الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Pregnancy affects essentially all aspects of kidney physiology. Acute kidney injury (AKI) was defined as an increase in serum creatinine within 2–7 days or oliguria. It affects 10%–20% of hospitalized adults and is associated with an increased risk of chronic kidney disease and further complications.
The development of AKI in pregnancy, termed pregnancy-related AKI (PRAKI) which is a heterogeneous disease entity that occurs due to a multitude of underlying etiologies. Regardless of the cause, it is an important obstetric complication associated with significant maternal and fetal morbidity and mortality.
The incidence of PR-AKI varies widely across the world, with reported incidence of 1 in 20,000 pregnancies to as much as 1 in 50 pregnancies. Many factors contribute to this variation in incidence, such as lack of uniform defining criteria, physiologic changes in pregnancy that affect interpretation of laboratory tests, and regional differences in factors contributing to acute kidney injury (AKI). In addition, AKI (a term that has replaced acute renal failure) is often under-recognized until it is severe. Often there is a lack of information on baseline pre-pregnancy serum creatinine (SCr) values in this population, which further poses a problem.
Some nations report a bimodal distribution with an early peak of AKI as a consequence of septic abortions and a second peak later in pregnancy from hypertensive disorders of pregnancy, along with obstetric complications such as hemorrhage. Although the etiology of PR-AKI varies based on the country of origin, in most regions, including low-income countries, preeclampsia and eclampsia account for 5% to 20% of cases, with one study reporting 36% of PR-AKI to be from hypertensive disorders of pregnancy. The risk of PR-AKI is higher in the setting of early-onset (<32 weeks gestation) preeclampsia. Other major causes of PR-AKI in developing countries include sepsis and severe hemorrhage, whereas primary renal disease, thrombotic microangiopathy (TMA), and acute fatty liver of pregnancy (AFLP) are more common in the developed nations. Pregnancy may also unmask underlying primary renal disease or modify the course of preexisting renal disease.
Although most women with AKI in pregnancy recover renal function, up to a third do not fully recover and can have serious long-term outcomes. Some may require RRT, and, when this option is unavailable (as in many parts of the world), it may result in mortality. Maternal and fetal outcomes, thus, depend on optimal management of AKI.
As understanding of the etiology and pathology of AKI has advanced, various biomarkers have been evaluated for the early and preclinical detection of AKI in different patients. These biomarkers include plasma and urine neutrophil gelatinase-associated lipocalin, urine interleukin 18, urine liver-type fatty acid-binding protein, and urine kidney injury molecule 1. However, none of these potential markers has been widely used in clinical practice because they do not exhibit acceptable accuracy for the early diagnosis of kidney injury and the early identification of at-risk patients.
In the US, the only Food and Drug Administration (FDA)-approved biomarkers for early AKI prediction are the cell-cycle arrest biomarkers (insulin-like-growth-factor–binding protein 7 [IGFBP7] and tissue inhibitor metalloproteinases-2 [TIMP-2]. Both TIMP-2 and IGFBP7 are markers of cellular stress in the early phase of tubular cell injury caused by a wide variety of insults. Furthermore, both molecules can initiate G1 cell-cycle arrest that prevents cells from dividing when potentially injured. The cut off values of 0.3 and 2.0 (ng/ml) ²/1000 for TIMP-2 and IGFBP7 were developed based on the sensitivity and specificity to determine the risk for AKI.
This study aimed to study the assessment of sensitivity and specificity of urinary biomarkers, tissue inhibitor of metalloproteinases-2 (TIMP-2), and insulin-like growth factor-binding protein 7 (IGFBP7) in early detection of PR-AKI, Maternal and fetal risk stratification.
It shows also most of the Pr-AKI patients presented in 3rd trimester (48%) in comparing to (22.5%) in post-partum period, (11.3%) in 1st trimester and (6.3%) in 2nd trimester, also It also shows statistical significance increase in obstetric complications that may lead to AKI as (61%) in Preeclamptic patients, (11.25%) in the patients presented with PPH, (13.75%) in patients presented with septic conditions and (5%) presented with hyperemesis and (2.5%) presented with severe abruption of placenta, TMA and lupus nephritis activity in its first presentation and only one case presented with post-renal AKI due to narrow pelvis a companied with (56.3%) fetal mortality and (22.5%) of the babies need admission in neonatal intensive care unit. The last and final diagnosis of the cause of AKI divided into several causes with (63.7%) due to preeclampsia per se, 25% due to ATN mostly after post-partum hemorrhage and septic conditions, 2.5% due to TMA, 5% due to hyperemesis with pre-renal affection, 2.5% for newly diagnosed lupus nephritis and one case presented with post-renal affection.
The study shows significant difference between the study groups in level of (TIMP-2). (IGFBP7). In patient group was 9.7±6.7 comparing to control group 0.2±0.1 with P value <0.001. The ROC shows 100% specificity and 97.5 sensitivity at cut off point > 0.33 with AUC 0.99 and P value <0.001.
Conclusion:
1- Two thirds of patients develop AKI in perinatal period.
2-The hypertensive disorders that complicate pregnancy including preeclampsia and eclampsia is the most common leading cause to Pr-AKI.
3-Pr-AKI lead to higher incidence of fetal mortality and neonatal ICU admission due to prematurity.
4- Most of patients require supportive management with 17.5% only requiring dialysis.
5-80 % of patients undergo complete resolution of renal function with 15% has incomplete recovery and 5% maternal mortality.
6-There is significant difference in level of TIMP-2.IGFBP-7 in patient group comparing to control group. This revels its higher sensitivity and specificity in diagnosis of Pr-AKI.