ARF complicates malaria in 1 – 5% of the natives in endemic areas but in non-immune visitors the figure goes up to 30%⁽⁵⁾ . It is mostly due to P. falciparum with P. vivax being the causative species in a minority of cases. The main features are oliguria and hypercatabolism in addition to the systemic effects of malaria. Mild proteinuria, <1gm/day, may occur but almost resolves completely after treatment. The urine sediment is usually negative. Hyperkalaemia is usually striking due to haemolysis, rhabdomyolysis and acidosis.

Histologically there is a mixture of ATN, interstitial nephritis and glomerulonephritis⁽⁶⁾. ATN is the most consistent finding. The glomerular lesions show prominent mesangial proliferation with modest mesangial matrix expansion. Segmental necrosis may occur due to occlusion of the capillaries by erythrocyte rosettes. Immunofluorescence show finely granular IgM and C3 deposits along the capillary walls and in the mesangium⁽⁷⁾.

Mortality depends on the urgency and facilities of treatment ranging from nil in well-equipped centers to as high as 45% when facilities are meager⁽⁸⁾.

A study of prognosis from Yemen reported that out of 64 children (4.2 – 11.2 years) who required dialysis for ARF secondary to falciparum malaria, 28 (43.8%) died. The group that died had significantly high plasma creatinine and BP and low urine output⁽⁹⁾.

Leptospirosis which is caused by several sero-types of Leptospira interrogans is a world wide disease. It is an uncommon cause of ARF in western countries^(10),(11) but plays an important role in tropical countries : for example it accounts for 24% of all cases of ARF in South East Asia ^(12),(13).

Almost in all cases the disease involves the kidney causing ARF of variable degrees.

The ARF occurring with Liptospirosis is usually mild and non-oliguric, in 60% of the cases. Urinary abnormalities range from mild protienuria and haematuria to haemoglobinuria, granular and bile pigment casts. In severe cases of Liptospirosis, ARF can be marked with rapid deterioration of renal function and raised serum uric acid. Acidosis may be severe due to bicarbonate wastage because of failure of absorption by proximal tubules. Also hypokalaemia may occur due to inhibition of potassium reabsorption in the medullary thick limb of HenLe. In certain cases Haemolytic Uraemic Syndrome may occur ^(14),(15).

Leptosprios causes necrotizing vasculitis causing severe glomerulonephritis in some patients while in others there is mild mesangioproliferative glumerulonephritis with IgM immunofluorescence deposit. Interstitial nephritis also occurs with focal or diffuse mononuclear cell infiltration. The organism is rarely seen in the renal biopsy.

Treatment is mainly directed towards treating the disease, Penicillin being the drug of choice; some patients may require dialysis before recovery of renal function. Plasma exchange is advocated by some workers in patients with severe jaundice⁽¹⁶⁾. Referring of ARF is almost invariable in patients who recover from the acute illness.

A number of mechanisms may lead to development of the ARF associated with tetanus, rhabdomyolysis⁽¹⁷⁾ and autonomic nervous system over activity⁽¹⁸⁾ being the most prominent. ARF due to tetanus is high in certain countries like Brazil⁽¹⁷⁾, where ARF is seen in 34% of cases. It is usually mild and non-oliguric.

Abnormal renal function is reported in about 16% of patients⁽¹⁹⁾ with salmonellosis. The main renal lesions are pyelonephritis, acute tubular necrosis and glomerulonephritis⁽²⁰⁾ which is exudative.

During the febrile phase haematuria and proteinuria, usually less than one gram, are common. The renal involvement is usually mild with full recovery within two weeks of typhoid treatment⁽²¹⁾. A more severe illness mimicking post infections glomerulonephritis was reported from South Africa with generalized oedema and hypertension ⁽²²⁾ . Renal biopsy showed mild to moderate mesangioproliferative glomerulonephritis with IgG and IgM deposits.

ATN may occur due to dehydation in severe infections. In a series reported by Bennish et al, out of 2018 patients ARF occurred in 26% of cases⁽²³⁾. Proliferative glomerulonephritis can occur. Shigellosis may also induce haemolytic uraemic syndrome (HUS) especially in children ⁽²⁴⁾. In such cases there may be cortical necrosis and diffuse fibrous deposits in the glomeruli. Mortality may be high in those patients.

ARF occurency in cholera is similar to that of shigellosis, being due to fluid and electrolytes loss. Hypokalaemia can be severe. In addition to ATN, proximal tubular vacoulation can occur due to hypokalaemia and cortical necrosis was noted in some patients⁽²⁵⁾.

ARF in haematobium infection occurs due to acute obstructive uropathy, usually on top of chronic disease. With mansoni infection, ARF may occur with late disease as ATN due to severe variceal bleeding or as hepatorenal syndrome associated with hepatic dysfunction.

ARF occurs in 5% of patients with Dengue Haemorrhagic Fever. It is mainly due to ATN which is associated with interstitial oedema and mononuclear cell infiltration. Mesangioproliferative glomerulonephritis may be seen with IgG, IgM and C₃ deposits. It is associated with mild proteinuria and abnormal urinary sediment.