ABSTRACT
This chapter describes acute kidney injury (AKI) and rhabdomyolysis. AKI occurs in 13–18% of hospitalised patients, usually as a result of systemic hypotension. Volume-responsive AKI is caused by failure to perfuse kidneys; glomeruli and renal tubules remain undamaged. Intrinsic AKI is caused by damage to glomeruli and nephrons. Extensive muscle damage, such as from crush injuries, major burns, severe infection/sepsis or prolonged immobilisation, can cause rhabdomyolysis, leading to acute kidney injury. Damage may be caused by: ischaemia, inflammation, and nephrotoxicity. Postrenal kidney injury is usually caused by mechanical obstruction to flow of urine – such as tumours, stones, strictures or enlarged prostate. There are many, but no ideal, ways to monitor renal function, including: urine volume, bloods, and urinalysis. Poorly managed volume-responsive AKI usually progresses to intrinsic AKI. Furosemide, a loop diuretic, blocks sodium reabsorption in the ascending loop of Henle; and as water follows sodium urine output is increased.
