Nephritic Syndrome with Aplastic Anemia: What Is the Unifying Diagnosis?

1Lutheran Medical Center, Wheatridge, CO

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

Abstract number: 409

Case Presentation:

A 51‐year‐old woman was admitted to the hospital with severe headaches, nausea, and vomiting. In the weeks preceding her admission, the previously healthy patient on no medications had developed headaches and saw her primary care physician. Accelerated hypertension (BP ∼180/110), hematuria, proteinuria (3+ on urinalysis), leukopenia [white blood cell count (WBC) 2.4] and anemia [hemoglobin (Hgb) 10] were discovered. She was started on carvedilol and saw a hematologist and nephrologist, who performed a bone marrow biopsy and secondary hypertension workup, respectively. Before she could follow up, her symptoms prompted admission to our service. On admission, her blood pressure was 1 69/1 12. The rest of her vitals were normal. Labs showed a normal Chem‐7, but WBC 0.9, Hgb 8.6 (normocytic indices), platelets 179. An MRI of the brain showed no cerebritis or vasculitis. Pleural effusions prompted a thoracentesis with normal fluid. Abdominal CT was normal with no splenomegaly and normal kidneys. A renal biopsy showed membranoproliferative glomerulonephritis type 1 (MPGN 1). Complement levels, ANCA, ANA with full profile, anti‐GBM antibody, hepatitis panels (HBsAg, Hepatitis C antibody), and antiphospholipid panel were all negative. Her bone marrow biopsy returned with aplasia of all cell lines but no abnormal cells. There was no evidence of infection, and 2 sets of blood cultures did not grow any organisms. She was noted to have mild renal failure (Cr 1.3‐1.7), but urine output would remain intact. On hospital day 5 her headaches, nausea, and vomiting were finally controlled. Her WBC was 1.9, Hgb 9.0, and blood pressures were better (140s/90s) on metoprolol, clonidine patch, and lisinopril. She was released. In follow‐up with her nephrologist, her anemia and leukopenia would improve slowly. Renal function would remain stable with Cr ∼1.6. Steroids would be started in light of her MPGN 1. Further questioning revealed that the patient worked as a dance instructor with children. Given this exposure, parvovirus B19 IgM, IgG, and polymerase chain reaction were sent on her serum and returned positive. The patient is now improving on steroids.


We describe a case of aplastic anemia and glomerulonephritis (MPGN type 1) from parvovirus B19 infection. Parvovirus B19 causes fifth disease in children and is a well‐described cause of aplastic anemia. It is not a well‐recognized cause of glomerulonephritis/nephritic syndromes.


Hospitalists often have the opportunity to manage nephritic syndromes. In this interesting diagnostic workup, systemic lupus erythematosus can cause aplastic anemia with acute glomerulonephritis. We add parvovirus B19 to that differential.


J. Strohecker ‐ none; D. Gillum ‐ none

To cite this abstract:

Strohecker J, Gillum D. Nephritic Syndrome with Aplastic Anemia: What Is the Unifying Diagnosis?. Abstract published at Hospital Medicine 2011, May 10-13, Dallas, Texas. Abstract 409. Journal of Hospital Medicine. 2011; 6 (suppl 2). Accessed April 8, 2020.

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