The A,b(19) and Cs of Acute Renal Failure

1Tulane University, New Orleans, LA

Meeting: Hospital Medicine 2011, May 10-13, Dallas, Texas.

Abstract number: 415

Case Presentation:

A 48‐year‐old man was referred from the clinic with worsening acute renal failure. He reported nausea without emesis but no other symptoms. His creatinine was 8.3 mg/dL (increased from his baseline of 1.4 mg/dL 12 days earlier). He denied a history of kidney disease but reported being hospitalized 2 weeks prior for an acute febrile illness with associated arthralgias, nausea with emesis, and diarrhea. During this time, he was treated with intravenous fluids and doxycycline and discharged. His blood pressure was 195/108 mm Hg; the remainder of his vital signs were normal. He was in no acute distress, and his physical examination was normal. Creatinine was 8.3 mg/dL and blood urea nitrogen 99 mg/dL. The remaining electrolytes were normal. A urinalysis showed 2– 5 white blood cells, 1 red cell, 200 mg of protein, and a few scattered fine granular casts. The urine drug screen was negative. An ultrasound of the kidneys showed mildly enlarged kidneys without evidence of hydronephrosis, mass, or renal artery stenosis. HbA1c was 5.9, and spot urine protein‐to‐creatinine ratio was 2.31. The C3 level was low at 84.3, with a normal C4 level of 28.4. ANA was < 1:20 (normal), C‐ANCA was < 1:20 (normal), P‐ANCA was 1:80 (high), and glomerular basement membrane antibody was <3.0 (normal). He had a kidney biopsy that showed a severe increase in mesangial matrix and edematous interstitium with fibrosis, tubular atrophy, and occasional inflammatory cells. Electron microscopy showed a thickened basement membrane, effacement of the foot processes, and an absence of deposits. Laboratory records from his hospitalization 2 weeks earlier revealed a positive parvovirus B19 IgM (4.31) and IgG (0.12). Based on these studies, the patient was diagnosed with acute renal failure secondary to parvovirus B19 infection and underlying diabetic nephropathy.


It is important for the general internist to recognize parvovirus B19 infection because this ubiquitous, human‐specific DNA virus causes a range of symptom severity depending on the age and health status of the human host. For infected adults, 25% are asymptomatic, 50% will present with fever and myalgia, and 25% will have fever, myalgia, arthralgia, and a lace‐like rash. In immunocompromised individuals (i.e., history of transplants, HIV, and diabetes mellitus), infection can result in a chronic anemia thus requiring intravenous immunoglobulin (IVIG) therapy. In this subset of patients, the typical rash or arthropathy may be absent. Parvovirus B19 has been implicated in nephritic and nephrotic syndromes.


Although there is no specific antiviral treatment for parvovirus B19, transfusions and IVIG therapy are useful in the settings of transient aplastic anemia or chronic infection, especially in immunocompro‐mised patients. Active parvovirus B19 infection is diagnosed in an immunocompetent individual by serologic testing for IgM, and viral DNA can be detected in the blood by PCR in immunocompromised individuals.


A. Tatum ‐ none; N. Whang ‐ none; W. Rothwell ‐ none

To cite this abstract:

Tatum A, Whang N, Rothwell W. The A,b(19) and Cs of Acute Renal Failure. Abstract published at Hospital Medicine 2011, May 10-13, Dallas, Texas. Abstract 415. Journal of Hospital Medicine. 2011; 6 (suppl 2). Accessed March 30, 2020.

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