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Table of Contents
CASE REPORT
Year : 2018  |  Volume : 12  |  Issue : 1  |  Page : 62-63

Early recurrence of IgA nephropathy in a young adult: Transplant recipient


Department of Nephrology, Madras Medical Mission Hospital, Chennai, Tamil Nadu, India

Date of Web Publication29-Mar-2018

Correspondence Address:
Dr. Georgi Abraham
Madras Medical Mission, 4A, Dr J.J Nagar, Mogappair, Chennai - 600 037, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijot.ijot_53_17

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  Abstract 


A 20-year-old male with hypothyroidism, chronic kidney disease Stage V due to hypertension, and Henoch–Schonlein purpura (IgA vasculitis) underwent a live-related renal transplant in 2015 with mother as a donor. He was inducted with single dose thymoglobulin 75 mg following which he was initiated on triple immunosuppressive therapy – prednisolone 25 mg once a day, tacrolimus 2.5 mg in the morning and 3 mg in the night, and mycophenolate mofetil 750 mg BID. On the 5th day of transplantation, he noticed purpuric rashes in the forearm and thigh associated with hematuria. He had good graft function. Renal allograft biopsy on sixth post operative day showed recurrence of IgA nephropathy (IgAN).

Keywords: Early recurrent IgA deposition, Henoch–Schonlein purpura, renal transplant


How to cite this article:
John MB, Kavalam GJ, George DS, Mathew M, Koshy P, Abraham G. Early recurrence of IgA nephropathy in a young adult: Transplant recipient. Indian J Transplant 2018;12:62-3

How to cite this URL:
John MB, Kavalam GJ, George DS, Mathew M, Koshy P, Abraham G. Early recurrence of IgA nephropathy in a young adult: Transplant recipient. Indian J Transplant [serial online] 2018 [cited 2019 Jul 21];12:62-3. Available from: http://www.ijtonline.in/text.asp?2018/12/1/62/228925




  Introduction Top


Henoch–Schonlein purpura (IgA vasculitis) with IgA deposition is not an uncommon cause of renal failure requiring renal replacement therapy.[1] The best treatment is renal transplantation.[2],[3] It is typically seen in younger age group.[2],[3] It is more prevalent in males than females. Identification of glomerulonephritis (GN) in the native kidneys and identification of the same disease affecting the transplant kidney define recurrent IgA nephropathy (IgAN). The diagnostic hallmark of IgAN is the predominant IgA deposits in the glomerular mesangium.

Here, we report a patient who developed recurrent IgAN on renal allograft on postoperative day 6 with normal allograft function.


  Case Report Top


A 20-year-old male was diagnosed with chronic kidney disease, systemic hypertension, Henoch–Schonlein purpura, and hypothyroidism in the year 2014. He was initiated on hemodialysis in August 2014 in our center meanwhile was being worked up for renal transplant. He is the only child of his parents. Preoperative investigations such as blood grouping, homologous leukocytic antibody typing, hemoglobin electrophoresis, and serology for HIV, hepatitis B, and C were negative. His mother who is O +ve is the donor of the kidney. CMV status of both the donor and recipient were IgG positive and IgM negative. Urine examination of the donor did not reveal hematuria. The patient underwent his renal transplant with mother as a donor on January 8, 2015 at our center in Chennai. He was inducted with single-dose thymoglobulin 75 mg following which, he was initiated on triple immunosuppressive therapy, which included prednisolone 25 mg once a day, tacrolimus 2.5 mg in the morning and 3 mg in the night, and mycophenolate mofetil 750 mg twice a day. On postoperative day 0, his creatinine was 4.93 mg/dl and urea was 38 mg/dl. On the 2nd postoperative day, creatinine became 0.86 mg/dl and urea was 21 mg/dl.

On the 5th postoperative day, he developed purpuric rashes without any abdominal pain or arthralgia. His platelet count was 200,000/mm 3, total white blood cell count was 5900 with 58% of neutrophils, and hemoglobin was 8.1 g/dl. Peripheral smear was not showing any features of hemolysis. His renal function was normal with blood urea of 18 mg/dl and serum creatinine of 0.9 mg/dl. Optic fundus was unremarkable. On the 6th postoperative day, urine examination was done and it revealed hematuria (red blood cell >50/high-power field [hpf]), leukocytes (15–20/hpf), with granular casts and trace albumin. Urine culture was sterile. Urine protein creatinine ratio was 2.61. Ultrasound of the graft showed normal allograft with no perinephric collection. Renal biopsy was done, and it revealed mild mesangial expansion with normal interstitium and tubules. Immunofluorescence [Figure 1] showed IgA2+ and IgA3+ positive and C4D negative. All the features were suggestive of recurrent IgAN in renal allograft. His renal function was monitored serially, and it was normal [Figure 2]. Serum IgA level was within normal limits, i.e., 2.3 g/l (0.7–4 g/l). Triple immunosuppressants were continued. He was followed up regularly. Currently, his renal allograft is functioning well with serum creatinine of 1.5mg/dL, 5-6 RBC in urine, no Proteinuria and no evidence of skin lesions.
Figure 1: (a) Glomerulus showing mild mesangial expansion (b) immunofluorescence showing IgA3+ over mesangial area

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Figure 2: Serial serum creatinine levels

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  Discussion Top


Initially, IgAN was considered as a benign disease, but in Indians, it is a malignant disease due to genetic and environmental factors. IgAN patients who had undergone renal transplant face the risk of recurrence in their kidney graft.[4] Recurrence of the original disease is now the third most frequent cause of allograft loss at 10 years after transplantation in patients with underlying GN. Clinical features of recurrent IgAN are persistent microhematuria as in our patient and proteinuria exceeding 0.5 g/day but usually remains below the nephrotic range. Gross hematuria associated with upper respiratory tract infections is seen less frequently.[5] Recurrence of IgAN should be proved histologically. Recurrent IgAN will show mesangial expansion with IgA deposits in the biopsy as in our patient. Very rarely, recurrent IgAN will present as crescentic GN with rapidly progressive renal failure. Observational studies of patients transplanted due to IgAN have shown that IgA recurs in up to 60% of patient's grafts as in our patient.[6],[7] Twenty-nine percent of patients with recurrent IgAN had graft dysfunction. Graft dysfunction was more in patients with a transplant from a live-related donor. The only established predictor of graft loss is the time elapsed since renal transplantation as rate of recurrence increases as time from transplant lengthens.[6] However, this is not the case with our patient.

Our patient had recurrence of IgA vasculitis as shown by purpuric rashes, active urinary sediments, and mild proteinuria. The diagnosis of IgAN recurrence requires histological evidence of IgA in the transplant kidney in a patient with biopsy-proven IgA disease in their native kidneys. As of now, no treatment has been shown to halt, or even slow down, the development of clinical IgAN recurrence. Biopsy of our patient taken on the 6th postoperative day was showing mesangial expansion, and immunofluorescence revealed IgA3+. This patient is a rare case of recurrence of IgAN within 6 days of allografting with long-term good outcome over 2 years of follow-up.


  Conclusion Top


We are presenting an interesting case in which IgAN recurred on the 6th postoperative day in a renal allograft recipient with adequate allograft function.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Wyatt RJ, Julian BA. IgA nephropathy. N Engl J Med 2013;368:2402-14.  Back to cited text no. 1
[PUBMED]    
2.
O'Shaughnessy MM, Montez-Rath ME, Lafayette RA, Winkelmayer WC. Patient characteristics and outcomes by GN subtype in ESRD. Clin J Am Soc Nephrol 2015;10:1170-8.  Back to cited text no. 2
    
3.
U.S. Renal Data System. USRDS 2013 Annual Data Report: Atlas of Chronic Kidney Disease and End-Stage Renal Disease in the United States. Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases; 2013.  Back to cited text no. 3
    
4.
Ortiz F, Gelpi R, Koskinen P, Manonelles A, Räisänen-Sokolowski A, Carrera M, et al. IgA nephropathy recurs early in the graft when assessed by protocol biopsy. Nephrol Dial Transplant 2012;27:2553-8.  Back to cited text no. 4
    
5.
Hariharan S, Johnson CP, Bresnahan BA, Taranto SE, McIntosh MJ, Stablein D, et al. Improved graft survival after renal transplantation in the United States, 1988 to 1996. N Engl J Med 2000;342:605-12.  Back to cited text no. 5
    
6.
Odum J, Peh CA, Clarkson AR, Bannister KM, Seymour AE, Gillis D, et al. Recurrent mesangial IgA nephritis following renal transplantation. Nephrol Dial Transplant 1994;9:309-12.  Back to cited text no. 6
    
7.
Frohnert PP, Donadio JV Jr., Velosa JA, Holley KE, Sterioff S. The fate of renal transplants in patients with IgA nephropathy. Clin Transplant 1997;11:127-33.  Back to cited text no. 7
    


    Figures

  [Figure 1], [Figure 2]



 

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