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SMP - Renal > Lecture 14 - Renal Function during Pregnancy > Flashcards

Lecture 14 - Renal Function during Pregnancy Flashcards

1
Q

What abnormal lab values are actually normal during pregnancy?

A
  1. Hyponatremia
  2. Hypokalemia
  3. Low plasma [HCO3-] and PCO2
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2
Q

What normal lab values are actually abnormal during pregnancy?

A
  1. BUN => renal insufficiency
  2. Plasma creatinine => renal insufficiency
  3. Plasma urea => hyperuricemia
  4. BP => HT
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3
Q

What is preeclampsia?

A

Hypertensive disorder with proteinuria unique to human pregnancy

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4
Q

Changes in CO during pregnancy? Cause?

A

50% increase, peaks at midpregnancy and is sustained through delivery

Due to increase in both SV and HR

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5
Q

Describe volume retention during pregnancy. What does this cause? What to note?

A
  • Weight gain averages 12.5 kg
  • ~8-9L increase in TBW (4-7L increase in ECF)
  • Cumulative retention of ~900mEq Na
  • Plasma volume increased ~42% to 3.7L

Can cause edemas

Volume expansion sensed as normal

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6
Q

BP changes during pregnancy? What to note? Provide an explanation.

A

Falls by 10 mmHg (even more so in women with underlying HT) due to dramatic systemic vasodilation with increased arterial compliance and venous capacitance

This occurs despite increased CO, volume retention, and RAA system activation

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7
Q

Describe 3 renal structural changes during pregnancy.

A
  1. Kidney length increases ~1cm
  2. Dilated collecting system (mimics obstruction response)
  3. GFR and ERPF both increase ~35-85% (peak effect by late 1st, early 2nd trimester) and RVR decreases
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8
Q

Does GFR vary in normal women?

A

Yes, during the menstrual cycle

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9
Q

Changes in plasma creatinine during pregnancy?

A

Falls due to increased GFR and its clearance

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10
Q

Normal Pcr in pregnant woman?

A

0.5 mg %

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11
Q

Do the changes in GFR in pregnant women happen to pregnant women with renal disease?

A

YUP

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12
Q

What is the increase in GFR during pregnancy due to exactly?

A

Balanced vasodilation of the afferent and efferent arterioles to increase flow and keep glomerular hydrostatic pressure constant => increase in SNGFR

Due to increase in relaxin => it binds to the relaxin receptor on afferent and efferent arterioles => increases MMPs (matrix metalloproteases) activity => MMPs cleave endothelin precursor (normally a potent vasoconstrictor) => alternate form binds to endothelial tissue (B receptor) causing the release of NO in endothelial cells => vasodilation causing increase in GFR, increase in RPF, and decrease in myogenic reactivity

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13
Q

Major role of relaxin during pregnancy?

A

Hormone that relaxes the pelvic ligaments in preparation for delivery

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14
Q

Describe the 5 acid base and tubular adaptations during pregnancy.

A
  1. Minute ventilation increased ~50% due to progesterone, resulting in compensated primary respiratory alkalosis (pH ~7.44) => normal pCO2~30, normal HCO3~18-20
  2. Urine often alkaline due to bicarbonate leak
  3. Modest glucosuria and aminoaciduria due to increased filtered loads
  4. Decreased uric acid (~2.8-3.0), due to increased renal clearance
  5. Absorptive hypercalciuria due to increased calcitriol (i.e., active vitamin D)
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15
Q

Describe calcium balance in pregnant women. Timing?

A

Increased vitamin D is because the placenta has 1-alpha hydroxylase just like the kidney => increased Ca++ absorption in GIT (needed to build the fetal skeleton - 25g of calcium transferred to fetus over pregnancy) => total plasma calcium is actually low due to high volume (ionized is normal) => hypercalciruia

Happens during all 3 trimesters

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16
Q

Do pregnant women get kidney stones due to increased plasma calcium?

A

NOPE - due to proteins made in the kidney during pregnancy that inhibits calcium crystallization

17
Q

Is increased load the only explanation for glucosuria in pregnant women?

A

Also small changes in Tm and splay, but it’s the predominant reason

18
Q

Albumin level in pregnant women?

A

Low because diluted by high volume

19
Q

Describe osmoregulation during pregnancy. What can this lead to?

A

Vasopressinase in the placenta breaks down AVP (even more during late pregnancy as placenta gets bigger) => hypo has to secrete more AVP => increased AVP secretion rate => shift to lower set point of AVP and thirst => shift to lower the set point of osmolality (“reset omostat”) => decrease in plasma osmolality (by about 10), including a decrease in plasma sodium (by about 5)

Can lead to gestational diabetes insipidus

20
Q

Is the fall in plasma [Na+] due to increased GFR?

A

NOPE

21
Q

Graphic representation of changes in osmoregulation in pregnant women?

A

Curve shift to the left of Posm vs plasma [AVP]

22
Q

Are the AVP levels elevated during pregnancy?

A

NOPE - normal

23
Q

Lab value of gestational diabetes insipidus?

A

Plasma [Na+] = 140 => hypernatremia

24
Q

Describe the functioning of the RAA system during pregnancy. What to note?

A
  1. Aldosterone increases dramatically even compared with someone who has an aldosterone tumor
  2. Potassium excretion is normal, even in the presence of exogenous aldosterone and salt, because progesterone binds to aldosterone receptors and acts as an antagonist
  3. Renin, angiotensinogen, angiotensin II increase, but no HT because less responsive to vasoconstrictor effects to Ang II

Note: pregnancy can mask hyperaldosteronism - post-partum the aldosterone levels fall back down and she becomes hypertensive and hypokalemic

25
Q

What % of pregnancies experience HT? Consequences?

A

15%

=> premature deliveries (15% of them due to this) and maternal/fetal morbidity

26
Q

Does preeclampsia resolve with delivery?

A

YUP

27
Q

What can preeclampsia progress to?

A

Convulsive phase: eclampsia

28
Q

What is the leading cause of maternal mortality?

A

Preeclampsia

29
Q

What is common with preeclampsia?

A

Target organ damage

30
Q

What can make preeclampsia hard to diagnose?

A

Pregnant patients with renal disease or HT

31
Q

% of first pregnancies with preeclampsia?

A

4-7%

32
Q

7 risk factors for preeclampsia?

A
  1. HT
  2. Diabetes
  3. Kidney disease of any cause or severity
  4. Obesity
  5. Insulin resistance
  6. Hyperhomocysteinemia
  7. Other markers of CV risk
33
Q

What does recurrent preeclampsia predict (in more than 1 pregnancy)? What to note?

A

Later CVD

BUT CVD risk lowest in women who have been pregnant, but never preeclamptic

34
Q

Normal pregnancy MAP? Range and value

A

81-89 => 83

35
Q

CO in women with preeclampsia? Why?

A

LOW

Because systemic vascular resistance is HIGH (double)

36
Q

Pathophys of preeclampsia? Effect on kidneys?

A
  1. Loss of resistance to angiotensin II (starts before preeclampsia HT) => hypersensitivity (when preeclampsia HT appears)
  2. Increase in sympathetic tone compared with all women regardless of pregnancy or not
  3. Endothelium-dependent relaxation is impaired in small arteries
  4. Glomerular endotheliosis is swollen and vacuolated => lumen occlusion (due to afferent vasoconstriction)

=> MAJOR INCREASE IN SVR

=> kidneys have lower GFR, ERPF and FF

37
Q

What is gestational hypertension due to?

A

Increased CO with normal TPR

38
Q

Ang II levels in preeclamptic women?

A

LOW

SMP - Renal (20 decks)

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