If in Doubt, Biopsy: Unexpected Renal Pathology Proves Critical to Patient Management in Two Interesting Cases
- AKI: Mechanisms - I
November 03, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 103 AKI: Mechanisms
- Madden, Michelle, University Hospital Waterford, Waterford, Waterford, Ireland
- Hamill, Mairead, University Hospital Waterford, Waterford, Waterford, Ireland
- O'Connell, Blathnaid, University Hospital Waterford, Waterford, Waterford, Ireland
- Casey, Robert William, University Hospital Waterford, Waterford, Waterford, Ireland
- Doyle, Brendan, Beaumont Hospital, Dublin, Ireland
- Brown, Catherine M., University Hospital Waterford, Waterford, Waterford, Ireland
- Leavey, Sean F., University Hospital Waterford, Waterford, Waterford, Ireland
We describe two patients who presented with an unexplained elevation in serum creatinine, inconclusive urinalysis and an unexpected rate of eGFR decline leading to kidney biopsy.
A seventy year-old man presented with several days of severe nausea, vomiting and diarrhoea. Creatinine was 8.92mg/dL, eGFR 6ml/min, a decline from a normal estimate when last checked one year prior. With intravenous fluids, creatinine fell to 4.03mg/dL but failed to improve further. Urinalysis was bland and urine ACR 3 mg/mmol. Kidney biopsy showed oxalate crystal deposition in the tubules and secondary acute tubular injury. The patient subsequently reported commencing a daily supplement of 550mg Vitamin C, more than five times the recommended allowance, eighteen months previously. Supplementation was discontinued and dietary counselling provided; twenty-four hour urine collection two weeks later showed a normal oxalate excretion of 27 mg/24 hour. Kidney function improved to stable stage 4, most recent creatinine 2.38mg/dL, nineteen months post biopsy.
An eighty year-old lady was referred by her GP for an eGFR that had fallen from >60 to 33ml/min. Serum creatinine at referral was noted to be 1.45mg/dL, compared to 1.1mg/dL twelve months prior and 0.68mg/dL eighteen months prior. She had no microalbuminuria or hematuria. She was on apixaban for paroxysmal atrial fibrillation. New medications introduced eighteen months prior were pantoprazole and amiodarone. Obstruction and myeloma were outruled and pantoprazole ceased, but creatinine rose further to 1.72mg/dL over three months and kidney biopsy was arranged. The biopsy revealed acute tubular injury with vacuolization of cells. This pattern of drug-induced injury is associated with amiodarone-related phospholipidosis and toxicity in the literature. Amiodarone was discontinued. The patient’s serum creatinine improved and is 1.43mg/dL, eGFR 35ml/min, eighteen months later.
In each of these cases, an unexpected kidney biopsy result critically and favourably altered management. Had these patients been left untreated, there was a significant likelihood of progression to end-stage kidney disease. Whether amiodarone may be an under-appreciated nephrotoxin deserves further research.