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.