Introduction and Background
An acute kidney injury (AKI), also known as acute kidney failure or acute renal failure, is a condition when kidneys suddenly stop working, with no ability to filter waste products found in the blood. In the United Kingdom (UK), a rise in AKI cases has been currently observed, but experts do not give clear explanations about this trend and continue investigating the field, including its pathophysiology and management.1 Despite its complex aetiology, AKI remains one of the main causes of morbidity and mortality, and much attention should be paid to primary-level care offered in an emergency department (ED).1
More the 67% of all reported cases are in adults, while only 2% occur in children.2 Thus, age becomes one of the critical risk factors in understanding the chosen disease. In addition, of approximately 500,000 UK citizens, AKI complaints are about 1.5 million, meaning that more than 17% of patients might have two episodes, and 7% have even more than two episodes.2 About 70 AKI cases are observed per 1,000 ED admissions, and 18% of people die within 30 days without proper treatment.2 These numbers prove the importance of learning AKI characteristics to prevent its progress, especially in older adults.
AKI has been a reason for multiple deaths for a long period, but its definitions and staging criteria were elaborated only in 2012. Its major symptoms include decreased urine output, fluid retention, fatigue, weakness, nausea, and confusion. The causes may be a specific condition that affects kidneys or direct physical damage. Hypertension, heart failure, diabetes, sepsis, and postoperative complications are common risk factors for AKI.3
The Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group offered the criteria to classify AKI complications in several stages (Table 1).3 Creatinine levels and urine output are the two elements to be regularly checked in patients with suspicion of AKI or other kidney problems. This project aims to discuss AKI pathophysiology, diagnosis, pharmacology, and treatment alternatives and improve overall knowledge of the disease.
Table 1 – KDIGO Classification Criteria for AKI
Discussion
Each element in the analysis of AKI in older adults plays an important role. Its pathophysiology shows what changes happen to the patient’s body. Diagnostic steps must be properly followed and explained so as not to miss a single point in clinical assessment at the ED. The discussion of pharmacology is necessary to identify which medications have the best effect. AKI treatment includes lifestyle changes, hospitalisation peculiarities, and understanding the impact of other health conditions on the AKI’s progress.
Pathophysiology
AKI’s pathophysiology is complex due to its spontaneous nature and the inability to predict the failure of kidney function. According to Yokota et al.3, three mechanisms should be identified: hemodynamic, oxidative stress, and inflammation. First, renal blood flow decreases and leads to acute cell injury/dysfunction. Second, oxidative stress or tubular ischaemia is characterised by the imbalance between reactive oxygen manifestation and antioxidant defence.4
Inflammatory cells provoke fluid loss and promote proinflammatory cytokine release.4 Vascular damage is hard to predict, but the injury of intrarenal vessels negatively affects renal perfusion. In addition to preventing the progression of vascular and tubular changes, it is important to repair the damaged areas and restore the body’s functions.
Diagnosis
Failures might provoke multiple physiological changes in the human body, while most patients remain asymptomatic. Thus, it is not always possible to diagnose AKI at an early stage. However, in the ED, people need to take blood and urine tests to check for abnormalities and recent changes. Many hospitals worldwide follow the KDIGO classification to identify the level of serum creatinine and the AKI stage at the moment of the first examination.5 Even if a small increase in 0.3 mg/dL within the next 48 hours is observed, a treatment should be initiated.5
In addition, attention is paid to urine output because if its decrease to 0.5 mL/kg/h during the next six hours is noticed, the patient is at risk for AKI.5 The National Institute for Health and Care Excellence6 admits that ultrasound is not commonly used to examine the urinary tract. Still, when it is impossible to identify the cause of AKI, and the risk of obstruction is possible, healthcare providers use ultrasound or computerised tomography to observe kidney changes.6 All these steps are necessary to predict AKI complications and choose the right course of treatment.
Pharmacology
Pharmacological treatment should promote improvements in several directions. First, vasopressor support is possible with Noradrenaline, Vasopressin, or Terlipressin.5 The second-line treatment focuses on the stabilisation of renal function and includes non-steroidal anti-inflammatory drugs (NSAIDs), aminoglycosides, or angiotensin-converting enzyme (ACE) inhibitors.6 If the levels of potassium or calcium are low, infusions are recommended. Finally, it is necessary to remove toxins from the body with the help of nephrotoxic drugs, including antibiotics.
Treatment
Treatment of patients with AKI must be based on shared decision-making and ethical standards of care. ED healthcare providers must inform the patient about the current condition, possible complications, and other factors affecting the recovery process. If an inadequate response to the offered medication is observed within the next 48 hours, new counselling with a nephrologist is required.6
To deal with hypovolemic complications, individualised fluid therapy and diuretics are prescribed intravenously.5 As soon as positive changes in vital signs and laboratory tests are observed, the dosage should be reorganised. Still, regular follow-ups, rest, and dietary improvements (decreased proteins and limited salt) should be underlined.
Conclusion
The evaluation of AKI pathophysiology and diagnosis proves that this condition is not always easy to identify. In most cases, people are diagnosed with AKI when they need care at the EDs. To classify the diagnosis and choose a treatment course, attention should be paid to creatinine levels and urinary output. Although mortality and morbidity rates are high in AKI patients, people can completely recover by following pharmacological and lifestyle recommendations.
References
- Bien, Z. et al. (2022) ‘Trends in hospital admission associated with an acute kidney injury in England 1998-2020: a repeated cross-sectional study’, SN Compr. Clin. Med., 4, article number 53 (9pp). Web.
- UK Renal Registry (2020) Acute kidney injury (AKI) in England – a report on the nationwide collection of AKI warning test scores from 2018. Web.
- Yokota, L. G. et al. (2018) ‘Acute kidney injury in elderly patients: narrative review on incidence, risk factors, and mortality’, Int J Nephrol Renovasc Dis, 11, pp. 217-224. Web.
- Blanco, V. E. et al. (2019) ‘Acute kidney injury pharmacokinetic changes and its impact on drug prescription’, Healthcare, 7(1), article number 10 (9pp). Web.
- Gameiro, J. et al. (2020) ‘Acute kidney injury: from diagnosis to prevention and treatment strategies’, J. Clin. Med. 9(6), article number 1704 (21pp). Web.
- National Institute for Health and Care Excellence (2019) Acute kidney injury: prevention, detection and management. Web.