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Acute kidney injury (AKI), also known as acute renal failure (ARF), is characterized by an abrupt decline in renal function, leading to a reduction in the glomerular filtration rate (GFR) and the subsequent accumulation of nitrogenous waste products in the body <ref name = "Ref15"> Lote, C.J., Harper, L. and Savage, C.O. (1996) ‘Mechanisms of acute renal failure’, British Journal of Anaesthesia, 77(1), pp. 82–89. doi:10.1093/bja/77.1.82.</ref>. The clinical signs of acute kidney injury (AKI) are characterized by either an elevation in serum creatinine levels, a decrease in urine output, or both [16]. <ref name = "Ref16">Ronco, C., Bellomo, R. and Kellum, J.A. (2019) ‘Acute kidney injury’, The Lancet, 394(10212), pp. 1949–1964. doi:10.1016/s0140-6736(19)32563-2</ref> The causes of this disorder can then be classified into three categories, namely, pre-renal, intrinsic renal or post renal <ref name = "Ref15"/>

Pre-renal kidney failure is a term used to describe the condition in which there is a systemic circulation disorder leading to a reduction in renal perfusion and subsequently a reduction in GFR [. <ref name = "Ref17"> Kellum, J.A. and Lameire, N. (2013) ‘Diagnosis, evaluation, and management of Acute Kidney Injury: A KDIGO summary (part 1)’, Critical Care, 17](1), p. 204. doi:10.1186/cc11454. </ref> Notable causes that can contribute to pre-renal kidney failure include reduced blood volume, peripheral vasodilation, reduced arterial pressure or impaired cardiac function, leading to a reduced cardiac output [17]. <ref name = "Ref17"/> Characterising a condition as pre-renal implies that addressing the root cause of the circulatory disorder, by improving cardiac function or replenishing lost volume, may lead to the restoration of GFR [16]. <ref name = "Ref16"/> However, in most cases, pre-renal failure is often followed by intrinsic renal failure where the GFR of a patient may not be restored, despite addressing pre-renal causes.

Intrinsic renal failure refers to direct damage to the kidney itself and is categorised by the location of the injury, most commonly occuring to the glomerulus or the tubule, and include the interstitial or vascular portions of the kidney [18]. <ref name = "Ref18"> Sharfuddin, A.A. et al. (2012) ‘Acute kidney injury’, Brenner and Rector’s The Kidney, pp. 1044–1099. doi:10.1016/b978-1-4160-6193-9.10030-2. </ref> The typical causes for each include the inflammation and structural damage of the glomerular cells (glomerulonephritis), interstitial cells (acute interstitial nephritis) or the tubular epithelial cells (acute tubular necrosis) [16]. <ref name = "Ref16"/> These conditions themselves can be a result of immune complexes from systemic illnesses, ischemic causes such as prolonged periods of severe hypovolemia or hypotension, nephrotoxic causes such as exposure to exogenous or endogenous toxins [18]<ref name = "Ref18"/>, or hypersensitivity reactions to medications such as antibiotics [19]. <ref name = "Ref19">Praga, M. and González, E. (2010) ‘Acute interstitial nephritis’, Kidney International, 77(11), pp. 956–961. doi:10.1038/ki.2010.89. </ref>

Post-renal failure or obstructive renal failure are caused by disease states downstream of the kidneys resulting in extrarenal obstruction of urinary flow [20]. <ref name = "Ref20">Raup, V.T., Chang, S.L. and Eswara, J.R. (2018) ‘Post-renal acute kidney injury: Epidemiology, presentation, pathophysiology, diagnosis, and management’, Core Concepts in Acute Kidney Injury, pp. 247–256. doi:10.1007/978-1-4939-8628-6_16. </ref> These can be related to neurogenic bladder conditions, obstructed urinary catheters, bladder stones, or cancers of the bladder, prostate or ureter [20].<ref name = "Ref20"/>

The GFR in mL/min can be calculated with the following formula: GFR = ( UX · V̇ ) / PX. Here, UX and PX are the concentrations of substance X in urine and plasma in mg/mL respectively, with V̇ being the urine flow in mL/min. Ideally X is a substance that is freely filtered but not secreted or reabsorbed by the kidneys, subsequently having the same concentration in the plasma and glomerular filtrate [21]. <ref name = "Ref21">Pocock, G., Richards, C.D. and Richards, D.A. (2013) Human physiology. Oxford: Oxford University Press.</ref>These criteria are largely met by creatinine, and the creatinine clearance (CCr) obtained from this formula is generally used to measure GFR in clinical practice [22]. <ref name = "Ref22">Delgado, C. et al. (2022) ‘A unifying approach for GFR estimation: Recommendations of the NKF-ASN task force on reassessing the inclusion of race in diagnosing kidney disease’, American Journal of Kidney Diseases, 79(2). doi:10.1053/j.ajkd.2021.08.003.</ref> Other diagnostic tools also include serum creatinine levels (SCr) as in the case of renal dysfunction, the creatinine clearance by the kidneys is reduced and therefore the creatinine concentration in the blood rises [21].<ref name = "Ref21"/>