Clinical case: 20-year-old man with a history of chronic kidney
disease of 4 years of evolution, in replacement treatment with hemodialysis
through a permanent catheter (left), with residual renal function of 100
ml/day. On 06/10/23 he was transplanted from cadaveric donor type, he received
Induction, Thymoglobulin 100 mg and Methylprednisolone 750 mg, He has high risk
for natural/acquired CMV and baseline creatinine 2.0, presented delayed graft
dysfunction requiring hemodialysis sessions, additional symptoms of urinary
tract infection with isolation of resistant K pneumoniae that required
in-hospital management for 7 days with carbapenem dose, was maintained with
treatment with Tacrolimus 1 mg 4-0-4, MMF 500 mg 2-0-2, Prednisone 15 mg 1-0-0,
TMP/SMX: 400/80 M-W-F 2 tablet, valganciclovir 1-0-1, Omeprazole 40 mg every 24
hr, in her zero biopsy: number of glomeruli 18. Acute Tubular Injury with
regenerative changes. Ramuzzi 1/12. Three months after his transplant, he
presented abdominal pain in the right upper quadrant with fever quantified at
38°, and presence of bicytopenia whit report Hb 4.6 gr/dl and lymphocytes of
200, additionally elevation creatinine levels 2.6 mg/dl. dl, he was started antibiotic
treatment with carbapenem due to a history of urinary infectious process,
however it was ruled out with blood and urine cultures taken, continued febrile
and with bicytopenia, pain and increased testicular volume were added to this
symptoms, in abdominal and pelvic CT scan showed lithiasis in the kidney graft
and with an increase in volume at the testicular level without collection data.
It was evaluated by urology where data was documented to orchiepidemitis. In
the complementary tests, iron 149, ferritin 1500, PCR 16, procalcitonin 0.5,
was discarded other causes of anemia and started a dose of erythropoiesis
stimulant was started without showing improvement in the levels. He completed 7
days of treatment with carbapenem, continued with anemia, lymphopenia and
fever. The normocytic, normochromic and hyporegenerative anemia with a pattern
of iron overload was suspected to be secondary to drug toxicity (valganciclovir
and trimetropim-sulfamethoxazole), which is why it was decided its suspension.
Due to persistence of symptoms, it was decided to
perform serology by PCR for more pathogens, whit negative result for EBV, CMV,
herpesviruses, hepatotropic viruses, rubella, varicella-zoster, Mycoplasma
pneumoniae, Coxiella burnetti, fungi and mycobacteria, the patient continuous
with anemia and lymphopenia and neutropenia data was added, it was decided to
perform a bone marrow aspirate (09/07/23) with culture and sample for GenXpert
for TB, 2PG was transfused due to the presence of hemoglobin of 3.5 gr/dl, PCR
was collected for Parvovirus B19 serum being positive, so the administration of
MMF was suspended and Immunoglobulin 0.75 was started every 3rd day until
treatment with 2 grams was completed, creatinine levels of 2.0 mg/dl and BUN of
39 mg/dl were maintained, and hemoglobin recovery at 8 gr/dl, neutrophils at
5.17 (10.3/ul), currently under continuous monitoring with doses of
immunosuppression with doses of Tacrolimus 1 mg 5-0-5 08:00 am and 20 pm MMF
500mg 1-0-1 , Prednisone 5 mg orally every 24 hours, report of last FK level
4.7 12.10.23.
Discussion: Parvovirus infection in the transplanted population is
rare, and the symptoms can be very subtle: anemia is the predominant
manifestation. Our patient was diagnosed with parvovirus B19 infection 3 months
after transplantation. Which debuted with abdominal pain and fever, added to
this was bicytopenia which became resistant to the administration of
stimulants. It is possible that the parvovirus infection comes from the donor,
for whom neither serology nor viral load is available. It could be a
reactivation of the virus caused by immunosuppression, but, since we do not
have the pre-transplant serological status of the recipient, we cannot To
ensure this, the anemia is characterized by being normocytic, severe
normochromic, non-regenerative, which does not respond to blood transfusions or
erythropoiesis-stimulating agents. Leukocytopenia, thrombocytopenia and
reactive hemophagocytic syndrome have also been related to parvovirus B19
infection. In our patient, normocytic and normochromic anemia was the main
manifestation throughout his evolution, with Hb levels of up to 3.5 g/dl, with
no response to erythropoiesis-stimulating agents. There are currently no
effective antiviral drugs available against parvovirus B19. In anemia
associated with infection by this virus, different therapeutic options can be considered:
reducing immunosuppression (reduction/withdrawal of drugs); change
immunosuppressant (replace tacrolimus with cyclosporine - some authors have
described defective clearance of the virus in patients treated with tacrolimus
or with the aim of providing neutralizing antibodies to the virus,
administration of IVIG at doses of 0.4-0.5 g/ kg, from 2 to 10 days13 with a
cumulative dose that usually ranges between 2 and 5 g/kg). Anemia is corrected
by more than 90% with just one cycle of treatment, but the risk of recurrence
ranges between 23 and 33%, which in this case improved with the transfusion of
red blood cells.