NDT Advance Access originally published online on September 30, 2006
Nephrology Dialysis Transplantation 2007 22(2):662-663; doi:10.1093/ndt/gfl599
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Acute renal failure in a patient with West Nile viral encephalitis
Email: brenerz{at}yahoo.comSir,
West Nile (WN) virus is increasingly recognized as an important human pathogen in the North America. Meningitis or encephalitis develops in approximately 1 in 150 infected persons. Rare extraneurological manifestations include myocarditis, pancreatitis and hepatitis. Acute renal failure (ARF) is a very rarely reported manifestation of WN virus infection. We describe a case of reversible ARF secondary to biopsy-proven acute tubular necrosis (ATN) in a patient with WN virus encephalitis. To our knowledge, this is the second report of ATN in a patient with WN virus infection.
Case
A 76-year-old man with known history of diabetic nephropathy and hypertension was admitted to hospital in New York City in October 2005 with fever and confusion. He reported fatigue and abdominal discomfort 3 days after being bitten by mosquitoes. Two weeks later he presented with high fevers, chills and confusion.
On examination, he was alert, but confused. His blood pressure was 170/80 mm Hg and temperature 39°C. The rest of the examination was unremarkable. Serum sodium was 127 mmol/l, potassium 4.8 mmol/l, urea 15.7 mmol/l and creatinine 168 µmol/l. His baseline creatinine level was 150 µmol/l. Complete blood counts were normal, and urinalysis showed haematuria and proteinuria. Computed tomography (CT) of the brain and chest were unremarkable. Intravenous antibiotics were started and stopped when cultures of cerebrospinal fluid (CSF), blood and urine remained negative after 72 h. On day 2 he became lethargic. Lumbar puncture showed clear CSF, with 0.7 g/l protein, 2.6 mmol/l glucose, 68 red cells per cubic millimeter, 154 white cells per cubic millimeter with 85% lymphocytes and negative Gram stain. New York State Department of Health subsequently reported WN virus IgM antibody from CSF by capture enzyme immunoassay. The patient remained confused and agitated with stable vital signs. MRI of the brain demonstrated cerebral atrophy. Four days later, serum creatinine rose to 583.4 µmol/l and urea to 26 mmol/l. Urine volume never decreased; urinalysis showed turbid colour, with proteinuria, 2–4 white cells, 22–24 red cells, 2–5 coarse granular casts per high-power field, no eosinophils and tested negative for myoglobin. Abdominal ultrasonography was normal. Renal biopsy on the ninth hospital day showed acute tubular necrosis (ATN) and early diabetic nephropathy (Figure 1). Over the next five days renal function and mental status returned to baseline and the patient did not require dialysis therapy. By day 12 the patient was ambulatory and was discharged home. The patient has remained well throughout the 7-month period of close clinical observation; he has been afebrile and his serum creatinine level has remained stable at 150 µmol/l.
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Comment
Most WN virus infections in humans are subclinical, with overt disease occurring in 1 out of every 100 infections. Rare manifestations include myocarditis, pancreatitis and fulminant hepatitis—the involved organs are sites of high viral replication [1]. Some support exists for a renal tropism of WN virus. WN virus has been detected in high titres by RNA assays in the kidneys of wild birds determined to have died from WN virus infection [2].
In contrast to a prior reported fatal case of WN virus encephalitis and renal failure [3], our patient had no traditional risk factors for ATN such as hypotension, clinically evident hypovolaemia, endogenous or exogenous nephrotoxins and he did not require dialysis.
The chronological sequence of renal failure and recovery in the context of WN encephalitis suggest that the renal injury is due to direct viral and/or immune-mediated damage. WN virus is an emerging infectious disease, and as more cases are reported, it is possible that renal involvement will be recognized among the presentations of WN virus infection. Our case report may help to elucidate the mechanisms of renal impairment in WN virus infection.
Conflict of interest statement. None declared.
References
- Southam CM and Moore AE. (1952) Clinical studies of viruses as antineoplastic agents, with particular reference to Egypt 101 virus. Cancer 5:1025–1034.[CrossRef][Web of Science][Medline]
- Kramer LD and Bernard KA. (2001) West Nile virus infection in birds and mammals. Ann NY Acad Sci 591:84–93.
- Huang C, Slater B, Rudd R, et al. (2002) First isolation of West Nile virus from a patient with encephalitis in the United States. Emerg Inf Dis 8:1367–1371.[Web of Science][Medline]
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