Synopsis
Recognise chronic tubular and interstitial kidney injury, distinguish analgesic-associated papillary disease from other causes, and prevent avoidable progression or obstruction.
- Chronic tubulointerstitial nephritis describes tubular atrophy and interstitial fibrosis caused by sustained toxic, metabolic, immune, infective, obstructive or inherited injury.
- Typical clues are slowly declining eGFR, relatively modest albuminuria, a bland or low-grade urinary sediment, concentrating impairment and tubular electrolyte or acid-base abnormalities.
- Review prescribed medicines, over-the-counter analgesics, combination products, supplements, occupational exposures and previous chemotherapy; a standard medication list may miss the cause.
Key red flags
Flank pain, visible haematuria, sterile pyuria or passage of tissue may indicate papillary necrosis, with sloughed material capable of obstructing the ureter.
Investigation priorities
Confirm chronicity and detect tubular or dangerous metabolic complications.
Management branches
Chronic kidney impairment has a tubular or bland-sediment pattern.
- Reconstruct prescribed and non-prescribed analgesic, lithium, antimicrobial, chemotherapy, supplement and occupational exposures with approximate dose and duration.
- Map creatinine, urine and electrolyte changes against exposure, dehydration, infection and obstruction events rather than relying on the latest result.
Key medicines
NSAID withdrawal or avoidanceDo not prescribe a replacement NSAID dose for suspected analgesic nephropathy; review indication and stop or minimise exposure with the responsible clinician.
ParacetamolIf appropriate, use the lowest effective licensed dose within the current BNF maximum and reduce or avoid it where liver disease, low body weight or interacting factors require.