PARVOVIRUS B19 INFECTION IN KIDNEY TRANSPLANT RECIPIENTS: A HIDDEN THREAT TO GRAFT SURVIVAL – A CASE SERIES

 

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https://storage.unitedwebnetwork.com/files/1099/1e189cd7838a88d61f37a1b4a1c8eb7f.pdf
PARVOVIRUS B19 INFECTION IN KIDNEY TRANSPLANT RECIPIENTS: A HIDDEN THREAT TO GRAFT SURVIVAL – A CASE SERIES

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Elizabeth Yasmine
Wardoyo
Elizabeth Yasmine Wardoyo elizabeth.yasmine@gmail.com International Society of Nephrology Fellow in Department of Nephrology, Post Graduate Institute of Medical Education and Research, Chandigarh, India Division of Nephrology, Department of Internal Medicine, Fatmawati Hospital, Jakarta, Indonesia. Jakarta Indonesia *
Shrinath Parmeshwar Mashale shrinathmashale10@gmail.com Post Graduate Institute of Medical Education and Research Department of Nephrology Chandigarh India -
Smita Divyaveer divyaveer.ss@gmail.com Post Graduate Institute of Medical Education and Research Department of Nephrology Chandigarh India -
Mini Singh minipsingh@gmail.com Post Graduate Institute of Medical Education and Research Department of Virology Chandigarh India -
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Parvovirus B19 (PVB19) infection can cause a range of clinical manifestations, most notably severe refractory anemia in kidney transplant recipients. Previous rejection episodes and intensified immunosuppression increase susceptibility. Management often requires reducing immunosuppression, which paradoxically raises the risk of rejection and graft loss.

We retrospectively reviewed kidney transplant recipients diagnosed with PVB19 infection at the Postgraduate Institute of Medical Education and Research, Chandigarh, India, between January 2020 and June 2025. Ten cases were identified and confirmed by PVB19 DNA PCR.

All 10 patients presented with weakness; 30% had fever and 10% had sore throat. Seventy percent of infections occurred within 6 months post-transplant. Eighty percent received thymoglobulin induction, and all were maintained on tacrolimus, mycophenolate mofetil, and steroids. All developed anemia, 60% had leukopenia, and none had thrombocytopenia. Bone marrow biopsy (n = 3) showed hypocellular marrow. Graft dysfunction was present in all cases. Forty percent had prior rejection, and 20% developed T-cell–mediated rejection after infection. All patients received intravenous immunoglobulin (IVIG) and red cell transfusions; mycophenolate was withheld in all. Forty percent were switched from tacrolimus to cyclosporine A, while the remainder had tacrolimus dose reductions. Five patients achieved complete resolution with IVIG (median time, 12 months), one died of sepsis, and two experienced graft loss due to rejection.

Table 1. Baseline characteristic of patients (n=10)

Parameter

Value

Male, %

100

Age (years), median (IQR)

33 (26-44)

Basic disease, %

·       FSGS

·       IgA nephropathy

·       Chronic glomerulonephritis

·       Diabetic kidney disease

·       Renal stone disease

·       Obstructive uropathy

·       Unknown

 

20

10

30

10

10

10

20

First kidney transplant, %

90

Kidney donor, %

·       Living donor

·       Deceased donor

 

90

10

ABO compatibility, %

·       ABO compatible

·       ABO incompatible

 

90

10

Induction, %

·       R-ATG (Thymoglobulin)

·       ATG-F (Grafalon)

·       No induction

 

80

10

10

FSGS = focal segmental glomerulosclerosis; R-ATG = rabbit antithymocyte globulin; ATG-F = antithymocyte globulin Fresenius.

 

Table 2. Characteristics and Outcomes of Parvovirus Infection (n=10)

Parameter

Value

Time to infection (months), median (IQR)

2.5 (2-10)

Time to infection, %

·       < 6 months

·       6-12 months

·       1-5 years

 

70

20

10

Symptoms, %

·       Weakness

·       Fever

·       Sore throat

 

100

30

10

Rejection prior to infection, %

40

Rejection after infection, %

20

Blood result at diagnosis, median (IQR)

·       Hemoglobin (g/dL)

·       White blood cell (cells/mL)

·       Platelet (cells/mL)

·       Urea (mg/dL)

·       Creatinine (mg/dL)

·       AST (IU/L)

·       ALT (IU/L)

 

6.0 (5.7-6.9)

4,550 (3,925-6,185)

193,000 (176,250-283,000)

54 (48-89)

2.2 (1.8-3.0)

27.5 (23-39.7)

21.5 (14.7-34.2)

Lowest hemoglobin during infection (g/dL), median (IQR)

4.9 (3.9-5.3)

Bone marrow examination, %

·       Hypocellular

30

100

Therapy, %

·       IVIG

·       Packed red cell transfusion

·       Erythropoietin

·       HIF-PHDi

 

100

100

40

20

Tacrolimus switch to Cyclosporin A, %

40

Time to resolution, median (IQR)

12 (10-13)

Graft loss, %

20

Death, %

10

AST = aspartate transaminase; ALT = alanine transaminase; IVIG = intravenous immunoglobulin; HIF-PHDi = hypoxia-inducible factor-prolyl hydroxylase inhibitor

PVB19 infection in kidney transplant recipients typically occurs early after transplantation and is associated with marked hematologic abnormalities and graft dysfunction. Immunosuppression reduction, though necessary for infection control, may predispose to rejection and graft loss. Timely diagnosis and management are vital for favorable patient and graft outcomes.

Kewords