Acute interstitial nephritis

Acute interstitial nephritis (AIN) is caused by acute inflammation of the renal tubulo-interstitium, commonly mediated by a hypersensitivity reaction to medications. Autoimmune diseases and infections are less common causes.

Usually drug-induced with >250 known triggering medications. Common classes include beta-lactam and fluoroquinolone antibiotics, proton-pump inhibitors, non-steroidal anti-inflammatory drugs (NSAIDs), and immune checkpoint inhibitors. Also occurs in inflammatory diseases such as sarcoidosis, Sjogren syndrome, IgG4-related diseases, and tubulo-interstitial nephritis with uveitis (TINU) syndrome. Various infectious agents (viruses, bacteria, fungi) and some malignancies can also cause AIN.

Presents with acute kidney injury or sub-acute loss of kidney function. The 'hypersensitivity triad' of rash, fever, and eosinophilia occurs rarely (<10%). Nephrotic syndrome may be present in cases triggered by NSAIDs.

Clinical diagnosis relies on maintaining a high index of clinical suspicion for this disease and performing a kidney biopsy to obtain tissue for histological diagnosis. Histological features of interstitial immune infiltrate, eosinophils, and tubulitis are considered characteristic of this disease.

May resolve once the triggering medication is discontinued. Corticosteroid therapy may be associated with greater recovery of kidney function.

Most patients have some residual renal impairment after an episode of acute interstitial nephritis.

AIN is a histological pattern of kidney inflammation, localised to the tubulo-interstitial space and usually triggered by medications.[1]Raghavan R, Eknoyan G. Acute interstitial nephritis - a reappraisal and update. Clin Nephrol. 2014 Sep;82(3):149-62. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4928030 http://www.ncbi.nlm.nih.gov/pubmed/25079860?tool=bestpractice.com See Acute kidney injury and Assessment of nephrotic syndrome.