26th June 2023

Pathophysiology of Acute interstitial nephritis (AIN)

Acute interstitial nephritis involves damage to the renal interstitium and accounts for approximately twenty-five percent of all drug-induced acute kidney injuries. 85% of the kidney is made up of the interstitium, and it consists of a collection of cells, extracellular matrix, and fluid surrounding the kidney and is essentially the structural support for the tubular architecture and participates in fluid and electrolyte exchange. Injury to renal cells leads to the expression of new antigens, inflammatory cell infiltration and activation of pro-inflammatory cytokines. The infiltrating inflammatory cells, including lymphocytes, macrophages and eosinophils, cause oedema and fibrosis within the interstitium. This can lead to impaired renal function, however, there is minimal or no damage to the glomeruli or blood vessels. The most prevalent cause of acute interstitial nephritis is drug-induced, most commonly secondary to NSAIDs or penicillin. Typical symptoms are fever, rash and arthralgia and other features include hypertension, renal impairment, and eosinophilia.