I recently skipped over a review article in the Dec 22, 2011 edition of the New England Journal of Medicine regarding recent advances in the understanding of the pathogenesis of focal segmental glomerulosclerosis (FSGS). I thought the article would be a complete snoozefest. When my attending assigned the article to me last night, I was less than excited about reading this article and procrastinated throughout the evening.
I found the article striking, however, as soon as I began reading about the ApoL1 gene on Chromosome 22 that is implicated in some genetically predisposed forms of FSGS. According to the article, this gene encodes the plasma factor Apoprotein L1, which has the incredible ability to lyse Trypanosoma brucei brucei - the parasite responsible for sleeping sickness. Naturally, the parasite also evolved. Presently, T. brucei rhodesiense and T. brucei gambiense are resistant to lysis by ApoL1 although some variants may still lyse the former parasite. How clever is nature!
This story is very reminiscent of the link between hemoglobinopathies and G6PD deficiency with malaria. Stumbling upon these type of evolutionary linkages and adaptive mechanisms further drive my love of medicine and, in this case, certainly bolstered the excitement with which I reported on FSGS this morning. The ways in which the world works, interacts, and reciprocates - from the genetic level to the population level astounds me.
Reference:
Vivette D. D'Agati, M.D., Frederick J. Kaskel, M.D., Ph.D., and Ronald J. Falk, M.D. N Engl J Med 2011; 365:2398-2411. December 22, 2011
I found the article striking, however, as soon as I began reading about the ApoL1 gene on Chromosome 22 that is implicated in some genetically predisposed forms of FSGS. According to the article, this gene encodes the plasma factor Apoprotein L1, which has the incredible ability to lyse Trypanosoma brucei brucei - the parasite responsible for sleeping sickness. Naturally, the parasite also evolved. Presently, T. brucei rhodesiense and T. brucei gambiense are resistant to lysis by ApoL1 although some variants may still lyse the former parasite. How clever is nature!
This story is very reminiscent of the link between hemoglobinopathies and G6PD deficiency with malaria. Stumbling upon these type of evolutionary linkages and adaptive mechanisms further drive my love of medicine and, in this case, certainly bolstered the excitement with which I reported on FSGS this morning. The ways in which the world works, interacts, and reciprocates - from the genetic level to the population level astounds me.
Reference:
Vivette D. D'Agati, M.D., Frederick J. Kaskel, M.D., Ph.D., and Ronald J. Falk, M.D. N Engl J Med 2011; 365:2398-2411. December 22, 2011
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