Tubulointerstitial Disease — Written Clinical Reasoning

Model answer — Part A: the PPI creatinine drift

Diagnostic reasoning. Frame it aloud: unexplained subacute AKI with sterile pyuria, modest proteinuria and normal-sized kidneys, four months into a new drug, is acute interstitial nephritis until proven otherwise — and the absence of rash, fever and eosinophilia is the expected modern presentation, not evidence against it [1]. PPIs are a leading culprit precisely because their latency is months and their course is silent; the nationwide case-control data put a severalfold increased risk on current users [5]. State what would refine the probability: the creatinine timeline against the drug chart, white-cell casts on urine microscopy, and exclusion of pre-renal, obstructive and glomerular causes [1]. Name the limits of eosinophiluria if asked — poor sensitivity and specificity, so it steers nothing on its own [3].

Immediate management. Stop the omeprazole today — withdrawal is the one intervention with consistent outcome data, and delay in withdrawal tracks with worse recovery [2]. Document the adverse drug reaction, reconcile the rest of the chart (amlodipine, atorvastatin and metformin are not AIN culprits — keep them, but review need), avoid further nephrotoxins, and monitor potassium, acidosis and urine output [1].

Steroids and deprescribing. Biopsy if the creatinine does not begin recovering after withdrawal, if it worsens, or before committing to steroids — biopsy is the only definitive test and grades the fibrosis that predicts recovery [3]. On steroids, give the examinable synthesis: the evidence is retrospective, benefit concentrates in early, biopsy-proven, significant AKI without contraindication, and a typical regimen is prednisone about 1 mg/kg with a taper over 8–12 weeks — offered as a shared decision in a patient of his age and comorbidity [2] [6]. Close with deprescribing: the PPI needs a genuine indication review and a non-PPI alternative if acid suppression is truly required, because casual re-prescription is how AIN recurs [5].

Model answer — Part B: checkpoint-inhibitor AKI

Assessment. AKI with sterile pyuria nine cycles into pembrolizumab is immune-related AIN until proven otherwise — AIN is the dominant biopsy finding in checkpoint-inhibitor AKI, typically appearing weeks to months into therapy, often alongside other immune-related adverse events [4]. The workup mirrors any AKI (exclude pre-renal, obstructive, sepsis and other nephrotoxins) but the prior probability sits firmly on the immunotherapy; biopsy is warranted if the diagnosis is uncertain or if severity demands certainty before prolonged steroids [4].

Management. Hold the pembrolizumab and start corticosteroids — multicentre data show most patients recover at least partial renal function with this approach [4]. Manage as an immune-related adverse event: document the grade, involve oncology early, and screen for other immune toxicities that travel with it [4].

Advising on further therapy. The strong answer is a negotiation, not a ban: among rechallenged patients, recurrent AKI occurs in a minority, so if pembrolizumab is her best cancer therapy, rechallenge after renal recovery is a legitimate shared decision with close creatinine surveillance and a pre-agreed plan for recurrence [4]. State the alternative plainly — if safer oncologic options exist, take them — and that the decision belongs to the patient, oncology and nephrology together [4].