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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Abstract titles should be brief and reflect the content of the abstract.
Primary adrenal insufficiency (PAI) is an uncommon and often overlooked cause of acute kidney injury (AKI). We report two patients referred for progressive renal dysfunction who were ultimately diagnosed with PAI, highlighting a hemodynamic mechanism of prerenal AKI and the reversibility of renal dysfunction with appropriate steroid replacement.
We conducted a descriptive review of two adults with AKI secondary to PAI, both of whom recovered with simple hydrocortisone supplementation.
Case 1: A man in his 80s was referred for evaluation of progressive renal dysfunction. He had loss of appetite and a 2.5-kg weight loss over six months. He had symptomatic hypotension of around 90/50 mmHg that had persisted for approximately one year. His renal function had gradually declined over 19 months, with eGFR decreasing from 50 to 28 mL/min/1.73 m². There was no serologic evidence of intrinsic nephritis. Plasma ACTH levels were markedly elevated, and PAI was suspected. Hydrocortisone replacement therapy was initiated at 15 mg/day, leading to rapid improvement in appetite and an increase in eGFR to 41 mL/min/1.73 m² within two weeks. Four months later, his body weight had returned to baseline, eGFR had risen to 45 mL/min/1.73 m², and blood pressure had improved.
Case 2: A man in his 70s achieved complete remission of follicular lymphoma with obinutuzumab (OBZ) plus bendamustine and received maintenance OBZ. eGFR declined gradually from 60 to 36 mL/min/1.73 m² over six months. He presented with hypotension of around 90/60 mmHg, anorexia, and an 8-kg weight loss over six months. Serum sodium was mildly decreased at 136 mEq/L, and laboratory tests revealed no abnormalities suggestive of glomerulonephritis. Plasma ACTH was 176 pmol/L, cortisol 118.6 nmol/L, and aldosterone was below the detection limit, consistent with PAI; a rapid ACTH stimulation test confirmed the diagnosis. Kidney biopsy showed mild tubulointerstitial injury, insufficient to account for the degree of dysfunction. Prednisolone 30 mg/day plus hydrocortisone 5 mg/day were given for 7 days, followed by hydrocortisone 20 mg/day. The therapy rapidly improved appetite, sodium, blood pressure, and eGFR to 50 mL/min/1.73 m², with subsequent weight gain of 5 kg.
Extracellular volume depletion from mineralocorticoid deficiency is a recognized contributor to PAI-related renal dysfunction; however, anorexia and low salt intake also contributed to prerenal physiology. Glucocorticoid deficiency can also reduce cardiac output, lowering renal perfusion. Although both patients had hypotension, such modest hypotension alone is unlikely to cause marked renal dysfunction. In both cases, the kidney function decline was relatively slow—atypical for simple dehydration or uncomplicated AKI—suggesting mixed acute-on-chronic prerenal factors.
As the use of immune checkpoint inhibitors increases, the incidence of PAI as an immune-related adverse event is rising, and it will become increasingly important to consider PAI as a potential cause of AKI.
When encountering a case of AKI with no apparent cause, PAI should be considered in the differential diagnosis.
