| Abstract|| |
Renal structural abnormalities in HIV/AIDS infected patients have been infrequently and incompletely reported in patients from sub-Saharan Africa. We report an immune complex glomerulonephritis with "lupus-like" features in a ten-year-old HIV+ boy who was evaluated at the University Hospital of Kinshasa. The light microscopic examination of the renal biopsy displayed a predominantly membranoproliferative glomerulonephritis with prominent focal segmental necrotizing injury, numerous wire-loops, and a spiky membranous nephropathy. In addition, there were prominent tubular injury, microcysts filled with periodic acid-Schiff (PAS) positive casts, edema and an inflammatory infiltrate of the interstitium, features of a classic HIV-associated nephropathy (HIVAN). Electron microscopy revealed large subendothelial, intra-membranous, subepithelial and mesangial deposits. The combination of these findings, while being consistent with lupus nephritis WHO grade IV/V, the tubulointerstitial HIVAN-like changes and the absence of clinical evidence of lupus disease favored an HIV-associated immune complex glomerulonephritis with "lupus-like features".
|How to cite this article:|
Pakasa NM, Binda P M. HIV-Associated immune complex glomerulonephritis with "lupus-like" features. Saudi J Kidney Dis Transpl 2011;22:769-73
|How to cite this URL:|
Pakasa NM, Binda P M. HIV-Associated immune complex glomerulonephritis with "lupus-like" features. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2020 Jan 27];22:769-73. Available from: http://www.sjkdt.org/text.asp?2011/22/4/769/82687
| Introduction|| |
Since the recognition of renal involvement in human immune-deficiency virus (HIV)/AIDS disease in 1984,  several abnormalities have been identified. They can be classified broadly into coincidental and specific disorders. The coincidental disorders include acute renal failure, fluid-electrolyte and acid-base disturbances, infections, and neoplasms such as lymphoma, Kaposi sarcoma, and metastatic malignancies. The specific abnormalities are heterogeneous. Although the HIV-related nephropathy (HIVAN) characterized by a combination of a collapsing focal segmental glomerulosclerosis (FSGS) and tubulointerstitial lesions far more predominates this category, increasingly, varieties of immune complex-mediated glomerulonephritis (GN) have been reported. ,,, Few studies have reported the so-called "HIV lupus-like GN". ,,, We report a case of HIV lupus-like GN.
| Case Report|| |
A 10-year-old boy from a remote area of the Democratic Republic of Congo (DRC) (Matadi, Bas-Congo) was seen at the outpatient pediatrics clinic of the University Hospital of Kinshasa in May 1991. The boy was referred by a primary care physician for investigation of persistent massive leg, abdominal, and facial edema unresponsive to protein-rich diet and diuretics. The past medical history was remarkable by the death of his single prostitute mother from HIV/AIDS. The boy was under the care of his uncle, a father of a large and extended African family.
The physical examination disclosed a fairly healthy-looking child with a 4+ pitting generalized edema. There was no evidence of orgamegaly or other pertinent abnormality.
Laboratory investigations revealed 4+ dipstick urinary protein consistent with the nephrotic syndrome. Routine blood and stool examinations were negative for anemia, malaria and common intestinal parasites. Systemic lupus erythematosus (SLE) and Hepatitis B and C serologies were not performed. However, the nephrologist decided to perform a percutaneous renal biopsy and rely on the pathology findings. The first histological impression was that of a pure membrano-proliferative GN (MPGN) with tubular microcyts and severe interstitial changes unusual for a pure MPGN. Enzyme-linked immunoadsorbent assay (ELISA) test was positive for HIV-1 infection.
Three corticomedullary cores were available for histological examination. The overall renal parenchyma architecture was severely disturbed. There were stripes of tubular atrophy and hypertrophy (grade III of IV) and fibrosis [Figure 1]A. A total of 35 glomeruli were present for evaluation, four of which were globally sclerotic. The remaining 31 were slightly enlarged and hypercellular. They showed diffuse, widened Bowman spaces [Figure 1]A-D. The vast majority of the glomeruli [Figure 1]B showed an increase of the mesangial matrix, proliferation of mesangial and endo-capillary cells, and presence of numerous inflammatory cells (monocytes and polymorpho-nuclear cells). The capillary walls were thickened and disclosed diffuse "double contour" pattern of the basement membrane with inter-mesangial matrix, cells and immune deposits ([Figure 1]C(a, b). There were occasional adhesions of the glomerular tufts to the Bowman capsule in three glomeruli [Figure 1]B.
|Figure 1: A: The specimen of the kidney biopsy in the study patient, displaying glomerular, tubular and interstitial structural abnormalities (Masson's trichrome, original magnification ×40).|
Figure 1: B: A glomerular lobular pattern with numerous "double contours", proliferation of resident cells, and immigration of inflammatory cells. A tubular microcyst is conspicuous (periodic acid-Schiff (PAS), original magnification ×150).
Figure 1: C: (a): Thickened basement membranes with numerous double contours and immune deposits.
Figure 1: C: (b): Dense immune deposits in immersion oil (white arrow) (Jones mathanamine stain with Masson's trichrome).
Figure 1: D: Focal and segmental necrotizing changes and wire loops (Masson's trichrome, original magnification ×150).
Figure 1: E: Subepithelial spikes (Jones silver stain, original magnification ×600).
Figure 1: F: A glomerular capillary thrombus (arrow) (Jones silver stain ×375).
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In one-fourth of the glomeruli, focal segmental necrotizing lesions and wire-loops were observed [Figure 1]D. The thickened basement membranes exhibited definite argyrophilic projections on silver stain in two glomeruli [Figure 1]E. A hyaline thrombus was identified in one glomerulus [Figure 1]F. There was a patchy moderate tubular atrophy and patchy marked tubular hypertrophy. Hypertrophied tubules showed prominent tubular cell changes often in single nephrons by the presence PAS positive pale hyaline casts-containing microcysts [Figure 1]B. Rare calcified crystals were also present, but overt acute tubular necrosis was absent. The interstitium showed mild edema, patchy moderate fibrosis, and patchy moderate to marked lymphocytic and plasma-cell infiltrates. The arteries and arterioles showed no conspicuous changes, whereas adjacent veinules were markedly dilated and contained lymphocytes. Electron microscopy on paraffin-embedded retrieval material [Figure 2] showed large mesangial, subendothelial, intramembranous and subepithelial dense deposits with spike formation. There was diffuse foot process effacement. Neither tubuloreticular structures nor deposits in the peritubular basement membranes were observed.
|Figure 2: Electron micrograph. Large subepithelial, intramembranous, subendothelial, and mesangial deposits (uranyl acetate and lead citrate, original magnification ×5.500)|
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| Discussion|| |
The current knowledge establishes three distinctive categories of glomerular involvement during the course of HIV-1/AIDS infection. The most prevalent lesion has been collectively called HIV-nephropathy (HIVAN) which affects about 60% of patients. Black adults are the most affected. They present with heavy proteinuria and hematuria, enlarged echogenic kidneys by ultrasonography, and a rapid progression to renal failure. Histologically, the HIVAN comprises a collapsing FSGN and related mesangiopathies. Secondly, about 10-15% patients develop an immune complex mediated glomerulopathy.  Several reports have demonstrated involvement of hepatitis B or C viral antigens.  IgA nephropathy in human immunodeficiency virus-infected patients has been described with increasing frequency.  Finally, some patients may develop hemolytic uremic syndrome/thrombotic thrombocytopenia purpura.  Additional tubulointerstitial diseases (about 7%) may include acute tubular necrosis, interstitial nephritis, renal involvement by diffuse infiltrative lymphocytes syndrome (DILS), renal infection by a host of pathogens, and renal neoplasms (including lymphoma and Kaposi's sarcoma). Around 3% of patients develop a peculiar immune complex GN, the so-called lupus-like nephritis. Light, immunofluorescence and electron microscopy features of this entity resemble those of classic lupus nephritis in the absence, however, of overt clinical SLE and related serologies. Haas et al  have provided a comprehensive review of this entity and a clinicopathologic study of 14 additional cases. In 1993, Nochy et al  described 10 out of 60 HIV-infected patients (four Blacks, six Whites) with a lupus-like nephritis. Similar findings have also been reported in other studies. ,, Srear and Peraldie  identified only one case of lupus-like nephritis, which completely remitted after six months treatment with antiproteases.
As shown by others,  renal outcome is poor. To the best of our knowledge, this is the first detailed report describing other type of renal involvement in the course of HIV/AIDS than the classic HIVAN from sub-Sahan Africans.
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Nestor M Pakasa
2 Rue du 24 Mars 1852, 69009 Lyon, France
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