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Care of the acute kidney injury patient

02 October 2023
14 mins read
Volume 14 · Issue 8
Figure 1. The four distinct phases of intravenous fluid therapy for humans with critical illness
Figure 1. The four distinct phases of intravenous fluid therapy for humans with critical illness


Acute kidney injury, previously called acute renal failure, indicates a sudden and often reversible reduction in kidney function as measured by glomerular filtration rate, increased serum and plasma creatinine concentration and changes in urine output. This article reviews the pathophysiology and common causes of acute kidney injuries, including pre-renal causes from hypovolaemia, intrinsic renal causes such as glomerular diseases and post-renal obstructive causes. Veterinary nurses should be aware of the common diagnostic tests used and how to deliver support to the hospitalised patient. While an acute kidney injury can be a serious condition for some patients, it is possible for others to recover and maintain a good quality of life with effective nursing care to help maximise the prognosis of these patients.

The primary purpose of the urinary system is to regulate the body's fluid balance, acid-base, electrolytes and regulate blood pressure. The kidneys also have a role in the excretion of metabolic waste and toxins, as well as in the secretion and metabolism of hormones.

Acute kidney injury is characterised by renal parenchymal injury. This represents an abrupt decline in glomerular filtration rate characterised by increased serum and plasma creatinine concentrations, uraemia (when severe enough) and, often, changes to urine output (Haskey, 2019). It is associated with decreased renal function, fluid, electrolyte and acid-base imbalances and retention of uraemic waste products (Bar-Nathan et al, 2022).

There are four phases of acute kidney injury based on pathophysiology (Monaghan et al, 2012):

The causes of acute kidney injury can be divided into three categories:

This occurs when renal blood flow is compromised due to certain conditions or situations such as dehydration, shock or congestive heart failure. It is important to remember the kidneys receive 20–25% of cardiac output (Waxman, 2020). In response, the kidneys conserve water and sodium, resulting in a reduction of urine output known as ‘physiological oliguria’. Local production of prostaglandins helps maintain renal blood flow, but this can be affected by drugs, including non-steroidal anti-inflammatories, and potentially lead to renal ischaemia. If left untreated, this can cause acute tubular necrosis and intrinsic renal failure. Therefore, it is crucial to recognise pre-renal failure promptly, identify and address the underlying cause and carefully choose drugs to avoid initiation.

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