Jun 5, 2024
Anatomical changes to the kidneys during pregnancy. Kidney size increases by a factor of one to 1.5. The progesterone's effect causing the pelvis to dilate. Pelvic dilatation-induced urine stasis increases the risk of urinary tract infection. The risk of pyelonephritis is higher on the right side. A renal volume increase of 30%.
Factor Effect Plasma volume ↑ till 32-34 weeks RBC, Plasma volume ↑/↑↑ - Dilutional anemia Cardiac Output ↑ by 40-50% Blood Pressure Reduces (Prostacyclin, Nitric Oxide, relaxin, Progesterone
Variations in hemodynamics during gestation. An rise in plasma volume of 32–34 weeks. Both an increase in plasma volume and an increase in RBC are factors in dilutional anemia.
A 40%–50% increase in cardiac output. Blood pressure is not raised by prostacyclin, relaxin, nitric oxide, or progesterone. Only during pregnancy does relaxin get produced.
Factor | Effect |
Renal Perfusion | ↑ |
Renal Plasma Flow | ↑ by 80% |
Glomerular Pressure | No increase |
GFR | ↑ by 50% by 2nd trimester |
Filtration Fraction | ↓ |
Serum Creatinine | ↓ (0.4-0.8) |
Modifications to the heart throughout gestation. Increased renal perfusion is the outcome of increased cardiac output and plasma volume. It is feasible to achieve a renal plasma flow increase of 80%. There is a steady state of Glomerular pressure. By the time the second trimester begins, GFR had increased by 50%.
The fraction of filtrate matter falls during pregnancy because renal plasma flow rises and exceeds GFR. Serum creatinine decreases with increased GFR and clearance. Creatinine levels in the range of 0.4 to 0.8 are considered normal during pregnancy. A creatinine level of 1 during pregnancy may be indicative of AKI.
Also Read: Tropical Acute Kidney Injury
RAAS is activated during gestation. Adrenaline increases plasma volume, which in turn increases uteroplacental flow.
The resistance of relaxin to the pressor effect of angiotensin II. Blood pressure remains unchanged even when RAAS is triggered. Products of angiotensin breakdown cause the blood wall to become resistant to the effects of angiotensin.
Feature Change Osmoregulation and sodium balance ↓ serum osmolality 270 mosm/Kg ↓ sodium 4-5 mmol/l Resetting of AVP secretion B-HCG and relaxin Potassium Lower limit of normal Aldosterone + mild alkalosis versus Progesterone Calcium Increased excretion Reduced Nephrocalcinosis - Magnesium, Citrate, Acid glycoprotein, Nephrocalcin Uric acid Early falls, Increases later Acid Base Chronic Mild Respiratory Alkalosis Urine Protein Increase Glucose Physiological Glycosuria
Also Read: Tropical Acute Kidney Injury
Osmoregulation and sodium balance: AVP production is inhibited, serum sodium decreases by 4-5, and serial osmolality falls to 270. But relaxin and beta HCG help the body release AVP once more.
Potassium: Progesterone maintains potassium within the lower range of normal by balancing the negative effects of aldosterone's kaliuresis.
Calcium: Although nephrocalcin (NCAM), citric acid, acid glycoproteins, and magnesium are natural inhibitors of urine stone formation that prevent calccinosis, higher GFR causes hypercalciuria.
Uric acid: Increased excretion results in an early drop that is later stabilized. Acid-base involvement: chronic respiratory alkalosis due to hyperventilation caused by the expanding uterus pressing on the diaphragm. Urine protein excretion increases with a greater GFR. Proof that physiological glycosuria exists.
Non Pregnant | Pregnant | |
Hematorict (%) | 41 | 33 |
Serum Protein (g/dl) | 7.0 | 6.0 |
Plasma osmolality (mOsm/kg) | 285 | 275 |
Serum Sodium (mmol/l) | 140 | 135 |
Serum creatinine (mg/dl, umol/l) | 0.8 (73) | 0.5 (45) |
Blood urea nitrogen (mg/dl) | 12.7 | 9.3 |
Serum urea (mmol/l) | 4.5 | 3.3 |
pH | 7.40 | 7.44 |
Arterial PCO2 (mmHg) | 40 | 30 |
Serum bicarbonate (mmol/l) | 25 | 20 |
Serum uric acid (mg/dl, μmol/l) | 4.0 (240) | 3.2 (190) early4.3 (260) late |
Systolic BP (mmHg) | 115 | 105 |
Diastolic BP (mmHg) | 70 | 60 |
Antinatriuretic |
Natriuretic |
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Hematocrit: in pregnant women, it decreases to roughly 33 from approximately 41 in non-pregnant women. Dilution causes serum protein, which is roughly 7 in non-pregnant women, to decrease to about 6 in pregnant women.
Dilution is the cause of the decrease in serum sodium and plasma osmolality. These chemicals are present at levels of about 285 in non-pregnant women and 275 in pregnant women, and 140 in non-pregnant women and 135 in pregnant women, respectively.
Serum Creatinine: a normal level for non-pregnant women is 0.8; during pregnancy, it falls to 0.5. Blood urea and blood urea nitrogen: these parameters measure roughly 12 in non-pregnant women and 12.7 in pregnant women.
In each scenario, the values decrease. pH: slightly increases due to chronic respiratory alkalosis; normal pH in pregnant women is about 7.4, but this increases to 7.44. Arterial PCO2 is decreased by hyperventilation and respiratory alkalosis. Reduced carbon dioxide causes a drop in serum bicarbonate.
Acid-Base imbalances: Respiratory alkalosis causes metabolic acidosis, which balances the alkalosis and resulting in a moderate acidosis. Serum uric acid: because of increased reabsorption, it first drops to around 4 in non-pregnant women then rises to roughly 4.3 in pregnant women. Throughout pregnancy, both the diastolic and systolic blood pressures drop.
All factors except pH drop during pregnancy because of dilution and respiratory alkalosis; this leads to a modest compensatory metabolic acidosis.
Also Read: Alport Syndrome and Familial Glomerular Disorders
Anti natriuretic factors |
Natriuretic factors |
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• A rise in the flow of renal plasma, an increase in heart rate.
• A rise in plasma volume.
• A rise in the rate of glomerular filtration.
• Serum sodium either doesn't change or does so marginally.
• The osmolality of plasma decreases.
• A decrease in serum protein levels.
• A decrease in creatinine in serum.
• A decrease in the resistance of the cystic arteries, Urea decreases.
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