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Optimized Negative Staining: a High-throughput Protocol for Examining Small and Asymmetric Protein Structure by Electron Microscopy

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Lipoprotein glomerulopathy associated with a mutation in apolipoprotein e.

Riccardo Magistroni¹, Marco Bertolotti², Luciana Furci¹

¹Department of Surgical, Medical, Dental and Morphological Sciences with Transplant Interest, Oncological and Regenerative Medicine, University of Modena and Reggio Emilia.

Clinical Medicine Insights. Case Reports

|December 19, 2013

Summary

Lipoprotein glomerulopathy, linked to rare apolipoprotein E (ApoE) mutations, involves lipid buildup in kidney capillaries. Effective treatment requires aggressive lipid lowering, apheresis, and antihypertensive therapy for remission.

Keywords:

APOE gene mutation glomerular lipid thrombi kidney lipoprotein glomerulopathy mixed hyperlipidemia proteinuria

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Transient Expression of Proteins by Hydrodynamic Gene Delivery in Mice

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Published on: May 5, 2014

Area of Science:

Nephrology
Genetics
Cardiovascular Medicine

Background:

Lipoprotein glomerulopathy is a rare kidney disease characterized by lipid deposits within glomerular capillaries.
It is often associated with specific mutations in apolipoprotein E (ApoE).

Observation:

A case study of a 51-year-old Italian patient with Type III hyperlipidemia and proteinuria.
Renal biopsy revealed capillary ectasia and intraluminal lipid deposits, indicative of lipoprotein glomerulopathy.
The patient was heterozygous for a novel ApoE mutation (Arg150Cys), termed apoEMODENA, leading to ApoE dimer formation.

Findings:

Standard hypolipidemic drugs failed to fully resolve proteinuria and worsened renal function.
Low-density lipoprotein apheresis combined with aggressive lipid-lowering and antihypertensive therapy achieved proteinuria remission and improved renal function.
Plasma filtration was less effective than low-density lipoprotein apheresis in managing renal damage.

Implications:

This case highlights the efficacy of LDL apheresis and comprehensive management in treating lipoprotein glomerulopathy.
The apoEMODENA mutation serves as a new genetic marker for this condition.
Aggressive therapeutic strategies are crucial for managing this complex lipid-related kidney disease.