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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
Year : 2011  |  Volume : 22  |  Issue : 6  |  Page : 1263-1265
Author's Reply

1 Renal Transplant Surgery, Riyadh Military Hospital, Riyadh, Saudi Arabia
2 Renal Transplant Pathology, Riyadh Military Hospital, Riyadh, Saudi Arabia
3 Renal Transplant Nephrology, Riyadh Military Hospital, Riyadh, Saudi Arabia

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Date of Web Publication8-Nov-2011

How to cite this article:
Khan T, Mirza A B, Haleem A, Zahid R, Hussaini H A, Sulaiman M A, Mousa D. Author's Reply. Saudi J Kidney Dis Transpl 2011;22:1263-5

How to cite this URL:
Khan T, Mirza A B, Haleem A, Zahid R, Hussaini H A, Sulaiman M A, Mousa D. Author's Reply. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2022 Nov 27];22:1263-5. Available from: https://www.sjkdt.org/text.asp?2011/22/6/1263/87252
To the Editor ,

We would like to thank Drs. Mubarak and Abbas for the detailed analysis [1] of our paper, [2] and we are hoping that this response will help in answering their questions.

The first point brought up is the question of delay caused by non-specific measures and tests in our first case; this also happened to have occurred in the early part of our program. As to the absence of chronological details, it is impossible to give a minute-by-minute narrative because of space constraints. It is sufficient it to say that treatment was delayed in this case by a combination of repeating labwork, IV fluid challenge, Doppler ultrasound, the timing of FK levels, empirical therapy, biopsy and C4d staining. We congratulate the authors for having a perfect response in place in their institution for "unexplained" rises in creatinine; in fact, it is this very unexplained part of the rise in creatinine that resulted in our delay. We would like to ask Drs. Mubarak and Abbas as to when their clinical colleagues label a serum creatinine as "unexplained"? This labeling is a process of exclusion and part of a clinical algorithm, from personal experience, a delay before a biopsy is performed and read is unavoidable even in the best of centers. It is this delay that was avoided in the second case because of increased LDH and NT at the time of renal impairment.

The authors challenge our claim of LDH being an "early" diagnostic marker with the argument that tissue necrosis and infarction is the end result of the antibody attack on allograft tissue. We found an increase in LDH and NT at the time of the increase in serum creatinine; in clinical terms at least, this would be considered early, not late. The pathological process may have been ongoing for longer but becomes "clinically" evident only after renal impairment is observed. Further evidence that LDH is an early marker is the observation of increases in LDH within 24 hours in kidney recipients when minor polar arteries are ligated during live donor nephrectomy [Figure 1]. The total area of necrosis following sacrifice of these minor polar arteries is small and is not enough to result in renal impairment, but the rise in LDH is undeniable and prompt. AMR, with its associated necrosis and infarction, [3] on the other hand involves the entire vascularized kidney that results in renal impairment and, in our experience, is reflected by a simultaneous increase in LDH and NT.

We would like to clarify that the increase in the TLC is entirely neutrophilic for two reasons; firstly, because of the profound lymphopenia with Thymoglobulin induction and secondly, because the complement-driven chemotaxis affects neutrophils.
Figure 1: Non-perfused area in allograft upper pole (small arrows) following ligation of minor polar artery during donor nephrectomy (long arrow). The small area involved is insufficient to cause renal impairment, but an increase in LDH is prompt.

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We regret the incorrect wording in the legend of (Figure 3), which should have read as afferent/ efferent vessel, and the omission of the leucocyte count in (Figure 5) is also regretted.

Regarding the second case, AMR was suspected by renal impairment with the increase in the early markers, LDH and NT, and immunoadsorption was carried out daily for four days with Globaffin (Fresenius Medical Care, Bad Homburg. Germany). We reiterate here, as we did in the paper, that early treatment for AMR played an important role in the final outcome and was possible only because of the early warning provided by increased LDH and NT. A recent situation reconfirmed our faith in the importance of a rising LDH and NT and early therapy. A sensitized female recipient with a high PRA and a negative FCXM with her sister became oliguric with a rising creatinine six days after transplantation along with increased LDH (900 IU/L from 230 IU/L) and NT (40 from 5.7×10 9 ). After confirming perfusion on Doppler, we initiated immuneadsorption therapy because, in our book, this association virtually confirms AMR, which was vindicated by the presence of DSA in serum and AMR on histology. Acute cellular rejection in this case was not a consideration because of a profound lymphopenia (0.3×10 9 ). We will go a step further and state that we feel that this triad of renal impairment, increased LDH and NT are pathognomonic of glomerular thrombotic AMR.

The authors quoted a poster abstract from their center by Nuhari et al. [4] We were unable to find a mention of the three cases of C4d-positive AMR they allude to. What is mentioned in the abstract is the acute rejection rate of 24%. This high rejection rate in their live related program for first transplants in a low-risk group would be a reason for concern, especially when re-transplants are not a priority! We are curious as to what their center offers the 29% of recipients with CAN who lose their first grafts? Did they consider the possibility that the acute tubular injury reported therein (23%) could be C4d-negative AMR?

We strongly believe that in transplant recipients, LDH and NT along with recent renal impairment and oliguria are early markers of thrombotic AMR. These are simple tests that can alert transplant clinicians about the possible diagnosis of AMR and prevent delays in early treatment to prevent graft loss. [5]

We would once again like to thank Drs. Mubarak and Abbas for their interest in our paper and hope that they can one day corroborate this triad.

   References Top

1.Mubarak M, Abbas K. Antibody-mediated rejection: Importance of lactate dehydrogenase and neutrophilia in early diagnosis. Saudi J Kidney Dis Transpl 2011;22(6):1261-5.  Back to cited text no. 1
2.Khan TT, Mirza AB, Zahid R, et al. Antibodymediated rejection: Importance of lactate dehydrogenase and neutrophilia in early diagnosis. Saudi J Kidney Dis Transpl 2011;22(3):525-30.  Back to cited text no. 2
3.Racusen LC, Haas M. Antibody-mediated rejection in renal allografts: Lessons from pathology. Clin J Am Soc Nephrol 2006;1:415-20.  Back to cited text no. 3
4.Nuhari MM, Kazi JI, Ahmed E, Akhtar F, Naqvi SA, Rizvi SA. Causes of renal graft dysfunction as detected in renal allograft biopsies in a live related renal transplant program. Transplantation 2008;86(2S):582.  Back to cited text no. 4
5.Bohmig GA, Wahrmann M, Regele H, et al. Immuneadsorption in severe C4d-positive acute kidney allograft rejection: A randomized controlled trail. Am J Transplant 2007;7:117-21.  Back to cited text no. 5

Correspondence Address:
Taqi Khan
Renal Transplant Surgery, Riyadh Military Hospital, Riyadh
Saudi Arabia
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Source of Support: None, Conflict of Interest: None

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