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General Considerations

Pregnancy is a transient physiologic state that alters kidney anatomy and physiology. It also causes changes in electrolytes, hemodynamics, water balance, and acid–base homeostasis that must be accounted for when evaluating a pregnant woman.


In a normal pregnancy, the kidneys increase in size by approximately 1 cm from dilation of the collecting system. Hormonal and urodynamic factors result in this physiologic hydronephrosis of pregnancy as early as 6 weeks’ gestation. Dilation of the renal calyces, renal pelvis, and ureters increases the capacity for urine volume in the kidney, which can hold up to 300 cc of urine in pregnancy.

While physiologic hydronephrosis of pregnancy is thought to increase the risk of ascending infection, most of the time it does not. The hydronephrosis is predominantly right-sided with normal function of that dilated kidney. However, pathologic hydronephrosis is also possible and again more common on the right; there are two anatomic reasons for this. First, the right ureter crosses the pelvic brim on top of the ovarian vein, which can exert a pressure that obstructs the ureter. On the left side, the ureter and ovarian vein run in parallel. Second, the rectosigmoid colon descends on the left side of the abdomen, which pushes the uterus slightly to the right (uterine dextrorotation), increasing its proclivity to directly obstruct the right ureter.


Pregnancy affects systemic and intrarenal hemodynamics. There is a dramatic rise in cardiac output and a fall in systemic vascular resistance and mean arterial pressure. An increase in blood volume leads to an increase in cardiac output (by up to 50% above baseline) and an increase in maternal heart rate. Because of the increased preload needed, cardiac output may be affected by postural changes or compression of the inferior vena cava by a gravid uterus.

At the end of the first trimester, there is a fall in systemic blood pressure, driven by a fall in systemic vascular resistance. Blood pressure decreases on average 10 mm Hg below baseline during the second trimester. By the third trimester, blood pressure returns to baseline.

Hormonal factors are responsible for these changes in vascular resistance. Specifically, diminished vascular resistance in pregnancy results from relative resistance to angiotensin II and norepinephrine, as well as increased production of vasodilatory nitric oxide and prostacyclin. With the fall in systemic blood pressure, the renin–angiotensin system (RAAS) is dramatically upregulated in pregnancy; in the first trimester, plasma renin levels can be up to four times above baseline levels. Renin continues to rise until around 20 weeks. The increased renin stimulates an increase in aldosterone levels that in turn leads to salt and water retention, resulting in the increase in blood volume.

Within the kidney, the hemodynamic changes described above lead ...

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