Tubular casts precipitate and “plug” the fine tubular system causing acute
tubular obstruction, back-leak into the interstitium, loss of epithelial
integrity and epithelial damage. Direct toxicity of myoglobin occurs when
the epithelial cells are exposed to free oxygen radicals originated from the
oxidation of ferrous oxide to ferric oxide.
In acute interstitial nephritis (AIN), the inflammatory infiltration of
extraglomerular structures (tubules and interstitium) and activation of
proinflammatory cytokines lead to acute epithelial injury and renal
dysfunction. This hypersensitivity process is usually secondary to the use
of medications. AIN is, however, self-limited most of the times and rarely
progresses to renal failure.
Radiocontrast dye imposes a high solute load to the tubular system which
in turn imposes high energy demands to the renal medulla due to
increased tubular activity. Since the renal medulla is an area of limited
blood flow, the enormous metabolic demand easily leads to interstitial
hypoxia and subsequent renal injury.[32]Causes of renal/parenchyma failure
Acute tubular necrosis
Shock states
Sepsis
Radiocontrast dye
Myoglobinuria
Acute tumor lysis syndrome
Segmental glomerulosclerosis
Cardiac and aortic surgery
Acute interstitial nephritis (AIN)