Renal Transplantation: Definition, Pathophysiology, and Management

Running Head: RENAL TRANSPLANTATION
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Renal Transplantation
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Introduction
In medical practice, despite the induction of immunosuppression and the utilization of
highly aggressive immunosuppressive regimens, incidences of acute allograft rejection following
renal transplants are several. These incidences pose significant therapeutic and diagnostic
challenges to health care providers and result in early mortalities and loss of graft. To add on,
acute allograft rejections initiate chronic alloimmune responses and inflammation of the centered
airway which predisposes patients to lung allograft dysfunctions that are chronic and
bronchiolitis obliterans syndrome which is collectively major sources of mortalities and
morbidities following a transplant.
This paper discusses Mrs. T who had received her first renal transplant in 6 weeks’ time
and a recent test revealed that she had a creatinine level of 240mmol/L. Nurses have a role in
assessing patients and instituting evidence-based interventions to improve health outcomes in
clinically unsuspecting patients with acute allograft rejection that have recently undergone a
renal transplant. This can be achieved by nurses having a proper understanding of the definition,
pathophysiology, and management of acute allograft rejection. Only then can nurses convey the
most appropriate health education and develop an effective plan of care for patients with acute
allograft rejection.
Comparison Of Acute Allograft Rejection With Chronic Allograft Nephropathy
Generally, there exist three forms of allograft rejection which are; acute, hyperacute and
chronic. Acute rejection occurs within the initial 6-12 months following transplantation which is
caused primarily by lymphocytes in the thymus (t-cells) (Benzimra, Calligaro & Glanville,
2017). Unless the suppression of the immune system is achieved usually by the use of drugs,
acute allograft rejection tends to occur in nearly all transplants apart from identical twins. Today,

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acute allograft rejection is still a prevalent issue in kidney transplantations. Generally, there are
incidences of 38% within the first year following transplants. Despite the fact that when they
occur by themselves they are rarely fatal, the indirect consequences have adverse effects on the
outcomes of transplantation (Moreau et al., 2013). Tissues that are highly vascularized such as
the liver, lungs, and kidneys host the earliest signs. In most cases, it is easy to identify acute
rejection episodes and appropriate treatment offered promptly to prevent the failure of organs.
However, when episodes recur, they lead to chronic allograft rejection/ nephropathy.
On the other hand, chronic allograft neuropathy defines the functional loss of
transplanted tissues through fibrosis. It is a term used to explain long-term morbidities in
recipients who have undergone transplantation and results from several factors including
lymphocytes and antibodies (Fletcher, Nankivell & Alexander, 2013). Chronic allograft
neuropathy also occurs from hypoperfusion, recurrent disease, and ischemia-reperfusion and
infections. However, its diagnosis is often made using a biopsy of a suspected organ with the
heart as the only organ that is exempted (Kloc & Ghobrial, 2014). In pediatric recipients of renal
transplants, chronic allograft neuropathy is the leading cause of the loss of renal allograft. As
outlined by Demetris et.al. (2014), chronic allograft neuropathy has great rates of survival with
improvements in immunosuppression. However, opportunistic infections present challenges.
Pathophysiology Of Acute Allograft Rejection
Acute allograft rejection is common during the first initial months following
transplantation. However, it may also occur during an allograft’s life. It is mediated by the t-
lymphocytes which are present in the circulation and may infiltrate an allograft via the
endothelium of a vascular tissue. Following infiltration of a graft with lymphocytes, cytotoxic
cells often start to target and kill the cells that function in an allograft (Ingulli, 2013).

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Simultaneously, the release of lymphocytes locally tends to attract and stimulate the presence of
macrophages to result in damage to tissues through a mechanism that is hypersensitive and
delayed. These series of inflammatory and immunologic events results in nonspecific signs and
symptoms such as lethargy, fever, pain and a tender graft site. Following kidney transplantation,
acute allograft rejection is likely to affect up to 20% of patients in the initial 6 months
(Benzimra, Calligaro & Glanville, 2017). This may be evidenced by the abrupt increase in the
concentration of serum creatinine to levels above 30 beyond the baseline.
Any transplanted organ may be rejected through primary mediation and activation of
alloreactive T cells and cells that present antigens such as dendritic, macrophages and
lymphocytes. Primarily, it should be noted that the infiltration of T cells to allograft results in an
acute allograft rejection that finally triggers cytotoxic and inflammatory effects (Benzimra,
Calligaro & Glanville, 2017). Should there be a failure to maintain immunosuppression;
complex interactions may exist between B cells, T cells, and CD4 cells which may result in
chronic allograft neuropathy and other complications.
Initial Management Of Acute Allograft Rejection
The initial management of an acute allograft rejection aims at improving clinical
outcomes and quality of life by addressing symptoms. Post-op, the overall health status of a
patient should be assessed including fluid status and urine output to check for dehydration.
Preferably, an input-output fluid chart can be used for this assessment with a urinary catheter in
situ (Leblanc et al., 2018). The patients wound should also be assessed daily to check for signs
of poor wound healing and immediately intervene when necessary. The wound should be kept
clean to avoid sepsis that would further result in more complications.