Obesity, acute kidney injury and outcome of critical illness

Abstract

Acute kidney injury is a heterogeneous clinical syndrome encompassing a spectrum of risk factors and acute insults, occurring in multiple settings and affecting both short-term and long-term outcomes. Obesity has become an epidemic. The available literature suggests that AKI is common in critically ill surgical or medical obese patients and that obesity is a novel risk factor for this acute renal syndrome. The pathophysiology of obesity-associated AKI is not completely understood. Obesity-related factors combined with the burden of other comorbidities in elderly obese patients may interact with known precipitating factors such as hypotension, nephrotoxins or sepsis and increase the susceptibility of this population to AKI. Whether or not obesity may counterintuitively be protective and associated with better survival of critically ill patients with AKI ("reverse epidemiology") is a subject for debate. Further investigations exploring the role of novel biomarkers and optimal management are needed urgently.

Class III obesity is a risk factor for the development of acute-on-chronic liver failure in patients with decompensated cirrhosis

“…(32) The connection between obesity and AKI is likely multifactorial in nature, with contributions from obesity-related glomerulopathy,(33) renal hypoperfusion, (34) and endothelial dysfunction from obesity associated oxidative stress. (30) Although the exact physiologic mechanism for AKI cannot be elucidated from this study, additional investigations are needed.…”

“…and is in fact an increasingly recognized phenomenon in critical care settings, (30) with studies demonstrating obesity to yield a greater risk of AKI (31) and requirement for renal replacement therapy in critically ill patients. (32) The connection between obesity and AKI is likely multifactorial in nature, with contributions from obesity-related glomerulopathy,(33) renal hypoperfusion, (34) and endothelial dysfunction from obesity associated oxidative stress.…”

A Case of Renal Cortical Necrosis in a 15-year-old Boy with Acute Kidney Injury

“…In a large Austrian study, severely obese patients had greater than 2fold increase in severe AKI than normal weighted patients 8) . Although the pathophysiology of obesityassociated AKI is not fully understood, obesity induced risk factors (glomerulopathy, lowgrade inflam mation, endothelial dysfunction, augmented oxidative stress, activation of the reninangiotensinaldosterone sys tem and increased sympathetic nervous system activity), obesityassociated risk factors (metabolic syndrome, hypertension, cardiovascular disease), and other common causes (hypotension, sepsis and nephrotoxins) can preci pitate AKI in critically ill obese patients 9) . A complex inter play between these different pathophysiologic mechanisms may underlie a predisposition of obese patients to more severe AKI.…”

Renal Sympathetic Nerve-Derived Signaling in Acute and Chronic Kidney Diseases

“…It has been proposed that the RAS activates the sympathetic nervous system and angiotensin-converting enzyme inhibition and angiotensin receptor blockade are antiadrenergic [78]. Obesity increases the susceptibility to AKI and subsequent progression to CKD [79,80]. Blockade using doxazosin, an α 1 -AR antagonist, clonidine, an α 2A -AR agonist, and atenolol, a β 1 -AR antagonist, lowered BP and heart rate in obese dog and human patients [81][82][83].…”