DENGUE VIRUS INFECTION PRESENTING AS ACUTE POSTINFECTIOUS GLOMERULONEPHRITIS

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DENGUE VIRUS INFECTION PRESENTING AS ACUTE POSTINFECTIOUS GLOMERULONEPHRITIS
Luis Miguel
Silvera
Veronica Petroff veronicapetroff42@hotmail.com Hospital Zonal de Frias Nefrologia Santiago del Estero
Maria Paula Dionisi dmaripau@gmail.com Clinica Privada Velez Sarsfield Nefrologia Cordoba
Rocio Escobar ro.esc12@gmail.com Clinica Privada Velez Sarsfield Nefrologia Cordoba
Paulo Gomez paulogomez003@gmail.com Clinica Privada Velez Sarsfield Nefrologia Cordoba
Maria Emilia Garcia Chiple emiliachiple@gmail.com Clinica Privada Velez Sarsfield Anatomia Patologica Cordoba
Gabriela Sambuelli gabysamb@gmail.com Clinica Universitaria Reina Fabiola Anatomia Patologica Cordoba
Marisol Rodriguez marisolrodper@gmail.com Clinica Privada Velez Sarsfield Nefrologia Cordoba
Maria Alejandra Quintero malequinti@gmail.com Clinica Privada Velez Sarsfield Nefrologia Cordoba
Carlos Idoria cidoria@gmail.com Clinica Privada Velez Sarsfield Nefrologia Cordoba
Rafael Alberto Maldonado ramaldonado@gmail.com Clinica Privada Velez Sarsfield Nefrologia Cordoba
 
 
 
 
 

According to the WHO, approximately 500 million people in America are at risk of contracting dengue.

In the first four months of 2023, 84,433 cases have been reported, 180% more than for the same period of the epidemic three years ago in Argentina.

The dengue virus is an arbovirus (genus Flavivirus, family Flaviviridae) transmitted by the female Aedes Aegypti mosquito, having the capacity to generate asymptomatic or symptomatic infections under a wide spectrum of clinical manifestations.

It is characterized by presenting as an acute febrile syndrome with systemic and multiorgan involvement. Within this spectrum of clinical manifestations, ''DAKI'' (Dengue-associated Acute Kidney injury) responds to multiple mechanisms, most often associated with hypovolemia, also to the cytopathic effect of the virus, by tubular damage due to myoglobinuria (due to rhabdomyolysis) or thrombotic microangiopathy, or less frequent due to glomerulonephritis.

We present a case of DAKI due to Postinfectious Glomerulonephritis (PIGN) diagnosed in April 2023.

65-year-old male patient with a history of benign prostatic hyperplasia.

He had a Dengue infection that required hospitalization due to dehydration, fever and anemia. Twenty days after discharge, he consulted by worsening of general condition. On physical examination, generalized edema, lungs with bibasal hypoventilation.BP: 140/80 mm Hg. Sat O2: 94% AA. Laboratory requested: Hematocrit: 32%, Hemoglobin: 11.35 mg/dl, white blood cells: 9500 mg/dl, Platelets: 150,000 mg/dl, Urea: 195 mg/dL, Creatinine: 2.9 mg/dL, CPK : 104 mg/dl, LDH: 515 mg/dl, Albumin: 3 mg/dl. Complete urine: Hematuria ++, Proteins ++. Sediment: cellular 1/c. Leukocytes: 1/c 2-3/c. Few hyaline and granular cylinders. Scant fatty oval bodies. FMV: P/C: 1 ; remaining lab unremarkable. Chest X-ray: grade I cardiomegaly with effacement of both costophrenic sinuses suggestive of bilateral pleural effusion, 12-hour urine: proteinuria: 1580 mg/dl, and abdominal ultrasound: liver compatible with mild steatosis, both kidneys of morphology and normal size with preserved corticomedullary differentiation without dilation of its excretors, absence of free fluid in the abdominal cavity.  It was decided to admit him to the hospital, give an IV drip infusion of furosemide (200 mg/day) and a renal biopsy (RB) was performed due to clinical suspicion of GN.


After improving generalized edema, sanatorium discharge was indicated, with Urea: 82 mg/dL and Creatinine: 1.38 mg/dL. 

Treatment at discharge: Valsartan 160 mg/24 hours, Furosemide 40 mg /8 hours and Terazosin 5 mg/24 hours.

The histopathology report (MO and IF) revelead an acute PIGN (see attached photos).

It is remarkable that most of the data on post-Dengue GN only come from isolated cases reported in the literature. Mesangial proliferation and immune complex deposition are the dominant histological features of Dengue-associated GN; some cases of TMA were also described.






Fig 1.Immunofluerence stain (IgG), Fig 2.Immunofluerescence stain (C3), Fig 3.Light microscopy (PAS), Fig 4. Light microscopy (Masson), Fig 5. Light microscopy (H&E).

PIGN is a rare complication of Dengue that can go unnoticed due to its wide range of clinical expression. 

We highlight the need for an adequate diagnosis using RB in cases of dengue with renal dysfunction and proteinuria as a part of an adequate management in order to avoid long-term complications.

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