While several hundred parasites – in fact 342 species – can infect humans, only 20 of them are associated with kidney disorders. Of these, plasmodia, schistosomes, filariae, and leishmanias are made responsible for noteworthy clinical or epidemiologic effects [1].

In S. haematobium infection, haematuria and dysuria due to ulceration of the bladder mucosa is well known, whereas proteinuria due to S. mansoni infection is not. Schistosomiasis-associated kidney disease is not frequently described in literature. The disease has a chronic evolution with variable severity. Glomerulonephritis is described in 10-12% of the cases in autopsy studies. Schistosomal glomerulopathy generally occurs in young, male patients and the glomerular lesions are of an immunological nature [2].

Malaria is one of the most prevalent infectious diseases in the world and was shown as the first to be clearly associated with nephrotic syndrome [3]. Kidney involvement is relatively frequent in infections by P. falciparum (Malaria tropica) and P. malariae (Malaria quartana), but has also been described in the infection by P. vivax (Malaria tertiana). With Malaria quartana, nephrotic syndrome commonly occurs in the course of a membranoproliferative type of glomerulonephritis, which is usually not reversible by treating the infection. In contrast to this, nephrotic syndrome or proteinuria is rare in P. falciparum-infected patients and disappears when the infection is brought under control. However, noteworthy is the appearance of acute renal failure due to tubulointerstitial damage such as tubular necrosis, haemoglobin and cellular casts in the tubuli, and interstitial oedema [4].

Leishmaniasis is caused by infections with protozoa and can manifest in three ways: cutaneous, mucocutaneous or visceral. Glomerular lesions are only observed with kala-azar, a distinct type of visceral leishmaniasis caused by Leishmania donovani, but not with any other cutaneous or mucocutaneous leishmaniasis. Study data elucidated mild proteinuria with benign changes in the urinary sediment in 60% of patients with kala-azar based on a mesangial proliferative to membranoproliferative glomerulonephritis with tubulointerstitial damage. Here, recovery from the glomerulopathy seems to set in with the cure of the infection [5].

1. Barsoum RS: Parasitic kidney disease: milestones in the evolution of our knowledge. Am J Kidney Dis. 2013 Mar; 61(3):501-13.
2. da Silva GB, Duarte DB, Guardão Barros EJ, and De Francesco Daher E: Schistosomiasis-associated kidney disease: A review. Asian Pac J Trop Dis. 2013 Feb; 3(1): 79–84.
3. Barsoum RS: Tropical parasitic nephropathies. Nephrol Dial Transplant. 1999; 14 Suppl 3:79-91.
4. da Silva GB, Pinto JR, Guardão Barros EJ, Nogueira Farias GM, and De Francesco Daher E: Kidney involvement in malaria: an update. Rev Inst Med Trop Sao Paulo. 2017; 59: e53.
5. van Velthuysen ML, Florquin S: Glomerulopathy associated with parasitic infections. Clin Microbiol Rev. 2000 Jan; 13(1):55-66.