Secondary Causes

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    Renovascular HTN

     

    • Typically when > 70% luminal narrowing of renal arteries
    • Suggest Renovascular HTN:
      • Suggesting renovascular HTN if: (≥ 2 of:)

         

        1. Sudden onset or worsening HTN at age >55 or < 30yo

        2. Abdominal bruit

        3. Resistant HTN (≥3 drugs)

        4. Increase in creatinine ≥ 30% with initiation of ACEi

        5. Atherosclerotic vascular dz in pts who smoke or have dyslipidemia

        6. Pulmonary edema with hypertensive surges

         

     

    • Exam:
      • Hear epigastric bruits (both atherosclerotic and FMD mechanisms)
    • Two types:
      • Atherosclerosis
        • Vascular risk factors (i.e. smoking, dyslipidemia)
        • Proximal renal arteries
      • Fibromuscular Dysplasia
        • Younger patients (women)
        • Distal renal arteries
    • Mechanism:
      • Unilateral --> Elevates BP through renin-mediate mechanism
      • Bilateral --> Sodium excess elevate BP
    • Diagnosis:
      • Captopril-enhanced radioisotope renal scan
        • Do not use in CKD (GFR < 60)
      • MRI Angiography (gadolinium)
      • CT angiography (for those with normal renal function) (Grade B).  (Grade D).
      • Renal Doppler
        • Recommended if GFR < 30 (cannot use iodinated or gadolinium contrast)
    • Treatment
      • Fibromuscular Dysplasia
        • Percutaneous renal angioplasty --> treatment of choice. 
      • Atherosclerotic Disease
        • Controversial!!!
        • ASTRAL Trial and STAR Trial do not support angioplasty over medical therapy. 
        • Recommendations:
          • Aggressive risk factor modification (BP control, dyslipidemia therapy, smoking cessation). 
          • Percutaneous stenting ONLY for those with refractory HTN despite extensive treatment, or progressive loss of renal function.
      • Bilateral Renal Artery Disease --> at risk of worsening renal function when treated with RAAS drugs (ACEi or ARBs).  Especially in those with aggressive diuretic use.  Be careful if serum creatine rises > 25% of baseline. 

     

    Hyperaldosteronism

     

    Suspect when:

    • Screening for hyperaldosteronism should be considered:

       

      1. HTN + spontaneous ↓K (K+ < 3.5 mmol/L);
      2. HTN + marked diuretic- induced ↓K (K+ < 3.0 mmol/L);
      3. Resistant HTN (≥ 3 drugs)
      4. HTN + incidental adrenal adenoma

     

    Diagnosis:

     

    • Step #1 Perform a Screening Test:  

     

    • Plasma aldosterone & plasma renin activity OR renin mass/concentration
      • Must collect in morning after patient ambulatory >2h (incl sitting/standing/walking)
      • Must be seated for 5-15min prior to blood draw
      • Hypokalemia should be corrected & sodium intake liberalized
      • Remove agents that affect testing (aldosterone antagonists, potassium sparing/wasting diuretics)  --> Must withdraw 4-6w prior
        • Medications not affecting test: slow-release verapamil, hydralazine, prazosin, doxazosin, terazosin)
      • If results nondiagnostic, remove: beta blockers, alpha-2-agonists, ARBs, ACEi, renin agonists, dihydropyridine CCB.
    • A. To estimate: B. From: Multiply (B) by:
      Plasma renin concentration (ng/L) Plasma renin activity (ng/mL/hr) 0.192
      Plasma renin activity (ng/L/sec) Plasma renin activity (ng/mL/hr) 0.278
      Plasma aldosterone concentration (pmol/L) Plasma aldosterone concentration (ng/dL) 28

     

    • Positive Screening Test: plasma aldo-to-renin activity ratio > 750 pmol/L/ng/ml/hr (or 144 pmol/L/ng/L when renin is measured as renin mass or concentration)

     

    • Step #2: If screening test positive, autonomous aldo secretion present:  Do Confirmatory test 

     

    • If adrenal mass present + eligible for surgery --> Adrenal venous sampling (assess for lateralization of secretion)
    1. saline loading tests (perform either):
      1. Administer 2L of normal saline IV over 4h with the patient in a recumbent position. Primary hyperaldosteronism is defined as a post-infusion plasma aldosterone >280 pmol/L. If <140 pmol/L, primary hyperaldosteronism is unlikely. Values in between are considered indeterminate;
      2. Administer PO sodium, 200 mmol/day x3 days, with primary hyperaldosteronism defined as a 24-hr urinary aldosterone >33 nmol/d (measured from the morning of Day 3 to the morning of Day 4). If <28 nmol/day, primary hyperaldosteronism is unlikely.
    2. a plasma aldosterone to PRA ratio greater than 1400 pmol/L/ng/ml/hr (or 270 pmol/L/ng/L), with a plasma aldosterone greater than 440 pmol/L.
    3. captopril suppression test: Administer 25-50mg captopril orally after the patient has been sitting or standing for 1 hour. While seated, renin and plasma aldosterone levels should be measured at time zero and 1-2 hours after ingestion. Primary hyperaldosteronism is unlikely if plasma aldosterone is suppressed by >30% following captopril ingestion. In primary hyperaldosteronism, plasma aldosterone remains elevated, while renin remains suppressed.

     

    • Step #3: Primary Hyperaldosteronism Subtype Classification

     

    • Adrenal CT or MRI to localize lesion
      • If lesion found & fit for surgery--> do adrenal venous sampling to see if it is source of hypersecretion
      • If imaging normal & fit for surgery
        • Adrenal Venous Sampling --> bilateral or unilateral production? for possible adrenalectomy
    • If family history of hyperaldosteronism or young stroke ≤40yo OR onset of HTN ≤ 20y and negative imaging --> test for Glucocorticoid Remediable Aldosteronism

     

    Management

    • Surgery? - find out if candidate (above testing) --> possible unilateral laparoscopic adrenalectomy
    • Medications:
      • Mineralocorticoid Receptor Antagonists (i.e. aldosterone)

     

     

    Pheochromocytoma

     

    • Increase BP through norepinephrine and epinephrine. 
    • Diagnosis requires a very high degree of suspicion
    • Suspect when:
      • Suspect Pheochromocytoma when:

        • Paroxysmal and/or severe (BP ≥ 180/110) sustained HTN refractory to anti-HTN therapy
        • HTN + symptoms suggesting catecholamine excess (headaches, palpitations, sweating, panic attacks, pallor)
        • HTN triggered by B-blockers, MAO Inhibitors, Micturition, abdominal pressure
        • HTN + incidentally discovered adrenal mass + MEN2A/2B or von Recklinghausen neurofibromatosis or von Hippel-Lindau disease
        • Positive biochemical screening tests --> Localize with MRI (preferred), CT if MRI unavailable, or I-131 scintigraphy.
    • Investigations:
      • Screening:
        • 24-hr urine total metanephrines and catecholamines (sn 90-95%)
          OR
          • 24-hr urine fractionated metanephrines (sn 100%) + 24hr urine creatinine (to confirm accurate collection)
        • Plasma metanephrine measurement and free normetanephrines, where available may be considered (sn 99%)
        • Urinary VMA measurements should not be used for screening
      • If borderline result, or possible false positive result
        • Repeat testing and/or clonidine suppression test.
      • Do biochemical testing BEFORE imaging (to avoid incidentalomas)
      • Imaging:
        • MRI (preferred)
        • CT (if MRI unavailable)
        • I-131 metaiodobenzylguanidine  scintigraphy  (aka MIBG)
    • Treatment:
      • Surgical removal!
        • Peri-operative management:
          • Alpha-blockers started 10-14d pre-op. (can include phenoxybenzamine (long-acting non-selective irreversible alpha-blocker), prazosin, doxazosin
          • Add Dihydropyridine CCB 
          • Add other anti-HTN agents
          • Avoid diuretics if possible
          • Encourage volume + salt intake pre-op (volume contraction is common)
        • Post-Op
          • Hold anti-HTN drugs
          • May need aggressive IV fluids 
        • Long-Term
          • Follow urinary or plasma metanephrines (screen for recurrence)
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