Key result
Gemfibrozil reduces glomerular foam cells despite worsening proteinuria in a familial dysbetalipoproteinemia case.
Why the study?
The potential role of lipid abnormalities in renal dysfunction in patients with familial dysbetalipoproteinaemia and proteinuria is not well characterized.
Does gemfibrozil improve glomerular lipid deposition in a patient with familial dysbetalipoproteinaemia?
Case Report (n=1)
Does gemfibrozil improve glomerular lipid deposition in a patient with familial dysbetalipoproteinaemia?
This case highlights the potential role of lipid abnormalities in renal dysfunction and demonstrates that lipid-lowering therapy can reduce glomerular lipid deposition, even if proteinuria worsens.
Gemfibrozil-associated histologic improvement in this apoE E2/E2 case leaves open whether lipid-lowering alters renal outcomes; prospective studies needed.
This report describes a male patient who was found to have proteinuria at age 31. Renal biopsy showed glomerular hypercellularity with enlarged, lipid-filled endocapillary cells. On subsequent lipid analysis there was elevation of cholesterol and triglyceride, with apolipoprotein E genotype E2/E2. The clinical course was complicated by pancreatitis and onset of diabetes. After treatment with gemfibrozil and some improvement of the lipid profile, a second renal biopsy showed marked reduction of the glomerular foam cells, despite an increased level of proteinuria. This case emphasizes the potential role that lipid abnormalities may play in renal dysfunction.
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BALSON et al. (1996) conducted a case report in Familial dysbetalipoproteinaemia with proteinuria (n=1). Gemfibrozil was evaluated on Glomerular lipid deposition and proteinuria. Treatment with gemfibrozil in a 31-year-old male with familial dysbetalipoproteinaemia reduced glomerular foam cells on repeat biopsy, despite an increased level of proteinuria.
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