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9. Plasma soluble fms-like tyrosine kinase 1 to placental growth factor ratio of 11.5 multiples of median predicts preeclampsia with severe features within 2 weeks of testing

Author

Espinoza, Jimmy, Calsavara, Vinicius F., Kilpatrick, Sarah, Rana, Sarosh, Costantine, Maged M., Boggess, Kim, Wylie, Blair J., Moore Simas, Tiffany A., Louis, Judette M., Gaw, Stephanie L., Murtha, Amy, Wiegand, Samantha, Gollin, Yvonne, Singh, Deepjot, Silver, Robert M., Durie, Danielle E., Panda, Britta, Norwitz, Errol R., Burd, Irina, Plunkett, Beth, Scott, Rachel K., Lemoine, Elizabeth, Thadhani, Ravi, and Karumanchi, S. Ananth

Published
2024
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14. Apixaban for Patients With Atrial Fibrillation on Hemodialysis: A Multicenter Randomized Controlled Trial

Author

Pokorney, Sean D., Chertow, Glenn M., Al-Khalidi, Hussein R., Gallup, Dianne, Dignacco, Pat, Mussina, Kurt, Bansal, Nisha, Gadegbeku, Crystal A., Garcia, David A., Garonzik, Samira, Lopes, Renato D., Mahaffey, Kenneth W., Matsuda, Kelly, Middleton, John P., Rymer, Jennifer A., Sands, George H., Thadhani, Ravi, Thomas, Kevin L., Washam, Jeffrey B., Winkelmayer, Wolfgang C., and Granger, Christopher B.

Published
2022
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17. Glycerol-3-phosphate is an FGF23 regulator derived from the injured kidney

Author

Simic, Petra, Kim, Wondong, Zhou, Wen, Pierce, Kerry A., Chang, Wenhan, Sykes, David B., Aziz, Najihah B., Elmariah, Sammy, Ngo, Debby, Pajevic, Paola Divieti, Govea, Nicolas, Kestenbaum, Bryan R., de Boer, Ian H., Cheng, Zhiqiang, Christov, Marta, Chun, Jerold, Leaf, David E., Waikar, Sushrut S., Tager, Andrew M., Gerszten, Robert E., Thadhani, Ravi I., Clish, Clary B., Juppner, Harald, Wein, Marc N., and Rhee, Eugene P.

Subjects
Thermo Fisher Scientific Inc., Phosphates -- Physiological aspects, Glycerol -- Physiological aspects, Fibroblast growth factors -- Physiological aspects, Liquid chromatography -- Physiological aspects, Mass spectrometry -- Physiological aspects, Scientific equipment industry -- Physiological aspects, Morbidity, Hormones, Chromatography, Spectroscopy, Proteomics, Homeostasis, Health care industry
Abstract

Fibroblast growth factor 23 (FGF23) is a bone-derived hormone that controls blood phosphate levels by increasing renal phosphate excretion and reducing 1,25-dihydroxyvitamin [D.sub.3] [1,25[(OH).sub.2]D] production. Disorders of FGF23 homeostasis are associated with significant morbidity and mortality, but a fundamental understanding of what regulates FGF23 production is lacking. Because the kidney is the major end organ of FGF23 action, we hypothesized that it releases a factor that regulates FGF23 synthesis. Using aptamer-based proteomics and liquid chromatography-mass spectrometry-based (LC-MS-based) metabolomics, we profiled more than 1600 molecules in renal venous plasma obtained from human subjects. Renal vein glycerol-3-phosphate (G-3-P) had the strongest correlation with circulating FGF23. In mice, exogenous G-3-P stimulated bone and bone marrow FGF23 production through local G-3-P acyltransferase-mediated (GPAT-mediated) lysophosphatidic acid (LPA) synthesis. Further, the stimulatory effect of G-3-P and LPA on FGF23 required LPA receptor 1 (LPAR1). Acute kidney injury (AKI), which increases FGF23 levels, rapidly increased circulating G-3-P in humans and mice, and the effect of AKI on FGF23 was abrogated by GPAT inhibition or Lpar1 deletion. Together, our findings establish a role for kidney-derived G-3-P in mineral metabolism and outline potential targets to modulate FGF23 production during kidney injury., Introduction Fibroblast growth factor-23 (FGF23) levels increase with both acute and chronic kidney disease (CKD) (1) and are a strong independent risk factor for adverse renal outcomes and mortality in [...]

Published
2020
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20. Impaired renal reserve contributes to preeclampsia via the kynurenine and soluble fms-like tyrosine kinase 1 pathway

Author

Dupont, Vincent, Berg, Anders H., Yamashita, Michifumi, Huang, Chengqun, Covarrubias, Ambart E., Ali, Shafat, Stotland, Aleksandr, Van Eyk, Jennifer E., Jim, Belinda, Thadhani, Ravi, and Karumanchi, S. Ananth

Subjects
Preeclampsia -- Development and progression -- Risk factors, Kidney diseases -- Complications and side effects -- Physiological aspects, Tryptophan metabolism -- Health aspects, Health care industry
Abstract

To understand how kidney donation leads to an increased risk of preeclampsia, we studied pregnant outbred mice with prior uninephrectomy and compared them with sham-operated littermates carrying both kidneys. During pregnancy, uninephrectomized (UNx) mice failed to achieve a physiological increase in the glomerular filtration rate and during late gestation developed hypertension, albuminuria, glomerular endothelial damage, and excess placental production of soluble fms-like tyrosine kinase 1 (sFLT1), an antiangiogenic protein implicated in the pathogenesis of preeclampsia. Maternal hypertension in UNx mice was associated with low plasma volumes, an increased rate of fetal resorption, impaired spiral artery remodeling, and placental ischemia. To evaluate potential mechanisms, we studied plasma metabolite changes using mass spectrometry and noted that L-kynurenine, a metabolite of L-tryptophan, was upregulated approximately 3-fold during pregnancy when compared with prepregnant concentrations in the same animals, consistent with prior reports suggesting a protective role for L-kynurenine in placental health. However, UNx mice failed to show upregulation of L-kynurenine during pregnancy; furthermore, when UNx mice were fed L-kynurenine in drinking water throughout pregnancy, their preeclampsialike state was rescued, including a reversal of placental ischemia and normalization of sFLT1 levels. In aggregate, we provide a mechanistic basis for how impaired renal reserve and the resulting failure to upregulate L-kynurenine during pregnancy can lead to impaired placentation, placental hypoperfusion, an antiangiogenic state, and subsequent preeclampsia., Introduction Pregnancy is an adaptive state of net sodium and volume expansion for the purpose of increasing perfusion of the placenta and fetus. Blood flow to the uterus can increase [...]

Published
2022
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21. UBD modifies APOL1 -induced kidney disease risk

Author

Zhang, Jia-Yue, Wang, Minxian, Tian, Lei, Genovese, Giulio, Yan, Paul, Wilson, James G., Thadhani, Ravi, Mottl, Amy K., Appel, Gerald B., Bick, Alexander G., Sampson, Matthew G., Alper, Seth L., Friedman, David J., and Pollak, Martin R.

Published
2018

35. Translation of mechanistic advances in preeclampsia to the clinic: Long and winding road.

Author

Thadhani, Ravi, Cerdeira, Ana Sofia, and Karumanchi, S. Ananth

Abstract

As one of the leading causes of premature birth and maternal and infant mortality worldwide, preeclampsia remains a major unmet public health challenge. Preeclampsia and related hypertensive disorders of pregnancy are estimated to cause >75 000 maternal and 500 000 infant deaths globally each year. Because of rising rates of risk factors such as obesity, in vitro fertilization and advanced maternal age, the incidence of preeclampsia is going up with rates ranging from 5% to 10% of all pregnancies worldwide. A major discovery in the field was the realization that the clinical phenotypes related to preeclampsia, such as hypertension, proteinuria, and other adverse maternal/fetal events, are due to excess circulating soluble fms‐like tyrosine kinase‐1 (sFlt‐1, also referred to as sVEGFR‐1). sFlt‐1 is an endogenous anti‐angiogenic protein that is made by the placenta and acts by neutralizing the pro‐angiogenic proteins vascular endothelial growth factor (VEGF) and placental growth factor (PlGF). During the last decade, this work has spawned a new era of molecular diagnostics for early detection of this condition. Antagonizing sFlt‐1 either by reducing production or blocking its actions has shown salutary effects in animal models. Further, in early‐stage human studies, the therapeutic removal of sFlt‐1 from maternal circulation has shown promise in delaying disease progression and improving outcomes. Recently, the FDA approved the first molecular test for preterm preeclampsia (sFlt‐1/PlGF ratio) for clinical use in the United States. Measuring serum sFlt‐1/PlGF ratio in the acute hospital setting may aid short‐term management, particularly regarding step‐up or step‐down of care, decision to transfer to settings better equipped to manage both the mother and the preterm neonate, appropriate timing of administration of steroids and magnesium sulfate, and in expectant management decisions. The test itself has the potential to save lives. Furthermore, the availability of a molecular test that correlates with adverse outcomes has set the stage for interventional clinical trials testing treatments for this disorder. In this review, we will discuss the role of circulating sFlt‐1 and related factors in the pathogenesis of preeclampsia and specifically how this discovery is leading to concrete advances in the care of women with preeclampsia. [ABSTRACT FROM AUTHOR]

Published
2024
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40. De novo NAD+ biosynthetic impairment in acute kidney injury in humans

Author

Poyan Mehr, Ali, Tran, Mei T., Ralto, Kenneth M., Leaf, David E., Washco, Vaughan, Messmer, Joseph, Lerner, Adam, Kher, Ajay, Kim, Steven H., Khoury, Charbel C., Herzig, Shoshana J., Trovato, Mary E., Simon-Tillaux, Noemie, Lynch, Matthew R., Thadhani, Ravi I., Clish, Clary B., Khabbaz, Kamal R., Rhee, Eugene P., Waikar, Sushrut S., Berg, Anders H., and Parikh, Samir M.

Published
2018
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46. DEVELOPING A BEDSIDE TEST FOR PREECLAMPSIA: OVERCOMING SISYPHUS.

Author

THADHANI, RAVI

Subjects
PREECLAMPSIA, PLACENTAL growth factor, VASCULAR endothelial growth factors, PREGNANCY complications, PRENATAL care, DIASTOLIC blood pressure
Abstract

This document is a list of references related to the topic of preeclampsia and the use of angiogenic biomarkers for diagnosis and prediction. The references include studies on the role of placental growth factor (PlGF) and soluble fms-like tyrosine kinase 1 (sFlt-1) in preeclampsia, as well as their potential use as diagnostic and prognostic markers. The studies mentioned cover various aspects of preeclampsia, including its differentiation from other conditions, prediction of adverse outcomes, and the clinical implementation of angiogenic biomarkers. The document also includes references to real-world studies and the use of angiogenic factors in the management of placental dysfunction. [Extracted from the article]

Published
2024

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