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Nonspecific: Nausea, fatigue, skin rash, fevers, arthralgia
Polyuria, polydipsia, enuresis (unable to concentrate urine)
Flank pain bilateral (inflamed kidney edema causing pain due to stretching of kidney capsule)
History of use of a new med within few weeks prior
Most common meds/drugs causing TIN: sulfa drugs (Bactrim, many diuretics), PPIs, beta-lactam Abx, NSAIDs, see other:
TIN is immune-mediated infiltration of the kidney interstitium by inflammatory cells, commonly due to hypersensitivity (allergic) reaction to medications. Glomeruli are not primarily affected. Tubular functions are lost (cannot concentrate urine, losses of glucose and protein in urine, Fanconi-like).
Stop offending medication
If sCr high treat with steroids, may need MMF
Ensure adequate hydration
BP is usually normal
KFP: high sCr, sAlb and other mainly normal
CBC: eosinophilia
Inflammatory markers: high ESR and CRP
UA “bland”: dilute, mild proteinuria (non-nephrotic, no albuminuria), glucosuria, no hematuria, may have many WBCs due to inflammation (sterile pyuria)
Urine eosinophil stain: may be positive
Urine Beta-2-microglobulin: high, marker of tubular damage
Complements, ANA, ANCA: negative in drug-induced TIN
Kidney US: shows enlarged kidneys
Biopsy:
usually not needed
indicated if no known offending drug, sCr very high and/or not improving
lymphocytic and eosinophilic tubulointerstitial inflammatory infiltrate
Mark offending med as “drug allergy”
Can resolve fully with or without steroids/MMF as offending med stopped
Irreversible damage/chronic TIN if offending drug ongoing
If no clear drug etiology, must look for other causes of TIN:
Systemic illness (i.e. IBD, sarcoidosis)
TINU Syndrome (TIN+uveitis, autoimmune)
Infectious (granulomatous areas on biopsy)
TIN is an under-recognized cause of AKI, remember to think of TIN if sCr disproportionately high + bland urine
[AMA formatted citations]
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