Hi,

You can probably check up these interesting works.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0138191

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4153290/

These are mostly from Animal models and the mice which were inoculated with Angiotensin II had reduced parasitemia.

Please, see PLoS ONE September 11, 2018 it is a excellent review

Silva LS, Peruchetti DB, Silva-Aguiar RP, Abreu TP, Dal-Cheri BKA, Takiya CM, et al. (2018)

The angiotensin II/AT1 receptor pathway mediates malaria-induced acute kidney injury. PLoS ONE 13

(9): e0203836

Malaria-induced acute kidney injury (MAKI) is a life-threatening complication of severe

malaria. By activation of the sympathetic nervous system has been observed, due to vasodilation, which in turn leads to stimulation of RAS and a consequent increase in the level of angiotensin II (Ang II) . The effects of Ang II are mediated by specific receptors: AT1 and AT2 . The Ang II/ AT1 receptor pathway plays a central role in the development of the glomerular and tubular injuries observed in AKI from different causes. This effect has been associated with the induction of a pro-inflammatory phenotype promoting immune cell infiltration and cytokine secretion in renal tissue . It has been shown that pro-inflammatory cytokine production is strongly associated with severe malaria . Previously, the Ang II/AT1 receptor pathway was implicated in the modulation of immune cells such as CD4+ and CD8+ T cells and brain damage in experimental CM, modulating the secretion of pro-inflammatory cytokines . Therefore, it is possible to postulate that the Ang II/AT1 receptor pathway is involved in the development of MAKI. To test this hypothesis, in this work we used a well-known murine model of severe malaria, C57BL/6 mice infected by P. berghei ANKA (PbA-infected mice) , treated or not with losartan or captopril, blockers of the Ang II/AT1 receptor pathway. The authors observed that these compounds abolished the increase in secretion of pro-inflammatory cytokines, such as interferon gamma (IFN-γ), interleukin (IL)-6, tumor necrosis factor alpha (TNF-α), and IL-17, avoiding the development of glomerular and tubular injuries in MAKI. These data help us to better clarify the molecular mechanism of pathogenesis of MAKI and suggest a potential strategy for adjuvant treatment with RAS inhibitors in human malaria.