Hypertension – a renal disease

K. Abirami*

Senior Consultant, Department of Nephrology & Urology Science, Kauvery Hospital, Salem, India

*Correspondence: Email: kishabi@yahoo.co.uk

Pathophysiology of Hypertension

From our first-year physiology lessons we know that blood pressure is product of cardiac output and peripheral vascular resistance. Cardiac output is governed by volume status and heart rate. Peripheral Vascular Resistance is determined by vasoconstriction/vasodilatation of the blood vessels. Sympathetic nervous system and Renin Angiotensin Aldosterone System are the 2 main neurohumoral factors which determine all the above said factors. Renin is secreted from the juxtaglomerular apparatus of the kidney and activates Angiotensinogen secreted from the liver forming Angiotensin II and Aldosterone. Aldosterone and AT-II mediate salt and water retention (both) and vasoconstriction (AT-II). AT-II also increases sympathetic nervous activity. Apart from that afferent sympathetic activity from the kidneys is increased in patients with renal disease which in turn leads to increased efferent sympathetic activity. So, it’s important to understand that kidneys through Renin Angiotensin Aldosterone System (RAAS) plays a pivotal role in initiating and sustaining hypertension. Clinically speaking also kidney disease is both a cause and effect of hypertension whereas cardiovascular system is predominantly not a cause of hypertension but affected by hypertension. This basic understanding of physiology also helps us to understand the place of each antihypertensive and why RAAS blockade has gained prominence for treatment of hypertension.

Diagnosis of Hypertension

What’s new in hypertension guidelines starts with the way we record Blood pressure. All the new guidelines talk about standardised office BP measurement. This stresses on the following parameters:

  1. Patient should be sitting at least for 5 min with back support and feet flat on ground
  2. No smoking or caffeine in the last half hour
  3. Bladder should not be full
  4. No talking
  5. No cloth covering the cuff area
  6. Record BP using standardised apparatus, could be oscillometric or manual
  7. Cuff should cover 80% of the circumference
  8. If manual palpatory method should precede auscultatory method.
  9. If manual deflate cuff by 2 mm of Hg every sec
  10. Take 3 readings and take average of the last 2 readings

Based on this standardised BP measurement ACC 2107 guidelines defines the following categories:

  1. Normal: SBP < 120 and DBP < 80
  2. Elevated: SBP 120–129 and DBP < 80
  3. Hypertension Stage1: SBP 130–139 or DBP 80–89
  4. Hypertension Stage 2: SBP ≥140 or DBP ≥ 90

Confirmation of diagnosis requires:

  1. Three readings over weeks to months or confirmation with home BP recording or ABPM
  2. It can be confirmed after first reading
    1. If BP > 180/120
    2. If presenting with HTN emergency or urgency
    3. If BP > 160/100 and patient has evidence for end organ damage (HMOD)

International Society of Hypertension has come up with newer guidelines in 2020 which are far less stringent but I prefer ACC guidelines.

Treatment of Hypertension

When to treat?

  1. All patients with elevated BP should be taught lifestyle modifications and reassessed in three months
  2. All patients with Stage 2 hypertension should start lifestyle modifications and pharmacologic therapy simultaneously
  3. All patients with Stage 1 hypertension should start lifestyle modifications.
    1. If associated cardiovascular disease or target organ damage or if calculated 10-year risk for CV disease is >10% then they should start pharmacologic therapy simultaneously

Goal of Treatment

  1. The outcome of SPRINT trial has lowered the BP targets.
  2. All adults with hypertension with CV disease or > 10% risk for CV disease in the next 10 years BP target should be < 130/80
  3. All patients with HTN but no risk factors still should try to achieve target BP of < 130/80
  4. Exceptions will be older patients with increased risk of falling, patients with orthostatic hypertension, patients with diastolic BP < 55–60 and patients with limited life expectancy

Which agents to use:

The preferred first line agents now would be ACE-I/ARB blockers (A), Long acting DHP Calcium Channel Blockers like Amlodipine (C) and Diuretics (D). The evidence for these drugs come from ASCOT and ACCOMPLISH trials.

In Stage 1, we can start with one drug either A or C. If BP not controlled then we add the second drug either A or C which was not used to begin with. Third step will be to add D.

In Stage 2, we start with A and C at low dose and titrate upwards. Third agent to be added will be a diuretic. If still not at target then add Mineralocorticoid Receptor antagonist.

Beta blockers are used preferentially in patients with AF and Fast ventricular rate, CAD, heart failure. In black’s better response is seen with diuretics and Calcium Channel blockers.

Specific agents:

Diuretics

  1. Thiazide diuretics are preferred if GFR > 30 ml/min
  2. Chlorthalidone and Indapamide over HCTZ mainly because they are long acting
  3. Loop diuretics – Torsemide has better oral bioavailability but equal efficacy to Frusemide and is used in patients with GFR less than 30

How to use ACEi-ARBs:

  1. Start with low dose and achieve maximum tolerated dose
  2. Check creatinine within 5 to 10 days of starting ACE/ARB in patients with CKD and within 2-4 weeks in patients with no CKD
  3. Stop if creatinine increases by > 30% in the first eight weeks of treatment
  4. ACE-I-5-20% incidence of cough. Less with ARBS
  5. Do not combine ACEi and ARBs
  6. Avoid other nephrotoxic drugs
  7. Hydration essential

Hypertension in CKD

  1. Hypertension in CKD is both a cause and effect. Hence its incidence increases with increasing stage of CKD. It has certain salient features:
  2. Increased incidence of white coat hypertension especially in earlier stages of CKD (up to 25%)
  3. Increased incidence of resistance HTN (25%)
  4. Salt sensitive HTN
  5. Non dipping in the night
  6. More likely to have increased systolic BP with increased pulse pressure

Goal of Hypertension therapy in CKD

From AASK, MDRD and SPRINT trial we have evidence that reducing BP to < 130/80 reduces mortality in CKD patients. It also retards progression of renal disease in proteinuric CKD patients. The current KDIGO guideline (2020) suggests target SBP of less than 120 in adult patients with CKD.

Agents of choice in CKD

Antihypertensives in CKD is based on presence or absence of proteinuria.

Proteinuric CKD Proteinuric CKD
Angiotensin inhibitors Diuretics- If GFR<30 then Loop diuretic or metolazone Diuretics if there is edema CCB or Angiotensin inhibitors
Non DHP CCB like Diltiazem Mineralocorticoid antagonists Alpha blockers and others Mineralocorticoid antagonists Alpha blockers Others

Conclusion

All of us have to adopt standardised office BP measurements. Without standardisation, BP readings can vary hugely depending on how and where is it recorded making it impossible to compare and have uniform recommendations. Antihypertensive therapy and goals have changed in the last decade because of our understanding of the central role played by RAAS and publication of large randomised control trials.

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