Introduction
Pregnancy causes structural and functional changes in maternal kidneys. The length of both kidneys increases by 1 to 1.5 cm during pregnancy1, and kidney volume increases by up to 30%2. Pregnancy also leads to increased renal plasma flow (RPF) and glomerular filtration rate (GFR)3. The physiological increase in GFR during pregnancy decreases serum creatinine concentrations during early pregnancy4. In a retrospective database study in Canada, the mean serum creatinine concentration decreased in the first trimester of pregnancy, leveled off in the second, and then gradually increased again in the third trimester to near pre-pregnancy levels5. Thus, a serum creatinine of 0.8 mg/dL (70.7 µmol/L) or higher, which may be normal in non-pregnant women, usually reflects renal impairment in pregnant women, and a slight increase in serum creatinine usually reflects a significant decrease in renal function. Therefore, to detect renal impairment during pregnancy, it is necessary to note even mild variation in serum creatinine levels.
The increase in GFR during gestation is primarily due to an increase in RPF6. RPF increases by up to 80% at 12 weeks of gestation7but decreases in the third trimester. Increased renal blood flow and GFR are caused by changes in the quantity of systemic blood flow (increased cardiac output) and systemic vasodilation8. Systemic vasodilation is induced mainly by the renin-angiotensin-aldosterone system (Angiotensin-1 receptors, causing vasoconstriction are down regulated, angiotensin-2 receptors, causing vasodilation are upregulated, and the levels of angiotensin-2 and aldosterone are increased)9, and progesterone, nitric oxide, and relaxin have been reported to play an important role in the hemodynamic changes in kidney function during pregnancy8-11. However, RPF begins to decrease in the second trimester and rapidly falls in the third trimester8,12. In addition, filtration fraction and proteinuria increase after 20 weeks of gestation8,13. Furthermore, an enlarged uterus negatively affects renal function by compression of the inferior vena cava (IVC), leading to decreased cardiac output, compression of the renal vein, and impaired ureteral transit due to ureteral dilation in the second half of pregnancy. These conditions can aggravate maternal renal dysfunction.
In this study we speculate that the effects of pregnancy on maternal renal function can differ between singleton and multiple pregnancies. However, to the best of our knowledge, no relevant scientific report investigating this hypothesis has been published. The purpose of this study was to examine the differences in maternal renal function between singleton and twin pregnancies in the second half of pregnancy.