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Acute tubulointerstitial nephritis (ATIN)
Acute tubulointerstitial nephritis (ATIN) is characterized by inflammation and edema in the kidney tubulointerstitium and can cause acute kidney injury (AKI). Definitive diagnosis is established by kidney biopsy, though this may not be necessary if the index of suspicion for ATIN is high.
A retrospective study done by Goicoechea showed that the incidence of ATIN, particularly ATIN in the elderly, has increased over the past decade due to a higher biopsy rate and/or an increased use of causative drugs, such as nonsteroidal antiinflammatory drugs (NSAIDs) and antibiotics.
8 Interesting Facts of Acute tubulointerstitial nephritis
1. ATIN accounts for up to one-third of AKI cases.
2. The classical triad of fever, maculopapular rash, and peripheral eosinophilia is seen in only a minority of cases (<10%) of ATIN.
3. The absence of eosinophiluria does not necessarily exclude the diagnosis of ATIN.
4. Drug-induced ATIN is not dose dependent. A repeat exposure to the same drug can potentially lead to a recurrence of the disease process. The most common offending drugs are NSAIDs, proton pump inhibitors, and antibiotics.
5. The majority of suspected cases of ATIN result in the recovery of kidney function in a few days to weeks.
6. Patients who do not recover kidney function within a few weeks of withdrawal of the offending agents may benefit from corticosteroids.
7. In chronic tubulointerstitial nephritis, depending on the culprit agent, the disease may have a particular predilection for either the proximal tubules or the distal tubules or both; the consequent functional abnormalities depend on the tubular site of involvement. The involvement of the proximal tubule often leads to hypophosphatemia, glycosuria, aminoaciduria, and hypomagnesemia.
8. Lithium-induced nephropathy is characterized by the formation of microcysts (cortical and medullary tubular cysts) in the distal convoluted tubules and collecting ducts.
