Acute Kidney Injury_AKI _ PATHOPHYSIOLOGY
شرح بالعربي : الفشل الكلوي الحاد باثوفسيولوجي
• AKI_Acute Kidney Injur...
Lecture Outline
-Incidence & importance
-Definition
-Causes
-Types & Pathophysiology of AKI
Renal physiology
AKI Incidence &Importance
Approximately 7% of all hospitalised patients
and 20% of acutely ill patients develop AKI.
In uncomplicated AKI mortality is low, however when it is associated with sepsis and multiple organ failure mortality is 50%-70%
and the outcome is usually determined by
the severity of the underlying disorder and other complications, rather than by kidney injury itself.
Definition
In AKI there is a sudden and often reversible loss of renal function
with rising serum urea and creatinine,
which develops over days or weeks
and is often accompanied by a reduction in urine volume.
Types & Pathophysiologyof AKI
1-‘Pre-renal’, when perfusion to the kidney is reduced
2-‘Renal’, when the primary insult affects the kidney itself
3-‘Post-renal’, when there is obstruction to urine flow at any point from the tubule to the urethra.
Causes of AKI
Pre-renal AKI &the renin-angiotensin-aldosterone system
Pre-renal AKI results from a reduction in renal perfusion, typically due to a reduction in systemic blood pressure.
The drop in renal perfusion activates the renin-angiotensin-aldosterone system, which promotes sodium retention in the kidney and systemic vasoconstriction in order to restore blood pressure.
Pre-renal AKI &the renin-angiotensin-aldosterone system
Angiotensin also preferentially constricts the glomerular efferent arteriole,
while prostaglandins are released locally to vasodilate the afferent arteriole.
The combined effect increases glomerular pressure to maintain GFR.
Renal AKI
If the drop in renal perfusion is severe or sustained, pre-renal AKI may progress to renal AKI as ischaemic injury causes Acute Tubular Necrosis (ATN),or bilateral cortical necrosis.
Histologically, the kidney shows inflammatory changes, focal breaks in the tubular basement membrane and interstitial oedema.
Dead tubular cells may also be shed into the tubular lumen, leading to tubular obstruction
A.T.N
While ischaemia is the most common cause of ATN in hospital, it may also be caused by
toxins and nephrotoxic drugs (Radiographic contrast media, Aminoglycosides, amphotericin, Paracetamol overdose).
The other common ‘renal’ cause of AKI is glomerulonephritis, in which there is direct inflammatory damage to the glomeruli.
COVID-19 infection is also associated with AKI in a significant proportion of patients.
Post-renal AKI
Obstruction to the renal tract leads to elevation of intraluminal ureteral pressure transmitted to the nephrons, with a subsequent fall in GFR.
The obstruction needs to be bilateral to cause renal failure, therefore it is unusual for renal stones to cause AKI, while obstruction of the bladder outlet is a much more common cause.
Post-renal AKI
If the obstruction is not relieved, the low GFR is maintained by a drop in renal perfusion via thromboxane A2 and angiotensin II which subsequently causes ischaemic injury
This leads to chronic renal injury over several weeks.
If obstruction is reversed, the extent of recovery of renal function is dependent on
the duration of obstruction and
the pre-morbid GFR.
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