Lipoprotein glomerulopathy: first case in a white European

Meyrier, Alain; Dairou, F.; Callard, P; Mougenot, B

doi:10.1093/ndt/10.4.546

Cited by 32 publications

(25 citation statements)

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“…As LRP1 is also involved in macrophage infl ammation and signaling ( 16,52,53 ), the impaired interaction of apoE Sendai with LRP1 may also have functional consequences involving lesion infl ammation. Clinical symptoms of LPG vary from mild proteinuria to nephrotic syndrome and chronic renal failure ( 20,54,55 ). LPG recurs in transplanted kidneys, implicating systemic rather than renal factors in the development of the disease ( 21,56 ).…”

Section: Discussionmentioning

confidence: 99%

Macrophage-derived apoESendai suppresses atherosclerosis while causing lipoprotein glomerulopathy in hyperlipidemic mice

Tavori

Fan

Giunzioni

et al. 2014

Journal of Lipid Research

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Section: Discussionmentioning

confidence: 99%

Macrophage-derived apoESendai suppresses atherosclerosis while causing lipoprotein glomerulopathy in hyperlipidemic mice

Tavori

Fan

Giunzioni

et al. 2014

Journal of Lipid Research

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“…Therefore, it seemed that the development of LPG was specific to chronic GVHD model in FcR␥ -/-mice. Actually, two clinical reports noted the recurrence of LPG in the transplanted kidney (4,16,17). Sustained inflammation induced by chronic GVHD might thus be a predisposing factor for LPG.…”

Section: Discussionmentioning

confidence: 99%

“…Many affected patients indeed have features of type III hyperlipidemia, characterized by elevated IDL and high apo E levels, and the glomerulopathy in Japanese patients has been shown to be associated with apo E polymorphism, especially a novel apo E variant (apo E Sendai) (3). However, the single European LPG patient was homozygous for apo E-III, the most common phenotype in whites (4,5). The pathogenic basis of LPG therefore remains unresolved.…”

mentioning

confidence: 99%

Chronic Graft-versus-Host Autoimmune Disease in Fc Receptor γ chain-deficient Mice Results in Lipoprotein Glomerulopathy

Kanamaru¹,

Nakao²,

Shirato³

et al. 2002

Journal of the American Society of Nephrology

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Abstract. Lipoprotein glomerulopathy (LPG) is a unique renal disease characterized by intraglomerular lipoprotein thrombi associated with severe proteinuria and frequent progression to renal failure. The histologic hallmark of LPG is the presence of laminated thrombi, consisting of lipid droplet, within the lumina of dilated glomerular capillaries. The findings of thrombi consisting of lipoproteins raised the possibilities that LPG might be related to a primary abnormality in lipid metabolism. However, the precise pathogenic basis of LPG remains unresolved. It was herein found that chronic graft-versus-host disease (GVHD) induced by the transfer of Ia-incompatible spleen cells from B6.C-H2 bm12 into coisogenic C57BL/6 mice with deficiency of Fc receptor ␥ chain (FcR␥) resulted in glomerulopathy that resembled LPG. The uptake of acetylated LDL was partially decreased in peritoneal macrophages isolated from FcR␥-deficient mice compared with wild-type mice, suggesting that partial impairment of modified LDL uptake might contribute to the development of LPG associated with chronic GVHD in FcR␥-deficient mice. LPG has been suggested to be a disorder of primary abnormality in lipid metabolism; these findings would therefore provide novel insight into the disease process.Lipoprotein glomerulopathy (LPG) is a unique renal disease that is characterized by intraglomerular lipoprotein thrombi associated with severe proteinuria and frequent progression to renal failure (1). Histologically, deposition of thrombus-like substances in markedly dilated glomerular capillaries is observed, which is positively stained for Sudan III or oil red O and contains apo B and apo E. Under electron microscopy, the lipid thrombi are finely, almost concentrically lamellated, with numerous small lipid vacuoles, suggesting that they have been serially deposited within the glomerulus.The findings of thrombi consisting of lipoproteins raised the possibilities that LPG might be related to a primary abnormality in lipid metabolism (2). Many affected patients indeed have features of type III hyperlipidemia, characterized by elevated IDL and high apo E levels, and the glomerulopathy in Japanese patients has been shown to be associated with apo E polymorphism, especially a novel apo E variant (apo E Sendai) (3). However, the single European LPG patient was homozygous for apo E-III, the most common phenotype in whites (4,5). The pathogenic basis of LPG therefore remains unresolved.It has been shown that the transfer of allogenic T cells recognizing a difference at the MHC class II loci into nonirradiated, non-autoimmune mice leads to chronic graft-versushost disease (GVHD), which resembles the clinical feature of SLE, with similar autoantibody specificities, Ig deposition, and renal pathology (6). We had been studying roles of Fc receptors (FcRs) in various disease processes; we therefore induced the chronic GVHD in Fc receptor ␥ chain (FcR␥)-deficient mice to determine whether FcRs contributed to the chronic autoimmune GVHD. FcRs (Fc␥RI, Fc␥RIII, and F...

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“…Apo E phenotypes detected in LPG were E2/E3 9, 11 −13, 15, 18, 23, 24) in the majority of the cases, although phenotypes E4/ E4 10) , E2/E2/E2 14) , E3/E3 16,28) , E4/EM 17) , E1/E3 19,21), E 2/E4 20) , and E2/E5 22) , were also detected (Table 2).…”

Section: A−1 Fabry's Diseasementioning

confidence: 97%