**5.7 Infection**

*Perioperative Care for Organ Transplant Recipient*

In transplant recipients who have established a good urine output post-operatively, the sudden development of oliguria or anuria should prompt a review of urinary catheter patency as well as raise the possibility of transplant vessel pathology. Early vascular pathology may be caused by structural or anatomical factors such as vessel kinking, anatomically disadvantageous configurations putting traction on the recipient vessels or thrombosis. Distinguishing between the various pathologies can be challenging clinically, with reliance on duplex ultrasound imaging and knowledge of donor vascular pathology through collaboration with

Renal transplant artery or vein thrombosis is a serious, although fortunately uncommon peri-transplant complication, with an incidence of 2–3%, classically occurring in the first week post-transplant [77]. Clinical features of transplant artery thrombosis are typically limited to the sudden onset of oligoanuria, while transplant vein thrombosis may cause allograft swelling, pain and frank haematuria in addition. Predisposing risk factors are decreased perfusion pressures and hypotension as well as donor factors—difficult bench surgery, multiple vessels, prolonged cold ischaemia time and vessel atherosclerosis [77, 88]. Rarer recipient risk factors, when present, can dramatically increase the risk of thrombosis, including in the transplant vessels. Recipients with thrombophilia, notably factor V Leiden mutation or anti-phospholipid antibodies, have been associated with higher risk (2.87 increased risk in one study) of adverse graft outcomes [89, 90]. Diagnosis of transplant vessel pathology may be obtained by urgent renal duplex ultrasonography; however, the abrupt onset of anuria in the early post-operative period is an indication for urgent surgical review and consideration of surgical re-exploration, due to the very short window after transplant arterial thrombosis before irretriev-

Renal transplant artery stenosis tends to be a later complication but can occasionally manifest in the perioperative period. The classical clinical features associated with stenosis of the transplant artery are hypertension, allograft dysfunction and fluid overload due to salt and water retention. Risk factors for early transplant artery stenosis tend to be donor related with atherosclerotic vessels or difficult bench surgery [77]. An association with acute rejection has also been described [91]. Diagnosis is by duplex scan showing increased velocity across the anastomotic sites and a flow differential between the aorta and

Intermittent vessel kinking caused by allograft nephroptosis can be diagnostically challenging due to the positional nature of the pathology [92]. Duplex scans may be non-diagnostic, and performing imaging in a non-prone position may assist in the diagnosis of positional vessel compression or kinking, and CT angiography

Ureteric pathology is more common than vascular pathology, but rarely affects graft survival [93]. The most common early urological complication is a urine leak with an estimated incidence of 8%, followed by ureteric stenoses with a similar incidence occurring later in the transplant course [77, 94]. Other complications of

Ureteric leaks, like vascular pathology, typically occur in first few weeks post-transplant and may present with localised pain or swelling at the site of the allograft, increased surgical drain output or a peri-transplant collection seen on

may provide additional diagnostic information in this situation.

vesicoureteric reflux and urolithiasis are uncommon [95].

**5.5 Renal vascular complication**

transplant surgeons.

able graft loss occurs.

transplant artery.

**5.6 Renal ureteric complications**

**24**

As a consequence of induction immunosuppression, transplant patients are particularly prone to infection in the perioperative phase. However, sepsis can be challenging to diagnose during this period because immunocompromised patients may not manifest the typical features of a systemic inflammatory response. Due to steroid therapy, most patients will exhibit a peripheral neutrophilia. In general, any change in physiological parameters, clinical deterioration or a temperature > 37.5°C should prompt consideration of sepsis, and a sepsis screen should be requested including [96]:


Although transplant recipients are susceptible to opportunistic pathogens such as CMV, EBV, mycobacteria, *Pneumocystis jiroveci* and fungi, these are unusual in the early post-transplant period. Infections occurring soon after transplantation are frequently nosocomial, associated with hospitalisation, intravenous and urinary catheters and intubation during surgery. In some instances, infection may be donor derived [97].

### *5.7.1 Bacterial infection*

Urinary tract infections (UTI) are the most common cause of bacterial infection requiring hospitalisation in transplant patients, followed by pneumonia,

surgical site infections and septicaemia [98]. Retrospective database studies have estimated a cumulative incidence of 17% in the first 6 months post-transplant, which rises to 60% for women and 47% for men at 3 years [99]. The presentation for UTI is similar to that of the general population and management identical to complicated UTIs with 7–14 days of antibiotic therapy, although the optimal duration has not been well established [98]. Management of post-transplant candiduria is controversial, without definite improvement in clinical outcomes following therapy [100]. Other bacterial pathologies are treated in the same way as in the general population with anticipated more frequent and longer duration antibiotic use due to physician concern over immunosuppressed state and propensity for more severe infection.

#### **5.8 Rejection**

In the early era of transplantation, hyperacute rejection due to the presence of preformed donor-specific antibodies (DSAs) occurring in the first minutes or hours after perfusion of the transplant was a significant risk. However, with the introduction of the complement-dependent cytotoxic cross-match, as described by Patel and Terasaki [101], and more recently solid phase assays that are able to detect DSAs with high sensitivity, hyperacute rejection is now extremely rare [102]. Nevertheless, early acute rejection remains a common occurrence, with a reported incidence of 7–25% depending on the level of immunological risk and choice of induction immunosuppression [21, 103–106]. Contemporary rejection rates in Australia and New Zealand are shown in **Table 9**.

In the perioperative period, DGF persisting beyond 4–5 days, decreasing urine output or an unexplained rise in creatinine by >15–20%, should prompt consideration of rejection as the underlying cause (Section 5.4). Unless there is a contraindication such as active bleeding or an unavoidable requirement for anticoagulation, the diagnosis requires a renal biopsy, both to exclude alternative causes of graft dysfunction and to characterise the histological pattern and severity of rejection. Rejection is classified histologically using the Banff criteria into borderline rejection, cell-mediated rejection, antibody-mediated rejection and mixed rejection [107, 108]. Treatment of cellular rejection would usually involve pulsed methylprednisolone 0.25–1.0 g daily for 3 days as first-line treatment, combined with a T-cell depleting therapy such as thymoglobulin/ATG if the rejection is histologically severe rejection (Banff class 2 or greater), or if there is a suboptimal response to methylprednisolone [109]. The optimal therapy for acute antibody-mediated rejection remains unclear, but would typically include pulsed methylprednisolone, plasma exchange (often combined with intravenous immunoglobulin at a dose of 0.1 g/kg following each exchange) outcomes [110–112]. Some centres also advocate the use of a B cell depleting antibody such as rituximab or the proteasome inhibitor bortezomib, although currently there is no strong evidence that these agents improve clinical outcomes [111, 113–115].


*Data from ANZDATA Registry. 41st Report, Chapter 7: Kidney Transplantation. Australia and New Zealand Dialysis and Transplant Registry, Adelaide, Australia. 2018. http://www.anzdata.org.au.*

**27**

**Author details**

Nil.

Sebastian Hultin1

provided the original work is properly cited.

University of Queensland, Brisbane, Australia

3 Translational Research Unit, Brisbane, Australia

\*Address all correspondence to: ross.francis@health.qld.gov.au

*Perioperative Care for Kidney Transplant Recipients DOI: http://dx.doi.org/10.5772/intechopen.84388*

operative monitoring and early complications.

have no conflict of interest to declare.

**Notes/thanks/other declarations**

Kidney transplantation has evolved from a highly experimental therapy to become recognised as the gold standard treatment for many patients with ESKD [116]. This progress has occurred through the many iterative developments in the surgical and medical management of transplant recipients, not the least of which being the introduction of highly effective immunosuppressive agents. Delivering high standards of clinical care during the perioperative period is a crucial step in achieving excellent allograft outcomes. This chapter provides an overview of the approach to assessing potential recipients admitted for transplantation, and guidance on typical perioperative medication and fluid prescriptions, as well as post-

David Johnson has previously received consultancy fees, research grants, speaker's honoraria and travel sponsorships from Baxter Healthcare and Fresenius Medical Care. He has also received consultancy fees from Astra Zeneca and travel sponsorships from Amgen. He is a current recipient of an Australian National Health and Medical Research Council Practitioner Fellowship. Carmel Hawley has received a research grant from Baxter Healthcare. Ross Francis has received honoraria and travel sponsorships from Novartis, Astellas and Amgen. The other authors

**6. Conclusions**

**Conflict of interest**

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

1 Department of Nephrology, Princess Alexandra Hospital, Brisbane, Australia

2 Australasian Kidney Trials Network, Centre for Health Services Research,

, Carmel M. Hawley1,2,3, David W. Johnson1,2,3 and Ross S. Francis1

\*

#### **Table 9.**

*Acute rejection rates in the first six months post-transplant.*
