# The Pathological Role of LDL in Membranous Nephropathy and Diabetic Nephropathy and the Protective Efficacy of LDL Apheresis: A Narrative Review

## TL;DR

This review discusses how LDL contributes to kidney diseases like diabetic and membranous nephropathy and how LDL apheresis can help treat these conditions.

## Contribution

The paper introduces LDL apheresis as a potential therapeutic strategy for refractory nephrotic syndrome in diabetic and membranous nephropathy.

## Key findings

- LDL, especially oxidized LDL, accelerates kidney injury and reduces immunosuppressant efficacy.
- LDL apheresis can induce remission in patients with refractory nephrotic syndrome due to diabetic and membranous nephropathy.
- A case report shows clinical improvement following LDL apheresis in a patient with concomitant DN and MN.

## Abstract

Diabetic nephropathy (DN) is the leading cause of end-stage kidney disease worldwide. One-third of patients with DN develop primary glomerulonephritis, and membranous nephropathy (MN) is the most common concurrent glomerulonephritis. Nephrotic syndrome (NS) due to DN and MN is often refractory to immunosuppressants because increased levels of low-density lipoprotein (LDL) not only accelerates kidney injury but also reduce the bioavailability of cyclosporine, a first-line immunosuppressant for MN. Given the pathological role of LDL, especially oxidized LDL, reducing LDL cholesterol levels can help achieve remission of NS and halt the progression of kidney injury. Although some lipoproteins are not excreted by the kidneys, excessive LDL, including oxidized LDL, can be considered uremic toxic-like factors that contribute to the development of NS or DN. We encountered a 74-year-old patient with concomitant DN and MN who achieved complete remission following additional LDL apheresis (LDL-A) with immunosuppressant therapy. Here, we provide a narrative review summarizing the role of LDL, especially ox-LDL, in the progression of DN and glomerulonephritis, including MN, and discuss the therapeutic rationale for LDL-A. We also present a representative case of concomitant MN and DN refractory to conventional immunosuppression who achieved clinical improvement following LDL-A.