爱肾分享 |HIV-Associated Immune Complex Kidney Disease...

AJKDAtlas of Renal Pathology: HIV-Associated Immune Complex Kidney Disease (HIVICK)

Agnes B. Fogo, MD,1 Mark A. Lusco, MD,1Behzad Najafian, MD,2 and Charles E. Alpers, MD2

Clinicaland Pathologic Features

Kidney disease is a common manifestation inHIV-infected patients. The spectrum of disease in HIV-infected patients varies,from HIV-associated nephropathy (HIVAN), which is manifest by collapsingglomerulopathy,to usual FSGS, minimal change disease, thromboticmicroangiopathy, and lupus-like HIVimmune complex kidney disease (HIVICK).Other immune complex diseases may also occur in HIV-infected patients,including IgA nephropathy and postinfectious glomerulonephritis, and are bestdiagnosed as those specific entities. We thus restrict the diagnosis of HIVICKto the lupus-like lesions that are seen in some HIV-infected patients, withoutserologic evidence of lupus. HIVICK varies in frequency depending on thepopulation studied. In HIV-infected patients of nonAfrican ancestry with kidneybiopsy, HIVICK appears to be more frequent than HIVAN. Patients with HIVICKhave varying kidney manifestations, depending on the location and extent ofglomerular deposits. A minority has concurrent HIVAN lesions. Proteinuria, whichmay be nephrotic, hematuria, reduced GFR, and low levels of complement arecommon. Patients may present at any age. Prognosis appears better than forHIVAN.

Light microscopy: Variable mesangial andfocal or diffuse endocapillary hypercellularity are seen, with an occasionalmembranous pattern with corresponding pinpoint-hole appearance and spikes ofthe glomerular basement membrane on silver stain. Immunofluorescencemicroscopy: “Full-house” staining with IgG, IgA, IgM, C3, and C1q granularstaining in the mesangium and capillary loops.

Electron microscopy: Variable deposits areseen, including mesangial, subendothelial, and subepithelial deposits, thelatter extensive in cases with a membranous pattern. Tubuloreticular aggregatesare present in endothelial cells. Tubuloreticular aggregates may be decreasedor even absent in patients with low viral loads being treated with combinationantiretroviral therapy.

Etiology/Pathogenesis

HIVICK is due to HIV infection, withaberrant immune regulation and increased gamma globulin contributing to immunecomplex formation. This may involve HIV p24 (capsid) and gp120 (envelope)antigens as targets. APOL1 risk allele variants, common in African Americans,are not associated with increased frequency of HIVICK.

DifferentialDiagnosis

Lupus nephritis has similar morphologicfeatures. Distinction must be made on clinical grounds. The “ball-in-cup”appearance of some subepithelial deposits is not, in our opinion, specific forHIVICK, and may also be seen in lupus nephritis with membranous features.

KeyDiagnostic Features

-Variable mesangial and endocapillaryhypercellularity, with occasional membranous features

-Tubuloreticular aggregates in endothelialcells

-“Full-house” staining byimmunofluorescence, with mesangial and variable capillary wall granulardeposits

-Immune complex deposits by electronmicroscopy; mesangial, subendothelial, and variable subepithelial locations

Figure1. HIV-associated immune complex kidney diseasewith mesangial proliferation (periodic acid–Schiff stain).

Figure2. HIV-associated immune complex kidney diseasewith “full-house” staining in the mesangium (immunofluorescence microscopy, IgGand C1q).

Figure3. HIV-associated immune complex kidney diseasewith mesangial deposits (electron microscopy).

Figure4. HIV-associated immune complex kidney diseasewith tubuloreticular aggregate present in endothelial cell (electronmicroscopy). - Atlas of Renal Pathology II e10 Am J Kidney Dis.;68(2):e9-e10

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