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PH-RN01

Acute kidney injury

How too little perfusion, injured tubules or a blocked outflow lower filtration over hours to days, and why creatinine, urea, potassium, acid and fluid then build up in the body.

By the end, you can

  • Describe how glomerular filtration depends on renal blood flow and on the tone of the afferent and efferent arterioles.
  • Distinguish pre-renal, intrinsic and post-renal acute kidney injury by where the problem lies.
  • Explain how ischaemic or toxic injury to tubular cells lowers the glomerular filtration rate.
  • Relate a falling filtration rate to rising creatinine and urea, hyperkalaemia, metabolic acidosis and fluid overload.
  • Recognise acute tubular necrosis, the KDIGO stages and the urine and blood tests that separate pre-renal, intrinsic and post-renal AKI, and explain how restoring perfusion, relieving obstruction, treating hyperkalaemia and dialysis act on the mechanism.

What it is

Acute kidney injury (AKI) is a fall in kidney function over hours to days, recognised by a rise in serum creatinine, a fall in urine output, or both. Its causes divide by site: pre-renal (too little perfusion of a structurally normal kidney), intrinsic (damage within the kidney, most often to the tubules) and post-renal (obstruction to the outflow of urine).

3 types to tell apart
Pre-renal
Low blood volume, low cardiac output or widespread vasodilatation reduce perfusion. The tubules work normally and conserve salt and water; prolonged, it can progress to tubular injury.
Intrinsic (acute tubular injury)
Ischaemia or toxins injure the tubular cells. Other intrinsic causes, with different mechanisms, include glomerulonephritis, acute interstitial nephritis and disease of the small renal vessels.
Post-renal
Obstruction to outflow, usually at the bladder outlet or in both ureters, raises pressure behind it and opposes filtration.

US spelling: litres → liters.

Normal function

Filtration depends on flow and pressure

The kidneys receive about a fifth of the cardiac output. In each nephron, blood enters the through the and leaves through the , whose resistance keeps capillary pressure high enough to push plasma into the . The total for both kidneys, the glomerular filtration rate (GFR), is about 120 mL/min in a young adult: some 180 litres of filtrate a day.

Autoregulation holds GFR fairly steady as blood pressure varies. The afferent arteriole constricts when stretched, and the adjusts it to the salt arriving at the end of the loop (tubuloglomerular feedback). When perfusion falls, prostaglandins widen the afferent arteriole and angiotensin II narrows the efferent one, keeping filtration pressure up.

The tubules then reabsorb about 99% of the filtered water and sodium. That work needs a great deal of ATP, and the and the straight end of the proximal tubule do much of it in the outer medulla, where oxygen is scarce.

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