Renal Transplantation Technique
- Author: Bradley H Collins, MD; Chief Editor: Ron Shapiro, MD more...
Kidneys are recovered from either living donors or deceased (brain-dead or donation after cardiac death) donors. Living-donor donation typically occurs between individuals who share an emotional bond but are not necessarily related. Good Samaritan living donors are altruistic (often anonymous) donors who wish to donate their kidney to individuals whom they do not know.
The incidence of living unrelated transplants (those performed between individuals who are not related by blood) is increasing. These living unrelated transplants generally have excellent outcomes that are superior to those of the best-matched deceased-donor transplants, though the results are still slightly inferior to those of human leukocyte antigen (HLA)-identical (HLA-ID) and haploidentical living-donor transplants.
Living donation is a scheduled event that offers the advantage of optimal preparation of both recipient and donor. Such scheduling allows better logistical control, which helps minimize organ preservation time. The total ischemia time from removal of the donor kidney to restoration of blood flow in the recipient can be less than 1 hour (although, in paired donation, may be considerably longer, without any compromise in the likelihood of immediate function). As a result, rates of initial poor graft function tend to be very low, with most grafts producing high volumes of urine within a few hours and a concomitant clearance of creatinine within the first day.
Previously, living donation required a flank incision, often accompanied by rib resection. However, the introduction of laparoscopic and laparoscopy-assisted techniques has proved to be a major improvement in surgery for living donation. Laparoscopic donor nephrectomy (see the video below) has many of the benefits associated with other laparoscopic procedures: It reduces donor postoperative hospital stays by several days and recovery time in motivated patients by several weeks.
In the authors’ experience, patients undergoing laparoscopic donor nephrectomy share the advantages noted in other programs, with less need for pain medication, earlier discharge (typically on the morning of postoperative day 1), and more rapid functional recovery than patients undergoing open donor nephrectomy.
Early experience has shown that laparoscopic donor nephrectomy is associated with a considerable increase in the willingness to donate. Transplant programs have noted increases in their overall kidney transplant volumes because potential donors face less postoperative morbidity and fewer economic disincentives when this technique is used.
Laparoscopic donor nephrectomy poses a number of surgical challenges. For instance, the pneumoperitoneum required for laparoscopic surgery may decrease venous return and compromise graft perfusion; however, with skillful anesthesia (and increased volume administration), this problem can be overcome.
Careful laparoscopic technique is required to recover grafts with adequate vessel length and with a well-preserved blood supply to the ureter. Given careful technique, the authors do not consider multiple renal arteries to be a contraindication to recovery, except in the rare case where four or more approximately equal-sized arteries are present. The left kidney is preferred because of implantation advantages associated with a longer renal vein; however, in some donors, the right kidney is preferable because of anatomic issues.
Whereas living donation typically occurs among persons who know each other, deceased donation is generally anonymous. Allocation of organs from deceased donors is based on a waiting list system, with special priorities given to the following:
HLA zero-mismatch pairings (because of their documented improved graft survival rate)
Pediatric recipients (to minimize the impact of chronic renal failure on growth)
Patients with a high panel-reactive antibody titer (to increase their probability of transplantation)
The list is managed by the United Network for Organ Sharing, based in Richmond, VA. A newly implemented kidney allocation system characterizes donors on a percent scale, using the kidney donor profile index, and allocates the 20% of deceased donor kidneys with the greatest expected posttransplant longevity to the 20% of candidates with the best expected posttransplant survival; kidneys that are not accepted are then offered to the remaining 80% of candidates.
Currently, most deceased-donor kidneys come from cadavers whose brains are dead but whose hearts are beating. The families of severely brain-injured patients may desire to withdraw support in conjunction with organ donation. Increasingly, donation after cardiac death (DCD), particularly in the controlled setting of withdrawal of support in the operating room, is becoming a source of kidney allografts. Outcomes for DCD allografts approach those obtained after brain death, especially if the DCD kidneys are preserved by pulsatile perfusion.
Contraindications to deceased-organ donation include most active infections, HIV infection (although this may change before too long), and extracranial malignancy. Relative contraindications include poor renal function in the donor, advanced donor age (especially if paired with hypertension or diabetes), and other factors likely to compromise long-term graft function.
Donors positive for hepatitis B core antibodies are routinely paired with recipients who have documented hepatitis B immunity as a result of immunization or prior infection. Kidneys from donors with chronic hepatitis C virus infection are frequently transplanted into recipients with hepatitis C and minimal hepatic damage (stage 2 fibrosis or less).
The donor operation is now typically part of a complex multiorgan recovery process that includes the kidneys, liver, pancreas, heart, and lungs (see Organ Procurement). Organ recovery essentially involves perfusion of the involved organs with cold (ie, 4°C) preservation solution. These solutions typically contain high levels of potassium to depolarize cell membranes, thereby reducing the metabolic demands associated with maintaining sodium and potassium gradients.
Organ preservation solutions may also contain impermeant sugars to prevent cell swelling, albumin or dextrans to maintain osmolality and to prevent swelling of the extravascular extracellular fluid compartment, and free radical scavengers and other agents (eg, allopurinol) to reduce reperfusion injury. The most commonly used preservation solution was first formulated by Folkert Belzer at the University of Wisconsin (UW).
After intravascular perfusion with a cold preservative solution, the kidneys are removed, with care taken to preserve the renal vasculature and the ureter with the blood supply contained in its investing tissue. The kidneys are packed sterilely in UW solution and kept at 4° C during transport to the appropriate transplant center. To provide target cells for the crossmatch, lymphoid tissue (eg, lymph nodes or spleen) is obtained at the time of organ recovery (see Organ Preservation).
The steadily increasing demand for renal transplantation has prompted consideration of ways to expand the pool of potential donors. Expanded living donation has had the greatest quantitative effect. Increased use of DCD donor kidneys and the efficient use of expanded-criteria donors (ECDs) can, to a lesser degree, increase organ availability. ECD kidneys come either from donors who are older than 60 years or from donors who are older than 50 years and have two of the following three characteristics:
History of hypertension
Cerebrovascular injury as the cause of death
Creatinine level higher than 1.5 mg/dL at any time
In routine use, ECD kidneys are associated with a significantly higher risk of nonfunction and delayed graft function. These kidneys are currently allocated in an expedited manner to patients who have agreed to accept these risks. They are often placed on pulsatile perfusion pumps to assess their flow and resistance to flow characteristics.
As the number of patients listed for kidney transplantation continues to increase, transplant professionals continue to search for methods of increasing the donor pool.
Transplanting across a positive crossmatch
A significant number of patients have preformed antibodies to potential living donors. The antibodies develop as the result of exposure to foreign antigens by prior transplantation, blood transfusions, or pregnancy. Consequently, these recipients have positive crossmatches against identified living donors.
Many transplant centers have protocols that enable these sensitized patients to receive kidneys from living donors against whom they have a positive crossmatch. This usually involves several pretransplant pheresis sessions to remove the offending antibodies and administration of intravenous immunoglobulin (IVIg) to inhibit the return of antibodies. The living-donor transplant is then performed when the crossmatch converts to negative. Postoperatively, the recipient usually receives additional pheresis treatments and IVIg infusions.
Another option for patients with a positive crossmatch with a potential donor is to enroll in a donor exchange program. Incompatible donor-recipient pairs are screened against other incompatible pairs to determine whether the donors could donate to another recipient. The most equitable method involves two recipients exchanging or swapping their donors, with both recipients receiving kidneys of equal quality. More complicated metrics have been proposed and used.
Implantation of Renal Allograft
Various approaches to kidney transplantation have been developed. The Gibson incision is the most common approach: it involves a curvilinear incision in a lower quadrant of the abdomen, with division of the muscles of the abdominal wall and dissection of the retroperitoneal space to expose the iliac vessels and the bladder. Occasionally, a midline incision is used; this approach is useful when a recipient has prior transplants in both lower quadrants or when a large kidney is to be placed in a small recipient.
The authors’ preferred approach involves direct end-to-side anastomosis of the renal artery to the external iliac artery (see the image below), though the common iliac may also be used. The inferior vena cava and aorta are accessible via the right-side approach. Anastomoses are typically performed with permanent vascular sutures (5-0, 6-0, or 7-0, as mandated by operating conditions). Numerous surgical options are available, including patch techniques, use of vascular autograft and allograft, and use of recipient hypogastric or epigastric arteries.
The ureter is anastomosed to the bladder through the formation of a ureteroneocystostomy. This procedure may involve bringing the ureter through a tunnel in the bladder submucosa (Leadbetter-Politano approach), or it may involve creating an anastomosis between the tip of the ureter and the bladder mucosa, then partially covering this with bladder muscularis (Lich approach). The standard of care for ureteral anastomosis in kidney transplant is via the extravesical approach.
The decision to use a ureteral stent to facilitate the ureteroneocystostomy and reduce the risk of obstruction in the early postoperative period is highly individualized. Some surgeons routinely place stents; others avoid them. The authors typically perform Lich ureteroneocystostomies and insert stents when ureter or bladder tissue appears marginal. Arranging for cystoscopic stent removal within a few weeks of transplantation is important: A forgotten stent can cause hematuria and become a nidus for stone formation and infection.
In rare clinical situations, anastomosis of the ureter to the bladder is not possible. If the donor ureter is devascularized during recovery and must be cut to a length that is too short to reach the bladder, then other options must be considered. In rare cases, it is impossible to mobilize the bladder sufficiently to allow creation of the standard anastomosis. Anastomosis of the donor ureter to the native ureter is a viable option.
Numerous complications are associated with kidney transplantation. These include the following:
Delayed graft function
Vascular thrombosis and stenosis
Delayed graft function
The incidence of delayed graft function (as defined by the need for dialysis in the first week after transplantation) varies according to donor, recipient, and transplant characteristics. Delayed graft function is rare with living donor grafts, probably because of the short cold ischemia time and the recovery of the kidney from a healthy live donor. For deceased donor kidneys, cold ischemia time remains the best predictor of delayed graft function.
While most delayed-graft-function kidneys eventually function, they do have a somewhat diminished lifespan compared with kidneys that function immediately. Delayed allograft function is associated with increased hospital stays and increased perioperative expense.
Vascular thrombosis and stenosis
Renal artery thrombosis occurs in about 1% of transplants, usually from small-caliber arteries. Nephrectomy is generally required if thrombectomy is unsuccessful. Arterial stenosis occurs in 2-10% of cases, may occur within months or years following transplantation, and is associated with hypertension. It is often suspected on the basis of findings from Doppler ultrasonography.
D efinitive diagnosis generally requires angiography to confirm the presence of the stenosis and exclude proximal vascular disease. One author has found carbon dioxide angiography to be useful, especially in the setting of renal insufficiency, because it eliminates the need to use nephrotoxic contrast material. Management of arterial stenoses has increasingly turned to percutaneous techniques, including angioplasty and stent placement.
Doppler ultrasonography can also be used to monitor for fluid formation, a potential sign of hematoma.
Venous thrombosis occurs in 0.5-4% of cases. In a few cases, thrombosis of the main renal vein has been successfully treated with thrombolytic agents, though the graft typically has undergone infarction by the time the thrombosis is detected. Graft infarction may occur with patent main arteries and veins, and nephrectomy is generally required. Graft thrombosis associated with sepsis carries a significant recipient mortality. Prompt nephrectomy is indicated.
With exception of infection, ureteral obstruction is the most common urinary tract problem associated with transplantation. It may occur early or late.
Early obstruction may result from clot, edema, or technical problems associated with the ureteroneocystostomy. If Foley catheter placement and expectant management do not resolve the problem, surgical revision of the ureteroneocystostomy over a stent may be required. Late obstruction, when not caused by external compression (eg, from lymphocele or pregnancy), is most commonly associated with fibrosis or nephrolithiasis. Management typically involves radiologic or cystoscopic stent placement and stricture dilatation.
Urine can leak at any level of the urinary tract, from the renal pelvis to the urethra. Suspect urinary leakage when a patient with good or improving graft function develops a fluid leak from the wound or abdominal pain or perineal swelling, typically within a month of transplantation. Fluid leaking from the wound can be collected and assayed for creatinine. Nuclear renal scanning is probably the most sensitive test for urinary leakage.
Small bladder leaks often can be managed by means of bladder decompression with a Foley catheter. Larger and more proximal leaks typically call for exploration and repair.
Leakage from perivascular lymphatic vessels can lead to significant collections of lymph between the lower pole of the transplanted kidney and the bladder. A lymphocele can manifest as swelling, pain, and impaired renal function within the first year after transplantation. Ultrasonography or computed tomography (CT) demonstrates the collection well and is used to facilitate treatment planning.
Aspiration occasionally resolves the problem, but prolonged catheter drainage is associated with a significant risk of infection. Sclerotherapy with 10% povidone-iodine solution may be successful in treating small nonloculated collections, but the lymphocele is highly likely to recur. Some early success has been obtained by instilling fibrin glue that contains gentamicin and iodine solution. However, the current standard of care is internal drainage of the lymphocele into the abdominal cavity. Increasingly, this procedure is performed laparoscopically.
The risk of opportunistic infections is increased after transplantation. These infections are typically caused by commonly encountered pathogens such as cytomegalovirus, BK virus, fungi, Pneumocystis jiroveci, and Legionella species. Early after transplantation, urinary tract infections are most common, and are often caused by Escherichia coli. For more information, see Infections After Solid Organ Transplantation.
With improved immunosuppression, acute rejection after transplantation has become less of a problem. In the first year after transplantation, acute rejection is observed in about 10-25% of patients. Rejection is usually asymptomatic, though it is sometimes associated with fever and pain at the graft site. It usually presents as an unexplained rise in serum creatinine levels and can be confirmed with biopsy. Typical biopsy findings include lymphoplasmacytic infiltration of the renal interstitial areas with occasional penetration of the tubular epithelium by these cells.
Most rejection episodes can be treated successfully with a short course of increased steroid doses. Failure to respond to steroid therapy for a particularly aggressive appearance determined by biopsy may prompt a change of treatment strategy (eg, use of antilymphocyte antibody agents).
"Chronic rejection" (termed interstitial fibrosis/tubular atrophy in the current literature) appears to have both immunologic and nonimmunologic components. Risk factors include initial poor function of the graft and a history of acute rejection episodes. Chronic rejection is not treatable.
Posttransplant diabetes, hypertension, and hyperlipidemia are all complications of immunosuppressive agents.
United Network for Organ Sharing (UNOS). Data. UNOS. Available at http://www.unos.org/donation/index.php?topic=data. August 28, 2015; Accessed: September 3, 2015.
Bartlett ST, Farney AC, Jarrell BE, et al. Kidney transplantation at the University of Maryland. Clin Transpl. 1998. 177-85. [Medline].
Frassetto LA, Tan-Tam C, Stock PG. Renal transplantation in patients with HIV. Nat Rev Nephrol. 2009 Oct. 5(10):582-9. [Medline].
Oellerich M, Shipkova M, Schutz E, et al. Pharmacokinetic and metabolic investigations of mycophenolic acid in pediatric patients after renal transplantation: implications for therapeutic drug monitoring. German Study Group on Mycophenolate Mofetil Therapy in Pediatric Renal Transplant Recipient. Ther Drug Monit. 2000 Feb. 22(1):20-6. [Medline].
Gallagher M, Jardine M, Perkovic V, Cass A, McDonald S, Petrie J, et al. Cyclosporine withdrawal improves long-term graft survival in renal transplantation. Transplantation. 2009 Jun 27. 87(12):1877-83. [Medline].
Kahan BD, Julian BA, Pescovitz MD, et al. Sirolimus reduces the incidence of acute rejection episodes despite lower cyclosporine doses in caucasian recipients of mismatched primary renal allografts: a phase II trial. Rapamune Study Group. Transplantation. 1999 Nov 27. 68(10):1526-32. [Medline].
Yakupoglu YK, Kahan BD. Sirolimus: a current perspective. Exp Clin Transplant. 2003 Jun. 1(1):8-18. [Medline].
Oberholzer J, John E, Lumpaopong A, et al. Early discontinuation of steroids is safe and effective in pediatric kidney transplant recipients. Pediatr Transplant. 2005 Aug. 9(4):456-63. [Medline].
Kramer BK, Krager B, Mack M, et al. Steroid withdrawal or steroid avoidance in renal transplant recipients: focus on tacrolimus-based immunosuppressive regimens. Transplant Proc. 2005 May. 37(4):1789-91. [Medline].
Berney T, Malaise J, Mourad M, et al. Laparoscopic and open live donor nephrectomy: a cost/benefit study. Transpl Int. 2000. 13(1):35-40. [Medline].
Ratner LE, Montgomery RA, Kavoussi LR. Laparoscopic live donor nephrectomy: the four year Johns Hopkins University experience. Nephrol Dial Transplant. 1999 Sep. 14(9):2090-3. [Medline].
Matas AJ, Smith JM, Skeans MA, Thompson B, Gustafson SK, Stewart DE, et al. OPTN/SRTR 2013 Annual Data Report: kidney. Am J Transplant. 2015 Jan. 15 Suppl 2:1-34. [Medline].
Huh KH, Kim MS, Ju MK, Chang HK, Ahn HJ, Lee SH, et al. Exchange living-donor kidney transplantation: merits and limitations. Transpl. Aug 2008. 86:430-435. [Medline].
Slagt I, Klop K, Ijzermans J. Intravesical versus extravesical ureteroneocystostomy in kidney transplantation: A systematic review and meta-analysis. Transplantation. October 2012.
Isoniemi H, Lehtonen S, Salmela K, Ahonen J. Does delayed kidney graft function increase the risk of chronic rejection?. Transpl Int. 1996. 9 Suppl 1:S5-7. [Medline].
Johnston TD, Thacker LR, Jeon H, et al. Sensitivity of expanded-criteria donor kidneys to cold ischaemia time. Clin Transplant. 2004. 18 Suppl 12:28-32. [Medline].
al-Aasfari R, Hadidy S, Yagan S. Infectious complications of kidney transplantation. Transplant Proc. 1999 Dec. 31(8):3204. [Medline].
Varon NF, Alangaden GJ. Emerging trends in infections among renal transplant recipients. Expert Rev Anti Infect Ther. 2004 Feb. 2(1):95-109. [Medline].
Adamska Z, Karczewski M, Cichańska L, Więckowska B, Małkiewicz T, Mahadea D, et al. Bacterial Infections in Renal Transplant Recipients. Transplant Proc. 2015 Jul-Aug. 47 (6):1808-12. [Medline].
- Table 1. Demographics of adult patients on the waiting list for kidney transplants, United States, 2012
- Table 2. Primary causes of ESRD in adult patients on the kidney transplant waiting list: United States, 2012
- Table 3. Demographics of pediatric patients awaiting kidney transplant: United States, 2012
- Table 4. Primary causes of end-stage renal disease in pediatric patients on the kidney transplant waiting list: United States, 2012
- Table 5. Five-year post-transplant survival with a functioning kidney graft: United States, 2012
|Patient Characteristic||Number of Patients||Percentage|
|Age 18-34 y||8811||9.5|
|Age 35-49 y||24,799||26.7|
|Age 50-64 y||40,523||43.6|
|Age 65-74 y||16,779||18.1|
|Age >75 y||1973||2.1|
|Cause of ESRD||Number of Patients||Percentage|
|Other or unknown cause||17||18.5|
|ESRD = End-stage renal disease|
|Age <1 y||1.0|
|Age 1-5 y||15.9|
|Age 6-10 y||14.1|
|Age 11-17 y||69.0|
|Other or unknown||1.8|
|Cause of Renal Failure||Percentage|
|Focal segmental glomerulosclerosis||12.0|
|Other or unknown||50.3|
|ESRD = End-stage renal disease|
|Age <11 y, deceased donor||75|
|Age <11 y, living donor||89|
|Age 11-17 y, deceased donor||67|
|Age 11-17, live donor||77|
|Adults, deceased donor||73|
|Adults, living donor||84|
|Adults transplanted for diabetes||71|
|Adults transplanted for hypertension||70|
|Adults transplanted for glomerulonephritis||77|
|Adults transplanted for cystic kidney disease||82|