Historically, the use of sevoflurane has been associated with the potential for production of renal toxic compounds, including inorganic fluoride ions [24], and the production of ‘compound A’ (a fluorinated ether) when interacting with CO₂ absorbers containing a strong base, such as NaOH [25, 26]. In reality, studies have not demonstrated development of nephrotoxicity from fluoride ions at the levels produced by sevoflurane, either in humans or animal models [27]. Animal studies in rats have, however, demonstrated the potential for temporary renal toxicity from the combination of sevoflurane, low fresh gas flow rates, and strong-base CO₂ absorbers. Since, in humans, the enzyme pathway utilized for transforming the rebreathed compound A into a nephrotoxic material is 10–30 fold less active than in rats, no studies have demonstrated a transient renal dysfunction stemming from sevoflurane use in humans [28, 29]. The FDA does suggest that the use of fresh gas flow over 2L/min when using sevoflurane for greater than 1 h, however, no other country has a similar restriction in place.

There are several advantages of a living donor (related or nonrelated) transplant over a cadaveric donor. The advantages include:

The overall outcome between living related versus living-unrelated kidney transplants is similar in terms of renal function decline over time and graft survival length [31, 32]. The major concern with an unrelated donor is in the frequency of rejection (see below), however, modern immunosuppression methods are quite effective in ‘hiding’ the HLA incompatibilities of nonrelated donors from the cellular response system.

In a kidney transplant, the principal types of rejections include:

Although plasmapheresis is occasionally utilized in patients receiving living kidneys from non-HLA matching donors, the principal method of decreasing rejection of the transplanted kidney is the use of immunosuppressants. A combination of monoclonal antibodies, steroids, calcineurin inhibitors, and TOR inhibitors are used to decrease the immune response over time [37, 38]. There are three phases of the immunosuppressive regimen:

Alemtuzumab (Campath) is a monoclonal antibody that was originally used in treatment of B-cell and T-Cell lymphoma [39]. It binds to the surface of lymphocytes and targets them for destruction. This function has been adapted for use in organ transplantation, since it effectively makes this medication an excellent immunosuppressant.

There are a number of surgical morbidities that are seen in patients who undergo renal implantation [40–42]. Since the kidney is a bridge between the circulatory and the urinary system, functional problems can occur with either of these components.

From a vascular point of view, the most immediately obvious would be an anastomotic failure of the renal vessels to the new kidney. Since each renal artery receives approximately 12–15% of the cardiac output, potentially hundreds of milliliters of blood loss per minute can occur in the event of vessel rupture. Fortunately, this is an uncommon occurrence in kidney transplant procedures. More commonly seen is renal artery thrombosis, which occurs from a low-flow state in the renal artery, stemming either from an inappropriately tight anastomosis causing obstruction, vascular ‘kinking,’ or significant hypotension. Arterial kinking presents as acute cessation of urine flow. If this complication is recognized quickly (by Doppler ultrasound), it is possible to salvage the organ. Doppler ultrasound is also utilized to diagnose complications in the venous connections of the kidney. An acute venous thrombosis can result in edema of the kidney, and also cause loss of the organ [43].

Although dialysis removes many waste products from the body and typically provides the benefit of normalizing electrolytes, the ultrafiltration component can result in major body fluid shifts, and hypovolemia is a significant possibility. Fluid boluses and increased rates of continuous infusions may be warranted [44].

The longer the ‘down time’ of an organ as it sits outside of the body, the more waste metabolites will build up. Cadaveric kidneys are typically placed in cold storage in a solution that contains high potassium (to prevent intracellular diffusion of potassium), and can remain viable for up to 40 h [45]. The goal for living donors is to have ischemic times less of than 30 min (when on ice), and no more than 3–5 min when warm [46, 47]. Without perfusion, toxic metabolites build up in the preserved organ quickly. Cooling shows the overall metabolism of the kidney and decreases waste product production. However, it does not stop cellular functioning altogether. Without oxygen, energy consumption within the cells is necessarily anaerobic, and if available fuel sources are exhausted, some cells will undergo apoptosis and rupture, releasing more toxic products. When perfusion is restored, the built up toxic metabolites are ‘washed’ into circulation. These waste products include potassium (which can cause the peaked T-waves seen in this question), and carbon dioxide, which is buffered by the bicarbonate system in the blood and breathed out of the lungs, increasing the etCO₂. Both of these effects are transient, and only seen very soon after connecting the transplanted organ to vascular support, unless the organ ischemia continues.

The primary concern for the new kidney is to avoid ischemia and acute tubular necrosis (ATN) [48]. This is principally achieved by keeping a positive fluid balance. Presuming that the patient does not have severe CHF or some other significant contraindication to high fluid balance, fluids are typically given to maintain a CVP between 10 and 15 mmHg, and PA pressure of 18–20 mm, in an effort to optimize renal blood flow. Since neither a CVP nor a PA catheter is commonly placed during a kidney transplant, and given that (until the graft is in place) the patient is anuric, other estimates of fluid balance must typically be used. Often patients will be ‘tanked up’ with crystalloid to the point where they can maintain a systolic blood pressure between 130 and 150 mmHg while under anesthesia. This usually requires fluid administration in the 10–20 ml/kg/h range [44, 49].

Typically, a form of crystalloid is utilized as the principal fluid. Although there is literature on the use of hexastarches and other artificial colloids, either normal saline or a combination of half-normal saline with bicarbonate (for isotonicity) is most often seen in transplant regimens. Traditionally, potassium-including solutions are not administered during these procedures, due to the fear of worsening the hyperkalemia seen in patients with inadequate graft perfusion. Since relying entirely on normal saline can lead to a hyperchloremic metabolic acidosis, the use of half-normal saline (with bicarb) interspersed with normal saline has come into favor. Several liters are expected to be infused during the case, in order to maximize the vascular fluid space. A blood volume >70 ml/kg is positively associated with faster return to function of the transplanted kidney [50].

Loop diuretics are commonly used to increase urine flow through the transplanted kidney. Mannitol, as an osmotic agent, improves renal blood flow (by increasing blood volume), and is associated with better outcomes in terms of initiating renal function from the transplanted organ. The only potential issue with diuretics would be in a patient who, due to severe comorbid disease, could not achieve an appropriate blood volume via crystalloid transfusion, and entered a hypovolemic state. This is unlikely when dealing with the urine volumes produced by a newly transplanted kidney, but can be seen in some cases where renal function is immediately established [51, 52].

Traditionally, use of any vasoactive with alpha-constrictor properties has been discouraged. As with any transplanted system, there is hesitation on the part of surgeons when considering the use of these vascular constricting mediations for fear of decreasing flow to the organ in question. Despite this intrinsic fear, the literature suggests that there may not be as significant of an impact in the use of low-dose phenylephrine or ephedrine in kidney transplantation as previously believed, and this question is still an ongoing investigation [53, 54].