23rd June 2023

Intrinsic renal AKI

This encompasses disease processes which affect the renal parenchyma. Causes can be stratified by the location affected:

• Vascular
  • Large vessel disease – renal artery occlusion (e.g. cholesterol embolus, thrombosis), renovascular disease or renal vein pathology (e.g. thrombus)
  • Small vessel disease and glomerulonephritis – glomerulonephritides (see Glomerular diseases section), thrombotic microangiopathies (e.g. haemolytic uraemic syndrome, thrombotic thrombocytopenic purpura), scleroderma, pre-eclampsia, malignant hypertension
• Tubulointerstitium
  • Acute tubular necrosis (see below), rhabdomyolysis, tumour lysis syndrome, cast nephropathy (e.g. due to myeloma), acute interstitial nephritis (e.g. drug-induced or secondary to infections), contrast nephropathy

Acute tubular necrosis (ATN)

Prolonged pre-renal AKI can lead to acute tubular necrosis; it can also be caused by intrinsic disorders, e.g. rhabdomyolysis, drugs, and contrast. The pathogenesis is complex, however centres around vascular supply to the renal tubules. Reduced blood flow results in vasoconstriction, leading to cell hypoxia; areas particularly vulnerable to this include the proximal convoluted tubule and the ascending loop of Henle. Cells die, and the resulting debris enters the tubular lumen, where it can form casts that cause obstruction. Other factors involved include backleak of filtrate through damaged tubules and injury to the vascular endothelium. Tubular structure and function can recover after some time once the blood supply has normalised; patients will frequently experience a period of polyuria before the tubules are able to concentrate urine again.