الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 131 |  |  |
| | | from | 131 | | |
Abstract
Glomerular hyperfiltration, altered tubular function, and shifts in
electrolyte-fluid balance are among the hallmark renal physiologic
changes that characterize a healthy pregnancy. These adjustments are not
only critical to maternal and fetal well being, but also provide the clinical
context for identifying gestational aberrations in renal function and
electrolyte composition. Systemic vasodilation characterizes early
gestation and produces increments in renal plasma flow and GFR, the
latter of which is maintained into the postpartum period. In addition renal
tubular changes allow for the accumulation of nutrients and electrolytes
necessary for fetal growth such that wasting of proteins, glucose, and
amino acids in urine is limited in pregnancy and total body stores of
electrolytes increase throughout gestation.
AKI in pregnancy remains a cause of significant fetomaternal mortality
and morbidity, particularly in developing countries. During the first
trimester of gestation, acute kidney injury develops most often due to
hyperemesis gravidarum or septic abortion.
AKI in late pregnancy includes hypertensive complications of pregnancy
(preeclampsia/eclampsia or hemolysis, elevated liver enzymes, and low
platelets count syndrome). Thrombotic microangiopathy is another
peculiar and devastating cause of AKI in pregnancy. During the last
decade, our management, of these causes of AKI in pregnancy has
dramatically improved. For instance, convincing data have linked preeclampsia/
eclampsia to an increase in circulating antiangiogenic factors
soluble Flt 1 and endoglin, which induce endothelial cell dysfunction,
hypertension, and proteinuria. Thrombotic microangiopathy, which can
present as hemolytic uremic syndrome or thrombotic thrombocytopenic
purpura.
In most cases, pregnancy is only a precipitating factor for thrombotic
microangiopathy. Treatment of thrombotic microangiopathy occurring
95
during pregnancy should be tailored to the underlying pathogenic
mechanism: (1) restoration of a disintegrin and metalloproteinase with
athrombospondin type 1 motif, member 13 serum activity in the setting of
thrombotic thrombocytopenic purpura through plasma exchanges and in
some cases, B cell-depleting therapy and (2) inhibition of complement
alter native pathway activation in atypical hemolytic uremic syndrome
using antiC5 blocking antibody (eculizumab).
Pre-pregnancy counseling should be available for all women with chronic
kidney disease (CKD) so that conception occurs at the right time in the
course of their disease and while they are on the right medications with
the aims of minimizing risks for both mother and fetus. Key areas to
consider are the factors which are associated with worse prognosis and
the influence underlying kidney conditions and their treatment.
Careful counseling of women with diabetic nephropathy before
pregnancy with estimation of the risk for the mother and fetus. Pregnancy
does not result in worsening of kidney function in women with important
diabetic nephropathy and serum creatinine, but pregnancy complications
such as pre-eclampsia and preterm delivery are common. Intensive
metabolic control before and during pregnancy, low-dose aspirin from12
gestational weeks onward, and intensive antihypertensive treatment are
important. Methyldopa, labetalol, and nifedipine are regarded safe in
pregnancy where as angiotensin converting enzyme inhibitors, AngII
antagonists, or statins should be paused before pregnancy. Case series and
pathophysiological studies support the use of a stringent goal for BP and
albumin excretion in pregnant women with diabetic nephropathy.
For LN, current recommendations advise that the affected woman achieve
a stable remission of her renal disease for at least 6months before
conception. Immunosuppressive therapy in pregnancy is control of
disease activity with medication that is relatively safe for a growing fetus.
Worsening proteinuria, which commonly occurs in proteinuric renal
diseases toward the end of pregnancy, should be differentiated from a
96
LN flare and/or preeclampsia, specific condition clinically characterized
by hypertension and proteinuria.
All women of child-bearing age should be counseled regarding the
possibility and risks of pregnancy after kidney transplantation. Although
pregnancy after kidney transplant is feasible, complications are relatively
high and this needs to be included in patient counseling and clinical
decision making.
Immunosuppressive medications should be used according The US Food
and Drug Administration (FDA) classification.