Plasmodium vivax presenting as acute glomerulonephritis in a 3-year-old child

Introduction

Malaria, a disease of global importance, is caused by Plasmodium, a protozoan parasite. ¹ In endemic regions, it can present with unusual features due to the development of immunity and an increasing resistance to anti-malarial drugs. ^1,2 In India, Plasmodium vivax is the predominant parasite and accounts for the majority of malarial cases. ³ Acute glomerulonephritis has been reported to be a rare complication of Plasmodium falciparum malaria. We report a case of malaria due to P. vivax presenting as acute glomerulonephritis in a child.

Case history

A three-year-old boy, born out of non-consanguineous marriage, presented with high grade fever associated with chills and rigors along with progressive swelling of the body for the previous seven days and a one-day history of vomiting. The swelling first appeared on his face and then progressed over next five days to the abdomen and legs. He had also begun to pass dark coloured urine the day before his admission. His past history and other clinical history were unremarkable.

On examination, he was febrile, with a 108/min heart rate, 24/min respiratory rate, his blood pressure was 109/68 mm mercury (>95th percentile). Severe pallor and generalized swelling of the body was present. His hepatosplenomegaly was remarkable (liver 6 cm and spleen 4cm below the subcostal margin). The remainder of the systemic examination was within normal limits.

Investigations revealed haemoglobin 5.6 g%, total leucocyte counts of 9000/m³ (68% polymorphs, 32% lymphocytes, 02% eosinophils), platelet count 80,000/m³, packed cell volume of 14.6 and a corrected reticulocyte count of 1.2%. His blood urea was 60 mg/dL, creatinine was 1.2 mg/dL and his liver function tests, serum electrolytes and proteins were normal. A urine examination was remarkable for red blood cells (RBCs) (20–30 RBCs/high power field) with more than 80% dysmorphic RBCs. However, no albumin or sugars were detected in his urine. A malaria antigen test was positive for P. vivax but negative for P. falciparum. A peripheral smear showed the presence of trophozoites of P. vivax. His blood culture was sterile. His C_3,C₄ was normal and the Widal, anti-nuclear antibody, anti-neutrophil cytoplasmic antibodies tests, Coomb's test, anti-streptolysin O test and anti-DNAase titres were negative. The dengue and leptospira serologies were negative. An ultrasonography of the abdomen confirmed the presence of hepatospleenomegaly with normal kidney echotexture.

He was started on intravenous artesunate, syrup paracetamol and enalapril. On day two of admission he became afebrile and his platelets increased to 120,000/mm³ but blood urea normalized to 32 mg/dL. The swelling disappeared completely by the 4th day of admission. However, haematuria persisted until the 10th day of admission and had disappeared by the 18th day during follow up.

Discussion

Severe and complicated malaria is usually caused by P. falciparum but it has been increasingly observed that P. vivax malaria, which was previously considered to be benign malaria, may also occasionally result in severe disease as with P. falciparum malaria. Renal involvement in falciparum malaria can present as: electrolyte abnormality; abnormal urinary sediments; increased urinary protein excretion; acute renal failure; etc. ⁴ Children are at an increased risk of acute glomerulonephritis associated with P. falciparum malaria. ⁵ Mild proteinuria, micro-haematuria and casts are reported in 20–50% of cases. ⁶ Nephrotic ⁷ and acute nephritic ⁸ syndromes are occasionally seen but hypertension is rare. Serum C3 and C4 may be reduced during the acute phase. Glomerular lesions are detected in approximately one fifth of autopsies on patients with falciparum malaria. They are characterized by prominent meningeal proliferation with many transit cells. Meningeal matrix expansion is modest and basement membrane changes are unusual. Deposition of an eosinophilic granular material has been noticed along the capillary walls, within the mesangium and in the Bowman's capsule. ⁹

Our case presented with fever, hepatosplenomegaly, oedema, anaemia, haematuria and hypertension and was confirmed as a case of P. vivax malaria causing acute glomerulonephritis by peripheral blood examination showing trophozoites of P. vivax along with urine showing more than 80% dysmorphic RBCs on a phase contrast microscopy. The patient was treated in accordance with World Health Organization (WHO) ¹⁰ guidelines and he had an uneventful recovery. To date only two cases of P. vivax malaria as a cause of acute glomerulonephritis have been reported. ^11,12

Conclusion

With the changing epidemiological pattern of malaria, especially in endemic areas, unusual complications such as acute glomerulonephritis may also be the clinical presentation of P. vivax malaria. Development of immunity and increasing resistance to anti-malarial drugs, along with the indiscriminate use of anti-malarial drugs, may be responsible for such complications. Early recognition and treatment with anti-malarial medicines is associated with a favourable outcome.

Competing interests: The authors declare that they have no competing interest.

Funding: None.