Hello and welcome to part 2 of KIDNEYS. If you haven't read up on the renal system, I'd recommend it and you can do that here. This post will be focusing on Acute Kidney Injury (AKI).
An acute kidney injury is a short-term injury to the kidney, defined as a sudden decrease in kidney function, which was previously known as acute renal failure. Because of its acute nature, AKIs are largely reversible with an expected return to normal function.
As a recap if you don't want to read my other post of renal functions, the functions of the kidney can be summarised with A WET BED (Travis, 2016; Dr Matt and Dr Mike, 2022):
Acid-base balance regulation Water balance Electrolyte regulation Toxins (metabolic waste products)
Blood pressure regulation Erythropoietin production D vitamin production
AKIs are most common in older people, who often have other comordibities and may have experienced a decrease overall in kidney functions due to conditions like hypertension and diabetes (NHS, 2022).
Around 7% of hospital inpatients will experience a hospital acquired AKI, largely due to dehydration or nephrotoxic medications like NSAIDS and aminoglycoside antibiotics (Dr Matt and Dr Mike, 2022; NHS, 2022).
AKI can be diagnosed using blood parameters like urea and creatinine, and by measuring urine output. Urea and creatinine are both metabolic waste products that are filtered from the blood by the kidneys, so increasing levels would indicate decreasing levels of filtration and clearance.
A normal creatinine level varies between men and women, but is usually expected to be less than 100µmol/L (Oxford University Hospitals, no date). Rising creatinine indicates that the kidneys are struggling to filter this waste product out of the blood. An increase in blood urea nitrogen (BUN) would also be seen, as urea also fails to be filtered out of the blood. Normal BUN is widely accepted as 3-9mmol/L, again differing between males and females (Oxford University Hospitals, no date). Creatinine cannot be reabsorbed, therefore if it is not being filtered into urine, it will continue to circulate in the blood. BUN can be reabsorbed in the nephron therefore is not a sensitive or specific marker for kidney filtration function (Parikh and Koyner, 2020). Creatinine, however, is produced at a consistent rate, and is filtered at a consistent rate so the normal
value of creatinine clearance can be theoretically known. This means that any changes in creatinine levels in the blood provides a clear and direct biochemical indication of kidney function (Dr Matt and Dr Mike, 2022).
Alongside an increasing serum creatinine and BUN level, a decrease in glomerular filtration rate may also be seen in AKI. Normal GFR is 90-120mL/min, but lower values may be seen with increasing age. Cause of concern starts when GFR drops below 90mL/min/1.73 m2 (Kaufman, Basit and Knohl, 2022) as this indicates that not enough blood is being filtered through the glomerulus of the kidney (again, you can see a recap of renal anatomy in this post). Increasingly low GFRs will be seen as chronic kidney disease progresses (more on that in this post).
Finally, a drop in urine output, also known as oliguria, can be observed. Oliguria is defined as urine output less than 20mL/hour in adults, or if more strictly monitoring, less than 0.5ml/kg/hr (Haider and Aslam, 2022). In a worst case scenario, patients may experience anuria, or no urine output, and this is a strong indicator of a very unhappy renal system as no filtration is taking place. In this case, you could also expect to see rises in potassium and sodium as it is not being excreted or reabsorbed as usual.
Generally (but specifically in ICU, as you wouldn't really know this information otherwise) it's important to maintain a MAP (mean arterial pressure) of 65mmHg (Badin et al., 2011; Sato, Luthe and Nasu, 2017). This acts as a minimum perfusing pressure needed to ensure adequate blood supply to the kidneys. With a MAP lower than this, blood is predominantly diverted to the more important organs like the brain and cardiac muscle and AKI will result due to a lower GFR and cause a pre-renal AKI (see below for more).
Staging or scoring of AKI is dependent on a) serum creatinine increases and b) urine output decreases. The scoring system is as follows, and has been developed by KDIGO (Kidney Disease- Improving Global Outcomes)
AKI can be classified into pre, intra or post renal based on what is affecting the GFR. Please enjoy the stunning visual below of the causes, created just for y'all.
Pre-renal- Nephrons in the kidneys are being under-perfused and therefore GFR is inhibited. This could be due to:
Severe dehydration
Decreased absolute fluid losses such as burns or vomiting/diarrhoea
Major haemorrhage with decreased absolute blood volume
Decreased cardiac output or heart failure
Shock with vasodilation and a decrease in relative blood volume
Issues with vessels going directly to the kidney (the renal artery) for example severe stenosis or thrombosis
Vasoconstriction of afferent blood vessels coming into the nephron for example NSAIDS that block prostaglandins.
Pre-renal presentation of AKI would present as a drop in GFR (due to hypoperfusion) with associated increases in creatinine secondary to impaired filtration and excretion. As there is impaired flow through the glomerulus, the renin-angiotensin-aldosterone system is activated and blood pressure increases will be seen as the kidney reabsorbs more sodium (and therefore water). A gradual decrease in urine output will be seen, and on urinalysis the osmolarity of urine will increase as urine becomes more concentrated secondary to water retention. Urine sodium would be low as sodium is retained as part of RAAS.
Resolution of pre-renal AKI will generally just involve correction of perfusion or hypovolaemia, and often there will be no damage to the actual kidney.
Intra-renal- Damage to the kidney cells or tissues themselves- this can follow the slightly dubious acronym 'Thank God It's Vriday' (Dr Matt and Dr Mike, 2022):
Tubule
Glomerulus
Interstitium
Vasculature
Overall aetiologies of intra-renal damage include:
Ischaemia- lack of oxygenation to tissues and cells.
Toxic product- build up of metabolic products or toxins introduced by bacterium or nephrotoxic drugs.
Inflammation- due to infection, direct damage or autoimmune conditions.
Tubule- Acute tubular necrosis (ATN) is the most common cause of AKI. It is an intra-renal form that can be due to drugs (such as aminoglycoside antibiotics such as vancomycin and IV contrast dyes), heavy metals, toxins (metabolic by-products, such as following rhabdomyolysis where products of muscle death lead to renal cell death), or secondary to poor perfusion pre-renally- if hypoperfusion is prolonged, it can lead to ATN developing with damage to the actual kidney.
Glomerulus- Glomerulonephritis is a form of inflammation in the glomerulus which impacts on the ability of the glomerulus to filter properly.
Interstitium- Acute tubular interstitial nephritis (ATIN) is commonly immune driven or medication driven, leading to hypersensitivity in the interstitium and inflammation in the functional tissue of the kidney.
Vasculature- Damage to microvessels within the nephron, such as vasculitis or direct trauma to the kidney itself.
Kidney damage may not be easily discernible (short of getting a biopsy). To measure kidney damage, other aspects can be considered such as looking at proteinuria or haematuria to establish if the filtration membrane has been damaged and is letting substances through that should not be excreted in urine. Sodium in urine could be normal or high as it is not being reabsorbed in the same manner as a pre-renal AKI. Sediment may also be noted in urine. BUN will not be reabsorbed in the usual manner due to nephron dysfunction (but wouldn't necessarily be expected to increase). Serum creatinine would still increase.
To determine if it is a pre or intra renal AKI, a fluid challenge can be given. If giving fluids resolves the issue, it can be assumed to be pre-renal as you have solved the hypovolaemia problems (yay!) however if the problem persists, it may be an intra-renal issue and the damage would not be reversed as rapidly.
Post-renal- Obstruction of urine getting out of urinary tract. A downstream problem from the kidney- anything from the ureters, bladder and urethra. A blockage in any of these pipes will lead to urine backing up into the kidney unless relived.
Causes can include:
Ureteric or bladder stones
Kidney stones (within the kidney/renal pelvis)
Bladder dysfunction
Urethral stricture/stenosis
Benign prostatic hyperplasia (BPH)
Pelvic or abdominal tumours causing compression
If fluid backs up into the kidney, it's known as hydronephrosis (literally 'water in kidney') and this can be seen on ultrasound- this would present as an enlarged kidney with increased pressure within the tubules and can result in issues with GFR. Initial presentation of a post-renal AKI could resemble pre-renal, with a GFR issue, but the presentation could develop into a problem that looks more like an intra-renal issue as renal cells become damaged.
Treatment involves removing whatever is blocking the tubes, and draining the urine to resolve the issue and prevent further back-up into the kidney.
General management to treat, or ideally prevent an AKI in the first place, will invplve management of fluid status and perfusion pressures, careful management of nephrotoxic medications (NSAIDS, some antibiotics), monitoring for drug overdoses due to impaired metabolism and excretion, monitoring serum creatinine and urine output, considering alternatives to IV contrast dyes (or avoiding them in the first place- if necessary, make sure hydration is maintained to flush them out) (Hulse and Davies, 2015).
If AKI is progressing, renal replacement therapy such as haemodialysis may be required to take the pressure off the kidneys and allow sufficient time for damage to heal.
Thank you so much for taking the time to read this post- coming soon is hopefully the 3rd in the kidney series, looking at chronic kidney disease, and also an overview of absolutely no-one's favourite system, RAAS.
As always, please like and leave a comment if you found this useful, and follow my socials- @christienursing on instagram and twitter
References
Badin, J., Boulain, T., Ehrmann, S., Skarzynski, M., Bretagnol, A., Buret, J., Benzekri-Lefevre, D., Mercier, E., Runge, I., Garot, D., Mathonnet, A., Dequin, P., Perrotin, D. (2011) 'Relation between mean arterial pressure and renal function in the early phase of shock: a prospective explorative cohort study' in Critical Care. 15(3)
Dr Matt and Dr Mike's Medical Podcast (2022) 'Acute Kidney Injury'. Available at: https://podcasts.apple.com/gb/podcast/acute-kidney-injury-aki/id1270681468?i=1000580240197
Haider, M., Aslam, A. (2022) 'Oliguria' in Statpearls. Available at: https://www.ncbi.nlm.nih.gov/books/NBK560738/ (Accessed 15-Jan-2
Hulse, C., Davies, A. (2015) 'Acute kidney injury: prevention and recognition' in Nursing Times, 111(30), pp. 12-15.
Kaufman, D., Basit, H., Knohl, S. (2022) 'Physiology, glomerular filtration rate' in Statpearls. Available at: https://www.ncbi.nlm.nih.gov/books/NBK500032/ (Accessed 15-Jan-2023)
NHS (2022) 'Acute Kidney Injury'. Available at: https://www.nhs.uk/conditions/acute-kidney-injury/#:~:text=Most%20cases%20of%20AKI%20are,or%20diarrhoea%2C%20or%20severe%20dehydration (Accessed 16-Jan-2023)
Oxford University Hospitals (no date) 'Clinical biochemistry- creatinine'. Available at: https://www.ouh.nhs.uk/biochemistry/tests/tests-catalogue/creatinine.aspx (Accessed 16-Jan-2023)
Oxford University Hospitals (no date) 'Clinical biochemistry- urea'. Available at: https://www.ouh.nhs.uk/biochemistry/tests/tests-catalogue/urea.aspx (Accessed 16-Jan-2023)
Parikh, C., Koyner, J. (2020) 'Biomarkers in acute and chronic kidney disease' in Brenner and Rector's 'The Kidney', Elsevier, Oxford.
Sato, R., Luthe, S., Nasu, M. (2017) 'Blood pressure and acute kidney injury' in Critical Care. 21(28). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5301320/
Travis, L. (2016) Renal physiology resources in Journal of Electronic Resources in Medical Libraries. 13(3)
UpToDate (2023) 'Criteria for acute kidney injury' https://www.uptodate.com/contents/image?imageKey=NEPH%2F83168 (Accessed 16-Jan-2023)