Rashad S Barsoum Magdi R Francis Visith Sitprija

Tropical nephrology is no longer a regional issue. With the enormous expansion of travel and immigration, the world has become a global village. Today, a health problem in a particular region has worldwide repercussions. Typical examples are the acquisition of malaria in European airports, renal disease associated with herbal medications, and increasing encounters of parasitic infections in immunocompromised persons [1-3].

Lessons learned from the study of tropical diseases have considerably enriched worldwide medical knowledge of the basic and clinical aspects of nontropical diseases. Examples include better understanding of macrophage function in vitro, the role of cytokines in acute renal failure, and the importance of immunoglobulin A deposits in the progression of glomerular disease [4-7].

The so-called typical tropical nephropathies are broadly classified as infective or toxic. Infective nephropathies include renal diseases associated with endemic bacterial, viral, fungal, and parasitic infections. Toxic tropical nephropathies include exposure to poisons of animal origin, such as snake bites, scorpion stings, and intake of raw carp bile, and plant origin, such as certain mushrooms and the djenkol bean [3].

Tropical bacterial infections often are associated with renal complications that vary according to the causative organism, severity of infection, and individual susceptibility. The principal acute infections reported to affect the kidneys are salmonellosis, shigellosis, leptospirosis, melioidosis, cholera, tetanus, scrub typhus, and diphtheria [8-16]. Renal involvement in mycobacterial infections such as tuberculosis and leprosy usually pursues a subacute or chronic course [17-19].

The clinical spectrum of renal involvement extends all the way from asymptomatic proteinuria or urinary sediment abnormalities to fatal acute renal failure. The respective renal pathologies include glomerular, microvascular, and tubulointerstitial lesions.

The pathogenesis of renal complications in tropical bacterial infections is multifactorial. The principal factors are direct tissue invasion by the causative organisms and remote cellular and humoral effects of bacterial antigens and endotoxins. The relative significance of the different pathogenetic mechanisms varies with the causative organism.

In tropical zones many viral nephropathies are endemic, such as those associated with human immunodeficiency virus and hepatitis A, B, and C viruses. These are addressed in Chapter 7. Here the focus is on an important viral disease endemic in Southeast Asia that often causes minor epidemics in Africa and other tropical countries, dengue hemorrhagic fever.

Mycotic infections are described in detail elsewhere. Discussed here is a fairly common mycotic infection, mucormycosis, which occurs in underdeveloped tropical regions, particularly among immunocompromised patients. Also described is ochratoxin, a fungal toxin often incriminated in the pathogenesis of Balkan nephropathy. Ochratoxin also contributes to progressive interstitial nephropathy in Africa [20].

Three ways exist by which parasitic infections cause renal disease: 1) direct physical invasion of the kidneys or urinary tract, as in schistosomiasis, echinococcosis, and filariasis; 2) renal injury as a consequence of the acute systemic effects of parasitic infection, eg, falciparum malaria; and 3) immunemediated renal injury resulting from the concomitant host-parasite interaction, eg, schistosomiasis, malaria, filariasis, leish-maniasis, trichinosis, echinococcosis, toxoplasmosis, and try-panosomiasis [21-32].

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