Acute glomerulonephritis in dengue hemorrhagic fever: A rare case report


An 11-year-old male child presented with fever, bodyache, swelling over the whole body, and oliguria. He had hypertension. Urine microscopy showed hematuria and glomerular casts. Renal functions were deranged and had low complement C3 level. Chest X-ray showed plural effusion and ultrasonography abdomen showed mild ascitis. The immunoglobulin (Ig)M and IgG enzyme-linked immunosorbent essay for dengue virus were positive. Diagnosis of dengue hemorrhagic fever with acute glomerulonephritis was made. He was managed with maintenance fluid, antihypertensive medicine and supportive care. He recovered gradually and was discharged 12 days after admission.

Keywords: Acute glomerulonephritis, dengue hemorrhagic fever, glomerular cast, hypertension, hematuria

How to cite this article:
Meena K R, Kumar P, Anita, Paul P. Acute glomerulonephritis in dengue hemorrhagic fever: A rare case report. Ann Trop Med Public Health 2013;6:581-2


How to cite this URL:
Meena K R, Kumar P, Anita, Paul P. Acute glomerulonephritis in dengue hemorrhagic fever: A rare case report. Ann Trop Med Public Health [serial online] 2013 [cited 2017 Nov 14];6:581-2. Available from:



Dengue fever, caused by dengue virus (RNA flavivirus) is currently the most important human mosquito borne viral infection of public health significance. It has been known to be endemic in India. In 2012, an estimated 37000 cases were detected all over India with 227 deaths. Renal injuries comprising glomarulonephtritis, acute kidney injury, and haemolytic uremic syndrome has been reported in dengue patients. [1] Till date, nearly all dengue hemorrhagic fever induced renal injuries in described cases had occurred in association with shock, sepsis, hemolysis, or rhabdomyolysis. [2]

Acute glomerulonephritis without these predisposing factors has rarely been reported. [1] Only one case has been reported till date. [3] We are reporting a case of dengue hemorrhagic fever presenting with acute glomerulonephritis.

Case Report

Previously healthy, 11-year-old male child was brought to our hospital with complaints of fever with bodyache (6 days), swelling of the whole body (2 days), and decreased urine output (1 day). There was no history of hematuria, burning micturition, rash, loose stool, vomiting, sore throat, icterus, or bleeding from any site. There was no history of boils in the last 3-4 weeks. There was no history of hypertension An epidemic of dengue fever was going on in the entire North India. On examination, the child was conscious, febrile (38.4°C), heart rate 120/min, respiratory rate 22/min, blood pressure was 140/110 mmHg (>95 th centile), facial puffiness, bilateral pitting pedal edema, decreased breath sound bilaterally in basal areas of lungs, hepatomagely (3 cm below right costal margin), and shifting dullness in abdomen was present. There was no icterus or cyanosis. Laboratory tests revealed hemoglobin 10.1 gm/dl, total leukocyte count 8800/cmm, differential leukocyte count-polymorphs 40%, lymphocytes 55%, monocytes 2%, eosinophils 3% and platelet count 1,00,000/cmm. Peripheral smear showed no evidence of haemolysis. Malaria parasite was negative. blood urea 120 mg/L, serum creatinine 3.9 mg/dL, serum Na+ 132 MEq/L, serum K+ 5.2 MEq/L, total bilirubin 0.3 mg/dl, SGOT 29 IU/L, SGPT 18 IU/L, alkaline phosphatase 396 IU/L, serum albumin 3.4 g/dL, and serum cholesterol 108 mg/dL. Urine analysis showed microscopic hematuria and proteinuria (++), RBC cast and was negative for myoglobin. ASLO and C-reactive protein (CRP) were negative. An abdominal ultrasonography showed normal size kidney with mild ascitis. Chest X-ray showed bilateral plural effusion. Echocardiography and renal Doppler were normal. Urine and blood culture were sterile. Serology [immunoglobulin (Ig)M and IgG enzyme-linked immunosorbent essay] against dengue virus was positive. Coagulation profile was normal. His complement C3 level was 20 mg/dL (normal range: 90-180).

Patient was treated conservatively with maintenance fluid, antihypertensive medicines (intravenous frusemide and oral enalapril), and supportive care. He gradually recovered with improving urine output and renal functions and discharged 12 days after admission. At the time of discharge, his repeat chest X-ray was normal, platelet count were 2, 50,000/cmm, serum creatinine was 0.6 mg/dL, and blood pressure returned to normal (off antihypertensive medicines). On follow-up visits, his blood pressure and kidney function test are normal.


The mechanism of glomerulonephritis in children with dengue hemorrhagic fever remains unclear. Various mechanisms are implicated in the pathogenesis of glomarulonephritis associated with viral infections. These include the direct cytopathic effects of viral proteins on glomarular and tubular cells, in situ immune-mediated mechanisms involving viral antigens bound to glomarular structures, injury due to circulating immune complexes composed of viral antigen and host antviral antibodies and injury due to various inflammatory mediators released in response to glomerular or tubular cytopathic effects. [2],[4]

It is not clear whether the virus causes direct damage by invasion of the kidneys. When dengue virus-2 was injected intra peritoneal in adult mice, proliferative glomerular lesions without urinary abnormalities developed by the 2 nd week and immune complex deposition was demonstrable in the glomaruli by the 3 rd week of infection. [5] Recent studies using immunehistochemistry techniques have established the presence of viral antigens in kidney tubules of patients with serologically or virologically confirmed dengue infections. [4] Histopathology has demonstrated the presence of IgG, IgM, and C3 deposition in the glomeruli and focal thickening of the glomerular basement membrane, with hypertrophy of mesangial cells at the sites of immune complex deposition in patients with renal insufficiency and dengue fever. [6]

It has been hypothesized that dengue virus infection elicits an immune response to viral antigens and results in immune complex deposit in the glomaruli. Immune complex deposits in immune complex mediated glomarulonephritis consist predominantly of IgG, IgM, and C3 and deposit in the mesangium in a coarse granular pattern. [7]

The low complement C3 levels in our case points toward a possible immune complex-mediated acute glomerulonephritis as the cause of glomerulonephritis.



1. Lima EQ, Gorayeb FS, Zanon JR, Nogueira ML, Ramalho HJ, Burdmann EA. Dengue haemorrhagic fever-induced acute kidney injury without hypotension, haemolysis or rhabdomyolysis. Nephrol Dial Transplant 2007;22:3322-6.
2. George R, Liam CK, Chua CT, Lam SK, Pang T, Geethan R, et al. Unusual clinical manifestations of dengue virus infection. Southeast Asian J Trop Med Public Health 1988;19:585-90.
3. Bhagat M, Zaki SA, Sharma S, Manglani MV. Acute glomarulonephritis in dengue haemorrhagic fever in the absence of shock, sepsis, haemolysis or rhabdomyolysis. Paediatr Int Child Health 2012;32:161-3.
4. Glassock RJ. Immune complex-induced glomarular injury in viral disease. An overview. Kidney Int Suppl 1991;35:S5-7.
5. Boonpucknavig S, Vittiviroj O, Boonpucknavig V. Infection of young adult mice with dengue virus type 2. Trans R Trop Med Hyg 1981;75:647-53.
6. Jessie K, Fong MY, Devi S, Lam SK, Wong KT. Localization of dengue virus in naturally infected human tissue by immunohistochemistry and in situ hybridization. J Infect Dis 2004;189:1411-8.
7. Upadhaya BK, Sharma A, Khaira A, Dinda AK, Agrawal SK, Tiwari SC. Transient IgA nephropathy with acute kidney injury in a patient with dengue fever. Saudi J Kidney Dis Transpl 2010;21:521-5.

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1755-6783.133749

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