Acute Kidney Injury Flashcards
What is AKI?
Rapid decline in kidney function occurring within a 48 hour window
Results in reduced ability to filter blood and manage waste products, electrolytes, and fluid balance
What are some high-risk populations for AKI?
- Trauma
- Shock
- Sepsis
High morality rates.
What are the types of AKI?
Prerenal AKI
Intrarenal AKI
Postrenal AKI
What is prerenal AKI?
Caused by decreased blood flow to the kidneys, often due to dehydration, shock, or heart failure.
Without adequate blood supply, the kidneys can’t filter blood effectively, leading to a decline in function.
50 - 60% of AKI cases - most common cause
What is Intrarenal AKI?
Results from direct damage to kidney structures, such as the nephrons and blood vessels due to toxins (like certain meds), infection, or ischaemia.
This type is often irreversible and requires intensive treatment
What is Postrenal AKI?
Caused by obstructions in the urinary tract, such as kidney stones, tumours, or an enlarged prostate.
The buildup of urine pressure can damage the nephrons and reduce kidney function.
What is the role of creatinine?
Creatinine is a waste product from muscle metabolism that kidneys filter out the blood,
When kidney function is compromised, creatinine accumulates in the blood, leading to elevated serum creatinine levels.
What does urine output as an indicator?
Reduce kidney function lowers urine output, as the filtration rate declines.
Monitoring urine output and serum creatinine levels are key in diagnosing and assessing the severity of AKI.
What is stage 1 of AKI severeity?
Stage 1 - Mild AKI
Serum Creatinine:
1.5 - 1.9 times baseline level
Urine Output:
Less than 0.5 ml/kg/hour for over 12 hours
What is Stage 2 of AKI severity?
Stage 2 - Moderate AKI
Serum Creatinine:
2.0 - 2.9 times baseline level
Urine Output:
Less than 0.5 ml/kg/hour for over 12 hours
What is stage 3 of AKI?
Stage 3 - Severe AKI
Serum Creatinine:
3.0 times baseline level or higher
Urine output:
Less than 0.3 ml/kg/hour for more than 24 hours, or complete absence of urine (anuria) for over 12 hours
What is Renal Hypoperfusion in prerenal AKI?
Without sufficient blood flow, the kidneys cannot maintain filtration rates, leading to a build up of waste products and disruption in fluid and electrolyte balance.
If untreated, prolonged hypoperfusion can lead to ischaemia and permanent kidney damage
Absolute Loss of Fluid is a mechanisms of Prerenal AKI. What is it and its cause?
Absolute Loss of Fluid:
This occurs when there is a significant physical loss of fluid from the body, reducing blood volume and consequently, renal perfusion.
Causes:
Major haemorrhage due to trauma, severe vomiting or diarrhoea and burns that can cause extensive fluid loss.
These conditions lead to a drop in blood pressure and overall blood volume, making it difficult for the kidneys to receive enough blood.
Relative Loss of Fluid is a mechanisms of Prerenal AKI. What is it and its cause?
Relative Loss of Fluid:
In this case, fluid moves out of the blood vessels and into tissues, but total body fluid remain unchanged. Blood volume decreases in the vessels, causing a relative loss of perfusion to the kidneys.
Causes:
Distributive shock (e/g sepsis) or congestive heart failure can cause fluid to shift from the bloodstream into surrounding tissues. This fluid shift reduces effective blood circulation to organs, including the kidneys, despite total fluid volume being adequate.
Direct Issue with Renal Artery is a mechanisms of Prerenal AKI. What is it and its cause?
Direct Issue with Renal Artery:
A physical blockage or narrowing of the renal artery limits blood flow to the kidneys directly, causing hypoperfusion
Cause:
An embolus can obstruct the renal artery, or the artery can become narrowed, reducing blood flow. This restricts the blood supply to the kidney, impairing function and potentially leading to ischemic injury
In prerenal AKI what happens to the GFR?
As renal blood falls, the GFR decreases, the amount of substances that are filtered (Na+, K+ etc) is reduced.
This can lead to deranged blood conditions (hyperkalaemia etc)
What happens to the Tubular Epithelial Cells (cells within the nephrons)
Tubular Epithelial Cells have high metabolic rate, therefore are affected most by lack of oxygenated blood. This can eventually lead to ischaemic tubular necrosis.
What are some causes of Intrarenal AKI?
Ischemia - often secondary to prolonged prerenal AKI
Sepsis - introduce harmful agents into the kidney
Nephrotoxic drugs - antibiotics, NSAIDs and chemo agents - that are toxic to kidney cells
Acute Intrarenal Infection - infections such as pyelonephritis can lead to inflammation and cellular damage within the kidneys.
What is Acute Tubular Necrosis (ATN)
A common result of intrarenal injury is acute tubular necrosis, where the tubular epithelial cells die due to a lack of oxygen or exposure to toxins
ATN impact on Kidney Function?
Necrosis of tubular cells causes blockages within the nephron, leading to an increase in intraluminal pressure and reduced GFR.
This back pressure can lead to further injury and reduced kidney efficient in filtering blood.
Ischemia in relation to ATN?
Ischemia:
Reduced renal blood flow leads to less o2 being delivered to tubular cells. Cells undergo necrosis, leading to tubular obstruction and increases pressure within nephron. Often secondary to prerenal conditions like shock, severe dehydration, BP reduced.
Sepsis in relation to ATN cause?
Sepsis:
Widespread vasodilation, leading to low BP and intrarenal hypoperfusion. Reduced blood flow to kidneys, causing ischemic conditions. Sepsis generated toxins that make tubular epithelial cells more susceptible to ischaemic damage. Sepsis causes both vascular changes and toxin release, making ATN more likely and more severe.
Nephrotoxic drugs in relation to cause of ATN?
Certain drugs can directly damage kidney tubules through various pathways, including renal vasoconstriction, direct cytotoxicity, or by causing obstructions with tubules
Aminoglycosides: Antibiotics that can cause tubular toxicity
NSAIDs (ibuprofen): Long-term use can reduce renal blood flow due to vasoconstriction, increasing ischemic risk
Chemo agents: Often toxic to rapidly dividing cells, including those in the kidneys
ACE inhibitors (Ramipril): Reduce renal perfusion by dilating efferent arterioles, which can decrease glomerular pressure
Diuretics (Furosemide): Though used to manage fluid, excessive use can strain kidney function, especially if underlying conditions exist.
Intrarenal infection in relation to ATN cause?
Infections within the kidney activate the completement system and attract immune cells like macrophages and neutrophils. These immune cells release enzymes that can damage podocytes within the glomerulus.
Podocytes form the filtration barrier, preventing large molecules (proteins, RBC) from entering the urine. When damaged, proteins and blood cells pass into the urine, resulting in proteinuria and haematuria detectable on urinalysis.
What is Cell Death and Tubular Obstruction in relation to ATN?
In ATN, the tubular epithelial cells die due to ischaemia, toxins, or other damage factors.
This cell death results in debris that obstructs and renal tubules.
The blockage within the tubules restricts the passage of filtrate, leading to an increase in intraluminal (internal tubular) pressure.
What is Intraluminal Pressure and GFR reduction?
The obstruction raises the pressure within the nephron’s tubules, opposing the filtration pressure generated in the glomerulus.
As a result GFR declines rapidly, causing a drop in urine output. With decreased filtration, metabolic waste accumulates in the bloodstream, leading to toxin build up, which can impair other organs.
What will happen when there’s Waste Accumulation?
The kidney’s ability to filter out metabolic waste products, such as urea and creatinine, is compromised, leading to their build up in the blood.
This accumulation causes electrolyte imbalances and metabolic acidosis, both of which can disturb the functions of the heart, brain and muscles.
What happens when there is fluid backflow and oedema?
Due to high intraluminal pressure, some of the filtrate that cannot pass through the tubules is forced back into the surrounding interstitial space and ultimately reabsorbed into the bloodstream.
This backflow of fluid contributes to systemic fluid overload, causing widespread swelling or oedema.
Oedema can be seen in extremities, around the lungs (pulmonary oedema) and in other tissues, worsening the patients condition
What are the main causes of postrenal AKI?
Compression of the Ureter or Urethra
Obstruction by Kidney Stones
What is Compression of the Ureter or Urethra?
Caused by an intra-abdominal tumour pressing against the ureter, or by benign prostatic hyperplasia, where an enlarged prostate gland restricts urine flow through the urethra in males
Impact of Compression:
Compression of the urinary tract prevents urine from draining properly, causing urine to accumulate above the site of obstruction, leading to increased pressure within the kidneys.
What is the mechanism and effect on the renal system on the obstruction by kidney stones?
Kidney stones or renal calculi can obstruct the ureter, restricting the flow of urine from the kidney to the bladder
The blockage caused by stones prevents urine from leaving the kidney, creating a backflow that increases intrarenal pressure, putting stress on the nephrons and impairing their function
What are the effects of urine backflow?
The obstruction creates a back pressure in the renal system, extending all the way up the nephrons in the kidney.
This increased pressure reduces the glomerular filtration rate as the resistance to filtration rises.
Prolonged backflow can damage nephrons and lead to chronic kidney damage if the obstructions is not promptly relived. It also creates a risk of infection due to stagnant urine in the urinary tract.
Urine is backed, and there is increased pressure within the lumen of the tubule, what happens now?
This balances out the pressure gradient between the capillary bed and tubule lumen, reducing the amount of waste that is filtrated.
The GFR is lowered, the blood becomes deranged due to the reduction in the filtration of waste and excess electrolytes from the blood.
What is the increased tubular pressure and disrupted filtration?
When urine backs up due to an obstruction in the urinary tract, the pressure within the tubules of the nephron rises.
This increased pressure in the lumen of the tubule opposes the natural pressure gradient that drives filtration from the capillaries in the glomerulus into the nephron.
What is the Pressure Gradient Balance in relation to Increased Tubular Pressure and Disrupted Filtration?
Filtration in the glomerulus relies on a pressure different between the blood in the glomerular capillaries and the fluid in the tubular lumen.
The backflow-induced rise in tubular pressure disrupts this gradient, balancing out pressure on both sides, which slows or stops the filtration process.
The Reduction in GFR in relation to Postrenal AKI?
The elevated pressure in the nephron tubules leads to decrease in GFR - the rate at which blood is filtered through the glomeruli.
With reduced GFR, the kidneys’ ability and eliminate metabolic waste and excess electrolytes from the blood declines sharply.
What are the consequences of lowered filtration?
As GFR drops, waste products such as urea and creatinine and excess electrolytes accumulates in the bloodstream.
This build up leads to metabolic imbalances, potentially causing symptoms like confusion, fatigue, and electrolyte abnormalities, which can be dangerous, particularly high potassium (hyperkalaemia) that affects heart rhythm.
What are some signs and symptoms of AKI?
- Sudden changes in mental status or mood
- Nausea, vomiting and/or diarrhoea
- Rapid onset of numbness or tingling, especially around the hands and feet
- Sudden onset of oedema to the feet and/or hands
- Rapid onset of hypertension
- Rapid decrease in urine output
- Muscle twitching
What is the management of AKI?
- Administer fluids as per JRCALC = slowly administered will reduced likelihood of fluid overload, common in AKI
- Consider furosemide if pulmonary oedema present
- Convergence necessary for definitive care, consider pre-alert based on presentation
- AKI kills
