Parasitic Kidney Disease: Milestones in the Evolution of Our Knowledge
2013; Elsevier BV; Volume: 61; Issue: 3 Linguagem: Inglês
10.1053/j.ajkd.2012.09.025
ISSN1523-6838
Autores Tópico(s)Parasite Biology and Host Interactions
ResumoOf the 342 parasites that infect humans, 20 are associated with kidney disease, yet of these, only schistosomes, plasmodia, filariae, and leishmanias are held responsible for significant clinical or epidemiologic impact. Reviewing the evolution of human knowledge for these parasites discloses a lot of similarities regarding their discovery, patterns of kidney injury, and pathogenic mechanisms. From a historical perspective, our relevant information may be classified into 4 phases: (1) disease documentation in ancient and medieval scripts as far back as 2000-3000 bce; (2) discovery of the parasites, their life cycles, and clinical correlates by European clinicians working in African and Asian colonies during the second half of the 19th century; (3) discovery and characterization of the renal manifestations of monoparasitic infections during the second half of the 20th century; and (4) recognition of the confounding effects of coinfection with bacteria, viruses, or other parasites. The spectrum of respective kidney diseases extends all the way from acute kidney injury to glomerulonephritis, amyloidosis, urologic disorders, and malignancy. Discovery of the common immunopathogenetic host response to parasitic infections has provided a knowledge core that explains the similarities, diversities, and interactions with regard to kidney injury. Of the 342 parasites that infect humans, 20 are associated with kidney disease, yet of these, only schistosomes, plasmodia, filariae, and leishmanias are held responsible for significant clinical or epidemiologic impact. Reviewing the evolution of human knowledge for these parasites discloses a lot of similarities regarding their discovery, patterns of kidney injury, and pathogenic mechanisms. From a historical perspective, our relevant information may be classified into 4 phases: (1) disease documentation in ancient and medieval scripts as far back as 2000-3000 bce; (2) discovery of the parasites, their life cycles, and clinical correlates by European clinicians working in African and Asian colonies during the second half of the 19th century; (3) discovery and characterization of the renal manifestations of monoparasitic infections during the second half of the 20th century; and (4) recognition of the confounding effects of coinfection with bacteria, viruses, or other parasites. The spectrum of respective kidney diseases extends all the way from acute kidney injury to glomerulonephritis, amyloidosis, urologic disorders, and malignancy. Discovery of the common immunopathogenetic host response to parasitic infections has provided a knowledge core that explains the similarities, diversities, and interactions with regard to kidney injury. By the turn of the present millennium, parasites had already acquired a prominent position on the list of agents that can cause kidney disease. Their importance stems not only from their clinical and epidemiologic importance in the tropics, but also because of their incremental spread into the industrialized world through travel and immigration. In addition, they can pose clinical challenges in immunocompromised patients at large,1Barsoum R.S. Parasitic infections in transplant recipients.Nat Clin Pract Nephrol. 2006; 2: 490-503Crossref PubMed Scopus (66) Google Scholar many of whom are within the domain of nephrology. There are 342 known parasites that may cause disease in humans, and about 20 of these may lead to kidney disorders (Fig 1).2Barsoum R.S. Tropical parasitic nephropathies.Nephrol Dial Transplant. 1999; 14: 79-91Crossref PubMed Scopus (25) Google Scholar However, the majority can cause merely subclinical or mild and self-limited disease that usually passes un-noticed, particularly if masked by more substantial extrarenal manifestations.3van Velthuysen M.L. Florquin S. Glomerulopathy associated with parasitic infections.Clin Microbiol Rev. 2000; 13: 55-66Crossref PubMed Scopus (70) Google Scholar Only 4 have attained significant clinical or epidemiologic importance, namely schistosomiasis, malaria, filariasis, and leishmaniasis. It took humankind more than 5,000 years to build up enough knowledge to link those sundry disorders and understand how they channel into a relatively narrow range of kidney injury. This review is an attempt to track the story of these 4 parasites from their early beginnings all the way to our present knowledge and understanding. Figure 2 chronicles the evolution of human knowledge for these parasites, displaying clear clustering of the important landmarks into 4 phases: (1) recognition and clinical description of respective diseases in ancient and medieval documents, (2) discovery of the causative parasites and their life cycles, (3) identification of kidney disease associated with monoparasitic infections, and (4) recognition of the important role of coinfection with other parasites, bacteria, or viruses. Scripts, embossments, statues, and tablets belonging to Egyptian, Chinese, Indian, and Sumerian civilizations dating back to 3000-2000 bce have documented the existence of many diseases that we now recognize as parasitic. However, a dynamic description of the respective clinical syndromes was not reported until the Middle Ages and Renaissance by European and Persian philosophers. The first written document on this disease is the Ebers papyrus (1550 bce),4Ghalioungui P. Magic and Medical Science in Ancient Egypt. Barnes and Noble Inc, New York, NY1965Google Scholar which is thought to be copied from more ancient papyri dating back to 3000 bce.5Cox F.C. History of human parasitic diseases.Infect Dis Clin North Am. 2004; 18: 171-188Abstract Full Text Full Text PDF PubMed Scopus (36) Google Scholar The Ebers and subsequently the Edwin Smith (1500 bce)6Breasted J.H. The Edwin Smith Surgical Papyrus: Published in Facsimile and Hieroglyphic Transliteration With Translation and Commentary in Two Volumes University of Chicago Oriental Institute publications, v 3-4. University of Chicago Press, Chicago, IL1991Google Scholar papyri contain an accurate description of "âââ" (bloody urine disease), with a "worm" pinpointed as its causative agent, and recommendations for its prophylaxis and treatment. The identification of âââ as urinary schistosomiasis was confirmed many centuries later when schistosomal ova were recovered from the bladders of Egyptian mummies dating 2000-1000 bce.7Ruffer M.A. Note on the presence of 'bilharzia haematobia' in Egyptian mummies of the Twentieth Dynasty (1250–1000 bc).Br Med J. 1910; 1: 16Crossref PubMed Scopus (153) Google Scholar Interestingly, ova also were found in contemporary mummies from China, which suggests the undocumented existence of the disease in Asia since ancient times. Its geographic limitation to Africa and Asia may explain the lack of further description of the disease during the Middle Ages and Renaissance. Paroxysmal febrile episodes associated with splenomegaly, typical of malaria, were described in the Nei Ching Chinese medical literature, dated as far back as 2700 bce.8Sivin N. Huang ti nei ching Loewe M Early Chinese Texts: A Bibliographical Guide. University of California Press, Berkeley, CA1993: 196-215Google Scholar Similar episodes also were alluded to in ancient Sumerian, Egyptian, and Indian texts.9Shah S. The Fever: How Malaria Has Ruled Humankind for 500,000 Years. Sarah Crichton Books, New York, NY2010Google Scholar The identity of the disease was elaborated in the Hippocratic Collection (460-377 bce) and Avicenna's Canon of Medicine (1025 ce).10Mehlhorn H. Encyclopedia of Parasitology. 3rd ed. Springer, New York, NY2008Crossref Google Scholar It was so highly prevalent in Italy that it initially was known as "Roman fever" and may have even contributed to the decline of the Roman Empire. Its current name is derived from Medieval Italian language, being composed of "mala" and "aria," referring to malus (bad), and aeris (air), thought to result from exposure to "poisonous air rising from marshes."11Dobson M.J. Malaria in England: a geographical and historical perspective.Parassitologia. 1994; 36: 35-60PubMed Google Scholar The first known record of lymphatic filariasis is a statue of Pharaoh Mentuhotep II (2000 bce) that renders him with irregularly swollen legs, suggestive of elephantiasis. Another typical feature of the disease, the "hanging scrotum," was depicted in artifacts from the Nok civilization in West Africa (500 bce). However, the first written document on filariasis was in 1590, when the Dutch merchant and historian Jan Huygen van Linschoten mentioned in his writings that natives in Goa, India, were "'all born with one of their legs and one foot from the knee downwards as thick as an elephants leg.'"12Cox F.E.G. History of human parasitology.Clin Microbiol Rev. 2002; 15: 595-612Crossref PubMed Scopus (274) Google Scholar Skin lesions were recognized many centuries before visceral involvement in leishmanial infection. They were displayed on tablets dating back to the 7th century bce at the time of the Assyrian King Ashurbanipal. It is believed that some of these were derived from texts as old as 1500-2000 bce. Detailed description of cutaneous leishmaniasis was provided in the 10th century ce by Avicenna, who gave the lesions the name "Balkh sore." Further description of such sores came from South America, India, and Africa and were given many names, including "oriental sore" and "white leprosy." Systemic illness was associated with such sores in the mid-18th century, being known as "valley sickness" or "Andean sickness" in South America and "Dumdum fever" or "black fever" (kala-azar) in India.12Cox F.E.G. History of human parasitology.Clin Microbiol Rev. 2002; 15: 595-612Crossref PubMed Scopus (274) Google Scholar The second half of the 19th century witnessed the discovery of most parasites. The main players were European clinicians and scientists working in the tropics during the era of political and military colonization. By 1825, when Antoine Clot, the French surgeon-in-chief of the Egyptian army, established the first organized medical service in the country, schistosomiasis had become so endemic that hematuria was considered a "sign of maturity" in teenagers. It was not uncommon for a father to take his son to the doctor if he did not "menstruate" by the age of 20! Clot imported young physicians from Europe to teach in the military medical school in the outskirts of Cairo. Among those was the German surgeon Theodor Bilharz, who eventually discovered the worm responsible for endemic hematuria.13Bilharz T. A study of human helminthography, derived from information by letter from Dr Bilharz in Cairo, along with remarks by Prof Th.V. Siebold in Breslaw.Z Wis Zool Leipzig. 1853; 4: 53-71Google Scholar The parasite initially was called after his name, "Bilharzia haematobia," until it acquired the formal name Schistosoma haematobium in 1858. Its life cycle was characterized 3 decades later,14Sonsino P. Discovery of the life history of Bilharzia haematobia.Lancet. 1893; 142: 621-622Abstract Scopus (7) Google Scholar thus paving the road for understanding schistosomal pathogenicity, prevention, and management. Other schistosomal species subsequently were discovered in humans, apes, cattle, and domestic animals. Of 21 known species, 7 were identified to infect humans, which differ in their geographic distribution and target-organ affinity. The parasite ultimately called plasmodium was first reported in the red blood cells of infected patients by the French physician Charles Laveran while working in Algeria in 1880. For this discovery, he was awarded the Nobel Prize for Physiology or Medicine in 1907. As early as the 7th century bce, the Indian physician Susruta had suggested that mosquitoes probably were responsible for the transmission of malaria. However, this hypothesis was not confirmed until the late 1800s by Scottish physician Sir Ronald Ross, also in India, for which he received the second Nobel Prize for discoveries in malaria in 1902.10Mehlhorn H. Encyclopedia of Parasitology. 3rd ed. Springer, New York, NY2008Crossref Google Scholar Many species have been identified, and the following cause disease in humans: Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale, and Plasmodium malariae. In 1863, French surgeon Jean-Nicolas Demarquay first described microfilariae in hydrocele fluid, and Brazilian physician Otto Wucherer described them in urine in 1868. Ten years later, while working in Brisbane, Australia, the British parasitologist Joseph Bancroft discovered the adult worm, which subsequently acquired the composite name Wuchereria bancrofti. The role of mosquitoes in parasite transmission and completion of the life cycle was established by George Carmichael Low in 1900.12Cox F.E.G. History of human parasitology.Clin Microbiol Rev. 2002; 15: 595-612Crossref PubMed Scopus (274) Google Scholar Seven other filarial nematodes were discovered in the following years, of which 3 are human pathogens; namely, W bancrofti, Loa loa, and Onchocerca volvulus. The Russian military surgeon Peter Borovsky was the first to discover the causative parasite of "Sart sore," as it is called in Russian, and published his observations in a local journal in 1898. This publication was overlooked for many years and not acknowledged until Borovsky's death in 1932. The credit went to William Leishman, a Glaswegian doctor who served with the British Army in India, who discovered the parasite in splenic aspirates from a patient with Dumdum fever in 1901. It took him 2 years to publish his findings, just a few weeks before Charles Donovan published similar observations on a patient with kala-azar. The identity of the organism in both discoveries was confirmed, hence the composite name "Leishman-Donovan bodies." Subsequently, the official name of the parasite became Leishmania donovani.12Cox F.E.G. History of human parasitology.Clin Microbiol Rev. 2002; 15: 595-612Crossref PubMed Scopus (274) Google Scholar The succeeding decades witnessed the discovery of 30 species of Leishmania, of which 21 infect humans, the best known being L donovani, Leishmania tropica, and Leishmania braziliensis. They are transmitted by 30 of the 500 known sandflies of the genera Phlebotomus and Lutzomyia. The disease is transmitted to humans from dogs or (rarely) cats in the Mediterranean region and China, rodents in Africa, and foxes in Brazil and Central Asia, whereas humans may serve as a reservoir for transmission in India and possibly other parts of the world where kala-azar is prevalent. Identification of almost the full spectrum of kidney disease attributed to parasitic infection took about a century, starting with the description of malarial nephropathy in the late 1800s and ending with the documentation of leishmanial kidney disease in humans in the mid-20th century. Egyptian pioneers in the early 1900s and Sudanese and Nigerian clinicians later on identified the lower urinary manifestations of S haematobium infection and their upstream sequelae. These were documented in Professor Naguib Makar's seminal monograph in which the bladder lesions were illustrated by detailed hand paintings, at a time when color photography was not available.15Makar N. Urological Aspects of Bilharziasis in Egypt. Societe Orientale de Publicite Press, Cairo, Egypt1955: 1-52Google Scholar The "granuloma," formed around single or multiple ova or worms, was soon identified as the basic histologic lesion throughout the urinary tract. Although active granulomas were blamed for some of the early manifestations of schistosomiasis, it was the healed lesions that induced peak morbidity, particularly by affecting the lower ureters. To the latter are attributed the upstream obstructive manifestations, infection and end-stage kidney disease.15Makar N. Urological Aspects of Bilharziasis in Egypt. Societe Orientale de Publicite Press, Cairo, Egypt1955: 1-52Google Scholar, 16Schistosomiasis.in: Barsoum R. Davison A. Cameron J.S. Ritz E. Oxford Textbook of Clinical Nephrology. 3rd ed. Oxford University Press, New York, NY2005: 1173-1184Google Scholar An epidemiologic study from Upper Egypt documented the occurrence of a transient immune-mediated acute glomerular injury in patients exposed to new S haematobium infection.17Ezzat E. Osman R.A. Ahmed K.Y. Soothill J.F. The association between Schistosoma hematobium infection and heavy proteinuria.Trans R Soc Trop Med Hyg. 1974; 68: 315-318Abstract Full Text PDF PubMed Scopus (29) Google Scholar The same also was reported in sporadic cohorts,18Rashed S.M. Khashaba A. Madwar M.A. Rafik M.M. Abul Fadl A.A. Shah A.M. Schistosomiasis and transient nephritis in children.J Egypt Soc Parasitol. 1989; 19: 611-615PubMed Google Scholar which seems to indicate that S haematobium glomerulopathy is relatively uncommon compared to Schistosoma mansoni (discussed later), of little clinical significance, and self-limited. A unique complication of urinary schistosomiasis, documented since those early descriptions, is bladder cancer. A cause-and-effect relationship had been proposed initially through postmortem observations in 40 Egyptian patients.19Ferguson A.R. Associated bilharziasis and primary malignant disease of the urinary bladder with observations on a series of forty cases.J Pathol Bacteriol. 1911; 16: 76-94Crossref Google Scholar This subsequently was confirmed on the basis of statistical association, characteristic clinicopathologic features, and the demonstration of ova within the neoplasm. The histopathologic pattern of "bilharzial cancer," as it often is called, has changed during the past half century from predominantly squamous cell20Ghoneim M.A. El-Mekresh M.M. El-Baz M.A. El-Attar I.A. Ashamallah A. Radical cystectomy for carcinoma of the bladder: critical evaluation of the results in 1,026 cases.J Urol. 1997; 158: 393-399Abstract Full Text Full Text PDF PubMed Scopus (373) Google Scholar to transitional cell carcinoma.21Gouda I. Mokhtar N. Bilal D. El-Bolkainy T. El-Bolkainy N.M. Bilharziasis and bladder cancer: a time trend analysis of 9843 patients.J Egypt Natl Canc Inst. 2007; 19: 158-162PubMed Google Scholar The role of S mansoni in causing kidney disease was discovered half a century later. The spark was a thesis submitted in 1964 at the Universidade de Minas Gerais in Brazil, where M. Lopez reported the association of hepatointestinal schistosomiasis with significant proteinuria and histologically documented glomerular lesions.22Lopez M. Aspectos renais da sindrome heaptoesplenica da esquistossomose mansonica [tese]. Universidade de Minas Gerais, Escola de Medicina, Belo Horizonte, Brasil1964Google Scholar This was confirmed by subsequent clinical, histopathologic, postmortem, and experimental observations in the same country.23Andrade Z.A. Queiroz A.C. Lesoes renais na esquistossomose hepatesplenica.Rev Inst Med Trop S Paulo. 1968; 10: 36-40PubMed Google Scholar, 24Andrade Z.A. Andrade S.G. Sadigursky N.I. Renal changes in patients with hepatosplenic schistosomiasis.Am J Trop Med Hyg. 1971; 20: 77-83PubMed Google Scholar Similar observations were made in Egypt by Sabbour et al,25Sabbour M.S. El-Said W. Abou-Gabal I. A clinical and pathological study of schistosomal nephritis.Bull World Health Organ. 1972; 47: 549-557PubMed Google Scholar who introduced the term "schistosomal nephritis." The clinical significance of schistosomal glomerulopathy, as it was called in later publications, subsequently was confirmed during the same decade by clinicopathologic studies in Africa and Central America.26Barsoum R.S. Schistosomal glomerulopathies.Kidney Int. 1993; 44: 1-12Crossref PubMed Scopus (72) Google Scholar Its burden was estimated in both Brazil and Egypt to range from 15%-20% of those with hepatointestinal schistosomiasis and to account for 3%-5% of patients undergoing regular dialysis in Egypt.27Barsoum R.S. The changing face of schistosomal glomerulopathy Nephrology Forum.Kidney Int. 2004; 66: 2472-2484Crossref PubMed Scopus (44) Google Scholar Many glomerular lesions were described in this context. In order to categorize the lesions into distinct clinicopathologic entities, a 5-tier classification was initially introduced and acknowledged by the African Association of Nephrology (AFRAN) as its official classification.26Barsoum R.S. Schistosomal glomerulopathies.Kidney Int. 1993; 44: 1-12Crossref PubMed Scopus (72) Google Scholar This was subsequently modified by adding a sixth tier to accommodate coinfection with hepatitis C virus (Table 1; Fig 3).Table 1Modified AFRAN Classification of Schistosomal GlomerulopathiesSources: Barsoum.26Barsoum R.S. Schistosomal glomerulopathies.Kidney Int. 1993; 44: 1-12Crossref PubMed Scopus (72) Google Scholar, 27Barsoum R.S. The changing face of schistosomal glomerulopathy Nephrology Forum.Kidney Int. 2004; 66: 2472-2484Crossref PubMed Scopus (44) Google ScholarClass: HistologyImmune DepositsEtiologic AgentPrevalenceClinical PictureTreatment of Kidney DiseaseI: MesangioproliferativeIgM, C3, schistosomal gut antigensS haematobium, S mansoni27%-60% of asymptomatic pts, 10%-40% of pts with overt kidney diseaseMicrohematuria, proteinuria?Antiparasitic treatmentII: Diffuse proliferative, exudativeC3, Salmonella antigensS haematobium/S mansoni, and SalmonellaUnknownAcute nephritic syndrome, toxemiaCombined antiparasitic and anti-Salmonella treatmentIII: Membranoproliferative (mesangiocapillary)IgG, IgA, C3, schistosomal gut antigensaNot always present.S mansoni, ?S haematobium7%-20% of asymptomatic pts; 80% of pts with overt kidney diseaseHepatosplenomegaly & NS, HTN, progressive CKDNone effectiveIV: FSGSIgM, IgG, IgAaNot always present.S mansoni11%-38%Hepatosplenomegaly & NS, HTN, progressive CKDNone effectiveV: AmyloidosisAmyloid A proteinS mansoni and/or S haematobium16%-39%Hepatosplenomegaly & NS, HTN, progressive CKDNone effectiveVI: CryoglobulinemicIgM, C3, fibrin, amyloid A proteinS mansoni and HCVUnknownCirrhosis, splenomegaly, NS, purpura, vasculitis, arthritis, HTN, progressive CKD?Interferon + ribavirin, corticosteroids, immunosuppression, plasmapheresisAbbreviations: AFRAN, African Association of Nephrology; CKD, chronic kidney disease; FSGS, focal segmental glomerulosclerosis; HCV, hepatitis C virus; HTN, hypertension; Ig, immunoglobulin; NS, nephrotic syndrome; pts, patients; S haematobium, Schistosoma haematobium; S mansoni, Schistosoma mansoni.a Not always present. Open table in a new tab Abbreviations: AFRAN, African Association of Nephrology; CKD, chronic kidney disease; FSGS, focal segmental glomerulosclerosis; HCV, hepatitis C virus; HTN, hypertension; Ig, immunoglobulin; NS, nephrotic syndrome; pts, patients; S haematobium, Schistosoma haematobium; S mansoni, Schistosoma mansoni. During 1884, malarial kidney disease was independently described for the first time in 2 geographically distant regions. Thus, P falciparum was held responsible for acute kidney injury (AKI) in South East Asia, whereas P malariae was held responsible for chronic kidney disease in West Africa. The Sierra Leonean doctor John Farrell Easmon was the first to relate kidney disease to malaria by describing "blackwater fever." Passage of black urine and subsequent anuria were attributed to massive intravascular hemolysis, mostly in patients treated with quinine. When the use of quinine was abandoned in 1950, blackwater fever became exceedingly rare and reappeared with the use of the drug in recent years for the treatment of multidrug-resistant malaria.28Bruneel F. Gachot B. Wolff M. et al.Backwater fever.Presse Med. 2002; 31: 1329-1334PubMed Google Scholar Less commonly, blackwater fever was reported later in patients treated with chloroquine or artemether compounds.29Myint P.T. Shwe T. A case of black water fever treated with peritoneal dialysis and artemether (quinghaosu derivative).Southeast Asian J Trop Med Public Health. 1987; 18: 97-100PubMed Google Scholar The role of falciparum malaria in causing AKI by its own right, regardless of any treatment, was disclosed during the years of withholding quinine therapy. Many reports estimated the incidence at ∼1% of infected patients.30Sitprija V. Nephropathy in falciparum malaria.Kidney Int. 1988; 34: 867-877Crossref PubMed Scopus (117) Google Scholar This suggests a global incidence of 4 million per year, based on the World Health Organization prevalence estimates. The work of Thai physicians during the last few decades of the 20th century attributed malarial acute renal failure to a combination of renal ischemia due to pooling of blood in the peripheral capillaries, interstitial kidney injury, and intravascular hemolysis.30Sitprija V. Nephropathy in falciparum malaria.Kidney Int. 1988; 34: 867-877Crossref PubMed Scopus (117) Google Scholar The main reason for the key hemodynamic perturbation turned out to be increased adhesiveness of parasitized red blood cell membranes due to surface expression of multiple parasite-related proteins.31Barsoum R.S. Malarial acute renal failure.J Am Soc Nephrol. 2000; 11: 2147-2154PubMed Google Scholar Acute immune-mediated glomerular lesions had been described later,32Berger M. Birch L.M. Conte N.F. The nephrotic syndrome secondary to acute glomerulonephritis during falciparum malaria.Ann Intern Med. 1967; 67: 1163-1171Crossref PubMed Scopus (48) Google Scholar mainly in patients who developed nephrotic syndrome as the sole manifestation of P falciparum nephropathy or after malarial acute renal failure. Malarial glomerulonephritis (GN) was first described by the American pathologist I.E. Atkinson, who introduced the term "Bright's disease of malarial origin" in Nigerian children with quartan malaria.33Atkinson L.E. Bright's disease of malarial origin.Am J Med Sci. 1884; 88: 149-163Crossref Google Scholar Similar reports were published from the same region in succeeding years, before G. Giglioli34Giglioli G. Malarial Nephritis: Epidemiological and Clinical Notes on Malaria, Blackwater Fever, Albuminuria and Nephritis in the Interior of British Guiana, Based on Seven Years' Continual Observation. Churchill, London, England1930Google Scholar published his comprehensive clinical monograph in 1930 on the renal manifestations of malaria in British Guiana. The disease was described as a progressive steroid-resistant nephrotic syndrome in children. The usual histologic pattern was immune-complex mediated mesangiocapillary GN with the formation of large intramembranous "lacunes" that were considered pathognomonic by some authorities (Fig 4).35Hendrickse R.G. Adeniyi A. Edington G.M. Glasgow E.F. White R.H.R. Houba V. Quartan malarial nephrotic syndrome: collaborative clinicopathological study in Nigerian children.Lancet. 1972; 1: 1143-1149Abstract PubMed Scopus (101) Google Scholar, 36Barsoum R.S. Malarial nephropathies.Nephrol Dial Transplant. 1998; 13: 1588-1597Crossref PubMed Scopus (64) Google Scholar Although the identity of quartan malarial nephropathy has been acknowledged for many decades, it recently was challenged on the basis of discrepancies in the pattern of glomerular injury in different geographic regions and the inconsistency of demonstrating malarial antigens in many studies.37Ehrich J.H. Eke F.U. Malaria-induced renal damage: facts and myths.Pediatr Nephrol. 2007; 22: 626-637Crossref PubMed Scopus (71) Google Scholar During the past 2 decades there has been a growing trend of P vivax causing malarial acute renal failure38Prakash J. Singh A.K. Kumar N.S. Saxena R.K. Acute renal failure in Plasmodium vivax malaria.J Assoc Physicians India. 2003; 51: 265-267PubMed Google Scholar or acute GN in India and China.39Sanghai S.R. Shah I. Plasmodium vivax with acute glomerulonephritis in an 8-year old.J Vector Borne Dis. 2010; 47: 65-66PubMed Google Scholar According to several clinical reports, the disease seems to be more common in children and is associated more often with thrombocytopenia and pulmonary complications compared with P falciparum disease. The English physician William Prout was the first to describe chyluria in 1849. He ascribed this condition to "the passage of lymph in urine,"40Prout W. On the Nature and Treatment of Stomach and Renal Diseases. John Churchill, London, England1840Google Scholar which was attributed later to obstruction of the central lymphatics by filarial worms. The occurrence of proteinuria in such patients traditionally has been considered an expression of lymphatic leakage. Even hematuria, reported in some cases, was attributed to capillary rupture into the dilated lymphatics.41Gulati S. Gupta N. Singh N.P. et al.Chyluria with proteinuria or filarial nephropathy? An enigma.Parasitol Int. 2007; 56: 251-254Crossref PubMed Scopus (16) Google Scholar It remained until the late 1970s for typical mesangioproliferative GN to be histologically documented in filarial infection,42Chugh K.S. Singhal P.C. Tewari S.C. Nath I.V.S. Datta B.N. Acute glomerulonephritis associated with filariasis.Am J Trop Med Hyg. 1978; 27: 630-631PubMed Google Scholar later attributed to deposition of immune complexes containing worm antigens.43Ngu J.L. Chatelanat F. Leke R. Ndumbe P. Youmbissi J. Nephropathy in Cameroon: evidence for filarial derived immune-complex pathogenesis in some cases.Clin Nephrol. 1985; 24: 128-134PubMed Google Scholar Although subsequent reports confirmed these observations, glomerular disease remains relatively rare in bancroftiasis compared with other filarial species. A fairly wide spectrum of glomerular lesions has been described since the early 1970s with L loa infection.44Pillay V.K. Kirch E. Kartzman N.A. Glomerulopathy associated with filarial loiasis.J Am Med Assoc. 1973; 225: 179-182Crossref Scopus (39) Google Scholar The most consistently reported is membranous nephropathy. Mesangio
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