A 36‐year‐old Caribbean male with a past medical history of type 2 diabetes mellitus and hypertension presented acutely to the hospital with syncope along with muscle aches, fevers to 104 degrees Fahrenheit (F) and profuse diarrhea after returning from a trip to Grenada. Two days prior he had presented to the emergency department with similar gastrointestinal complaints. He was given intravenous fluids and discharged on ciprofloxacin for presumed traveler’s diarrhea. Upon returning to the hospital, his exam was notable for a temperature of 101.6 degrees F, no rashes, and a distended but soft and non‐tender abdomen. His labs were remarkable for a hematocrit of 53.4, platelets of 107, creatinine of 3.3, ALT/AST of 80/123, and albumin of 2.6. He was started on intravenous ciprofloxacin and metronidazole with resolution of all gastrointestinal symptoms by hospital day 3. All stool cultures returned negative as did IgM and IgG antibodies to dengue. His creatinine continued to uptrend despite aggressive intravenous hydration and peaked at 5.5. A 24 hour urine collection yielded 7.2 grams of protein. A renal biopsy was performed and showed collapsing focal segmental glomerulosclerosis as well as widespread acute tubular injury. He was started on high dose prednisone. A week following his hospitalization repeat studies for dengue IgM and IgG antibodies returned positive.
Dengue fever is a self‐limited, systemic viral infection of great global impact transmitted to humans through mosquito vectors and should be considered in the differential diagnosis for all returning travelers with a fever. In addition to fevers greater than 101.3 degrees F, presenting symptoms often include headache, myalgias, joint pain and vomiting. The clinical course varies from a mild febrile illness to multi‐organ failure and death. Diagnosis is often confirmed with dengue serologies, but require at least 4 days after the onset of fever for ELISA detection. The incidence of renal failure is higher in patients with severe disease; typically resulting in acute tubular necrosis (ATN) from capillary leak syndrome, hemorrhage or shock. Other processes published in case reports include acute glomerulonephritis, thrombotic microangiopathy, and rhabdomyolysis. Our patient was discovered to have HIV‐ negative collapsing focal segmental glomerulosclerosis (FSGS). Dengue fever has no known association with FSGS, which is most linked with HIV‐1, parvovirus B19, SV40, EBV and CMV. These latter viruses are thought to infect podocytes and tubular cells, inducing collapse through induction of cell arrest and apoptosis. Our patient’s renal failure appears to have been multifactorial including ATN and collapsing FSGS.
Dengue fever should be considered in the differential diagnosis for any returning traveler with fever. The natural history of the disease is quite variable. Careful observation and supportive therapy is required as severe manifestations including hemorrhage, capillary leak and shock may occur. Renal failure may result from severe disease. The etiology of renal failure associated with dengue fever is not well understood, but likely varies depending on the clinical scenario. To our knowledge, this is the first case of dengue fever associated with collapsing FSGS.