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| Year : 2002 | Volume
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| Issue : 4 | Page : 511-512 |
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| The New Molecular Revelations of Recurrent Focal Segmental Glomerulosclerosis in Renal Allografts |
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Anil K Saxena
Post-Graduate Department of Medicine, King Fahad Hospital, Hofuf, Al-Hasa 31982, Saudi Arabia
Click here for correspondence address and email
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How to cite this article:
Saxena AK. The New Molecular Revelations of Recurrent Focal Segmental Glomerulosclerosis in Renal Allografts. Saudi J Kidney Dis Transpl 2002;13:511-2 |
How to cite this URL:
Saxena AK. The New Molecular Revelations of Recurrent Focal Segmental Glomerulosclerosis in Renal Allografts. Saudi J Kidney Dis Transpl [serial online] 2002 [cited 2023 Feb 9];13:511-2. Available from: https://www.sjkdt.org/text.asp?2002/13/4/511/33108 |
To the Editor:
I would like to share with you the new developments in the understanding of the pathogenesis of recurrent focal segmental glomerulosclerosis (FSGS) in the renal allografts in light of the reported experience of the transplant unit in Bahrain by Ratnakar et al, [1] which was recently published in your journal. In that article, the authors reported 9.5% (2/21) graft failures due to recurrence of focal segmental glomerulosclerosis. FSGS tends to recur in 20-40% of patients receiving first kidney transplantation with graft failure in approximately 50% of affected kidneys (10-20%). [2]
It is amazing that a lesion histologically localized to <50% of glomeruli (focal) which involve just segments of glomeruli (segmental) has such a disproportionately devastating impact on the renal allograft survival. Fogo et al showed that the real percentage of glomeruli affected by sclerosis ranged from 30 to 50% in adults. Moreover, they found that 62% of these biopsies when examined meticulously, demonstrated a mixed pattern of lesions. [3] The platelet aggregation studies by LASER aggregometry, platelet Thrornboxane-B2 (TXB2) levels by radioimmunoassay and cyclic AMP (cAMP) levels by binding assays have demonstrated increased platelet aggregability and Thromboxane-B2 release that may possibly be implicated in the pathogenesis of FSGS. By virtue of being potent vasoconstrictor, TXB2 may have an impact on the progression of glomerular damage by augmented vasoconstriction and increased intraglomerular pressure. [4] Savin et al described a circulating factor in serum from FSGS patients that induced increased glomerular permeability (glomerular permeability factor) to albumin. [2] Koyama et al reported a vascular permeability factor (VPF), a postulated lymphokine, which induced nephrotic syndrome by impairing the glomerular basement membrane (GBM) anionic charges. Despite the fact that both, the biochemical nature and the ultimate targets of this factor remain unknown, it reflects a disorder of lymphocyte function, most likely T-lymphocyte. Oliveira et al, described recurrence of FSGS as early as two weeks following renal allograft placement. They also demonstrated strong interleukin-2 (IL-2) and transforming growth factor beta (TGF-i?) synthesis induced by graft infiltrating initiation and progression of early fibrosis and thus glomerulosclerosis. [5] Nevertheless, the above studies may throw some light on the new developments in the understanding of the FSGS pathogenesis.
 References | |  |
| 1. | Ratnakar KS, George S, Datta BN, et al Renal transplant pathology: Bahrain experience. Saudi J Kidney Dis Transplant 2002;13:71-6.  |
| 2. | Savin VJ, Sharma R, Sharma M, et al. Circulating factor associated with increased glomerular permeability to albumin in focal segmental glomerulosclerosis. N Engl J Med 1996;334:878-83. [PUBMED] [FULLTEXT] |
| 3. | Fogo A, Glick AD, Horn SL, Horn RG. Is focal segmental glomerulosclerosis really focal? Distribution of lesions in adults and children. Kidney Int 1995;47:1690-6. |
| 4. | Bereczki C, Turi S, Sallai E, Torday C, Mohacsi G, Sonkodi S. Increased platelet thromboxane release in focal segmental glomerulosclerosis. Nephrol Dial Transplant 1998;13:1604-5. |
| 5. | Koyama A, Fujisaki M, Kobayashi M, Igarashi M, Narita M. A glomerular permeability factor produced by human T cell hybridomas. Kidney Int 1991;40:453-60. [PUBMED] |
Correspondence Address:
Anil K Saxena
Post-Graduate Department of Medicine, King Fahad Hospital, Hofuf, Al-Hasa 31982
Saudi Arabia
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 17660677 
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