We report the case of a 65-year-old man with a history of hypertension secondary to primary hyperaldosteronism and chronic kidney disease since 1999 with nephrotic proteinuria secondary to chronic glomerulonephritis.
The patient was treated with hemodialysis from May 2012 to September 30, 2014, when a cadaveric donor kidney transplant was performed with 6 unaffected kidneys.
The donor biopsy, with 41 granules, reveals the existence of 7.3% of sclerotic glomeruli, mild hyaline thickening gl less than 25% and interstitial fibrosis less than 25%.
The induction treatment was performed with basiliximab, tacrolimus, mycophenolate mofetil (MMF) and steroids.
In the immediate post-transplant period, the patient has effective diuresis and no need for dialysis.
Complications include post-transplant diabetes mellitus and a surgical bed hematoma with anemization, which requires transfusion of 5 concentrates.
At discharge, the following values were observed: plasma creatinine (Crp): 1.56 mg/dl; hemoglobin (Hb): 8.2 g/dl; hematocrit: 25.5%; leukocytes: 11.300/1.000.
Treatment consisted of prednisone 25 mg/day, tacrolimus 5.5 mg/day and MMF 2 g/day.
Valganciclovir is prescribed as prophylaxis.
The patient evolved without symptoms, with a reduction in Crp levels to 1.2 mg/dl in the first 15 days after transplantation.
It maintains its Hb around 8-9 g/dl with progressive increase in the requirements of erythropoietin and fluctuating lymphopenia, but without other anomalies.
56 days after transplantation (26/11/2014), due to an increase in proteinuria of up to 1.2 g/day without deterioration of renal function, a graft biopsy was performed, with findings consistent with mild tubular toxicity, isolated tubular interstitial inflammation and segmental anticalcer lymphocytes.
Immunofluorescence revealed mild positivity for IgM and C3, and C4d staining was negative.
The asymptomatic patient did not show deterioration of renal function (Crp: 1-1.2 mg/dl), with optimal levels of immunosuppression, anti-HLA class I and II antibodies of 0% and virological studies without ultrasound abnormalities.
It was decided to maintain a narrow control, during which a progressive reduction of proteinuria was observed.
On December 2, 2014, at 64 days of age, the patient developed hyperthermia without focality, malaise, asthenia, hypoxia and body weight reduction, accompanied by anemization with Hbdl of up to 206%.
In complementary tests the following stand out: absence of primary leucocyte a.17 mg; normal levels of procalcitonin (0.15 ng/ml); elevated LDH: 321-397 mEq/l and increased C-reactive protein (7dl);
From the point of view of renal function, plasma creatinine does not exceed 1.05 mg/dl.
During this first admission, the complete serology of the following pathogens: EBV, CMV, herpesvirus, hepatotropic viruses, rubella, varicella zoster, parvovirus B19, CMV and mycoplasmaetti pneumoniae negative, C
Clinically, fever stands out only on the first day of admission, with subsequent persistence of fever.
He received treatment with quinolones and third generation cephalosporins, which were suspended at discharge.
Normocytic, hyporegenerative and normocytic anemia with a pattern of iron overload is related to heptazoles, deciding toxicity (valgan vir and trimethoprim-sulfamethoxa suspension).
Upon discharge, an analytical was requested, which showed a serology suggestive of acute Q fever, with positive IgM antibodies by IFI of Coxiella burni, so treatment was initiated with corticosteroids for 10 days.
Percutaneous fever and anemia were ruled out 4 months after transplantation.
During this second admission, the imaging tests performed (chest X-ray, abdominal ultrasound, CT scan of the abdomen, PET-CT, echocardiography, gastroscopy and ultrasound) revealed no significant abnormalities.
Tumor markers and serological studies (including determination of antibodies [IFI] for parvovirus B19 and for Coxiella VBV, whole virus HSV-8H) were negative, as well as cultures for tuberculosis and virus (HSV-1, respectively).
Therefore, the diagnosis of Q fever as the origin of the clinical picture is ruled out.
It was a false positive, since there was no seroconversion in the second sample and fever persisted despite treatment.
The patient remains febrile with marked deterioration of his general condition, anemia and lymphopenia, so it was decided to perform 23/2/2015 a bone marrow biopsy in which a hypocellular eosinophilic marrow with intense decrease of red blood cells was observed.
All this suggests parvovirus B19 infection, which is confirmed by PCR with positive results in this tissue.
At the same time, it was decided to perform a new blood PCR determination for parvovirus B19, which is positive this time.
1.
After confirming parvovirus B19 infection, the patient was discharged with MMF and started treatment with daily intravenous immunoglobulin of 0.5 g/kg/dose (10 doses) with adequate tolerance, disappearance of fever and normalization of Hb in March 2015.
At the end of the treatment and after checking that Hb remains stable and the patient remains afflicted, it was decided to reintroduce MMF at low doses.
However, 6 months after discharge, the patient presented mild renal function impairment: Crp up to 1.55 mg/dl and proteinuria 2.1 g/24 h (previous 0.6-0.8 g/24 h).
obscure vacuol, an immunological event derived from the decrease in immunosuppression in order to control viral replication, we decided to perform a second renal biopsy in November 2015 in which we observed acute interstitial tubular rejection suggestive of
Inflammatory cells are mostly intraparietal and few of them subendothelial.
C4d staining and immunofluorescence were negative.
After verifying the stabilization of parvovirus viral load, it was decided to optimise immunosuppression by increasing the MMF dose from 500 to 750 mg/24 h and tacrolimus (to maintain proteinuria levels around 7-8 ng/dl).
After one year of treatment, the patient continues to suffer from constipation with increased appetite and increased body weight.
Analytically, Hb levels are 15.2 g/dl without erythropoietin requirements, with renal function stability with proteinuria below 1 g/day (controlled with double RAAS blockade).
Anti-HLA antibodies class I and II remain negative.
Regarding plasma PCR for parvovirus B19, the laboratory of our hospital validates the quantitative technique for parvovirus B19.
We do not have viral load at the time of diagnosis, and the first quantitative is September 2015 (7 months approximately after treatment confirmation) with <50 copies/ml.
We inferred that although we were not able to completely eliminate the virus, probably the viral load before treatment was much higher, given the improvement observed both clinically and analytically.
Current viral load is maintained below 100 copies/ml, and a thorough clinical and analytical follow-up is performed including periodic determinations with PCR in order to detect a possible relapse.
