Dexmedetomidine protects against acute kidney injury in patients with septic shock

Emerging benefits and drawbacks of α2‐adrenoceptor agonists in the management of sepsis and critical illness

“…However, a recent subgroup analysis focussed on 104 severe septic patients with Acute Physiology and Chronic Evaluation II (APACHE II) scores of ≥23 and reported reductions in serum creatinine, improvements in renal sequential organ failure assessment (SOFA) subscores, and a reduction in 28‐day mortality rate (22% vs. 42%) (Nakashima et al, 2020). In agreement with such findings, a single‐centre clinical trial in 200 septic patients also reported reductions in serum creatinine and urinary injury biomarkers in those receiving dexmedetomidine compared with propofol, an effect which was accompanied by decreases in plasma inflammatory cytokines (TNF‐α and IL‐1) (Liu et al, 2020). Despite a current lack of convincing clinical evidence to prove the renal benefits of dexmedetomidine in sepsis, it is possible that therapeutic strategies which protect the kidneys from ischaemic and hypoxic injury may not only mitigate AKI, but also its subsequent transition to chronic kidney disease and end‐stage renal disease (Lankadeva, Okazaki, et al, 2019).…”

“…It is possible that a reduction in renal tubular sodium reabsorption induced by α 2adrenoceptor agonists will reduce the metabolic demand, oxygen utilization and further contribute to the preservation of renal medullary oxygenation in septic AKI (Figure 3). an effect which was accompanied by decreases in plasma inflammatory cytokines (TNF-α and IL-1) (Liu et al, 2020). Despite a current lack of convincing clinical evidence to prove the renal benefits of dexmedetomidine in sepsis, it is possible that therapeutic strategies which protect the kidneys from ischaemic and hypoxic injury may not only mitigate AKI, but also its subsequent transition to chronic kidney disease and end-stage renal disease (Lankadeva, Okazaki, et al, 2019).…”

Is the Sympathetic System Detrimental in the Setting of Septic Shock, with Antihypertensive Agents as a Counterintuitive Approach? A Clinical Proposition

“…In sepsis, beta-blockers or alpha-2 agonists minimize the inflammation [ 183 , 262 ], the systemic vasodilation [ 9 , 10 , 11 , 183 , 196 , 198 ], the emergence delirium [ 301 ], the delayed emergence from conventional sedation, the duration of controlled mechanical ventilation [ 302 ], the CCU stay [ 172 , 298 , 303 ], and the mortality [ 111 , 162 , 163 , 164 , 165 , 166 , 167 , 168 , 169 , 170 , 171 ].…”

“…In the setting of CABG + CPB, clonidine (4 μg·kg −1 ) increased urine output and prevented the decrease in creatinine clearance [ 296 ]. In addition, clonidine (20 μg·kg −1 × 4 days) suppressed protein catabolism following esophagectomy in alcoholic patients [ 297 ], possibly minimizing RRT [ 298 ].…”

“…A meta-analysis reported a reduced incidence of AKI trending toward lowered mortality ( p = 0.13) [ 171 ]. In the setting of septic shock, dexmedetomidine was associated with lower creatinine, preserved creatinine clearance, lowered incidence of AKI, RRT, and shortened CCU stay (AKI: 38% vs. 60%; RRT: 9% vs. 14%; stay: 14 vs. 19 d, n = 100 × 2) [ 298 ]. To sum up, following alpha-2 agonists, animal [ 149 ] and clinical data suggest an improvement of the renal microcirculation.…”