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Kidney Week

Abstract: SA-PO863

Steroid-Responsive FSGS Secondary to Bisphosphonate Use

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • Ali, Omar, Albany Medical Center, Albany, New York, United States
  • Pal, Aman, Albany Medical Center, Albany, New York, United States
  • Faddoul, Geovani, Albany Medical Center, Albany, New York, United States
  • Monrroy, Mauricio, Albany Medical Center, Albany, New York, United States
Introduction

Focal segmental glomerulosclerosis (FSGS) is a histopathologic renal injury pattern with varying clinical features that poses diagnostic and management challenges. Current KDIGO guidelines recommend immunosuppression to treat primary FSGS, which is associated with nephrotic syndrome and diffuse podocyte effacement (DPE). Secondary FSGS presentations are highly variable, allowing primary and secondary FSGS to have overlapping features. Our case highlights an excellent response to steroids in a patient with secondary FSGS with DPE.

Case Description

A 71-year-old female presenting with an acute on chronic kidney disease stage 3 in the setting of a 2-week history of persistent nausea, vomiting, and diarrhea. Her creatinine was 15.68 mg/dL from a baseline of 1.3mg/dL, with nephrotic-range proteinuria of 4.96g/day and hypoalbuminemia. She started emergent dialysis for acute renal failure and had a renal biopsy showing collapsing FSGS with 100% foot process effacement. Genetic testing revealed a heterozygous mutation for Fanconi anemia. She was on ibandronate for postmenopausal osteoporosis, which was discontinued. She started daily prednisone 60mg and came off dialysis after one month of treatment, with creatinine returning to 1.2mg/dL. A few months later, she continued to have an adequate urine output with appropriate creatinine levels and was tapered to 10mg of prednisone daily. She has remained off dialysis since then and was recently transitioned to oral tacrolimus 0.5mg twice daily due to concerns of steroid-induced myopathy.

Discussion

In our case of FSGS secondary to ibandronate use, the biopsy revealed DPE. Bisphosphonates' exact mechanism of nephrotoxicity remains unclear. However, it was found to directly induce podocytes' loss of differentiation and loss of vital cytoskeletal proteins. This direct insult is similar to the postulated podocyte-toxic factor injury in primary FSGS. The prevalence of bisphosphonate-induced FSGS is well documented. However, its treatment with steroids and immunosuppressants is uncommon. There are reports of successful steroid treatment of secondary FSGS. Our patient demonstrated remarkable recovery after discontinuing ibandronate and starting steroids. She remained off dialysis and returned to her baseline renal function within a few weeks. More studies are needed to validate the role of steroids in secondary FSGS with diffuse podocyte involvement.