Background: Renal interstitial foam cells (FCs) are occasionally observed in various renal diseases. The goal of the present study was to determine the relationship between the formation of renal interstitial FCs and the degree of proteinuria and hyperlipidemia, as well as the progression of these diseases. Methods: 125 patients with Alport syndrome (AS), 192 patients with idiopathic membranous nephropathy (IMN), 388 patients with IgA nephropathy (IgAN), and 137 patients with focal segmental glomerulosclerosis (FSGS) were investigated retrospectively. Results: FCs were observed in various glomerular diseases. The frequency of interstitial FCs was 64.8% in AS, 21.4% in MN, 12.4% in IgAN, and 36.5% in FSGS. Regardless of the pathologic diagnosis of the glomerular disease, segmental glomerular sclerosis occurred more frequently in patients with FCs than in patients without FCs. In the AS or IgAN group, interstitial fibrosis was more severe, and levels of proteinuria and serum lipids were significantly higher in FC-positive patients than in patients without FCs. Conclusion: FC formation in renal interstitium is associated with the degree of proteinuria and hyperlipidemia in patients with AS and IgAN. The presence of FCs in renal interstitium may contribute to the progression of glomerular diseases.

Keywords:
Foam cells, Alport syndrome, Glomerulonephritis, Proteinuria, Hyperlipidemia
1.
Risdon RA, Sloper JC, De Wardenner HE: Relationship between renal function and histological changes found in renal biopsy specimens from patients with persistent glomerular nephritis. Lancet 1968;2:363–366.
2.
Nath KA: The tubulointerstitium in progressive renal disease. Kidney Int 1998;54:992–994.
3.
Mackensen-Haen S, Bader R, Grund KE, Bohle A: Correlation between renal cortical interstitial fibrosis, atrophy of proximal tubules and impairment of glomerular filtration rate. Clin Nephrol 1981;15:167–171.
4.
Bazzi C, Petrini C, Rizza V, Arrigo G, Beltrame A, D’Amico G: Characterization of proteinuria in primary glomerulonephritides. SDS-PAGE patterns: clinical significance and prognostic value of low molecular weight (‘tubular’) proteins. Am J Kidney Dis 1997;29:27–35.
5.
Eddy AA: Interstitial nephritis induced by protein-overload proteinuria. Am J Pathol 1989;135:719–733.
6.
Mezzano SA, Barria M, Droguett MA, Burgos ME, Ardiles LG, Flores C, Egido J: Tubular NF-κB and AP-1 activation in human proteinuric renal disease. Kidney Int 2001;60:1366–1377.
7.
Nakatsuji S, Yamate J, Sakuma S: Macrophages, myofibroblasts, and extracellular matrix accumulation in interstitial fibrosis of chronic progressive nephropathy in aged rats. Vet Pathol 1998;35:352–360.
8.
Sean Earley K, Cockwell P: Macrophages and progressive tubulointerstitial disease. Kidney Int 2005;68:437–455.
9.
Magil AB: Intertitial foam cells and oxidized lipoprotein in human glomerular disease. Mod Pathol 1999;12:33–40.
10.
Nolasco F, Cameron JS, Reuben R, Hartley B, Carvalho F, Coelho RA: Interstitial foam cells in the nephrotic syndrome belong to the monocyte/macrophage lineage. Proc Eur Dial Transplant Assoc Eur Ren Assoc 1984;21:666–671.
11.
Kurihara I, Saito T, Soma J, Sato H, Hotta O, Taguma Y, Ito S: Clinicopathological characteristics of interstitial foam cells in membranous nephropathy. Kidney Int Suppl 1999;71:S144–S146.
12.
Poucell S, Thoner P, Balfe JW, Baumal R: Interstitial foam cells in renal biopsies: an aid in differentiating idiopathic membranoproliferative glomerulonephritis (type I) and membranoproliferative glomerulonephritis associated with systemic lupus erythematosus. Child Nephrol Urol 1988–89;9:106–111.
13.
Kurihara I, Hotta O, Taguma Y, Kurosawa K, Sudo K, Horigome I, Munakata T, Hirai M, Soma J, Sato H, Oguchi K, Saito T: A case of IgA nephropathy with numerous interstitial foam cells – analysis of infiltrating mononuclear leucocytes in renal tissue. Jpn J Nephrol 1994;36:774–778.
14.
Franco M, Schmitt F, Rejaili WA, Viero RM, Bacchi CE: Renal interstitial foam cells are macrophages. Histopathology 1992;20:173–176.
15.
Pasqui AL, Bova G, Maffei S, Auteri A: Immune factors in atherosclerosis. Ann Ital Med Int 2005;20:81–89.
16.
Choudhury RP, Lee JM, Greaves DR: Mechanisms of disease: macrophage-derived foam cells emerging as therapeutic targets in atherosclerosis. Nat Clin Pract Cardiovasc Med 2005;2:309–315.
17.
Kriszbacher I, Koppan M, Bodis J: Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med 2005;353:429–430.
18.
Bobryshev YV: Monocyte recruitment and foam cell formation in atherosclerosis. Micron 2006;37:208–222.
19.
Yoshimoto K, Wada T, Furuichi K, Sakai N, Iwata Y, Yokoyama H: CD68 and MCP-1/CCR expression of initial biopsies reflect the outcomes of membranous nephropathy. Nephron Clin Pract 2004;98:c25–c34.
20.
Schwartz CJ, Valente AJ, Sprague EA, Kelley JL, Nerem RM: The pathogenesis of atherosclerosis: an overview. Clin Cardiol 1991;14(suppl 1):I1–I16.
21.
Watanabe T, Hattori F, Tanaka K: An experimental study on the origin of foam cells in glomerulonephritis. Acta Pathol Jpn 1982;32:371–383.
22.
White RH, Raafat F, Milford DV, Komianou F, Moghal NE: The Alport nephropathy: clinicopathological correlations. Pediatr Nephrol 2005;20:897–903.
23.
Berfield AK, Abrass CK: IGF-1 induces foam cell formation in rat glomerular mesangial cells. J Histochem Cytochem 2002;50:395–403.
24.
Hansson GK: Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med 2005;352:1685–1695.
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