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Nephrology 19, Suppl. 3 (2014) 45–48
Brief Communication
Early recurrence of active IgA nephropathy after kidney transplantation YASUHIRO OTSUKA, ASAMI TAKEDA, KEIJI HORIKE, DAIJYO INAGUMA, NORIHIKO GOTO, YOSHIHIKO WATARAI and KUNIO MOROZUMI Department of Nephrology and Transplantation Center, Japanese Red Cross Nagoya Daini Hospital, Nagoya, Japan
KEY WORDS: early recurrence, IgA nephropathy, recurrent glomerulonephritis, recurrent IgA nephropathy, renal transplantation. Correspondence: Dr Yasuhiro Otsuka, Department of Nephrology and Transplantation Center, Japanese Red Cross Nagoya Daini Hospital, Nagoya, Japan. Email: [email protected] doi:10.1111/nep.12252 Conflict of interest: None declared.
ABSTRACT: IgA nephropathy (IgAN) is recurrent after transplantation; however, its time of recurrence is unpredictable. To date, factors influencing IgAN recurrence have not been elucidated. We present a case of a 23-year-old man with end-stage renal disease (ESRD) who underwent living-related ABOidentical pre-emptive kidney transplantation (PEKT) using his 57-year-old mother as a donor. IgAN started when the patient was 19 years old, and renal biopsy revealed the usual pathological findings of IgAN. In spite of steroid therapy including steroid pulse and tonsillectomy, the patient developed nephrotic syndrome and progressed to ESRD in 4 years. Protocol biopsy on day 19 following PEKT revealed active recurrent IgAN. Nephroticrange proteinuria and mild deterioration of kidney function developed regardless of strong immunosuppressive therapy such as steroid pulse, double filtration plasmapheresis and rituximab. We report a case of refractory IgAN that recurred 19 days after transplantation. This case is considered of value to elucidate factors leading to active IgAN recurrence.
IgA nephropathy (IgAN) is the most common primary glomerulonephritis that causes end-stage renal disease (ESRD) in 20–40% of patients.1 The success rate of kidney transplantation for patients with IgAN-induced ESRD was believed to be good. However, few data are available on the long-term outcome of IgAN patients with renal transplantation. Moroni et al.2 reported that death-censored graft survival at 15 years was approximately 10% lower in IgAN patients than in controls, suggesting that the culprit is IgAN recurrence. In fact, IgAN is one of the most common recurrent glomerulonephritis. The majority of recurrent IgAN is not clinical but pathological. Factors deciding the activity of recurrent IgAN remain unclear. It is unpredictable when IgAN recurs and why these recurrences occur immediately after transplantation. We report a case of active IgAN that recurred 19 days after transplantation.
A CASE OF REFRACTORY IgAN THAT RECURRED 19 DAYS AFTER TRANSPLANTATION A 23-year-old man with ESRD underwent living-related ABO-identical pre-emptive kidney transplantation (PEKT) from his 57-year-old mother. At the age of 18, his urinalysis © 2014 Asian Pacific Society of Nephrology
was normal. However, at the age of 19, 3+ proteinuria and 2+ occult blood were detected by annual physical examination. The abnormality on his urinalysis was diagnosed as IgAN by renal biopsy, which showed mild to moderate mesangial hypercellularity, with fibrocellular crescent in 1 of 10 glomeruli (Fig. 1a). Subsequently, tonsillectomy was performed and steroid pulse therapy was initiated. However, unfortunately, nephrotic-range proteinuria still developed. The patient then progressed to ESRD regardless of the treatment with steroid pulse therapy, cyclosporine (CyA), prednisolone, a renin– angiotensin system inhibitor, an antiplatelet agent, and anticoagulation therapy. He was referred to our hospital to undergo PEKT from his mother. Laboratory data revealed ESRD with a serum creatinine concentration of 8.53 mg/dL, haemoglobin of 8.8 g/dL and serum albumin of 3.54 g/dL. Urinalysis showed 3+ proteinuria and microscopic haematuria. PEKT was performed when the patient was 23 years old. Initial immunosuppressive therapy consisted of prednisolone, mycophenolate mofetil, CyA and basiliximab, and the transplantation procedure was successful. Allograft biopsy performed 1 h after transplantation revealed normal glomeruli and an immunofluorescence study showed negativity for IgA and C3. The second biopsy was performed 19 days 45
Y Otsuka et al.
a
b
Fig. 1 (a) Native kidney biopsy at the age of 19. A mild to moderate mesangial hypercellularity can be seen, and fibrocellular crescent was observed in 1 of 10 glomeruli. An immunofluorescence study showed strong positivity in the mesangial area for IgA, IgG and C3. Moreover, mesangial and paramesangial deposits were observed by electron microscopy. (b) Fourth allograft biopsy performed 195 days after transplantation. This biopsy showed mild mesangial hypercellularity and endocapillary proliferation. Cellular crescent with tuft necrosis was observed in 1 of 21 glomeruli. An immunofluorescence study showed strong positivity in the mesangial area for IgA and C3.
a
b
Fig. 2 (a) Allograft biopsy performed 19 days after transplantation. Mesangial proliferation was not observed. Tuft necrosis with fibrin deposits and clustered leukocyte fragments was observed in 1 of 18 glomeruli. (HE stain). (b) Direct immunofluorescence using anti-IgA antibody performed 19 days after transplantation. Strong positivity can be seen in the mesangial area and capillaries. Strong positivity was also observed for C3 (data not shown).
after transplantation to elucidate the cause of the increasing proteinuria (1.1 g/day) and serum creatinine (1.80 mg/dL). This biopsy showed segmental tuft necrosis with fibrin (Fig. 2a), and an immunofluorescence study showed strong positivity for IgA and C3 (Fig. 2b). Neither acute rejection nor CyA nephrotoxicity was observed. These pathological findings and negative results for MPOANCA and PR3-ANCA completed the diagnosis of recurrent IgAN. The patient received steroid pulse therapy, double filtration plasmapheresis (DFPP), and anticoagulation therapy with warfarin. However, he developed nephroticrange proteinuria and the serum creatinine concentration increased gradually. A cytomegalovirus infection made it 46
inevitable to reduce the immunosuppressive agents. The fourth biopsy performed 195 days following transplantation after increasing proteinuria reached to 4.4 g/day and the serum creatinine concentration reached to 2.38 mg/dL revealed high activity of IgAN (Fig. 1b). The patient received 200 mg of rituximab. However, he continued to exhibit nephrotic-range proteinuria and increasing serum creatinine concentration (Fig. 3).
DISCUSSION Graft survival is better in IgAN patients than in controls during the first 5 years after transplantation.3,4 However, © 2014 Asian Pacific Society of Nephrology
Early IgAN recurrence
Fig. 3 Clinical course. The second biopsy performed 19 days after transplantation revealed recurrent IgAN. Regardless of steroid pulse therapy, DFPP and warfarinization, the serum creatinine concentration increased and nephrotic-range proteinuria developed rapidly. After an opportunistic infection by cytomegalovirus, 200 mg rituximab was used for recurrent IgAN. Rituximab was also ineffective against the increasing serum creatinine concentration and the accompanying proteinuria. Laboratory data obtained 622 days after transplantation revealed a serum creatinine concentration of 3.59 mg/dL and proteinuria of 3.4 g/day (data not shown). ANCA, anti-neutrophil cytoplasmic antibody; BXM, basiliximab; CMV-ag, cytomegalovirus antigen; CyA, cyclosporine; DFPP, double filtration plasmapheresis; GCV, ganciclovir; MMF, mycophenolate mofetil; MPO-ANCA, myeloperoxidase-ANCA; OB, urinary occult blood; POD, postoperative day; PR3ANCA, proteinase 3-ANCA; PSL, prednisolone; RBx, graft biopsy; RTx, renal transplantation; sCr, serum creatinine; UP, urinary protein; VGCV, valganciclovir.
graft survival at 12 years becomes worse in IgAN patients than in controls.5 Death-censored graft survival at 15 years was approximately 10% lower in IgAN patients than in controls (63% vs 72%),2 suggesting that the culprit is IgAN recurrence. The reported frequency of histological or clinically significant recurrence of IgAN varies from 13% to 60%.3,4,6–8 This large variation showed in the reported literature is attributed to the differences in the duration of follow-up and in the biopsy policy. Longer follow-ups have higher probabilities to find recurrent IgAN than shorter ones, and the frequency of histological recurrence of IgAN increases when protocol biopsy is performed7,8 because histological recurrence without evidence of clinical manifestation is common. Ortiz et al.8 reported that 52% of the IgAN recurrences diagnosed by protocol biopsies were not accompanied by proteinuria or haematuria. © 2014 Asian Pacific Society of Nephrology
IgAN recurrence is associated with several possible risk factors, such as (i) living-related donor; (ii) specific HLA alleles in the recipient including HLA-B35, HLA-DR4, HLA-B8 and DR3; (iii) good HLA match; and (iv) high serum IgA concentration. The impact that an immunosuppressive regimen has on recurrence is also equivocal. The case described herein is the one with the earliest recurrence of IgAN after transplantation. Bumgardner et al.9 reported that the mean time to diagnose recurrence and report subsequent graft loss is 31 and 63 months, respectively. Obviously in our case, IgAN recurred unusually early. No episode including upper respiratory tract infection occurred during the early postoperative period. Recurrent IgAN occurs more frequently in younger patients.6,10–12 Patients who develop ESRD at a younger age might have a shorter duration of renal failure before transplantation. Patients who had a rapidly progressive course to 47
Y Otsuka et al.
ESRD in the native kidney tend to have early recurrences with clinically significant manifestations.9,13–15 One of the possible reasons for early IgAN recurrence in the present case is that the onset of IgAN in the patient was at the age of 19 and he had a rapidly progressive course to ESRD. Factors related to IgAN onset are well investigated. Genetic factors related with the structure of IgA, races, HLA, and some of bacterial infections are known to play important roles in IgAN onset. However, factors related to IgAN severity remain unclear. There is no known data showing that PEKT causes early IgAN recurrence. However, long duration of dialysis has the potential to prevent IgAN recurrence by lowering the activity of the disease. The native IgAN of the present case was undistinguished histologically; however, the clinical manifestations were significant. A few reports16–18 show that crescent IgAN may lead to early graft failure. However, the fourth biopsy performed 195 days after kidney transplantation in our patient showed that cellular crescent was observed in only 1 of 21 glomeruli (4.8%). In addition, the patient developed nephrotic-range proteinuria, had renal function deterioration, and showed refractory IgAN despite the common IgAN histology. It is well known that high levels of serum soluble urokinase plasminogen activator receptor (suPAR) can be found as a circulating factor in some patients with primary focal segmental glomerulosclerosis. Such circulating factors have not yet been reported in IgAN patients. However, our case of early IgAN recurrence cast a new light on the possible existence of a circulating factor in IgAN patients.
REFERENCES 1. Levy M, Berger J. Worldwide perspective of IgA nephropathy. Am. J. Kidney Dis. 1988; 12: 340–47. 2. Moroni G, Longhi S, Quaglini S et al. The long-term outcome of renal transplantation of IgA nephropathy and the impact of recurrence on graft survival. Nephrol. Dial. Transplant. 2013; 28: 1305–14. 3. Kim YS, Moon JI, Jeong HJ et al. Live donor renal allograft in end-stage renal failure patients from immunoglobulin A nephropathy. Transplantation 2001; 71: 233–8.
48
4. Andresdottir MB, Hoitsma AJ, Assmann KJ, Wetzels JF. Favorable outcome of renal transplantation in patients with IgA nephropathy. Clin. Nephrol. 2001; 56: 279–88. 5. Choy BY. Renal transplantation in patients with primary immunoglobulin A nephropathy. Nephrol. Dial. Transplant. 2003; 18: 2399–404. 6. Ponticelli C, Traversi L, Feliciani A, Cesana BM, Banfi G, Tarantino A. Kidney transplantation in patients with IgA mesangial glomerulonephritis. Kidney Int. 2001; 60: 1948–54. 7. Odum J, Peh CA, Clarkson AR et al. Recurrent mesangial IgA nephritis following renal transplantation. Nephrol. Dial. Transplant. 1994; 9: 309–12. 8. Ortiz F, Gelpi R, Koskinen P et al. IgA nephropathy recurs early in the graft when assessed by protocol biopsy. Nephrol. Dial. Transplant. 2012; 27: 2553–8. 9. Bumgardner GL, Amend WC, Ascher NL, Vincenti FG. Single-center long-term results of renal transplantation for IgA nephropathy. Transplantation 1998; 65: 1053–60. 10. Han SS, Huh W, Park SK et al. Impact of recurrent disease and chronic allograft nephropathy on the long-term allograft outcome in patients with IgA nephropathy. Transplant. Int. 2010; 23: 169–75. 11. Bantis C, Heering PJ, Aker S, Schwandt C, Grabensee B, Ivens K. Influence of interleukin-10 gene G-1082A polymorphism on recurrent IgA nephropathy. J. Nephrol. 2008; 21: 941–6. 12. Floege J. Recurrent IgA nephropathy after renal transplantation. Semin. Nephrol. 2004; 24: 287–91. 13. Frohnert PP, Donadio JV, Velosa JA, Holley KE, Sterioff S. The fate of renal transplants in patients with IgA nephropathy. Clin. Transplant. 1997; 11: 127–33. 14. Freese P, Svalander C, Nordén G, Nyberg G. Clinical risk factors for recurrence of IgA nephropathy. Clin. Transplant. 1999; 13: 313–17. 15. Ohmacht C, Kliem V, Burg M et al. Recurrent immunoglobulin A nephropathy after renal transplantation: A significant contributor to graft loss. Transplantation 1997; 64: 1493–6. 16. Brensilver JM, Mallat S, Scholes J, McCabe R. Recurrent IgA nephropathy in living-related donor transplantation: Recurrence or transmission of familial disease? Am. J. Kidney Dis. 1988; 12: 147–51. 17. Díaz-Tejeiro R, Maduell F, Diez J et al. Loss of renal graft due to recurrent IgA nephropathy with rapidly progressive course: An unusual clinical evolution. Nephron 1990; 54: 341–3. 18. Streather CP, Scoble JE. Recurrent IgA nephropathy in a renal allograft presenting as crescentic glomerulonephritis. Nephron 1994; 66: 113–14.
© 2014 Asian Pacific Society of Nephrology
Nephrology 19, Suppl. 3 (2014) 45–48
Brief Communication
Early recurrence of active IgA nephropathy after kidney transplantation YASUHIRO OTSUKA, ASAMI TAKEDA, KEIJI HORIKE, DAIJYO INAGUMA, NORIHIKO GOTO, YOSHIHIKO WATARAI and KUNIO MOROZUMI Department of Nephrology and Transplantation Center, Japanese Red Cross Nagoya Daini Hospital, Nagoya, Japan
KEY WORDS: early recurrence, IgA nephropathy, recurrent glomerulonephritis, recurrent IgA nephropathy, renal transplantation. Correspondence: Dr Yasuhiro Otsuka, Department of Nephrology and Transplantation Center, Japanese Red Cross Nagoya Daini Hospital, Nagoya, Japan. Email: [email protected] doi:10.1111/nep.12252 Conflict of interest: None declared.
ABSTRACT: IgA nephropathy (IgAN) is recurrent after transplantation; however, its time of recurrence is unpredictable. To date, factors influencing IgAN recurrence have not been elucidated. We present a case of a 23-year-old man with end-stage renal disease (ESRD) who underwent living-related ABOidentical pre-emptive kidney transplantation (PEKT) using his 57-year-old mother as a donor. IgAN started when the patient was 19 years old, and renal biopsy revealed the usual pathological findings of IgAN. In spite of steroid therapy including steroid pulse and tonsillectomy, the patient developed nephrotic syndrome and progressed to ESRD in 4 years. Protocol biopsy on day 19 following PEKT revealed active recurrent IgAN. Nephroticrange proteinuria and mild deterioration of kidney function developed regardless of strong immunosuppressive therapy such as steroid pulse, double filtration plasmapheresis and rituximab. We report a case of refractory IgAN that recurred 19 days after transplantation. This case is considered of value to elucidate factors leading to active IgAN recurrence.
IgA nephropathy (IgAN) is the most common primary glomerulonephritis that causes end-stage renal disease (ESRD) in 20–40% of patients.1 The success rate of kidney transplantation for patients with IgAN-induced ESRD was believed to be good. However, few data are available on the long-term outcome of IgAN patients with renal transplantation. Moroni et al.2 reported that death-censored graft survival at 15 years was approximately 10% lower in IgAN patients than in controls, suggesting that the culprit is IgAN recurrence. In fact, IgAN is one of the most common recurrent glomerulonephritis. The majority of recurrent IgAN is not clinical but pathological. Factors deciding the activity of recurrent IgAN remain unclear. It is unpredictable when IgAN recurs and why these recurrences occur immediately after transplantation. We report a case of active IgAN that recurred 19 days after transplantation.
A CASE OF REFRACTORY IgAN THAT RECURRED 19 DAYS AFTER TRANSPLANTATION A 23-year-old man with ESRD underwent living-related ABO-identical pre-emptive kidney transplantation (PEKT) from his 57-year-old mother. At the age of 18, his urinalysis © 2014 Asian Pacific Society of Nephrology
was normal. However, at the age of 19, 3+ proteinuria and 2+ occult blood were detected by annual physical examination. The abnormality on his urinalysis was diagnosed as IgAN by renal biopsy, which showed mild to moderate mesangial hypercellularity, with fibrocellular crescent in 1 of 10 glomeruli (Fig. 1a). Subsequently, tonsillectomy was performed and steroid pulse therapy was initiated. However, unfortunately, nephrotic-range proteinuria still developed. The patient then progressed to ESRD regardless of the treatment with steroid pulse therapy, cyclosporine (CyA), prednisolone, a renin– angiotensin system inhibitor, an antiplatelet agent, and anticoagulation therapy. He was referred to our hospital to undergo PEKT from his mother. Laboratory data revealed ESRD with a serum creatinine concentration of 8.53 mg/dL, haemoglobin of 8.8 g/dL and serum albumin of 3.54 g/dL. Urinalysis showed 3+ proteinuria and microscopic haematuria. PEKT was performed when the patient was 23 years old. Initial immunosuppressive therapy consisted of prednisolone, mycophenolate mofetil, CyA and basiliximab, and the transplantation procedure was successful. Allograft biopsy performed 1 h after transplantation revealed normal glomeruli and an immunofluorescence study showed negativity for IgA and C3. The second biopsy was performed 19 days 45
Y Otsuka et al.
a
b
Fig. 1 (a) Native kidney biopsy at the age of 19. A mild to moderate mesangial hypercellularity can be seen, and fibrocellular crescent was observed in 1 of 10 glomeruli. An immunofluorescence study showed strong positivity in the mesangial area for IgA, IgG and C3. Moreover, mesangial and paramesangial deposits were observed by electron microscopy. (b) Fourth allograft biopsy performed 195 days after transplantation. This biopsy showed mild mesangial hypercellularity and endocapillary proliferation. Cellular crescent with tuft necrosis was observed in 1 of 21 glomeruli. An immunofluorescence study showed strong positivity in the mesangial area for IgA and C3.
a
b
Fig. 2 (a) Allograft biopsy performed 19 days after transplantation. Mesangial proliferation was not observed. Tuft necrosis with fibrin deposits and clustered leukocyte fragments was observed in 1 of 18 glomeruli. (HE stain). (b) Direct immunofluorescence using anti-IgA antibody performed 19 days after transplantation. Strong positivity can be seen in the mesangial area and capillaries. Strong positivity was also observed for C3 (data not shown).
after transplantation to elucidate the cause of the increasing proteinuria (1.1 g/day) and serum creatinine (1.80 mg/dL). This biopsy showed segmental tuft necrosis with fibrin (Fig. 2a), and an immunofluorescence study showed strong positivity for IgA and C3 (Fig. 2b). Neither acute rejection nor CyA nephrotoxicity was observed. These pathological findings and negative results for MPOANCA and PR3-ANCA completed the diagnosis of recurrent IgAN. The patient received steroid pulse therapy, double filtration plasmapheresis (DFPP), and anticoagulation therapy with warfarin. However, he developed nephroticrange proteinuria and the serum creatinine concentration increased gradually. A cytomegalovirus infection made it 46
inevitable to reduce the immunosuppressive agents. The fourth biopsy performed 195 days following transplantation after increasing proteinuria reached to 4.4 g/day and the serum creatinine concentration reached to 2.38 mg/dL revealed high activity of IgAN (Fig. 1b). The patient received 200 mg of rituximab. However, he continued to exhibit nephrotic-range proteinuria and increasing serum creatinine concentration (Fig. 3).
DISCUSSION Graft survival is better in IgAN patients than in controls during the first 5 years after transplantation.3,4 However, © 2014 Asian Pacific Society of Nephrology
Early IgAN recurrence
Fig. 3 Clinical course. The second biopsy performed 19 days after transplantation revealed recurrent IgAN. Regardless of steroid pulse therapy, DFPP and warfarinization, the serum creatinine concentration increased and nephrotic-range proteinuria developed rapidly. After an opportunistic infection by cytomegalovirus, 200 mg rituximab was used for recurrent IgAN. Rituximab was also ineffective against the increasing serum creatinine concentration and the accompanying proteinuria. Laboratory data obtained 622 days after transplantation revealed a serum creatinine concentration of 3.59 mg/dL and proteinuria of 3.4 g/day (data not shown). ANCA, anti-neutrophil cytoplasmic antibody; BXM, basiliximab; CMV-ag, cytomegalovirus antigen; CyA, cyclosporine; DFPP, double filtration plasmapheresis; GCV, ganciclovir; MMF, mycophenolate mofetil; MPO-ANCA, myeloperoxidase-ANCA; OB, urinary occult blood; POD, postoperative day; PR3ANCA, proteinase 3-ANCA; PSL, prednisolone; RBx, graft biopsy; RTx, renal transplantation; sCr, serum creatinine; UP, urinary protein; VGCV, valganciclovir.
graft survival at 12 years becomes worse in IgAN patients than in controls.5 Death-censored graft survival at 15 years was approximately 10% lower in IgAN patients than in controls (63% vs 72%),2 suggesting that the culprit is IgAN recurrence. The reported frequency of histological or clinically significant recurrence of IgAN varies from 13% to 60%.3,4,6–8 This large variation showed in the reported literature is attributed to the differences in the duration of follow-up and in the biopsy policy. Longer follow-ups have higher probabilities to find recurrent IgAN than shorter ones, and the frequency of histological recurrence of IgAN increases when protocol biopsy is performed7,8 because histological recurrence without evidence of clinical manifestation is common. Ortiz et al.8 reported that 52% of the IgAN recurrences diagnosed by protocol biopsies were not accompanied by proteinuria or haematuria. © 2014 Asian Pacific Society of Nephrology
IgAN recurrence is associated with several possible risk factors, such as (i) living-related donor; (ii) specific HLA alleles in the recipient including HLA-B35, HLA-DR4, HLA-B8 and DR3; (iii) good HLA match; and (iv) high serum IgA concentration. The impact that an immunosuppressive regimen has on recurrence is also equivocal. The case described herein is the one with the earliest recurrence of IgAN after transplantation. Bumgardner et al.9 reported that the mean time to diagnose recurrence and report subsequent graft loss is 31 and 63 months, respectively. Obviously in our case, IgAN recurred unusually early. No episode including upper respiratory tract infection occurred during the early postoperative period. Recurrent IgAN occurs more frequently in younger patients.6,10–12 Patients who develop ESRD at a younger age might have a shorter duration of renal failure before transplantation. Patients who had a rapidly progressive course to 47
Y Otsuka et al.
ESRD in the native kidney tend to have early recurrences with clinically significant manifestations.9,13–15 One of the possible reasons for early IgAN recurrence in the present case is that the onset of IgAN in the patient was at the age of 19 and he had a rapidly progressive course to ESRD. Factors related to IgAN onset are well investigated. Genetic factors related with the structure of IgA, races, HLA, and some of bacterial infections are known to play important roles in IgAN onset. However, factors related to IgAN severity remain unclear. There is no known data showing that PEKT causes early IgAN recurrence. However, long duration of dialysis has the potential to prevent IgAN recurrence by lowering the activity of the disease. The native IgAN of the present case was undistinguished histologically; however, the clinical manifestations were significant. A few reports16–18 show that crescent IgAN may lead to early graft failure. However, the fourth biopsy performed 195 days after kidney transplantation in our patient showed that cellular crescent was observed in only 1 of 21 glomeruli (4.8%). In addition, the patient developed nephrotic-range proteinuria, had renal function deterioration, and showed refractory IgAN despite the common IgAN histology. It is well known that high levels of serum soluble urokinase plasminogen activator receptor (suPAR) can be found as a circulating factor in some patients with primary focal segmental glomerulosclerosis. Such circulating factors have not yet been reported in IgAN patients. However, our case of early IgAN recurrence cast a new light on the possible existence of a circulating factor in IgAN patients.
REFERENCES 1. Levy M, Berger J. Worldwide perspective of IgA nephropathy. Am. J. Kidney Dis. 1988; 12: 340–47. 2. Moroni G, Longhi S, Quaglini S et al. The long-term outcome of renal transplantation of IgA nephropathy and the impact of recurrence on graft survival. Nephrol. Dial. Transplant. 2013; 28: 1305–14. 3. Kim YS, Moon JI, Jeong HJ et al. Live donor renal allograft in end-stage renal failure patients from immunoglobulin A nephropathy. Transplantation 2001; 71: 233–8.
48
4. Andresdottir MB, Hoitsma AJ, Assmann KJ, Wetzels JF. Favorable outcome of renal transplantation in patients with IgA nephropathy. Clin. Nephrol. 2001; 56: 279–88. 5. Choy BY. Renal transplantation in patients with primary immunoglobulin A nephropathy. Nephrol. Dial. Transplant. 2003; 18: 2399–404. 6. Ponticelli C, Traversi L, Feliciani A, Cesana BM, Banfi G, Tarantino A. Kidney transplantation in patients with IgA mesangial glomerulonephritis. Kidney Int. 2001; 60: 1948–54. 7. Odum J, Peh CA, Clarkson AR et al. Recurrent mesangial IgA nephritis following renal transplantation. Nephrol. Dial. Transplant. 1994; 9: 309–12. 8. Ortiz F, Gelpi R, Koskinen P et al. IgA nephropathy recurs early in the graft when assessed by protocol biopsy. Nephrol. Dial. Transplant. 2012; 27: 2553–8. 9. Bumgardner GL, Amend WC, Ascher NL, Vincenti FG. Single-center long-term results of renal transplantation for IgA nephropathy. Transplantation 1998; 65: 1053–60. 10. Han SS, Huh W, Park SK et al. Impact of recurrent disease and chronic allograft nephropathy on the long-term allograft outcome in patients with IgA nephropathy. Transplant. Int. 2010; 23: 169–75. 11. Bantis C, Heering PJ, Aker S, Schwandt C, Grabensee B, Ivens K. Influence of interleukin-10 gene G-1082A polymorphism on recurrent IgA nephropathy. J. Nephrol. 2008; 21: 941–6. 12. Floege J. Recurrent IgA nephropathy after renal transplantation. Semin. Nephrol. 2004; 24: 287–91. 13. Frohnert PP, Donadio JV, Velosa JA, Holley KE, Sterioff S. The fate of renal transplants in patients with IgA nephropathy. Clin. Transplant. 1997; 11: 127–33. 14. Freese P, Svalander C, Nordén G, Nyberg G. Clinical risk factors for recurrence of IgA nephropathy. Clin. Transplant. 1999; 13: 313–17. 15. Ohmacht C, Kliem V, Burg M et al. Recurrent immunoglobulin A nephropathy after renal transplantation: A significant contributor to graft loss. Transplantation 1997; 64: 1493–6. 16. Brensilver JM, Mallat S, Scholes J, McCabe R. Recurrent IgA nephropathy in living-related donor transplantation: Recurrence or transmission of familial disease? Am. J. Kidney Dis. 1988; 12: 147–51. 17. Díaz-Tejeiro R, Maduell F, Diez J et al. Loss of renal graft due to recurrent IgA nephropathy with rapidly progressive course: An unusual clinical evolution. Nephron 1990; 54: 341–3. 18. Streather CP, Scoble JE. Recurrent IgA nephropathy in a renal allograft presenting as crescentic glomerulonephritis. Nephron 1994; 66: 113–14.
© 2014 Asian Pacific Society of Nephrology
