Acute kidney injury (AKI) is a relatively common complication of cardiothoracic surgery and has both short- and long-term survival implications, even when AKI does not progress to severe renal failure. Given that currently, there are no active effective treatments for AKI, other than renal replacement therapy when indicated, the focus of clinicians ought to be on prevention and risk factor management. In the AKI-surgery literature, there exists this general consensus that intraoperative hypotension (IH) following hypotensive anesthesia (HA) or controlled hypotension (CH) in the operating room has no significant short-term and long-term impacts on renal function. In this review, we examine the basis for this consensus, exposing some of the flaws of the clinical study data upon which this prevailing consensus is based. We then describe our experiences in the last decade at the Mayo Clinic Health System, Eau Claire, in Northwestern Wisconsin, USA, with two selected case presentations to highlight the contribution of IH as a potent yet preventable cause of post-operative AKI. We further highlight the causative although neglected role of IH in precipitating postoperative AKI in chronic kidney disease (CKD) patients. We show additional risk factors associated with this syndrome and further make a strong case for the elimination of IH as an achievable mechanism to reduce overall, the incidence of hospital acquired AKI. We finally posit that as the old saying goes, prevention is indeed better than cure.
Journal of Injury and Violence Research, Vol 7, No 1 (2015)
Acute kidney injury is a frequent and serious complication in hospitalized patients. Mortality rates have not substantially been decreased during the last 20 years. In most patients AKI results from transient renal hypoperfusion or ischemia. The consequences include tubular cell dysfunction/damage, inflammation of the organ, and post-ischemic microvasculopathy. The two latter events perpetuate kidney damage in AKI. Clinical manifestations result from diminished excretion of water, electrolytes, and endogenous / exogenous waste products. Patients are endangered by cardiovascular complications such as hypertension, heart failure, and arrhythmia. In addition, the whole organism may be affected by systemic toxification (uremia). The diagnostic approach in AKI involves several steps with renal biopsy inevitable in some patients. The current therapy focuses on preventing further kidney damage and on treatment of complications. Different pharmacological strategies have failed to significantly improve prognosis in AKI. If dialysis treatment becomes mandatory, intermittent and continuous renal replacement therapies are equally effective. Thus, new therapies are urgently needed in order to reduce short- and long-term outcome in AKI. In this respect, stem cell-based regimens may offer promising perspectives.
Rev Med Chil. 2015 Sep;143(9):1114-20. doi: 10.4067/S0034-98872015000900003.
BACKGROUND: Acute Kidney Injury (AKI) increases morbidity, mortality and hospital stay in critical patients units (CPU).AIM: To determine the incidence and mortality of AKI in CPU.
MATERIAL AND METHODS: Review of electronic medical records of 1,769 patients aged 61 ± 20 years (47% males) discharged from a CPU during one year. Acute Kidney Injury diagnosis and severity was established using the Acute Kidney Injury Network (AKIN) criteria. RESULTS: A history of hypertension and Diabetes Mellitus was present in 44 and 22% of patients, respectively. APACHE II and SOFA scores were 14.6 ± 6.8 and 3.6 ± 2.1 respectively. AKI incidence was 28.9% (stage I, 16.7%, stage II, 5.3% and stage III, 6.9%). Mortality during the first 30 days and during the first year was 8.1 and 20.0% respectively. Patients with stage III AKI had the highest mortality (23.8 and 40.2% at 30 days and one year respectively). Compared with patients without AKI, the Odds ratio for mortality at 30 days and one year of patients with AKI stage III was 3.7 and 2.5, respectively. CONCLUSIONS: Thirty percent of patients admitted to UPC develop an AKI, which influences 30 days and one year mortality.