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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2017  |  Volume : 28  |  Issue : 6  |  Page : 1421-1426
Infection-related glomerulonephritis in a renal allograft

1 Department of Nephrology, Madras Medical College and Rajiv Gandhi Government General Hospital, Chennai, Tamil Nadu, India
2 Renopath Center for Renal and Urological Pathology Pvt Ltd., Chennai, Tamil Nadu, India

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Date of Web Publication18-Dec-2017


Infection-related glomerulonephritis (IRGN) is an immune-mediated glomerulo-nephritis, most commonly caused by bacterial infections. Although there is an increased incidence of infectious episodes in renal transplant recipients, IRGN as a cause of de novo glomerulonephritis is rarely seen probably due to impaired immunity. We hereby report a 28-year-old male renal transplant recipient, who developed IRGN following impetigenous skin lesions after six years of transplant. He developed rapid worsening of allograft function and was started on hemodialysis. Allograft renal biopsy showed diffuse exudative endocapillary proliferation with crescents. Electron microscopy revealed large subepithelial hump-like deposits. Despite pulse steroid therapy, he became dialysis dependent. Our patient is unique in the way that poststreptococcal glomerulonephritis in an adult after renal transplantation has not been reported so far. We conclude that IRGN after renal transplant, though rare is a possible etiology for allograft dysfunction. There is no definitive treatment protocol for this de novo glomerulonephritis which has an overall poor prognosis.

How to cite this article:
Gopalakrishnan N, Jeyachandran D, Abeesh P, Dineshkumar T, Kurien AA, Sakthirajan R, Balasubramaniyan T. Infection-related glomerulonephritis in a renal allograft. Saudi J Kidney Dis Transpl 2017;28:1421-6

How to cite this URL:
Gopalakrishnan N, Jeyachandran D, Abeesh P, Dineshkumar T, Kurien AA, Sakthirajan R, Balasubramaniyan T. Infection-related glomerulonephritis in a renal allograft. Saudi J Kidney Dis Transpl [serial online] 2017 [cited 2022 Dec 4];28:1421-6. Available from: https://www.sjkdt.org/text.asp?2017/28/6/1421/220864

   Introduction Top

Posttransplant glomerulonephritis may be either due to recurrence of native disease which is more common or due to de novo glomerulonephritis.[1],[2] Posttransplant recipients in immunocompromised milieu, have increased risk for infections of varying etiology. However,acute glomerulonephritis due to infections among these patients has been rarely reported. We present here a male patient who had crescentic infection-related glomerulonephritis (IRGN) as a cause of late renal allograft dysfunction.

   Case Report Top

A 28-year-old gentleman was on maintenance hemodialysis (HD) for two years, and his native kidney disease was secondary vesicoureteric reflux due to hypospadias. He underwent live-related renal transplantation with the father as donor in September 2007. No induction therapy was given and was under triple immunosuppressive drugs (prednisolone, azathioprine, and cyclosporine) with normal graft function. At two years after transplant, he had biopsy-proven acute cellular rejection. He was treated with three doses of methyl prednisolone, and tacrolimus was substituted for cyclosporine. He had stable graft function with serum creatinine of 2.4 mg/dL for next four years.

On October 2013, he presented with fever, oliguria, and one episode of macrohematuria. On examination, he had leg edema and multiple healing impetigenous skin lesions over the right leg and gluteal region. His vitals were normal. Laboratory investigations showed urinalysis: 50–100 red cells/hpf, red cell casts, 3+ proteinuria, urine protein creatinine ratio: 7.9; hemoglobin: 8.8 g/dL; total white cell count: 4800/mm3; blood sugar: 102 mg/dL; blood urea nitrogen: 99 mg/dL; serum creatinine: 7.7 mg/dL; C3 level: 28 mg/dL (normal 90–180 mg/dL); C4 level: 24 mg/dL, and antistreptolysin O (ASO): 1:248 Todd units (normal <200). Viral serologies were negative. No organism was grown in urine and blood.

Renal biopsy was done on day 3 after admission. Light microscopy revealed nine glomeruli, of which five were globally sclerotic. There was endocapillary proliferation and a neutrophilic infiltration with early cellular crescents in three of the four viable glomeruli [Figure 1]a. There were no spikes, no necrotizing lesions, no tubulitis or vasculitis. Edema and a mild inflammatory infiltrate were seen in the interstitium. Immunofluorescence showed C3 (3+) and IgG (3+) positivity. C4d was negative. Ultrastructural examination revealed severe hypercellularity involving both mesangium and glomerular capillary loops. There were frequent large hump-like subepithelial deposits [Figure 1]b without basement response and mesangial deposits. Diagnosis of Infection related glomerulonephritis in a renal allograft was made.
Figure 1a: Renal allograft biopsy showing endocapillary proliferation with neutrophilic infiltration and cellular crescents (H and E).

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Figure 1b: Electron micrograph showing multiple, large, discrete, subepithelial electron dense deposits (subepithelial humps indicated by arrow) 12,000× magnification.

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The patient was started on HD and received pulse intravenous methylprednisolone 500 mg/ day for three days. Although months, his graft function did not improve and his serum C3 level was normalized after two became dialysis dependent.

   Discussion Top

The incidence of de novo glomerulonephritis in renal transplant recipients is around 2%–3%, most common being membranous glomerulopathy.[1],[2] IRGN is an immune complexmediated disease occurring most commonly after bacterial infections such as group A streptococcus and staphylococcal infection.[3] Rarely, viral infection such as Epstein–Barr, human immunodeficiency virus, parvovirus B19, and influenza A are also linked with the occurrence of IRGN.

Acute IRGN in renal allograft were reported rarely, and to the best of our knowledge, only 13 cases[4],[5],[6],[7],[8],[9],[10],[11] of IRGN in renal allograft has been reported in literature [Table 1] till date, ours being the first case report of IRGN following streptococcal infection in an adult after renal transplantation. Of total 13 cases, 11 were males. The mean age and time of presentation after renal transplant was 41.1 ± 18.3 years and 69.3 ± 53.1 months, respectively. Among causative organisms staphylococcus (4/13) was commonest, followed by streptococcus (1/13),  Escherichia More Details coli (1/13), Enterococcus (1/13), and cytomegalovirus (1/13). Low C3 was seen in five patients. Endocapillary proliferation with neutrophilic infiltration was the most common histopathology (10/13). Crescents were seen in three. Six patients received steroid pulse therapy. Seven patients had some renal recovery, five became dialysis dependent, and one patient died. Among three patients who had crescents, two became dialysis dependent, and one expired.
Table 1. Infection related glomerulonephritis in renal transplant recipients reported in literature.

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The pathogenesis of IRGN after transplantation is poorly understood.[12] Although there is an increased incidence of infection posttrans-plantation, de novo glomerulonephritis due to infections has been reported rarely. Most of the reported cases had severe clinical course. It is surmised that long-term immunosuppressive drugs affect the immune response of T-cell function, antibody production, and immune complex formation. Benefits of cytotoxic agents and corticosteroids in native kidney IRGN and IRGN posttransplantation are not clear.[13]

Our patient presented with worsening graft function at six years of the posttransplant period, preceded by impetigo. He had low C3 and elevated ASO titer. Renal histology showed proliferative glomerulonephritis with glomerular neutrophilic infiltration and cellular crescents with intense C3 deposits. EM revealed large subepithelial hump-like deposits. These findings confirmed the diagnosis of IRGN due to streptococcal infection. He had severe clinical course requiring HD during the presentation and subsequently ended up with graft loss. Although steroid has no definite role, intravenous pulse methyl prednisolone was tried as he had cellular crescents.

To conclude, IRGN should also be considered as the differential diagnosis for post transplant graft dysfunction, particularly when associated with infections. A high index of suspicion is necessary for the diagnosis. The exact role of corticosteroids and augmentation of the existing immunosuppressive therapy is uncertain.

   Acknowledgment Top

We thank Prof. Patrick D Walker MD, Director, NEPHROPATH, Arkansas, for his help in electron microscopic evaluation of renal biopsy.

Conflict of interest: None declared.

   References Top

Ivanyi B. A primer on recurrent and de novo glomerulonephritis in renal allografts. Nat Clin Pract Nephrol 2008;4:446-57.  Back to cited text no. 1
Cameron JS. Recurrent primary disease and de novo nephritis following renal transplantation. Pediatr Nephrol 1991;5:412-21.  Back to cited text no. 2
Nasr SH, Radhakrishnan J, D’Agati VD. Bacterial infection-related glomerulonephritis in adults. Kidney Int 2013;83:792-803.  Back to cited text no. 3
Sanfilippo F, Croker BP. The possible occurrence of staphylococcal postinfectious glomerulonephritis in a renal allograft. Transplantation 1983;35:25-9.  Back to cited text no. 4
Nebeker HG, Hercz G, Feld GK, et al. Postinfectious glomerulonephritis in a renal allograft associated with a mycotic aneurysm of a coronary artery. Am J Med 1984;76:940-2.  Back to cited text no. 5
Schwarz A, Krause PH, Offermann G, Keller F. Recurrent and de novo renal disease after kidney transplantation with or without cyclosporine A. Am J Kidney Dis 1991;17:524-31.  Back to cited text no. 6
Sorof JM, Weidner N, Potter D, Portale AA. Acute post-streptococcal glomerulonephritis in a renal allograft. Pediatr Nephrol 1995;9:317-9.  Back to cited text no. 7
Moroni G, Papaccioli D, Banfi G, Tarantino A, Ponticelli C. Acute post-bacterial glomerulonephritis in renal transplant patients: Description of three cases and review of the literature. Am J Transplant 2004;4:132-6.  Back to cited text no. 8
Plumb TJ, Greenberg A, Smith SR, et al. Postinfectious glomerulonephritis in renal allograft recipients. Transplantation 2006;82: 1224-8.  Back to cited text no. 9
Gaspert A, Lüthi B, Mueller NJ, et al. Subacute allograft failure with dysuria and hematuria in a kidney transplant recipient. Am J Kidney Dis 2009;54:154-8.  Back to cited text no. 10
Alsaad KO, Aloudah N, Alhamdan HM, Alamir A, Fakeeh K. Acute diffuse proliferative postinfectious glomerulonephritis in renal allograft – A case report and literature review. Pediatr Transplant 2014;18:E77-82.  Back to cited text no. 11
Moroni G, Pozzi C, Quaglini S, et al. Long-term prognosis of diffuse proliferative glomerulonephritis associated with infection in adults. Nephrol Dial Transplant 2002;17:1204-11.  Back to cited text no. 12
Roy S 3rd, Murphy WM, Arant BS Jr. Post-streptococcal crescenteric glomerulonephritis in children: Comparison of quintuple therapy versus supportive care. J Pediatr 1981;98:403-10.  Back to cited text no. 13

Correspondence Address:
Dhanapriya Jeyachandran
Department of Nephrology, Madras Medical College and Rajiv Gandhi Government General Hospital, Chennai, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-2442.220864

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