Abstract
Post-operative acute kidney injury (AKI) is a common complication of surgery. Rates vary according to type of surgery, ranging from 13% following gastrointestinal surgery and 10% after orthopaedic surgery to 26% following cardiac surgery [1–3].
Understanding the aetiology of post-operative AKI is vital to peri-operative optimization. However, the pathogenesis is complex and usually multifactorial (Figure 1). Renal hypoperfusion plays an important role in post-operative AKI. This can occur as a result of a number of different factors including hypovolaemia, loss of autoregulation during anaesthesia, cardiogenic shock, sepsis and high-risk medicines such as non-steroid anti-inflammatory drugs (NSAIDs) and inhibitors of the renin–angiotensin system.
Understanding the aetiology of post-operative AKI is vital to peri-operative optimization. However, the pathogenesis is complex and usually multifactorial (Figure 1). Renal hypoperfusion plays an important role in post-operative AKI. This can occur as a result of a number of different factors including hypovolaemia, loss of autoregulation during anaesthesia, cardiogenic shock, sepsis and high-risk medicines such as non-steroid anti-inflammatory drugs (NSAIDs) and inhibitors of the renin–angiotensin system.
| Original language | English |
|---|---|
| Pages (from-to) | 757-759 |
| Number of pages | 3 |
| Journal | Nephrology Dialysis Transplantation |
| Volume | 34 |
| Issue number | 5 |
| Early online date | 11 Sept 2018 |
| DOIs | |
| Publication status | Published - May 2019 |
ASJC Scopus subject areas
- Nephrology
- Transplantation