Early Course of the Patient With a Kidney Transplant

Perioperative Management

A patient’s journey to a successful kidney transplant begins long before the patient meets the surgical and anesthesiology teams, at the time of diagnosis of chronic kidney disease where the patient and his or her nephrologist discuss and initiate the process of waitlist candidacy. Surgical management of the kidney transplant recipient begins in the immediate preoperative period. The initial evaluation includes a careful history and physical examination to determine whether potential contraindications to transplantation exist. For instance, the presence of significant cardiac disease may preclude successful surgery. Characteristics such as tobacco use, diabetes, obesity, hypertension, and dyslipidemia have all been shown to be independent predictors of cardiovascular disease in kidney transplant recipients and should prompt further cardiac evaluation, particularly in the symptomatic preoperative candidate. The Revised Cardiac Risk Index has also been demonstrated to be a useful perioperative tool for evaluating adverse cardiac event risk in kidney transplant recipients, particularly for those older than age 50. In addition, peripheral vascular disease and vascular insufficiency are more common in end-stage renal disease (ESRD) patients and represent a barrier to successful transplantation, with a higher incidence of postoperative renal transplant artery stenosis, graft failure, and mortality. Thus a simple pulse examination before surgery with ankle brachial indices in select patients can help stratify perioperative risks of vascular morbidity in kidney transplant recipients. Assessment of the recipient’s pretransplant fluid status and electrolyte levels to determine the need for dialysis is also important in the perioperative period. However, routine hemodialysis immediately before transplantation is not warranted except in cases of metabolic derangements (e.g., hyperkalemia) or fluid overload because preoperative hemodialysis has been associated with an increased risk of delayed graft function. Knowledge of the donor status is also helpful in the early postoperative management of the transplant recipient. With an ideal deceased donor or a living related donor, the expected outcome is an immediately functioning transplant that may preclude posttransplant dialysis. Kidneys procured from high KDPI donors or donation after circulatory death (DCD) donors have a higher likelihood of DGF, which can lead to volume overload and the need for urgent dialysis. Technical considerations include the need for vascular reconstruction, which may prolong surgery and contribute to postoperative DGF. Recipient factors also affect the early postoperative course. Significant risk factors for early posttransplant dysfunction include pretransplant sensitization, obesity, younger or older age, and anatomic considerations that complicate the surgery.

In the early perioperative period, attention to fluid and electrolyte balance is crucial. Careful monitoring of urine output is essential, and any decrease in urine flow must be evaluated. The Kidney Disease: Improving Global Outcomes (KDIGO) guidelines recommend measuring urine volume every 1 to 2 hours for at least 24 hours after transplantation and daily until graft function is stable. In addition, serum creatinine should be measured daily until hospital discharge, and frequently thereafter. For example, creatinine should be measured two to three times per week for a month, and a tapering frequency of measurements in ensuing weeks. A decrease in urine volume may be a result of acute tubular necrosis, hypovolemia, urinary leak, ureteric obstruction or, most significantly, vascular thrombosis or acute rejection. Assessment of the patient’s volume status may help eliminate hypovolemia as a cause of decreasing urine output. DGF can be ascertained further with duplex ultrasonography to assess perfusion of the graft and to exclude renal artery or vein thrombosis. Duplex ultrasonography also allows the diagnosis of a urinary complication such as obstruction or leak.

Measures to decrease the likelihood of DGF often are used during the operative procedure and in the perioperative period. Maintenance of adequate blood pressure and fluid status may be accomplished with intravenous albumin or crystalloid. There is no evidence for the superiority of one type of fluid during kidney transplant; however, the use of normal saline is associated with a higher incidence of acidosis. Shorter cold ischemia or pulsatile perfusion of the donor organ also may decrease the likelihood of postoperative DGF, and there is ongoing evaluation of normothermic perfusion techniques in this context. Some centers have used intraarterial calcium channel blockers, such as verapamil, to improve renal blood flow. It is common practice to administer mannitol (12.5 g) about 10 minutes before the kidney is reperfused, which helps trigger an osmotic diuresis and might be protective. Loop diuretics are also commonly used at the time of renal reperfusion. Oral calcium channel blockers have been used to decrease the incidence of DGF. There is controversy about the early initiation of CNIs because of the potential for nephrotoxicity. Some centers delay the use of CNIs until there is established diuresis. If additional immunosuppression is desired, polyclonal or monoclonal anti–T-cell antibodies may be used as induction therapy.

Graft Dysfunction

Early complications of renal transplantation may be mechanical/surgical or medical. Early medical problems are more common than posttransplant surgical problems ( Table 14.1 ). The most common early posttransplant medical problem is DGF, which occurs in 20% of patients who received kidneys from ideal deceased donors and in nearly 40% of patients in whom the donors were older than age 55 years. After or concomitant with DGF, acute rejection may become a significant clinical problem. Other reasons for early medical complications include acute cyclosporine or tacrolimus nephrotoxicity, prerenal azotemia, other drug toxicity, infection, and early recurrent disease. An uncommon but serious posttransplantation medical problem is thrombotic microangiopathy (discussed later). Thrombotic microangiopathy may be induced by rejection or as a secondary consequence of cyclosporine, tacrolimus, or sirolimus therapy. CNI blood levels should be measured regularly during the immediate postoperative period until target levels are reached, as this measurement may indicate the likelihood of CNI toxicity versus rejection in the diagnosis of graft dysfunction. The level of mammalian target of rapamycin (mTOR) inhibitor should also be measured regularly if this class of drugs is used.

Mechanical problems usually are the result of complications of surgery or specific donor factors, such as multiple arteries, that lead to posttransplantation dysfunction. Mechanical/surgical factors include obstruction of the transplant, hematuria, urine leak or urinoma, and vascular problems such as renal artery or vein stenosis or thrombosis. Postoperative bleeding is another potential complication that may cause compression of the transplant because the transplant usually is placed in the retroperitoneal space. Posttransplant lymphoceles are another common cause of early transplant dysfunction. Lymph drainage from transected lymphatic channels accumulates in the perivascular and periureteral space and can cause ureteral obstruction or lower-extremity swelling from iliac vein compression.

Urinary Problems

Urinary Obstruction

After implantation of a living donor kidney transplant, urine output begins immediately or within minutes. (See Chapter 29 for a more complete discussion of urinary problems.) The same is not generally true of deceased donor kidneys, in which urine output may not be apparent for 1 hour or more after implantation and may be sluggish or nonexistent for days if the kidney has been injured (DGF) by donor factors or preservation. If a kidney that was formerly making urine slows down or stops and does not respond to fluid administration, urinary obstruction must be considered in the differential diagnosis. The initial evaluation is to check the patient’s vital signs and physical examination to ensure adequate hydration and to check that the Foley catheter is functioning correctly. Obstruction of the Foley catheter by blood clots easily may occur and can be cleared by gentle irrigation. If these problems are not present, renal transplant ultrasound is the fastest, most accurate, and least expensive method to assess the renal pelvis for obstruction. Pelvicaliceal and/or ureteral dilation seen by ultrasound implies distal obstruction. If the bladder is collapsed rather than full, the problem is likely to be ureteral obstruction. Treatment should be immediate decompression of the renal transplant pelvis by percutaneous insertion of a nephrostomy tube. Subsequently (usually 1 or 2 days later to allow blood and edema to clear after nephrostomy tube placement), a nephrogram can be obtained to evaluate the ureter for stenosis or obstruction. The diagnosis is confirmed by a decline in the serum creatinine level after decompression of the renal pelvis.

After the Foley catheter is removed, the most common cause of urinary obstruction is not ureteral stenosis, but rather bladder dysfunction. This problem is particularly common in diabetic patients with neurogenic bladders. Initial management is replacement of the Foley catheter and a trial of an alpha-blocker, such as tamsulosin, doxazosin, or terazosin. If bladder dysfunction persists after one or two such trials, it may be necessary to start intermittent self-catheterization. In rare instances in which bladder dysmotility is severe and urinary tract infections are common, it may be preferable to drain the transplant ureter into an ileal conduit to the anterior abdominal wall. Ideally, a patient with a neurogenic bladder should have been evaluated before transplantation with urodynamic studies, and a decision should have been made about management at that time (see Chapter 12, Chapter 4 ).

During the first 1 or 2 weeks after transplantation, obstruction usually is caused by a technical problem related to surgery (see Chapter 29 ). If a ureteral stent was placed at the time of surgery, it is highly unusual to have obstruction. Indeed, the incidence of major urologic complications after kidney transplant in patients who had a prophylactic stent placed during surgery is significantly lower compared with those who did not have a ureteral stent placed during the transplant. However, placement of ureteral stents during transplant carries a higher risk of infection so it is recommended that a sulfa-based antibiotic prophylaxis be administered to these patients. Possible explanations for obstruction are a twisted ureter or anastomotic narrowing. Generally, obstructions appear several weeks postoperatively, after the stent has been removed, and occur most frequently at the anastomosis between ureter and bladder. Usually, these obstructions can be crossed by a guidewire and dilated percutaneously by an interventional radiologist ( Fig. 14.1 ). If the nephrostogram shows a long (>2 cm) stricture, especially a proximal or midureteral stricture, it is likely to be a result of ischemia and is not usually amenable to balloon dilation, necessitating surgical repair ( Fig. 14.2 ). The operation of choice for a long stricture or one that has failed balloon dilation is ureteroureterostomy or ureteropyelostomy using the ipsilateral native ureter. The spatulated ends of the transplant and native ureters are anastomosed using running 5-0 absorbable suture. This anastomosis can be done over a 7 French double-J stent, which is left in place for 4 to 6 weeks. If no ipsilateral ureter is available, it may be necessary to use the contralateral ureter. If neither the ipsilateral ureter nor the contralateral ureter is available, alternatives include bringing the bladder closer to the kidney using a psoas hitch or fashioning a Boari flap, but these measures are seldom necessary. Another method is endoureterotomy; experience with this method is growing. Even if urinary obstruction is clinically silent (i.e., the patient is asymptomatic with a normal creatinine value), urinary obstruction manifested by dilation of the pelvis and calices on ultrasound should be treated because it ultimately leads to thinning of the renal cortex and loss of renal function. Urinary obstruction should be treated immediately to minimize damage to the transplanted kidney.

Vascular Problems