Quarten malarial nephropathy is associated with plasmodium malariae infection. It has been reported from British Guyana, Uganda, Nigeria, Kenya, Ivory Coast, Sumatra, New Guinae and Yemen.

The disorder predominently affects children and young adults. A peak incidence is seen at 5-8 years of age. Nephrotic syndrome develops several weeks after onset of quarten fever. Non-selective proteinuria is observed in 80% of cases and urine microscopy often reveals hematuria. Serum complement (C3) levels are usually within normal range. Disease may progress slowly to end stage renal failure in 3-5 years. Parasites are detected in 75% of cases in the early stage.

Anti-malaria therapy does not alter the course of renal disease. Of the few patients with highly selective proteinuria, less than 50% respond to predenisolone.Cyclophosphamide may also be associated with remission in some cases. Renal histological changes are shown in table 2.

Glomerulopathy in P. falciparum malaria

Plasmodium falciparum is widely prevalent in several tropical countries of the world and is of great clinical importance because of many serious complications. A transient glomerulonephritis commonly occurs soon after the onset of fever but remains undetected because of absence of overt clinical manifestations. Non nephrotic proteinuria, microscopic hematuria and casts are seen in 20-50% patients. Serum complement (C3 and C4) levels are decreased and P. falciparum soluble antigen, antibody to P. falciparum and circulating immune complexes are present. Glomerular changes are listed in the table 3. Renal lesions resolve within 4-6 weeks of anti malarial therapy.

Schistosomal glomerulopathy

Schistosoma mansoni infection is endemic in Africa, Aden, Saudi Arabia, Yemen and Brazil. Approximately 5% of patients have a heavy worm load and develop hepatosplenic schistosomiasis after several years. Of these, about 15% (or 0.75% overall) develop overt glomerulopathy. Some patients, however, may have subclinical renal disease.

60% of patients present with a nephritic syndrome; the remaining patients have non-nephrotic proteinuria. Proteinuria is poorly selective. Hypertension develops in less than 50% of patients.

Renal histology reveals a membrano-proliferative glomerulonephritis. Mesangial expansion and lobular accentuation are usually seen. Focal glomerulosclerosis, mesangial proliferative, membranous, diffuse proliferative and crescentic glomerulonephritis have also been reported. Immunofluorescence reveals deposits of IgG, IgM and C3 in the mesangium and along the capillary walls.

Filarial Nephropathy

Glomerulonephritis has been observed following infection with filarial nematodes - Wuchereria bancrofti, Onchocerca volvolus, and Loa loa. Bancroftian filariasis is endemic in Africa and South-East Asia, onchocerciasis in South America and tropical subsaharan Africa, and loiasis in West central Africa.

Renal involvement is frequently associated with nephrotic syndrome but an acute presentation has been described. In loiasis, membranous, mesangio-capillary and chronic sclerosing glomerulonephritis have been reported. In onchocercal infection, minimal change, mesangiocapillary, mesangio-proliferative and chronic sclerosing lesions have been observed. Glomerular deposition of onchocercal antigen has been demonstrated in 50% of patients (Table 4).

Studies in dogs infected with Dirofilaria immitis have shown development of glomerular lesions similar to those seen in human beings (Table 5).

Diethylcarbamazepine therapy leads to recovery of nephritic lesions but patients with nephrotic syndrome generally do not respond.

Mycobacterial infections

Leprosy : Leprosy is widely prevalent in Africa, India, South America, China and many other countries of South East Asia. Worldwide there are about 5.5 million cases of leprosy. The two major renal lesions in leprosy include secondary amyloidosis and glomerulonephritis. While patients with secondary amyloidosis present with a nephrotic syndrome, most of those with glomerulonephritis have only asymptomatic urinary abnormalities. In rare instances, oliguric acute renal failure may occur when crescentic glomerulonephritis develops. Hypertension is uncommon. Gradual progression of renal failure is the rule in amyloidosis.

While less than 2% of patients are suspected to have glomerulonephritis on clinical evaluation, renal biopsies have revealed glomerulonephritis in as many as 13-71% in different studies. The most common glomerular lesions observed in leprosy include those of mesangioproliferative, diffuse proliferative, MPGN and crescentic glomerulonephritis. Organisms consistent with Mycobacterium leprae have been identified in histological studies. Vascular lesions resembling microscopic polyarteritis nodosa have been documented (Table 6).

Amyloidosis develops in 2-8% of patients. It is far more frequent in lepromatous than in tuberculoid leprosy. The occurrence of repeated episodes of erythema nodosum leprosum in lepromatous leprosy may predispose to the development of amyloidosis since each episode is associated with a marked and persistent elevation of serum amyloid A protein which is the amyloid fibril precursor protein.

Tuberculosis Glomerular involvement in tuberculosis is usually associated with chronic infection which results in amyloidosis. Many aspects of formation, deposition and persistence of amyloid fibrils are not yet understood but some are evidentally important. Chief amongst these is production of a fibril precursor protein. A newer diagnostic approach SAP scintigraphy has been found to be of great help in evaluating the amount of amyloid deposited in various organs and for determining progression or resolution of the disease. Resolution of early amyloid may occur with cure of tuberculosis (Table 7).

References

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