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Renal Week 2 > HTN and the Kidneys > Flashcards

HTN and the Kidneys Flashcards

1
Q

What percentage of HTN is Primary?

Secondary (Many factors case BP elevation by influencing CO or SVR)

A

~90%

~10%

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2
Q

What is often the age of onset for primary HTN?

A

40s-50s

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3
Q

What is often the age of onset for secondary HTN?

A

less than 30 or older than 50

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4
Q

Does primary HTN likely have a genetic component?

A

Yes. 70-80% of individuals have positive family history

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5
Q

What are some candidate genes for primary HTN?

A

very polygenic disease

M235T variant in the angiotensinogen gene,

ACE gene,

β2-adrenergic receptor gene

the environment affects greatly

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6
Q

What is the eqn for MAP?

A

CO x TPR or

SV x HR x TPR

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7
Q

What things increase SV?

A
  • increased preload (Frank Starling)

- increased contractility

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8
Q

T or F. Increase in essential HTN does not persist.

A

T, eventually the reason for the HTN is the elevated TPR (see cardio cards)

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9
Q

The development of sustained hypertension depends on what?

A

The impairment in kidney ability to excrete excess sodium and, therefore, water.

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10
Q

Importante info about the role of kidney function in HTN

A

The transplantation of kidney from a hypertensive donor will induce hypertension in a normotensive recipient.

The transplantation of kidney from a normotensive donor will reverse hypertension in a hypertensive recipient.

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11
Q

What is Guyton’s Theory of Long-term BP Control?

A

Inability of kidneys to appropriately excrete sodium loads play central role in the development of essential hypertension

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12
Q

What is pressure natriuresis?

A

When perfusion pressure increases, renal sodium output increases and extracellular fluid and blood volumes contract by an amount sufficient to return arterial blood pressure to baseline.

Natriuresis driven by pressure provides a primary and powerful means of stabilizing total body sodium and blood pressure over a wide range of sodium intakes

Therefore, impairment in pressure-natriuresis is essential for elevated BP to persist

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13
Q

At what MAP does pressure natriuresis normally kick in?

A

Normally when MAP approaches 100 mg, Na excretion will increase exponentially (very steep) so that further increase in MAP is buffered almost completely

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14
Q

How does pressure natriuresis change in primary HTN?

A

The kidneys are still able to maintain normal volume by excreting excess Na but at higher levels of baseline BP (reset) and they are less efficient (Na+ is given off more slowly)

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15
Q

What are the pros of Guyton’s theory?

A

It allows for a normal blood volume despite an elevated pressure, in keeping with most volume measurements in hypertensive patients

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16
Q

What are the cons of Guyton’s theory?

A
  • Ignores role of Autonomic Nervous System in the development of HTN
  • Fails to explain BP↑ in prehypertension, where↑ CO is mainly driven by activation of SNS
17
Q

Autoregulation note

A

Increased volume increases CO which increases BP.

18
Q

What does ouabain do?

A

inhibits the Na/K ATPase

19
Q

a

A

a

20
Q

What is Brenner’s hypothesis of essential HTN?

A

The development and maintenance of hypertension must involve a renal factor favoring sodium retention, thereby preventing pressure-induced natriuresis from restoring blood pressure toward normal levels.

Since nephron numbers in the normal population range from 300,000 to 1,100,000 or more, it was reasoned that a congenital deficit in nephron endowment itself could be the renal risk factor for hypertension:

21
Q

Is there data that supports Brenner’s Hypothesis?

A

Demographic groups in whom HTN is unusually prevalent tend to have smaller kidneys, implying fewer nephrons. This argues that recent independent observations in humans relating low birth weight to both increased risk of hypertension in later life and the formation of fewer nephrons at birth lend strong support to the nephron number hypothesis.

22
Q

Where is the number of nephron theory strongly supported in relation to HTN?

A

Best demonstrated in chronic kidney disease that in turn leads to secondary HTN

23
Q

T or F. AAs are more sensitive to salt intake than caucasians

A

T.

24
Q

What is salt sensitivity?

A

the situation that exists when a patient sees ↑ in BP on high salt diet and ↓ in BP with low salt diet

25
Q

What other population is at increased salt sensitivity?

A

elderly (increases with age). At older ages, the HTN is more driven by upper systolic pressure with normalish diastolic pressure

26
Q

HTN (MAP) is also affected by changes TPR. Name some vasoconstrictors involved in elevating MAP.

A 
Angiotensin II (ATII), 	norepinephrine (NE), endothelin, 
ADMA
27
Q

Name some vasodilators involved in lowering MAP.

A

NO, prostacyclin, PGE2 and PD2, adenosine

28
Q

What does increased NaCl delivery to the thick ascending limb cause?

A

Increased adenosine secretion which binds to adenosine receptors on the juxtaglomerular cells, inhibiting the release of renin

29
Q

T or F. Renin is elevated in everyone with primary HTN

A

F.

  • 20% high PRA (plasma renin activity)
  • 30% low PRA
  • 50% normal PRA
30
Q

What is Laragh’s hypothesis of nephron heterogenesity?

A

Some nephrons are ischemic and produce high renin, while others are not but will have impaired natriuresis from ATII. Total PRA is “diluted” and may be normal

31
Q

How does CKD cause 2ndary HTN?

A

by impairing Na excretion due to reduced nephron mass

32
Q

What is the Goldblatt model I of unilateral renal artery stenosis?

A

HTN due to unilateral RAS is associated with both increased SVR and right shift in pressure natriuresis in the contra-lateral “normal” kidney

The “Normal” kidney is able to excrete excess Na, therefore volume does not play additional role in BP

ACE-inhibitors reduce BP

33
Q

What is the Goldblatt model II of unilateral renal artery stenosis?

A
  • A clip is applied to 1 renal artery in an animal with 1 functioning kidney

Total kidney mass hypoperfusion
No off-setting pressure natriuresis (flash pulmonary edema)

  • Intolerance to ACE-Inhibitors
34
Q

How prevalent is renal artery stenosis?

A
  • in non referred populations ~1%
  • 4% blacks and 32% whites with
    DBP >125mmHg
35
Q

What are the most common causes of renal artery stenosis?

A
  • Atherosclerosis (85%)

- Fibromuscular dysplasia (10%)

36
Q

What are the clinical features of RAS?

A

Onset of HTN in younger (

37
Q

What are some kidney and endocrine causes of 2ndary HTN?

A
  • Aldosterone Excess
  • Glucocorticoid Excess
  • Pseudohyperaldosteronism:
    • 11β-Hydroxysteroid -Dehydrogenase inhibition
    • Liddle’s Syndrome
  • Psedohypoaldosteronism type 2 (Gordon syndrome)

All characterized by salt-sensitive hypertension
All, except aldosterone excess, characterized by low renin and low aldosterone
All, except Gordon syndrome, are associated with hypokalemia and metabolic alkalosis

Renal Week 2 (13 decks)

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