Acute kidney injury

Abstract

Acute kidney injury (AKI) represents a medical emergency associated with poor clinical outcomes. The international guideline group Kidney Disease: Improving Global Outcomes (KDIGO) has defined AKI according to rises in serum creatinine and/or reductions in urine output. Any patient who meets the criteria for AKI should be reviewed to ascertain the cause of AKI and the severity of the injury should be staged. Patients with more severe AKI are at greater risk of progression to chronic kidney disease (CKD). The 2009 National Confidential Enquiry into Patient Outcomes and Death (NCEPOD) reported that only 50% of patients who died with a diagnosis with AKI received good care. The mortality from AKI has remained unchanged for the last four decades and there are currently no specific therapies for the majority of cases of AKI. Patients with rarer forms of AKI need urgent renal referral for specific therapy. At present, serum creatinine and urine output remain the best biomarkers for detecting AKI. However, significant kidney damage has usually occurred by the time changes in these biomarkers are manifest and newer biomarkers are under investigation. Management of AKI is based upon general supportive measures, which includes treatment of the underlying cause and the initiation of renal replacement therapy (RRT) in patients with complications refractory to medical management. The optimal choice of intravenous fluid therapy remains controversial. There is currently renewed interest in more specific therapies for AKI secondary to hypoperfusion and/or sepsis, which have been previously unsuccessful. A number of therapeutic strategies are presently being explored in clinical trials.

A prospective study of the demographics, management and outcome of patients with acute kidney injury in Cape Town, South Africa

“…A large proportion of these patients (62.4%) also had sepsis, which was associated with mortality (p-value 0.005). It may be that earlier detection and management of sepsis in these in-hospital patients could have prevented the development of AKI, similarly to findings of a National Confidential Enquiry into Patient Outcome and Death report in the United Kingdom [17]. …”

Enhanced renoprotective effect of IGF-1 modified human umbilical cord-derived mesenchymal stem cells on gentamicin-induced acute kidney injury

“…The clinical symptoms of AKI manifest as a rapid loss of the ability of the kidney to concentrate urine, excrete wastes, and maintain fluid and electrolyte homeostasis 1 2 3 . Although advances have been made to improve the therapy effect of AKI in recent years, this disease remains a high risk factor for morbidity and mortality 4 5 . Current clinical therapeutic options for AKI are limited to the application of supportive measures and dialysis.…”

The impact of the NHS electronic-alert system on the recognition and management of acute kidney injury in acute medicine

“…AKI was defined according to the KDIGO definition. 7 As per 2011 Renal Association guidelines, 9 and recent articles, [22][23][24][25] baseline creatinine was defined as the lowest creatinine level recorded within 3 months. If a 3-month creatinine was not available, then AKI was not diagnosed, assuming other criteria were not met.…”

“…When creatinine rises occur in the preceding 12 months, this approach can miss AKI, which may explain the high proportion of stage 1 AKI that was missed by the e-alert system. Currently, there is a limited evidence base to support any definition of the baseline creatinine, which is acknowledged in the literature 22,31 and by KDIGO. 7 A further limitation of this study was the decision to judge the standards solely based on documentation.…”