Minimal Change Disease with Progression to Focal Segmental Glomerulosclerosis - Support for an Immune-Mediated Disease Continuum

Sep 28, 2026

Minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) are among the most common causes of primary nephrotic syndrome in adults. A 32-year-old woman with biopsy-proven MCD developed worsening renal function unresponsive to first-line corticosteroids. Repeat biopsy showed collapsing FSGS. The patient was effectively treated with plasmapheresis (PLEX), suggesting MCD and FSGS may represent a continuous spectrum of podocyte injury. The case emphasizes earlier consideration of PLEX in nephrotic syndrome with IgG dusting.

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Case Reports Minimal Change Disease with Progression to Focal Segmental Glomerulosclerosis: Support for an Immune-Mediated Disease Continuum Ritika Muthyala, BS1, Abhinav R Thummala, MD2, Michael Neinast, DO3, Justin D Peterson, MD2 1 Texas College of Osteopathic Medicine, University of North Texas Health Science Center, 2 Department of Medicine, David Geffen School of Medicine, 3 Division of Nephrology, David Geffen School of Medicine Journal of Brown Hospital Medicine Vol. 5, Issue 1, 2025 Article Information Keywords: minimal change disease, focal segmental glomerulosclerosis, plasmapheresis, FSGS, MCD [https://doi.org/10.56305/001c.154640](https://doi.org/10.56305/001c.154640) Submitted: August 19, 2025 EST Accepted: December 19, 2025 EST Published: January 01, 2026 EST Abstract Minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) are among the most common causes of primary nephrotic syndrome in adults. A 32-year-old female with diagnosed MCD, characterized by podocyte effacement and immunoglobulin G (IgG) dusting on initial biopsy, developed worsening renal function unresponsive to first-line treatment with corticosteroids. Persistence of symptoms led to repeat biopsy, which identified collapsing FSGS that was effectively treated with plasmapheresis (PLEX). This case explores the hypothesis that MCD and FSGS lie along a continuous spectrum of podocyte injury and emphasizes the need for early consideration of PLEX in the management of nephrotic syndrome associated with IgG dusting. abbreviations MCD: minimal change disease FSGS: focal segmental glomerulosclerosis PLEX: plasmapheresis AKI: acute kidney injury Immunoglobulin G: IgG background Nephrotic syndrome, which is characterized by significant proteinuria secondary to defects in the glomerular filtration barrier, commonly manifests in patients as hypoalbuminemia and periorbital and/or peripheral edema.1 Minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) are two common causes of nephrotic syndrome that are caused by injury to the renal podocytes. While historically described as distinct disease processes, an expanding body of clinical and translational evidence over the last decade supports a continuum of pathology between MCD and immune-mediated FSGS, with MCD representing an early stage of this continuum.2 The recent identification of anti-nephrin antibodies, which are associated with both MCD and immune-mediated FSGS, further supports this continuum and may link the two conditions pathophysiologically.2,3 case presentation A 32-year-old female with a known history of MCD presented to the emergency department at the recommendation of her outpatient nephrologist with symptoms of volume overload, worsening renal function, and emesis. She was diagnosed with MCD via renal biopsy seven months prior (Figure 1) and was initially maintained on furosemide and dual immunosuppressant therapy of cyclosporine and prednisone (down-titrated to 20 mg daily due to prior complications of steroid-induced psychosis and hallucinations). A month prior to admission, she received care at an outside hospital for acute kidney injury (AKI) in the setting of volume overload with a serum creatinine of 8.0 mg/dL on admission (baseline 0.80 mg/ dL, reference 0.5-1.2 mg/dL) . The AKI was thought tobe multifactorial secondary to recent trimethoprim/sulfamethoxazole use for a finger infection and pre-renal injury in the setting of persistent emesis and furosemideuse. Both cyclosporine and furosemide were discontinued during that hospitalization, and she was dischargedon prednisone monotherapy at 40 mg daily. Although her renal function initially improved and creatinine levels stabilized at 3.30 mg/dL, the patient gradually developed recurrent anasarca. This edema was refractory to both escalation of prednisone to 60 mg daily and reinitiation offurosemide at 10 mg daily per outpatient nephrology, prompting t

FAQs

How did the patient’s disease progress from minimal change disease to focal segmental glomerulosclerosis?

The patient initially had biopsy findings consistent with MCD and later developed worsening renal function and persistent symptoms. A repeat biopsy identified collapsing FSGS, indicating progression along a podocyte injury continuum.

Why was plasmapheresis (PLEX) used, and what was the result?

The case supports an immune-mediated disease continuum between MCD and FSGS. The patient was treated effectively with plasmapheresis (PLEX) after the collapsing FSGS diagnosis.

What features suggested an immune-mediated process and IgG involvement?

Initial biopsy showed podocyte effacement with IgG dusting, and repeat biopsy showed punctate IgG podocyte cytoplasmic staining. Despite no clear immune-mediated process on repeat biopsy, the IgG-associated findings motivated early consideration of PLEX.

Sep 28, 2026

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