Tubulointerstitial Disease — Viva Defence

Opening statement (SASPOP, delivered aloud)

"Mrs Marsh is a 76-year-old woman with biopsy-proven acute interstitial nephritis, almost certainly induced by ten months of omeprazole, presenting as a silent creatinine rise without any allergic features — the typical modern phenotype of drug-induced AIN [5]. Her problems are: significant AKI with partial early improvement since drug withdrawal; polypharmacy in an older adult, where deprescribing is both treatment and prevention; a decision about corticosteroids on incomplete evidence; and the need for honest counselling about slow and possibly incomplete renal recovery. My priorities are to consolidate drug withdrawal, finish the steroid decision with her, protect her from re-exposure, and arrange structured renal follow-up." [1] [2]

Structured problem list

1. Biopsy-proven AIN with significant AKI — active inflammation with only mild fibrosis, which is the histology most likely to benefit from early treatment [2].
2. Iatrogenic drug injury (omeprazole) — requires permanent withdrawal, adverse-reaction documentation and pharmacovigilance reporting; PPIs carry a severalfold increased AIN risk and a characteristically silent, late presentation [1] [5].
3. Polypharmacy in an older adult — the medication chart needs a formal indication-by-indication review, not just removal of the culprit [1].
4. Reflux management without a PPI — a genuine symptom need that must be addressed deliberately, not by casual re-prescription [5].
5. Recovery uncertainty and CKD risk — long-term series show incomplete recovery is common even with treatment, so follow-up is part of the therapy [3].

Integrated management plan

• Consolidate withdrawal: confirm omeprazole is ceased everywhere — GP record, pharmacy, discharge summary — and recorded as an adverse drug reaction with a do-not-rechallenge note, because AIN is immune-mediated and re-exposure can trigger recurrence [2].
• Steroid decision, shared: offer prednisone about 1 mg/kg with an 8–12 week taper, framed honestly — the evidence is retrospective, benefit concentrates in early biopsy-proven disease like hers, and prolonged courses add nothing [2] [4]. In a 76-year-old, I would explicitly weigh diabetes risk, infection, delirium and myopathy, and document her view [3].
• Deprescribing review: amlodipine, atorvastatin, metformin and alendronate are not AIN culprits — continue with indication checks; the discipline is reviewing each agent for ongoing need at her age and eGFR (metformin dosing, alendronate renal thresholds) [1].
• Reflux plan: trial of withdrawal with alginate/H2-blocker cover if needed, lifestyle measures, and a clear statement that PPI re-introduction requires specialist discussion [5].
• Follow-up: creatinine through the recovery arc over weeks to months, blood pressure and proteinuria surveillance, and nephrology review if function plateaus below baseline — because CKD after AIN is a real outcome, not a failure of the admission [3].

Probing questions with model answers

"She had no rash, no fever, normal eosinophils. Why did you even suspect AIN?" — "Because that is what modern AIN looks like. The classic triad is present in only a small minority of biopsy-proven drug-induced cases; the consistent signal is the drug timeline with a subacute creatinine rise and sterile pyuria. Her ten months of omeprazole with an otherwise unexplained drift was the diagnosis waiting for a biopsy." [5] [1]

"Defend giving steroids to a 76-year-old when there is no trial." — "I defend it as a shared, explicit decision, not a reflex. Three retrospective anchors: González showed early steroid treatment improved recovery; the large multicentre series found benefit concentrated in those treated early; and the duration study found prolonged courses added nothing. She is early, biopsy-proven, significantly injured, and has only mild fibrosis — the profile with the most to gain. I would tell her plainly that drug withdrawal is the proven part and steroids the uncertain part, and I would respect a decision either way." [2] [3] [4]

"Why did you biopsy rather than just stop the drug and watch?" — "Her AKI was significant and I was contemplating immunosuppression in an older adult — that decision deserves histology. Biopsy confirmed the diagnosis, excluded granulomatous or IgG4-related disease that would change management, and graded the fibrosis, which is the strongest predictor of how much function she gets back." [2] [3]

"What stops this happening again?" — "Three things: the reaction is documented and reported so no prescriber restarts a PPI blindly; her chart is reconciled so every agent has an indication; and she leaves understanding that her kidney injury was drug-related, what the early warning was, and that her creatinine needs checking through recovery." [1] [5]

"Her creatinine plateaus at 140. What do you tell her?" — "That this is within the expected range of outcomes — recovery from AIN runs over weeks and is often incomplete, and the long-term series show many patients keep some CKD. It does not mean the treatment failed: it means inflammation scarred some of the interstitium before it was treated. We protect what remains — blood pressure, avoiding nephrotoxins, no re-exposure — and follow her formally." [3] [2]

Communication points

• Open disclosure: an iatrogenic injury is named, explained and apologised for, with the learning documented [1].
• Shared decision-making on steroids: observational evidence stated as such, her risks and priorities weighed [2] [4].
• Recovery counselling: slow, possibly incomplete — set the expectation early rather than at the plateau [3].