Retinal findings in a patient with mesangial proliferative glomerulonephritis
DOI:
https://doi.org/10.70313/2718.7446.v18.n3.434Keywords:
mesangial proliferative glomerulopathy, retina, optical coherence tomography, glomerulonephritisAbstract
Objective. Mesangial proliferative glomerulopathy (MPG) is characterized by the proliferation of mesangial cells with extracellular matrix accumulation. The aim of this article is to describe retinal findings in the fundoscopy of a patient with MPG.
Case report. A 34-year-old female presented for a routine check-up. She had a medical history of bronchial asthma, hypertension (HTN), and MPG with IgM deposits, which required renal transplantation. On examination, her visual acuity was 10/10 in both eyes. Fundoscopy revealed multiple round lesions smaller than ¼ of the optic disc diameter in the posterior pole, affecting the macula, perifoveal areas, and 360° of the peripheral retina. Optical coherence tomography (OCT) showed posterior profile alterations consistent with drusen-like deposits at the retinal pigment epithelium (RPE), and multiple hyperreflective images indicative of RPE alterations were observed in the retinofluoresceinography. Additionally, visual field studies revealed isolated scotomas in both eyes, and the electroretinogram showed normal characteristics.
Conclusion. As demonstrated in this case, retinal findings in MPG provide valuable information about ocular involvement in mesangial proliferative glomerulopathy and enable the monitoring of these patients for early detection and/or prevention of potential complications.
Downloads
References
1. Yang Y, Zhang Z, Zhuo L, Chen DP, Li WG. The spectrum of biopsy-proven glomerular disease in China: a systematic review. Chin Med J (Engl) 2018; 131(6): 731-735. doi:10.4103/0366-6999.226906.
2. Woo KT, Chan CM, Chin YM et al. Global evolutionary trend of the prevalence of primary glomerulonephritis over the past three decades .Nephron Clin Pract 2010; 116(4): c337-c346. doi:10.1159/000319594.
3. Zhou FD, Zhao MH, Zou WZ, Liu G, Wang H. The changing spectrum of primary glomerular diseases within 15 years: a survey of 3331 patients in a single Chinese centre. Nephrol Dial Transplant 2009; 24(3): 870-876. doi:10.1093/ndt/gfn554.
4. Couser WG, Johnson RJ. Mechanisms of progressive renal disease in glomerulonephritis. Am J Kidney Dis 1994; 23(2): 193-198. doi:10.1016/s0272-6386(12)80971-1.
5. Kashgarian M, Sterzel RB. The pathobiology of the mesangium. Kidney Int 1992; 41(3): 524-529. doi:10.1038/ki.1992.74.
6. Cebeci Z, Bayraktar S, Oray M, Kir N. Multimodal imaging of membranoproliferative glomerulonephritis type II. Saudi J Ophthalmol 2016; 30(4): 260-263. doi:10.1016/j.sjopt.2016.11.005.
7. Mansour AM, Lima LH, Arevalo JF et al. Retinal findings in membranoproliferative glomerulonephritis. Am J Ophthalmol Case Rep 2017; 7: 83-90. doi:10.1016/j.ajoc.2017.06.011.
8. Ulbig MR, Riordan-Eva P, Holz FG, Rees HC, Hamilton PA. Membranoproliferative glomerulonephritis type II associated with central serous retinopathy. Am J Ophthalmol 1993; 116(4): 410-413. doi:10.1016/s0002-9394(14)71397-2.
9. D’souza YB, Jones CJ, Short CD, Roberts IS, Bonshek RE. Oligosaccharide composition is similar in drusen and dense deposits in membranoproliferative glomerulonephritis type II. Kidney Int 2009; 75(8): 824-827. doi:10.1038/ki.2008.658.
10. Bai J, Geng W, Mei Y et al. Effect of Huaier on the proliferation of mesangial cells in anti-thy-1 nephritis. Cell Physiol Biochem 2017; 42(6): 2441-2452. doi:10.1159/000480198.
11. Striker LJ, Doi T, Elliot S, Striker GE. The contribution of glomerular mesangial cells to progressive glomerulosclerosis. Semin Nephrol 1989; 9(4): 318-328.
12. Lai KN, Wang AY. IgA nephropathy: common nephritis leading to end-stage renal failure. Int J Artif Organs 1994; 17(9): 457-460.
13. Zhang A, Han Y, Wang B, Li S, Gan W. Beyond gap junction channel function: the expression of Cx43 contributes to aldosterone-induced mesangial cell proliferation via the ERK1/2 and PKC pathways. Cell Physiol Biochem 2015; 36(3): 1210-1222. doi:10.1159/000430291.
14. Gómez-Guerrero C, Hernández-Vargas P, López-Franco O, Ortiz-Muñoz G, Egido J. Mesangial cells and glomerular inflammation: from the pathogenesis to novel therapeutic approaches. Curr Drug Targets Inflamm Allergy 2005; 4(3): 341-351. doi:10.2174/1568010054022169.
15. Tamouza H, Chemouny JM, Raskova Kafkova L et al. The IgA1 immune complex-mediated activation of the MAPK/ERK kinase pathway in mesangial cells is associated with glomerular damage in IgA nephropathy. Kidney Int 2012; 82(12): 1284-1296. doi:10.1038/ki.2012.192.
16. Chiang CK, Sheu ML, Hung KY, Wu KD, Liu SH. Honokiol, a small molecular weight natural product, alleviates experimental mesangial proliferative glomerulonephritis. Kidney Int 2006; 70(4): 682-689. doi:10.1038/sj.ki.5001617.
17. Gao J, Wu L, Wang Y et al. Knockdown of Cxcl10 inhibits mesangial cell proliferation in murine habu nephritis via ERK signaling. Cell Physiol Biochem 2017; 42(5): 2118-2129. doi:10.1159/000479914.
18. Duvall-Young J, Short CD, Raines MF, Gokal R, Lawler W. Fundus changes in mesangiocapillary glomerulonephritis type II: clinical and fluorescein angiographic findings. Br J Ophthalmol 1989; 73(11): 900-906. doi:10.1136/bjo.73.11.900.
19. Duvall-Young J, MacDonald MK, McKechnie NM. Fundus changes in (type II) mesangiocapillary glomerulonephritis simulating drusen: a histopathological report. Br J Ophthalmol 1989; 73(4): 297-302. doi:10.1136/bjo.73.4.297.
20. Han DP, Sievers S. Extensive drusen in type I membranoproliferative glomerulonephritis. Arch Ophthalmol 2009; 127(4): 577-579. doi:10.1001/archophthalmol.2009.38.
21. Pauleikhoff D, Barondes MJ, Minassian D, Chisholm IH, Bird AC. Drusen as risk factors in age-related macular disease. Am J Ophthalmol 1990; 109(1): 38-43. doi:10.1016/s0002-9394(14)75576-x.
22. Guigui B, Leveziel N, Martinet V et al. Angiography features of early onset drusen. Br J Ophthalmol 2011; 95(2): 238-244. doi:10.1136/bjo.2009.178400.
23. Gass JD. Stereoscopic atlas of macular diseases. St Louis: C. V. Mosby, 1977.
24. Leys A, Vanrenterghem Y, Van Damme B, Snyers B, Pirson Y, Leys M. Fundus changes in membranoproliferative glomerulonephritis type II: a fluorescein angiographic study of 23 patients. Graefes Arch Clin Exp Ophthalmol 1991; 229(5): 406-410. doi:10.1007/BF00166300.
25. Stone EM, Lotery AJ, Munier FL et al. A single EFEMP1 mutation associated with both Malattia Leventinese and Doyne honeycomb retinal dystrophy. Nat Genet 1999; 22(2): 199-202. doi:10.1038/9722.
26. Pager CK, Sarin LK, Federman JL et al. Malattia leventinese presenting with subretinal neovascular membrane and hemorrhage. Am J Ophthalmol 2001; 131(4): 517-518. doi:10.1016/s0002-9394(00)00821-7.
27. Piguet B, Haimovici R, Bird AC. Dominantly inherited drusen represent more than one disorder: a historical review. Eye (Lond) 1995; 9 (Pt 1): 34-41. doi:10.1038/eye.1995.5.
28. Mullins RF, Aptsiauri N, Hageman GS. Structure and composition of drusen associated with glomerulonephritis: implications for the role of complement activation in drusen biogenesis. Eye (Lond) 2001; 15(Pt 3): 390-395. doi:10.1038/eye.2001.142.
29. Mullins RF, Russell SR, Anderson DH, Hageman GS. Drusen associated with aging and age-related macular degeneration contain proteins common to extracellular deposits associated with atherosclerosis, elastosis, amyloidosis, and dense deposit disease. FASEB J 2000; 14(7): 835-846.
30. Einbock W, Moessner A, Schnurrbusch UE, Holz FG, Wolf S; FAM Study Group. Changes in fundus autofluorescence in patients with age-related maculopathy. Correlation to visual function: a prospective study. Graefes Arch Clin Exp Ophthalmol 2005; 243(4): 300-305. doi:10.1007/s00417-004-1027-3.
31. D’souza Y, Short CD, McLeod D, Bonshek RE. Long-term follow-up of drusen-like lesions in patients with type II mesangiocapillary glomerulonephritis. Br J Ophthalmol 2008; 92(7): 950-953. doi:10.1136/bjo.2007.130138.
Downloads
Published
Issue
Section
License
Copyright (c) 2025 Consejo Argentino de Oftalmología

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
Con esta licencia no se permite un uso comercial de la obra original, ni la generación de obras derivadas. Las licencias Creative Commons permiten a los autores compartir y liberar sus obras en forma legal y segura.