One of the most common causes of allograft dysfunction is a rejected kidney graft, despite It’s became less prevalent

CLINICAL MANIFESTATIONS AND DIAGNOSIS OF ACUTE RENAL ALLOGRAFT REJECTION

 

One of the most common causes of allograft dysfunction is a rejected kidney graft, despite It’s became less prevalent since the admission of more robust immunosuppressive strategies, especially the calcineurin inhibitors (CNI). Certain rejected grafts, however, cannot resume its function again despite the administration of maximum antirejection agents. The recurrence of acute rejection attacks may negatively affect the long-term allograft outcome. The two major types of acute rejection episodes are the cellular type and antibody mediated one.
Another subclinical form can be present if there’re histologic criteria in allograft biopsy with no associated allograft dysfunction.

Acute episodes of rejection can be observed through the first 6 months post-transplant. Rejection episode after 6 months, is primarily related to patient’s non-compliance or due to rapid   immunosuppressives reduction/withdrawal. Historically, the classic clinical manifestations may include pyrexia, malaise, oliguria (low urine output), locally tender/painful allograft, allograft swelling and hypertension (HT), however, with the advent of the new immunosuppressive protocols, this presentation is not common and many kidney transplant recipients (KTRs) mostly present only with a rise in serum creatinine levels (SCR) that suggest the possibility of a rejection episode.  

 

 

CLINICAL FEATURES

Despite the attacks of acute rejection mostly observed during the 1^st 6 months post-transplant, many episodes can be seen immediately post-operative. As KTRs are usually asymptomatic, a diagnosis of acute rejection can be suspected only via a rise in the SCr levels.  

Lab manifestations

KTRs with acute episode of graft rejection can present with an acute elevation in the SCr.  A step rise in SCr level, however, can be observed lately in the course of the rejection episode, its presence, however, may indicate the finding of a currently significant histopathological lesions. Pus cell in urine (Pyuria) or new or increasing proteinuria can be also observed.

Radiographic manifestations

The role of kidney imaging in the diagnosis of acute rejection is limited and nonspecific. However, they can be utilized in exclusion of other pathology that may associate acute allograft injury. U/S (Ultrasonography) may show enlarged allograft size, with lost cortico-medullary differentiation, prominently hypoechoic pyramid and diminished echogenicity upon the kidney sinuses. Nuclear medicine kidney scanning may declare a kidney visualization delay. Doppler study may declare an increased resistance index (RI), however, this finding can also be seen with the following:

1)    Ureteric occlusion,

2)    ATN (acute tubular necrosis),

3)    Renal vein thrombosis,

4)    Acute PN (Pyelonephritis), and

5)    CyA toxicity.

v A suggested monitoring schedule for rejection episodes follow up is suggested, via measuring SCr, urinalysis, urinary protein/Cr ratio and the vital signs:

• Twice weekly in the 1^st month after transplant.
• Weekly for the 1^st to the 4^th month.
• Every other week for the 4^th to the 12^th month.
• Monthly, after the 1^st y. forever.

Surveillance biopsy is NOT generally recommended.

The diagnosis is usually made by an allograft biopsy. Before biopsy, other common causes of AKI (acute kidney injury) must be excluded. Plasma CNI  should be measured as well as an U/S prior to graft biopsy. Patients presented with pyrexia, malaise, low urine output, and allograft pain and/or tenderness and HT, their major DD (differential diagnoses) are viral infections, (BK, CMV virus, and adenovirus) or bacterial PN, urinary leak, and obstructive uropathy.

Most KTRs however are no symptomatizing and may show only a rise in SCr. DD will depend upon post-transplant timing, including pre-renal, post-renal and intrinsic renal etiologies.  

https://dx.doi.org/10.5500/wjt.v7.i6.301

http://www.jesnt.eg. net/text. asp? 2019/19/2/31/260214

https://www.wjgnet.com/2220-3230/full/v8/i6/203.htm

 

 N.B. This Blogger is created to declare the clinical picture and management in acute allograft rejection.

 

REFERENCES

 

§  Solez K, Colvin RB, Racusen LC, et al. Banff '05 Meeting Report: differential diagnosis of chronic allograft injury and elimination of chronic allograft nephropathy ('CAN'). Am J Transplant 2007; 7: 518.

§  Pham, PTT, Nast, et al. Diagnosis and therapy of graft dysfunction. In: Chronic kidney disease, dialysis and transplantation, 2, Periera, BJG, Sayegh, et al. (Eds), Elsevier Saunders, Philadelphia 2005. p.641.

§  Schwarz A, Gwinner W, Hiss M, et al. Safety and adequacy of renal transplant protocol biopsies. Am J Transplant 2005; 5:1992.

§  Desvaux D, Le Gouvello S, Pastural M, et al. Acute renal allograft rejections with major interstitial oedema and plasma cell-rich infiltrates: high gamma-interferon expression and poor clinical outcome. Nephrol Dial Transplant 2004; 19:933.

§  Poduval RD, Kadambi PV, Josephson MA, et al. Implications of immunohistochemical detection of C4d along peritubular capillaries in late acute renal allograft rejection. Transplantation 2005; 79:228.

§  Solez K, Colvin RB, Racusen LC, et al. Banff 07 classification of renal allograft pathology: updates and future directions. Am J Transplant 2008; 8: 753.

§  Mengel M, Sis B, Haas M, et al. Banff 2011 Meeting report: new concepts in antibody-mediated rejection. Am J Transplant 2012; 12: 563.