after 4-8 wk as BP normalizes). Do not combine with salicylates. Eplerenone 25 mg bid is an expensive alternative.

References

Kotliar C, Inserra F, Forcada P, et al. (2010) "Are plasma renin activity and aldosterone levels useful as a screening test to differentiate between unilateral and bilateral renal artery stenosis in hypertensive patients?" J Hypertens 28(3):594-601.

* Laragh J (2001) “Lesson I: A brief history of hypertension research: Renin is twice rejected” Am J Hypetension 14:186-194.

* Young WF (2007) “Primary aldosteronism: Renaissance of a syndrome” Clin Endocrinol 66:607-618.

Important Abbreviations

ACEi = angiotensin converting enzyme inhibitor

ARB = angiotension receptor blocker

BP = blood pressure

PRA = plasma renin activity

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