Tubulo-interstitial kidney disorders
Acute and chronic tubulointerstitial nephritis beyond drugs (TINU, sarcoid, Sjögren, IgG4), the tubular syndromes that give it away (Fanconi, RTA, concentrating defects), papillary necrosis, analgesic and lithium nephropathy, and ADTKD.
Tier 2Condition
Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made
At a glance
- Tubulointerstitial disease injures the tubules and interstitium rather than the glomeruli. It causes about 15 to 20% of AKI biopsies and a share of CKD with bland urine.
- Acute interstitial nephritis (AIN) is drug-induced in about 70%. The drug culprits, steroid dosing and urine eosinophils are covered in Drug-related nephrotoxicity; this note covers the rest.
- Clues: sterile pyuria, low-grade proteinuria, AKI without much haematuria, and tubular dysfunction out of proportion to the GFR (RTA, potassium or phosphate wasting, polyuria).
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Sources
- Therapeutic Guidelines: Kidney and UrinaryAU/NZTherapeutic Guidelines Ltd, 2026
- KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney International Supplements 2012;2:1-138Kidney Disease Improving Global Outcomes, 2012 (2026 AKI/AKD update: public review completed, final not yet published)
- Perazella MA, Markowitz GS. Drug-induced acute interstitial nephritis. Nat Rev Nephrol 2010;6:461-70Nature Reviews Nephrology, 2010
- Eckardt KU et al. Autosomal dominant tubulointerstitial kidney disease: diagnosis, classification, and management. A KDIGO consensus report. Kidney Int 2015;88:676-83Kidney Disease Improving Global Outcomes, 2015
- Wallace ZS et al. The 2019 ACR/EULAR classification criteria for IgG4-related disease. Ann Rheum Dis 2020;79:77-87Annals of the Rheumatic Diseases, 2019
- Last updated
- 14 November 2026
What changed
- 14 November 2026 Turnstile bot check on sign-in and signed-out feedback