#NephMadness 2022: Intradialytic Hypotension – The Bad and the Ugly
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Etienne Macedo @EtienneMacedo
Etienne Macedo is a Assistant Professor of Medicine in the Division of Nephrology at the University of California, San Diego. Her research has focused on acute kidney injury, dialysis initiation, and critical care nephrology.
Competitors for the Hemodialysis Region
Intradialytic Hypotension vs Intradialytic Hypertension
Small Molecules vs Middle Molecules

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Fluid mobilization and removal with intermittent hemodialysis can be challenging and often complicated by intradialytic hypotension (IDH). During ultrafiltration, the decline in plasma osmolality in the setting of impaired cardiac and sympathetic nervous system compensatory mechanisms can result in decreased blood pressure (BP) levels. Even in the absence of occluding coronary disease, the presence of left ventricular hypertrophy (LVH) and reduced peripheral arterial compliance, two conditions highly prevalent in patients with end-stage kidney disease (ESKD), can predispose to a reduced coronary vasodilator reserve and demand ischemia. A proof-of-concept study in patients without severe coronary stenosis showed that myocardial perfusion during dialysis was reduced in the absence of hypotension. In hypotensive patients during conventional intermittent hemodialysis, recurrence of transient regional wall motion abnormalities has been shown to lead to the development of dialysis-associated heart failure.
These long-term effects of IDH may not be restricted to cardiac complications. A similar process is occurring in the cerebrovascular system, resulting in peri-dialysis changes in cerebral blood flow (CBF) that may contribute to long-term neuropsychological decline via repeated episodes of cerebral ischemia. Intradialytic cerebral ischemia has been shown to correlate with mean arterial pressure during dialysis. More recently, studies using positron emission tomography–computed tomography and Doppler ultrasound demonstrated a significant decrease in cerebral blood flow during dialysis and that ultrafiltration rate plays a critical role.
Despite this evidence, the long-term consequences of repetitive episodes are not well-established. A small 3-year prospective study with 32 nondiabetic patients with no previous symptomatic neurologic lesions documented a significant inverse correlation between the progressive frontal lobe atrophy and the number of IDH episodes. A large prospective ongoing study, KIDBRAIN (Cohort Study of Morphological Changes of the Brain by MRI in CKD Patients) is designed to prove the hypothesis that IDH plays a key role in developing morphological changes in the brain and that these changes have a negative influence on cognitive function. In a cross-sectional analysis of the study, the number of sessions with a decrease of 20 mm Hg in pre-dialysis SBP was an independent predictor of white matter and hippocampus volume, which have been shown to correlate with global cognitive function (GCF). These findings are still lacking causality proof but highlight the role of hypoperfusion in the pathophysiology of cognitive impairment.

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Another concern of IDH, mainly in critically ill patients, is the increased risk for intestinal ischemia, which may predispose to bacterial translocation. A retrospective study using data from the US Renal Data System assessed the risk for hospitalized mesenteric ischemia events among 626 maintenance HD patients and 2,428 controls. The occurrence of IDH in ≥ 30% of HD sessions in the 30 days before the event resulted in an 82% increased risk for the development of mesenteric ischemia.
Althought midodrine can effectively increase BP, it may not be the answer. Midodrine is an α-adrenergic agonist that causes arteriolar and venous vasoconstriction, increasing the peripheral vasculature resistance and venous return to the heart, resulting in increased cardiac output. However, in the setting of pre-existing vascular disease, vasoconstriction may also be harmful by impairing tissue perfusion and possibly aggravating the effects of decreased organ perfusion, including heart, brain, and intestines.
While there is no single intervention that will reduce the risk of IDH, longer and more frequent dialysis sessions have been shown to be effective. We should always consider all the options currently available for treating patients with ESKD, especially those at higher risk for organ hypoperfusion. It may challenge our practice, but in order to decrease the burden of heart failure and cognitive impairment, we need to increase the use of other dialysis modalities and evaluate methods to lessen the hemodynamic effects of IDH. These very important clinical implications of team Intradialytic Hypotension make it a huge contender in this year’s competition and a worthy winner of NephMadness 2022.
– Guest Post written by Etienne Macedo @EtienneMacedo
As with all content on the AJKD Blog, the opinions expressed are those of the author of each post, and are not necessarily shared or endorsed by the AJKD Blog, AJKD, the National Kidney Foundation, Elsevier, or any other entity unless explicitly stated.
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