1. Introduction
Following Kidney Transplant, recurrent and de novo glomerulonephritis are possible causes of renal dysfunction.
Recurrent glomerulonephritis occurs much more frequently than De novo, but the exact prevalence remains unknown, in 1% - 12% [1] , due to the lack of allograft biopsies, and also to unknown initial kidney disease.
Any glomerulonephritis can recur. Segmental and focal hyalinosis, membranous nephropathy and atypical UHS are the most reported ones.
On the other hand, membranous nephropathy and HCV-associated membranoproliferative glomerulonephritis are the most frequent types of de novo glomerulonephritis. Rare cases of minimal change nephropathy and crescentic glomerulonephritis in Alport’s syndrome have been described.
Postinfectious acute glomerulonephritis (PIGN) is one of the most rarely reported de novo glomerulonephritis with only 18 cases previously described [2] . It’s due to an immunological process that affects the kidney after or during an ongoing infection (Infection—Associated glomerulonephritis).
2. Case Report
We report the case of a 47-year-old North African woman with end-stage renal disease (ESRD) due to unknown kidney nephropathy. She underwent hemodialysis for 11 years, and received the first kidney transplantation from her sister in 2017.
We used thymoglobulin as immunosuppressive induction, associated with Tacrolimus, mycophenolate and prednisone. Baseline serum creatinine was 0.9 mg/dl with normal urinalysis.
On March 2023, she is hospitalized for fever and dysuria. On admission, blood pressure was 155/85 mmHg with peripheral edema and the temperature was 38.5˚C with macroscopic hematuria.
Biological tests showed a leukocytosis (WBC 13,500 per cmm), acute kidney injury with serum creatinine at 3.5 mg/dl, a nephrotic syndrome with a serum albumin 25 g/l, urin protein excretion of 4 g/day, and a consumption of C3 and C4. Cryoglobulins were absent.
Urinalysis showed severe hematuria with 1200 red blood cells (RBC), 150 WBC, and urine culture was positive to Echerichia coli. Intravenous Ceftriaxone was given for 10 days.
The graft biopsy, performed 7 days after fever appeared, revealed in the light microscopic examination, a diffuse endocapillary cell proliferation in all glomeruli (Figure 1), an extracapillary proliferation in 3 glomeruli (Figure 2), with a preponderant deposit of C3 in direct fluorescence (Figure 3).
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Figure 1. Light microscopy ×40 (Hematoxylin eosin). Diffuse endocapillary cell proliferation and neutrophil exudation.
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Figure 2. Light microscopy (Hematoxylin eosin ×40): Extra capillary proliferation.
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Figure 3. (Direct Fluorescence) intense staining of C3.
The patient was treated with one intravenous pulse of Methylprednisolone and Cyclophosphamid.
The serum creatinine normalized after 3 months; Hematuria disappeared after 2 months. The complement was normalized after 10 weeks.
Proteinuria slowly decreased and had completely disappeared 4 months later.
The particularity of our clinical case, in addition to the rarity of the entity, is the favorable evolution contrary to the data in the literature.
3. Discussion
The immunosuppressive regimen of the organ transplant recipients increases the rate of infection complications. Both bacterial and viral infections are very common and may have indirect effects on the patient and graft. However, despite the high incidence of post-transplant infections, PIAGN is a rare entity. It’s an unusual cause of renal allograft dysfunction.
This could be due the ongoing immunosuppressive therapy that decreases antibody production or simply to the lack of biopsies during such events.
The few cases of PIGN in renal transplant reported in the literature were secondary to a wide variety of organisms; G. Moroni and al. described 3 heterogeneous types due to Echerichia coli bacteremia, a skin abscess, and cholangitis [3] . Some cases secondary to Staphylococcus aureus [4] [5] [6] , Cytomegalovirus [2] and polyomavirus [7] were also reported.
Regarding glomerulonephritis (GN) and bacterial infections, 2 different entities should be considered: a postinfectious GN with usually a latent period, and infection-associated GN developed in same time of an active ongoing infection. Our Patient developed the GN in the same time of an Echerichia coli pyelonephritis; Troy. J et al. described one case of PIGN in renal graft, 3 days after dysuria empirically treated with levofloxacin [2] .
In 2003, a new form of PIGN characterized by IgA dominant immunocomplex deposit has been described [8] . In kidney transplant, two cases of graft dysfunction related to IgA dominant PIGN were reported, the first one is a staphylococcus Infection-Associated GN developed 18 years post Kidney transplantation [4] , the second one reported 5 years after kidney transplantation, was an Influenza A secondary PIGN [3] .
PIGN usually presents as a nephritic syndrome with C3 hypocomplementemia; as for our patient who developed a nephrotic syndrome with a C3 but also C4 hypocomplementemia. The renal allograft biopsy found a diffuse proliferative Glomerulonephritis with extensive neutrophil infiltrate into the glomerular capillaries. Direct Immunofluorescence typically shows dominant staining for C3 predominantly mesangial, and less intensely for IgG, IgM and C1q.
Unlike the typical form of post-streptococcal GN, there is no established method in treating PIGN in renal transplant recipients. Some authors speculate a potential benefit of short course of intravenous corticosteroid; others use plasma exchange associated to steroid when crescents are present [6] . Despite that treatment, graft loss occurs in up to 60% of cases [9] . Some papers consider that using an immunosuppression can increase the risk of septicemia, especially in forms with active ongoing infection associated GN [10] .
In our case, we decided to associate an antimicrobial therapy with Corticosteroid and intravenous Cyclophosphamid because of the presence of crescents in the graft biopsy. Complete recovery was achieved 4 months later.
4. Conclusion
PIGN is surely a rare entity in renal graft patients, but any transplant clinician should know of its possible occurrence after or during any ongoing infection.
Renal biopsy needs to be considered during any graft dysfunction because of the amount of information it can provide.