Hyperacute rejection occurs almost immediately following organ implantation and necessitates immediate explant of the organ. Hyperacute rejection is uncommon with pre-transplantation cross-matches and screening. Hyperacute rejection (HAR) of the kidney was first recognized 20 years ago in cases of donor-recipient incompatibility for the major blood group and tissue antigen systems. Classic pathological changes described include early accumulation of PMNs in glomeruli and peritubular capillaries, progressive glomerular thrombosis, tubular necrosis, and eventual cortical necrosis. Reaction of host humoral antibodies with antigens on donor cells serves as one trigger of the clotting mechanism, which then proceeds in a nonspecific fashion.

Antigen systems other than the ABO groups that contribute to HAR reactions are leukocyte antigens, endothelial and monocyte antigens, and B cell antigens. It is also documented that glomerular thrombosis identical to HAR may occur secondary to endothelial damage after pulsatile perfusion. However, in such cases no specific deposition of immunoglobulins and complement is detected.

Lymphocele has been defined as a lymph-filled collection in the retroperitoneum without an epithelial lining. In kidney transplanted patients, lymphocele is a pseudocystic entity with lymph content covered with a hard fibrous capsule frequently localized around the graft. Lymphocele is one of the most common complications after kidney transplantation. It is usually asymptomatic, but can cause pressure on the kidney transplant, ureter, bladder, and adjacent vessels with deterioration of graft function, ipsilateral leg oedema, and external iliac vein thrombosis. Peritoneal fenestration is a well-established method for treatment.

Allograft is a tissue graft from a donor of the same species as the recipient but not genetically identical.

Isograft Graft – tissue between two individuals who are genetically identical

Autograft – transplantation of organs or tissues from one part of the body to another in the same individual

Xenograft – tissue transplanted from another species

Renal vein thrombosis (RVT) is the formation of a clot in the vein that drains blood from the kidneys, ultimately leading to a reduction in the drainage of one or both kidneys and the possible migration of the clot to other parts of the body.

Venous thrombosis is a rare occurrence, occurring in 0.5% of kidney transplants. With aggressive treatment,
i.e. thrombectomy, the chances of success are very poor, but treatment is successful in rare cases. More often, patients are treated with transplantectomy.

The left side is preferred for live donor transplants due to longer renal vein while right side has been associated with renal vein thrombosis and shorter vessels.

With the iliac artery anatomically located lateral to iliac vein, one would need a longer vein in the graft to enable the graft placement in the iliac fossa, its final location. Most renal transplant surgeons would intuitively prefer to implant a graft harvested from the left side. The right kidney has a simpler anatomy for retrieval, with no adrenal or lumbar veins to tackle. However, a long artery and short vein make this kidney’s anatomy skewed for grafting. Studies on cadavers have shown significantly shorter right renal vein length (average 13.7%) on the right side. With its weak posterior wall, there is an added risk of tear of the right renal vein if there is tension during anastomosis. Overzealous manoeuvres and stretching of a short vein during retrieval, or handling during allografting may also risk intimal damage, a possible aetiology for some early reports of right grafts lost to renal vein thrombosis following laparoscopic harvest.

Recommendations:
• On the right, lengthen the renal vein with the infra renal vena cava in order to avoid an anastomosis
under tension.
• Carry out a large venous anastomosis; at declamping, if the renal vein is tight, re-do the venous anastomosis.

As a class, NSAIDs are known to have direct nephrotoxic effects including afferent vasoconstriction leading to reduced glomerular filtration; allergic reactions leading to tubulointerstitial nephritis; nephrotic syndromes, which commonly include minimal change disease and membranous glomerulonephropathy; fluid and sodium retention; worsening of pre-existing hypertension; papillary necrosis and various electrolyte disturbances, including hyponatremia, hyperkalaemia and type 4 renal tubular acidosis.
The use of NSAIDs should be minimized among patients with Stage 3 CKD and avoided in those with Stage 4 or Stage 5 CKD with residual kidney function or recipients of kidney transplant regardless of CKD stage. It is conceivable that compromised intraglomerular hemodynamic may be potentiated with concurrent use of NSAIDs and calcineurin inhibitors in the transplant setting.
Diclofenac which is an NSAID should therefore be avoided in this patient.

Rejection is related primarily to activation of T cells, which, in turn, stimulate specific antibodies against the graft. Various clinical syndromes of rejection can be correlated with the length of time after transplantation.

Hyperacute rejection
Hyperacute rejection of the renal allograft happens in the operating room within hours of the transplant, when the graft becomes mottled and cyanotic. This type of rejection is due to unrecognized compatibility of blood groups A, AB, B, and O (ABO) or to a positive T-cell crossmatch (class I human leukocyte antigen [HLA] incompatibility).
It is thought that IgG antibodies from the host bind to HLA-1 antigen of the donated organ.
No treatment exists, and nephrectomy is indicated.

Acute rejection
Acute rejection appears within the first 6 months after transplantation and affects approximately 15% of transplanted kidneys. Rejection is secondary to prior sensitization to donor alloantigens (occult T-cell crossmatch) or a positive B-cell crossmatch.
Acute tubular interstitial cellular rejection is the most common type of rejection reaction, with an incidence of approximately 20-25%. Typically, it occurs between 1 and 3 months after transplantation. It is T-cell mediated, and injury is directed to the renal tubules. The standard for diagnosis is renal allograft biopsy. Mild rejections may be successfully reversed with corticosteroids alone, whereas moderate or severe rejections may require the use of anti–T-cell antibodies, either polyclonal or monoclonal.
Late acute rejection is strongly correlated with the scheduled withdrawal of immunosuppressive therapy 6 months after transplantation.

Chronic rejection
Chronic rejection occurs more than 1 year after transplantation and is a major cause of allograft loss. It is a slow and progressive deterioration in renal function characterized by histologic changes involving the renal tubules, capillaries, and interstitium. Its precise mechanism is poorly defined and is an area of intense study. Diagnosis is by renal biopsy, and treatment depends on the identified cause if any. Application of conventional antirejection agents (e.g., corticosteroids or anti–T-cell antibodies) does not appear to alter the progressive course.

For this procedure:
Following the preparation of the patient, a Rutherford-Morison incision was made at the right or left iliac fossa to access to the iliac vessels. Heparin (2500-4000 IU bolus) was given intravenously prior to the clamping of the iliac vessels. The renal artery was first anastomosed in an end-to-side fashion to the external iliac artery. The corner sutures (6/0 Prolene) were placed while the kidney allograft was first placed at the medial side of the incision. The lateral side of the renal artery was anastomosed by continuous suture using the 6/0 Prolene suture. The kidney allograft was then flipped to the lateral side and the medial side of the renal artery was anastomosed to the external iliac artery. The anastomosis was checked by placing a small vascular bulldog to the renal artery and the vascular clamp was released over the external iliac artery.

Following the renal artery anastomosis, the renal vein was anastomosed in an end-to-side fashion to the external iliac vein. Two corner sutures (5/0 Prolene) were placed first, then the lateral side of renal vein anastomosis was performed with continuous sutures from inside the lumen, and then a medial side anastomosis was performed by continuous sutures from the outside of the lumen (Figure ​(Figure2).2). Similarly, the anastomosis was checked by placing a vascular clamp over the renal vein and then releasing the vascular clamp on the external iliac vein.

Transplant renal artery stenosis (TRAS) is a well-recognized vascular complication after kidney transplant. It occurs most frequently in the first 6 months after kidney transplant, and is one of the major causes of graft loss and premature death in transplant recipients. Transplant renal artery stenosis (TRAS) is the narrowing of the transplant renal artery, impeding blood flow to the allograft. It accounts for 1–5% cases of post-transplant hypertension. Patients with TRAS have activated RAAS and usually present with worsening or refractory hypertension, fluid retention and/or allograft dysfunction without evidence of rejection.
Percutaneous transluminal angioplasty with stent placement is generally the first-line therapy to correct hemodynamically significant stenosis in TRAS, especially for lesions that are short, linear and distal to the anastomosis.

Corticosteroids are responsible for an array of side effects. However, necrosis has a different pathophysiology and is not usually linked with corticosteroid usage.

In this patient, a blocked catheter is the case because the urine is flowing into the urostomy bag but it is not able to pass through the catheter.
It is recommended that in cases without hypotension, a bladder washout should be done if there is clot retention. The catheter may also be changed.

Prolonged cold ischemia time (CIT) may contribute to the perception of the graft as being suboptimal since donation after circulatory death (DCD) kidneys may be considered less tolerant of CIT. In fact, previous reports recommend restriction of CIT to 12 to 18 hours when transplanting DCD kidneys and a recent UK registry analysis identified increased risks of DCD graft failure with CIT longer than 12 hours.
The donated kidney in this case had a CIT of 26 hours and the patient presented with symptoms 10 days later which would lead to acute rejection.

Transplantation is a process by which cells, tissues, or organs (a graft) from the donor are transplanted into a host (or recipient). The immune system’s ability to recognize and respond to foreign antigens bring challenges to transplantation.
Type IV hypersensitivity is characterized by cell-mediated response rather than antibodies as in other types of hypersensitivity reactions. Specifically, the T lymphocytes are involved in the development of the sensitivity, hence called cell-mediated hypersensitivity.
After exposure to antigens, through a series of biochemical events, the T-cells will be activated. By releasing some chemicals, the T-cells activate other white blood cells to mount an immune response.
Rejection of transplant occurs months to years later. In chronic rejection, there is intimal fibrosis with vascular thickening, leading to ischemic changes. Mononuclear infiltrates with prominent plasma cells are present.

Antibody-mediated rejection (AMR) is defined as allograft rejection caused by antibodies of the recipient directed against donor-specific HLA molecules and blood group antigens. Although the mechanism by which HLA I antibodies promote inflammation and proliferation has been revealed by experimental models, the pathogenesis of HLA II antibodies is less defined. Antibodies to HLA II frequently accompany chronic rejection in renal transplants. AMR has been recognized as the leading cause of graft loss after kidney transplant if there is a donor-host antigenic disparity. Antibodies can be produced against epitopes of the antigen that differ from self by as little as one amino acid. Pre-existing antibodies or the development of de novo antibodies after transplantation has become a biomarker for AMR graft loss. HLA antibodies are risk factors for hyperacute, acute, and chronic allograft rejections.

The specificity of HLA antibodies can be determined using single-antigen luminex beads that consist of fluorescent microbeads conjugated to single recombinant HLA class I and class II molecules. Complement-fixing ability would be assessed by the binding of C1q to HLA antibodies present in the serum. In several studies, C1q-positive DSA had associated with antibody-mediated rejection in renal transplantation compared with antibodies identified only by IgG. Complement-fixing ability is relevant to hyperacute and acute rejections. Hyperacute rejection is predominantly complement-mediated severe allograft injury occurring within hours of transplantation. It is caused by high titre of pre-existing HLA or non-HLA antibodies in presensitized patients. But the incidence of hyperacute rejection is reduced due to improved DSA detection methods and desensitization protocols.

Acute renal artery thrombosis is a devastating complication of renal transplantation that can result in graft loss if not detected early. Surgical and technical errors are the major cause of renal artery thrombosis. Renal artery thrombosis usually presents with sudden onset oliguria or anuria accompanied by pain and tenderness over the graft site. Patients may develop thrombocytopenia due to platelet aggregation at the thrombosis site. The imaging modality of choice for diagnosis of renal artery thrombosis is colour Doppler sonography. Conventional, computed tomography (CT) and magnetic resonance (MR) angiography may also be used to confirm the presence of renal artery thrombosis. Although there are reports of successful resolution of post-transplant acute renal artery thrombosis with endovascular and surgical modalities such as percutaneous thrombus aspiration, intra-arterial injection of fibrinolytic agents and surgical thrombectomy, renal artery thrombosis usually results in ischemic necrosis and graft loss.