LDL Apheresis Facilitates Dialysis Independence in Podocytopathy-Associated Acute Kidney Injury: Two Case Reports

Minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) are podocytopathies that can lead to nephrotic syndrome (NS) and acute kidney injury (AKI) in severe cases. Although low-density lipoprotein apheresis (LDL-A) is employed for refractory NS, its effectiveness in dialysis-dependent AKI, particularly in elderly or comorbid patients, remains uncertain. This study presents two cases that illustrate the utility of LDL-A in complex scenarios.

We describe two female patients (48 and 76 years) with biopsy-proven podocytopathies (MCD and FSGS) who presented with NS and severe AKI requiring intermittent hemodialysis (HD). AKI was defined according to the KDIGO criteria, and dialysis was initiated due to anuria and volume overload. The clinical course, kidney histology, treatment, and outcomes were reviewed.

Case 1 (MCD, 48 years old; history of MCTD and breast cancer): The patient developed NS and AKI following gastroenteritis-like symptoms after seafood intake. Kidney biopsy confirmed MCD. Methylprednisolone pulses (500 mg/day ×3) started on day 5 of hospitalization, followed by oral prednisolone 60 mg/day. Rituximab was administered on days 17 and 24. Worsening proteinuria (urinary protein 30 g/gCr) and renal dysfunction required HD starting on day 24. A second steroid pulse on day 33 was ineffective. LDL‑A was initiated on day 60 (LDL cholesterol level (LDL-C), 259 mg/dL). After five LDL-A sessions, proteinuria and kidney function improved, allowing for HD cessation on day 73 of hospitalization. By day 115, partial remission of NS (urinary protein, 3.23 g/gCr) and recovery of renal function (serum creatinine, 1.0 mg/dL) were achieved.

Case 2 (FSGS, 76 years): The patient developed rapid-onset NS and AKI in the absence of malignancy or autoimmune disease. Kidney biopsy confirmed FSGS. She received methylprednisolone pulses (500 mg/day ×3) on day 12, followed by oral prednisolone (40 mg/day). Renal function declined, leading to anuria and volume overload, which required the initiation of HD on day 14. Given her age and the risk of infection, LDL‑A was initiated on day 20 (LDL‑C, 301.6 mg/dL). From day 24, proteinuria and kidney function improved significantly. HD was stopped on day 29 after four LDL‑A sessions, with near baseline renal function (serum creatinine, 0.9 mg/dL) and partial remission of NS (urinary protein, 1.01 g/gCr) by day 41. Steroid-induced diabetes and cytomegalovirus antigenemia were treated with temporary insulin and ganciclovir, respectively. 

In two cases of podocytopathy-associated nephrotic syndrome complicated by dialysis-dependent acute kidney injury, LDL-apheresis promoted improvement in proteinuria and renal function, allowing for the withdrawal of dialysis. These results suggest that LDL-apheresis may facilitate renal recovery by mitigating lipid-induced podocyte and endothelial injury. LDL-apheresis not only removes lipoproteins but may also improve glomerular microcirculation and enhance the response to corticosteroid therapy. This modality may support individualized therapy in older or high-risk patients by enabling earlier steroid tapering and reducing the need for additional immunosuppression therapy. Further studies are needed to clarify patient selection, optimal timing, and comparative efficacy.