**2. Chagas disease**

Chagas disease (or American trypanosomiasis) is the infection caused by the flagellated protozoan *Trypanosoma cruzi* and transmitted by insects of the family Triatominae, the *Triatoma infestans*, known as "kissing bugs" (in Brazil: "barbeiro"; in Argentina, Bolivia, Chile, and Paraguay: "vinchuca"; in Colombia: "pito"; in Venezuela: "chipo"; and in Central America: "chinche") [2]. The transmission occurs through the inoculation of *T. cruzi* in the blood of the host, through the insect stool left next to the site of the bites. The infection can also occur through the ingestion of the infected insects (contaminated food), blood transfusion, organ donation, or vertical transmission [3]. Kidney involvement in Chagas disease is seldom described and rarely studied [4].

The disease is endemic in 21 Latin American countries, and the highest prevalence is registered in Bolivia, Argentina, Paraguay, Ecuador, El Salvador, and Guatemala [3]. In Brazil, there was a significant decrease in incidence due to the vector control program, and now the disease is predominantly seen as chronic cases with cardiac or gastrointestinal manifestations [5, 6].

Clinical manifestations of Chagas disease can be divided into acute and chronic phase [3, 4]. The acute phase manifests with fever, signs of inflammation at the inoculation site, unilateral palpebral edema (Romaña sign), lymphadenopathy, and hepatosplenomegaly [3]. Severe acute Chagas infection is rare and occurs in less than 5% of the cases, manifesting with acute myocarditis, pericardial effusion, and meningoencephalitis [3]. The chronic phase develops in 10–30% of infected individuals and is characterized by heart disease and gastrointestinal disease (megaesophagus and megacolon) [7, 8].

*T. cruzi* has the ability to act as a parasite to a great variety of cells, including kidney cells [4]. There is evidence of functional and structural kidney abnormalities after *T. cruzi* infection, associated with reduction in renal blood flow, proximal tubular damage, and inflammatory interstitial infiltrate. An observation is made of an increased production of pro-inflammatory cytokines and nitric oxide, as well as renal function loss associated with high parasitic load [9–12]. In the acute phase, the renal lesion is related to cardiovascular dysfunction, due to a transitory decrease in renal blood flow, which was demonstrated in experimental models [11, 13]. Glomerulonephritis is reported in *T. cruzi* infection and also demonstrated in experimental studies [14, 15]. The pathophysiology of kidney involvement in Chagas disease is associated with immunological process and includes autoantibodies production [16, 17]. There are reports that in the chronic phase of the disease, glomerular deposits of IgM occur at early stages, with intense inflammatory response, resulting in immune complex formation, which leads to glomerulonephritis [9]. The exact mechanism by which *T. cruzi* causes kidney disease is still to be elucidated [4].

Treatment of Chagas disease is based on antitrypanosomal drugs, which is indicated for all acute and congenital cases, reactivated cases, and chronic disease in individuals <18 years [3]. Specific treatment is currently recommended even for patients with the chronic forms of the disease, despite achieving lower cure rates than in acute phase [6]. The main available drugs are benznidazole (dose for adults: 5 mg/kg/day; for children: 5–10 mg/kg/day) and nifurtimox (dose for adults: 8–10 mg/kg/day; for children: 15 mg/kg/day), for 60 days.
