Kidney–placenta crosstalk in health and disease

Abstract

Organ crosstalk allows the interaction between systems to adapt to a constant changing environment, maintaining homeostasis. The process of placentation and the new hormonal environment during pregnancy trigger physiological changes that modulate kidney function to control extracellular volume, acid-base balance, and filtration of metabolic waste products. The bidirectional communication means that acute or chronic dysfunction of one organ can compromise the other. Abnormal placentation in pregnancy-related hypertensive disorders such as pre-eclampsia and HELLP (haemolysis, elevated liver enzymes and low platelet count) syndrome leads to the release of antiangiogenic factors that may cause kidney injury (thrombotic microangiopathy, glomeruloendotheliosis, mesangiolysis and vasoconstriction of peritubular vessels). These hypertensive disorders are a key cause of kidney injury in gestation, which increases maternal morbi-mortality and adverse foetal outcomes. Conversely, prior kidney injury or causes of kidney injury (diabetes, lupus, glomerulonephritis or other form of chronic kidney disease) increase the risk of developing hypertensive pregnancy disorders, providing a baseline higher risk. Inherited kidney diseases are a special concern, given the potential for genetic predisposition to kidney disease in the foetus. Understanding the bidirectional potential for compromise from placenta to kidney and vice versa provides a better framework to limit damage to both organs and improve maternal and foetal outcomes.

Pregnancy-associated changes in urinary uromodulin excretion in chronic hypertension

“…Previous research, including our own, has identified Stroke-Prone Spontaneously Hypertensive rats as a suitable model for investigating chronic hypertension during pregnancy [ 23 , 25 – 27 ]. Abnormal placentation leads to the release of antiangiogenic factors that may cause subclinical kidney injury [ 28 ]. We and others have shown abnormal placentation with release of antiangiogenic factors and kidney injury in Stroke-Prone Spontaneously Hypertensive rats [ 26 , 29 , 30 ].…”