0587 Pancreas Kidney Transplantation - Aetna · 11/10/2017 · The American Diabetes Association...

http://www.aetna.com/cpb/medical/data/500_599/0587.html 08/28/2019

Page 1 of 21

(https://www.aetna.com/)

Pancreas Kidney Transplantation

Clinical Policy Bulletins Medical Clinical Policy Bulletins

Policy History Last

Review

08/15/2019

Effective: 02/12/200

Next Review:

06/12/2020

Review History

Definitions

Additional Information

Number: 0587

Policy *Please see amendment for Pennsylvania Medicaid at the end of this CPB.

Simultaneous Pancreas-Kidney (SPK) and Pancreas and Living-Donor Kidney (SPLK) Transplantation

Aetna considers simultaneous pancreas-kidney (SPK) transplantation and

simultaneous cadaver-donor pancreas and living-donor kidney (SPLK)

transplantation medically necessary for members with diabetes and end-stage renal

disease (ESRD) who meet the transplanting institution's selection criteria. In the

absence of an institution's selection criteria, Aetna considers SPK transplantation

and SPLK transplantation medically necessary in persons with diabetes and ESRD

when all of the following selection criteria are met, and none of the following

absolute contraindications is present:

1. Member has a creatinine clearance (Clcr), calculated by the Cockcroft-Gault

formula (see Appendix), of less than 20 ml/min, or a directly measured

glomerular filtration rate (GFR) of less than 20 ml/min; and

2. Member has ESRD and requires dialysis or is expected to require dialysis in the next 12 months.

http://www.aetna.com/cpb/medical/data/500_599/0587.html

https://www.aetna.com/


Page 2 of 21

Aetna considers SPK and SPLK transplantation not medically necessary for

persons with poorly controlled HIV infection. HIV infection is considered poorly

controlled if any of the following is present:

HIV-1 RNA (viral load) is not at undetectable levels; or

Member has not been on stable anti-viral therapy for at least 3 months; or

Member has opportunistic infections or neoplasms; or

Member's CD4 count has not been 200 cells/mm3 or greater for at least 6

months.

Because of the success of protease inhibitors, the literature indicates the HIV-

positive person may be a candidate for transplant if the CD4 count is more than 200

cells/mm3 for greater than 6 months, on stable anti-viral therapy more than 3

months, no opportunistic infections or neoplasms, and viral load is zero.

Aetna considerrs SPK and SPLK transplantation not medically necessary for

members with any of the following absolute contraindications:

Inability to adhere to the regimen necessary to preserve the transplant

Malignant neoplasm (other than non-melanomatous skin cancer or low

grade prostate cancer) that has a significant risk of recurrence

Ongoing or recurrent active infections that are not adequately treated

Persistent substance abuse

Severe uncorrectable cardiac disease (e.g., coronary angiographic evidence of

significant non-correctable coronary artery disease, refractory congestive heart

failure, ejection fraction below 40 %, myocardial infarction less than 3 months

ago) (cardiac status should be re-evaluated annually while on waiting list)

Unresolvable current psychosocial problems.

Aetna considers SPK and SPLK transplantation medically necessary for persons

with any of the following relative contraindications if the attending physician

determines and documents that the potential benefits of SPK or

SPLK transplantation outweigh the risks. Relative contraindications to SPK and

SPLK transplantation include:

Chronic liver disease



Page 3 of 21

Clinical evidence of severe cerebrovascular or peripheral vascular disease (e.g.,

ischemic ulcers, previous amputation secondary to severe peripheral vascular

disease, severe iliac disease, blindness). Adequate peripheral arterial supply

should be determined by standard evaluation in the vascular laboratory

including Doppler examination and plethysmographic readings of systolic blood

pressure.

Past psychosocial abnormality

Persons with body mass index (BMI) of 35 or higher and type 2 diabetes

(bariatric surgery should be considered)

Structural genito-urinary abnormality or recurrent urinary tract infection.

Substance abuse history (other than persistent substance abuse)

Treated malignancy (SPK or SPLK transplantation is considered medically

necessary in persons with malignant neoplasm if the neoplasm has been

adequately treated and the risk of recurrence is small)

Uncontrolled hypertension.

Aetna considers measurement of donor-derived cell-free DNA of transplant

recipients for monitoring of rejection experimental and investigational because the

effectiveness of this approach has not been established.

Note: For isolated kidney transplant,

see CPB 0493 - Kidney Transplantation (../400_499/0493.html). For pancreas

after kidney (PAK) transplant,

CPB 0601 - Pancreas Transplantation Alone (PTA) and Islet Cell Transplantation

see (../600_699/0601.html)

.

Background

Diabetes mellitus is the most common endocrine disease worldwide and is the

leading chronic disease in children. Despite the success of exogenous insulin

therapy, numerous long-term sequelae develop in patients with diabetes, including

end-stage renal failure, cardiovascular disease, autonomic and somatic

neuropathy, and blindness. Chronically abnormal lipid metabolism, accelerated

atherosclerosis, and destruction of the microvascular system result in global

vascular disease, leading to amputations and premature death from myocardial

infarctions and cerebrovascular accidents. Occurring in approximately 1 % of the



Page 4 of 21

population, diabetes accounts for more than 160,000 deaths annually in the United

States. According to the United States End-Stage Renal Disease (ESRD) Registry,

diabetic patients between the ages of 20 and 45 who have to undergo dialysis as

their only treatment option have less than 20 % survival after 10 years. Solitary

renal transplantation with continued administration of exogenous insulin for glucose

control is a good option for diabetic recipients as it has 5-year survival rates

approaching 70 % for cadaveric renal transplants and 85 % for living related donor

(LRD) transplants; however, the diabetic state remains associated with poor patient

survival.

Reported in 1993, the Diabetes Control and Complications Trial Study conclusively

showed that tight glucose control significantly decreases nephropathy, retinopathy,

and neuropathy in patients with type 1 diabetes, and this provided the impetus for

combining pancreas transplantation with kidney transplantation. In selected

patients and without compromising survival rates, both diabetes and ESRD can be

eliminated by simultaneous pancreas and cadaver kidney (SPK) transplantation

and LRD kidney transplantation alone followed by a solitary cadaver-donor

pancreas transplant (sequential pancreas after kidney [PAK] transplantation). SPK

transplantation is more widely used than PAK, because SPK is a single operation

and there is an "immunologic advantage" for the pancreas because the kidney can

serve as a reliable marker for rejection of the pancreas. However, some advocate

PAK transplantation if there is a willing LRD. Use of a well-matched living-donor

kidney offers the potential benefits of shorter waiting time, expansion of the organ

donor pool, and improved short-term and long-term renal graft function. SPK

pancreas graft survival has historically exceeded that of solitary pancreas

transplantation; however, recent improvements in solitary pancreas transplant

survival rates have narrowed the advantage seen with SPK. Both SPK and PAK

impose greater immunologic risks over kidney transplant alone.

The goal of these transplants is to produce a lasting normoglycemic state that

enhances quality of life and prevents, arrests, or perhaps even reverses the

otherwise inexorable progression of the destructive effects of diabetes. As

demonstrated in a number of studies, this resumption of normal glucose

homeostasis achieved provides several benefits: (i) quality of life is improved

since it usually removes dependence on both insulin and d ialysis; (ii)

recurrence of diabetic nephropathy is attenuated; (iii) diabetic retinopathy is

reduced; (iv) progression of diabetic neuropathy may be halted and in some

cases reversed, including improvements in autonomic neuropathy, enhancing



Page 5 of 21

both cardiac reflex function and gastric motility in some cases; and (v)

beneficially affects patient survival even though this glycemic control is given as

a late intervention in a diabetic patient's lifetime. More importantly, studies show

that diabetic patients who receive a successful SPK transplant do not develop

diabetic complications in their newly transplanted kidney, unlike persons with

diabetes who receive a kidney transplant alone. Even diabetic vesicopathy has

been shown to improve after transplantation, as well as attenuation of diabetic

cardiovascular disease.

The American Diabetes Association (2003) has concluded that pancreas-kidney

transplantation is indicated in patients with insulin-dependent diabetes and end

stage renal disease: “Pancreas transplantation should be considered an acceptable

therapeutic alternative to continued insulin therapy in diabetic patients with

imminent or established end-stage renal disease who have had or plan to have a

kidney transplant, because the successful addition of a pancreas does not

jeopardize patient survival, may improve kidney survival, and will restore normal

glycemia.”

An assessment by the Institute for Clinical Systems Improvement (ICSI, 2003)

stated that “[n]early all uremic diabetics are candidates for a kidney transplant and

most should also receive a pancreas either simultaneously (SPK) or sequentially

(PAK). For those who have a living donor for a kidney, PAK is preferable to waiting

years for a cadaver SPK". The ICSI assessments notes that experience with

pancreas transplant for type 2 diabetes is more limited than for type 1 diabetes.

The assessment reports that approximately 6 % of pancreas transplants are done

in patients with type 2 diabetes and about 94 % are done in patients with type 1

diabetes. The ICSI guideline describes an unpublished study by Elkhammas et al

(1999) of SPK transplantation in 299 patients with type 2 diabetes who received

pancreas transplants from 1994 to 1999. The study noted that, at 5 years, 86 % of

patients survived, 73 % of pancreas grafts survived, and 75 % of kidney grafts

survived.

Nath et al (2005) reported on the results of pancreas transplant in 17 patients with

type 2 diabetes transplanted between 1994 through 2002. Of the 17 transplants, 7

(41 %) were a SPK, 4 (24 %) were a PAK, and 6 (35 %) were a pancreas

transplantation alone (PTA). One recipient died during the peri-operative period

because of aspiration. The other 16 recipients became euglycemic post-transplant

and had a functional graft at 1 year post-transplant. After a mean follow-up of 4.3



Page 6 of 21

years post-transplant, the patient survival rate is 71 % (12 of 17). The investigators

reported that the 4 additional deaths were due to sepsis (n = 2), suicide (n = 1), and

unknown cause (n = 1). The investigators noted that all 4 of these recipients were

insulin-independent at the time of death, although 1 was on an oral hypoglycemic

agent. The investigators reported that, of the 12 recipients currently alive, 11

remain euglycemic without requiring insulin therapy or oral hypoglycemic agents,

and 1 recipient began insulin therapy 1.2 years post-transplant.

Light and Barhyte (2005) reported on 10- to 15-year results of SPK transplants in

135 type 1 and type 2 patients who were dependent on insulin. Twenty-eight

percent of the patients in the cohort had type 2 diabetes. The investigators

reported that, at 5 and 10 years, pancreas survival for type 1 diabetes was 71 %

and 49 %; for type 2 diabetes it was 67 % and 56 % (p = 0.52). Kidney survival at 5

and 10 years for patients with type 1 diabetes was 77 % and 50 %; for patients with

type 2 diabetes, it was 72 % and 56 % (p = 0.65). Patient survival at 5 and 10

years with 85 % and 63 % for patients with type 1 diabetes mellitus, and was 73 %

and 70 % for patients with type 2 diabetes (p = 0.98). The investigators concluded

that the outcomes of SPK transplants are equivalent regardless of diabetes type.

The pros and cons of SPK and PAK must be weighed in each individual patient to

determine proper treatment. The graft survival rate of living related kidney

allografts significantly exceed that of cadaveric renal transplants because they have

less immunologic disparity and comparatively minimal preservation injury.

However, in the setting of diabetes, with the possibility of recurrent diabetic

nephropathy and other disabling complications, the medical literature indicates that

the addition of a pancreas transplant might provide benefits that outweigh the

advantages of LRD renal transplantation. SPK transplantation is associated with

excess initial morbidity and an uncertain effect on patient survival when compared

with solitary cadaveric or living donor renal transplantation. Recent studies show

rejection rates after SPK transplantation have now diminished to less than 5 %

within the first 6 months. The results also show that SPK has long-term transplant

survival rates, which are equal to or even better than survival rates of kidneys from

the very best matched live donors. Certainly, survival of SPK transplants is

superior to cadaver kidney transplants alone in the diabetic population.

Largely because of these results, and because of the distinct advantages of living

kidney donation, some centers have developed a new approach for uremic diabetic

patients: simultaneous cadaver-donor pancreas and living-donor kidney



Page 7 of 21

transplantation (SPLK). As a single procedure, SPLK has obvious advantages over

the standard living-donor kidney transplant followed by PAK. Moreover, because

the SPLK kidney is from a living donor, there may be both short-term and long-term

benefits over SPK transplantation. Potential benefits of SPLK for diabetic uremic

patients include a shorter waiting time for transplantation and better early and long-

term renal graft function. Generalized use of SPLK transplantation would expand

the renal organ donor pool, thus benefiting all patients waiting for a kidney

transplant. The main drawback to SPLK -- coordination of a living donor

nephrectomy with a cadaver pancreas transplant -- is easily overcome.

With improved surgical technique and better organ preservation, the remaining

obstacle was a high rejection rate of both the kidney and the pancreas. However,

with the introduction of more immunosuppressant alternatives, rejection rates have

now been reduced. The addition of mycophenolate mofetil (CellCept) and

tacrolimus (Prograf) have been extremely helpful options in the immunosuppressive

management. Furthermore, induction protocols utilizing basiliximab (Simulect) or

daclizumab (Zenapax) are less complicated and have been shown to be better

tolerated than the previous induction protocols with anti-lymphocyte globulin (ALG)

or OKT3 (Muromonab-CD3). The reported 1-year pancreas graft survival rate for

SPK transplantation is now 83 %. The results of PAK have lagged behind the

excellent results of SPK transplantation. During the past 3 to 4 years, the reported 1

year pancreas graft survival rate for PAK recipients has improved from 54 % survival

to 71 %, shrinking the "immunologic advantage" of combining a cadaver pancreas

with a kidney from the same donor.

Members referred for SPK transplantation, who are acceptable candidates by all

criteria, should be counseled about possible living donor kidney transplantation.

Since there is an extreme shortage of cadaver kidneys in the United States and

because living donor kidneys have a survival advantage over cadaver kidneys,

generally accepted guidelines state that persons with diabetes with ESRD referred

for SPK transplantation should consider living donor kidney transplant alone

(LDKTA) followed by a pancreas after kidney (PAK) procedure. Studies show that

the LDKTA and PAK option carries equal pancreatic transplant success as SPK

transplantation combined with the added survival advantage of LDKTA.

Margreiter et al (2013) systematically reviewed the relevant literature with regard to

various biomarkers, imaging techniques, and pathologic evaluation of allograft

tissue following pancreas transplantation. More recent studies including graft



Page 8 of 21

histology demonstrated the low specificity of pancreatic enzymes as a marker of

acute rejection. On the other hand, most blood and serum markers are indicative of

an activated immune status rather than rejection. Interestingly, the concomitantly

transplanted kidney from the same donor does not seem to be a reliable surrogate

marker. Although computed tomography or ultrasound-guided percutaneous

biopsies of the pancreas are performed more frequently at present, the

complication rate is still as high as 11 %. In contrast, cystoscopic and enteroscopic

biopsies of the duodenal part of the graft are associated with almost no

complications. The few clinical studies dealing with the duodenum as surrogate

marker for the pancreas report a high correlation between duodenum mucosal and

pancreas parenchymal histology. The authors concluded that pancreatic graft

parenchymal biopsy remains the gold standard in diagnosing pancreatic rejection,

as clinical parameters, pancreatic enzymes, non-invasive biomarkers, and

surrogate renal biopsies are not reliable tools. Endoscopically obtained duodenal

cuff biopsies are a less invasive alternative to percutaneous biopsies.

Kobayashi et al (2014) studied and compared clinical and functional outcomes after

simultaneous deceased donor pancreas and kidney transplantation (SPK DD),

simultaneous deceased donor pancreas and living donor kidney transplantation

(SPK DL), and simultaneous living donor pancreas and kidney transplantation (SPK

LL). From January 1, 1996 to September 1, 2005, a total of 8,918 primary SPK

procedures were reported to the International Pancreas Transplant Registry. Of

these, 8,764 (98.3 %) were SPK DD, 115 (1.3 %) were SPK DL, and 39 (0.4 %)

were SPK LL. These researchers compared these 3 groups with regard to several

end-points including patient and pancreas and kidney graft survival rates. The

1-year and 3-year patient survival rates for SPK DD were 95 % and 90 %, 97 %

and 95 % for SPK DL, and 100 % and 100 % for SPK LL recipients, respectively (p

≥ 0. 07). The 1-year and 3-year pancreas graft survival rates for SPK DD were 84

% and 77 %, 83 % and 71 % for SPK DL, and 90 % and 84 % for SPK LL

recipients, respectively (p ≥ 0.16). The 1-year and 3-year kidney graft survival rates

for SPK DD were 92 % and 84 %, 94 % and 86 % for SPK DL, and 100 % and 89

% for SPK LL recipients, respectively (p ≥ 0.37). The authors concluded that

patient survival rates and graft survival rates for pancreas and kidney were similar

among the 3 groups evaluated in this study.

In a Cochrane review, Montero et al (2014) noted that pancreas or kidney-pancreas

transplantation improves survival and quality of life for people with type 1 diabetes

mellitus and kidney failure. Immunosuppression after transplantation is associated



Page 9 of 21

with complications. Steroids have adverse effects on cardiovascular risk factors

such as hypertension, hyperglycemia or hyperlipidemia, increase risk of infection,

obesity, cataracts, myopathy, bone metabolism alterations, dermatologic problems

and Cushingoid appearance; whether avoiding steroids changes outcomes is

unclear. These investigators evaluated the safety and effectiveness of steroid early

withdrawal (treatment for less than 14 days after transplantation), late withdrawal

(after 14 days after transplantation) or steroid avoidance in patients receiving PTA,

SPK or PAK. They searched the Cochrane Renal Group's Specialised Register (to

June 18, 2014) through contact with the Trials' Search Co-ordinator. They hand-

searched: reference lists of nephrology textbooks, relevant studies, recent

publications and clinical practice guidelines; abstracts from international

transplantation society scientific meetings; and sent emails and letters seeking

information about unpublished or incomplete studies to known investigators. These

researchers included randomized controlled trials (RCTs) or cohort studies of

steroid avoidance (including early withdrawal) versus steroid maintenance or

versus late withdrawal in pancreas or pancreas with kidney transplant recipients.

They defined steroid avoidance as complete avoidance of steroid

immunosuppression, early steroid withdrawal as steroid treatment for less than 14

days after transplantation and late withdrawal as steroid withdrawal after 14 days

after transplantation. Two authors independently assessed the retrieved titles and

abstracts, and where necessary the full text reports to determine which studies

satisfied the inclusion criteria. Authors of included studies were contacted to obtain

missing information. Statistical analyses were performed using random effects

models and results expressed as risk ratio (RR) or mean difference (MD) with 95 %

confidence interval (CI). Cohort studies were not meta-analyzed, but their findings

summarized descriptively. A total of 3 RCTs enrolling 144 participants met the

inclusion criteria: 2 compared steroid avoidance versus late steroid withdrawal and

1 compared late steroid withdrawal versus steroid maintenance. All studies

included SPK and only 1 also included PTA. All studies had an overall moderate

risk of bias and presented only short-term results (6 to 12 months). Two studies

(89 participants) compared steroid avoidance or early steroid withdrawal versus late

steroid withdrawal. There was no clear evidence of an impact on mortality (2

studies, 89 participants: RR 1.64, 95 % CI: 0.21 to 12.75), risk of kidney loss

censored for death (2 studies, 89 participants: RR 0.35, 95 % CI: 0.04 to 3.09), risk

of pancreas loss censored for death (2 studies, 89 participants: RR 1.05, 95 % CI:

0.36 to 3.04), or acute kidney rejection (1 study, 49 participants: RR 2.08, 95 % CI:

0.20 to 21.50), however results were uncertain and consistent with no difference or

important benefit or harm of steroid avoidance/early steroid withdrawal. The study



Page 10 of 21

that compared late steroid withdrawal versus steroid maintenance observed no

deaths, no graft loss or acute kidney rejection at 6 months in either group and

reported uncertain effects on acute pancreas rejection (RR 0.88, 95 % CI: 0.06 to

13.35). Of the possible adverse effects only infection was reported by 1 study.

There were significantly more UTIs reported in the late withdrawal group compared

to the steroid avoidance group (1 study, 25 patients: RR 0.41, 95 % CI: 0.26 to

0.66). These researchers also identified 13 cohort studies and 1 RCT that

randomized tacrolimus versus cyclosporine. These studies in general showed that

steroid-sparing and withdrawal strategies had benefits in lowering HbAc1 and risk

of infections (BK virus and CMV disease) and improved blood pressure control

without increasing the risk of rejection. However, 2 studies found an increased

incidence of acute pancreas rejection (HR 2.8, 95 % CI: 0.89 to 8.81, p = 0.066 in 1

study and 43.3 % in the steroid withdrawal group versus 9.3 % in the steroid

maintenance, p < 0.05 at 3 years in the other) and 1 study found an increased

incidence of acute kidney rejection (18.7 % in the steroid withdrawal group versus

2.8 % in the steroid maintenance, p < 0.05) at 3 years. The authors concluded that

there is currently insufficient evidence for the benefits and harms of steroid

withdrawal in pancreas transplantation in the 3 RCTs (144 patients) identified. The

results showed uncertain results for short-term risk of rejection, mortality, or graft

survival in steroid-sparing strategies in a very small number of patients over a short

period of follow-up. Overall the data was sparse, so no firm conclusions are

possible. Moreover, the 13 observational studies findings generally concur with the

evidence found in the RCTs.

Gruessner and colleagues (2017) stated that pancreas transplantation remains the

best long-term treatment option to achieve euglycemia and freedom from insulin in

patients with labile diabetes mellitus. It is an approved procedure for type 1

diabetes mellitus (T1DM), but it is still considered controversial for type 2 diabetes

mellitus (T2DM). These investigators analyzed all primary deceased donor

pancreas transplants in patients with T2DM reported to IPTR/UNOS between 1995

and 2015. Characteristics, outcomes, and risk factors over time were determined

using uni-variate and multi-variate methods. The focus was on SPK transplants,

the most common pancreas transplant category. Patient, pancreas, and kidney

graft survival rates increased significantly over time and reached 95.8, 83.3, and

91.1 %, respectively, at 3 years post-transplant for transplants performed between

2009 and 2015. The authors concluded that SPK is a safe procedure with excellent



Page 11 of 21

pancreas and kidney graft outcome in patients with T2DM. The procedure restored

euglycemia and freedom from insulin and dialysis. They stated that based on these

findings, SPK should be offered to more uremic patients with labile T2DM.

Measurement of Donor-Specific Cell-Free DNA for Monitoring Transplant Recipients for Rejection

Knight and colleagues (2019) noted that there is increasing interest in the use of non

invasive biomarkers to reduce the risks posed by invasive biopsy for monitoring of

solid organ transplants (SOTs). One such promising marker is the presence of

donor-derived cell-free DNA (dd-cfDNA) in the urine or blood of transplant recipients.

These investigators systematically reviewed the published literature investigating the

use of cfDNA in monitoring of graft health following SOT. Electronic databases were

searched for studies relating cfDNA fraction or levels to clinical outcomes, and data

including measures of diagnostic test accuracy were extracted. Narrative analysis

was performed. A total of 95 articles from 47 studies met the inclusion criteria (18

kidneys, 7 livers, 11 hearts, 1 kidney-pancreas, 5 lungs, and 5 multi-organs). The

majority were retrospective and prospective cohort studies, with 19 reporting

diagnostic test accuracy data. Multiple techniques for measuring dd-cfDNA were

reported, including many not requiring a donor sample; dd-cfDNA fell rapidly within 2

weeks, with baseline levels varying by organ type.

Levels were elevated in the presence of allograft injury, including acute rejection

and infection, and return to baseline following successful treatment. Elevation of

cfDNA levels was observed in advance of clinically apparent organ injury.

Discriminatory power was greatest for higher grades of T cell-mediated and acute

antibody-mediated rejection (AMR), with high negative predictive values (NPVs).

The authors concluded that cell-free DNA is a promising biomarker for monitoring

the health of SOTs. These researchers stated that future studies will need to define

how it can be used in routine clinical practice and determine clinical benefit with

routine prospective monitoring.

Appendix

The Cockcroft-Gault formula for calculation of creatinine clearance is now generally

accepted as superior to actual measured creatinine clearance as determined by a

24-hour urine collection, due to inherent inaccuracies and collection difficulties.

The formula is as follows:


Page 12 of 21


CPT Codes / HCPCS Codes / ICD-10 Codes

Information in the [brackets] below has been added for clarification purposes. Codes requiring a 7th character are represented by "+":

CPT codes covered if selection criteria are met:



Page 13 of 21

Code Code Description

50323 Backbench standard preparation of cadaver donor renal allograft prior to

transplantation, including dissection of allograft and removal or

perinephric fat, diaphragmatic and retroperitoneal attachments, excision

of adrenal gland, and preparation of ureter(s), renal vein(s), and renal

artery(s), ligating branches, as necessary

50325 Backbench standard preparation of living donor renal allograft (open or

laparoscopic) prior to transplantation, including dissection and removal

of perinephric fat and preparation of ureter(s), renal vein(s), and renal

artery(s), ligating branches, as necessary

50327 Backbench reconstruction of cadaver or living donor renal allograft prior

to transplantation; venous anastamosis, each

50328 arterial anastamosis, each

50329 ureteral anastamosis, each

50340 Recipient nephrectomy (separate procedure)

50360 Renal allotransplantation, implantation of graft, excluding donor and

recipient nephrectomy

50365 with recipient nephrectomy

50370 Removal of transplanted renal allograft

50380 Renal autotransplantation, reimplantation of kidney

50547 Laparoscopic nephrectomy; donor nephrectomy from living donor

(excluding preparation and maintenance of allograft

Other CPT codes related to the CPB:

90935 - 90999 Dialysis, hemodialysis, and end-stage renal disease services

HCPCS code covered if selection criteria are met:

S2065 Simultaneous pancreas kidney transplantation

Other HCPCS codes related to the CPB:

J7513 Daclizumab, parenteral, 25 mg

S9339 Home therapy; peritoneal dialysis, administrative services, professional

pharmacy services, care coordination and all necessary supplies and

equipment (drugs and nursing visits coded separately

ICD-10 codes covered if selection criteria are met:



Page 14 of 21

Code Code Description

E10.21 - E10.29

E11.21 - E11.29

E13.21 -E13.29

Diabetes mellitus with renal manifestations

N18.5 Chronic kidney disease, Stage V

N18.6 End stage renal disease

ICD-10 codes contraindicated for this CPB:

A00.0 - B99.9 Infectious and parasitic diseases [ongoing or recurrent active infections

that are not adequately treated]

C00.0 - C75.9,

D00.0 - D09.9

Malignant neoplasms and carcinoma in situ [other than melanoma]

[other than melanoma and low-grade prostate cancer]

E66.01, E66.1,

E66.8, E66.9

Obesity unspecified or morbid obesity [BMI of 35 or higher]

F10.10 - F19.99 Alcohol and drug dependence and nondependent abuse [persistent

substance abuse]

I05.0 - I52 Chronic rheumatic heart disease, hypertensive disease, ischemic heart

disease, diseases of pulmonary circulation, and other forms of heart

disease [severe uncorrectable cardiac disease]

I60.00 - I69.998 Cerebrovascular disease [severe]

I70.201 - I70.92 Atherosclerosis of the extremities

I73.0 - I73.9 Other peripheral vascular diseases

I79.8 Other disorders of arteries, arterioles and capillaries in diseases

classified elsewhere

K70.0 - K74.69,

K76.89

Diseases of liver

L89.000 - L89.95

L97.101

L97.929

L98.411

L98.499

Chronic ulcer of skin [ischemic ulcer]

N36.0 - N36.9,

N39.0

Other disorders of urethra and urinary tract [structural genitourinary

abnormality or recurrent urinary tract infection]

Q50.01 - Q64.9 Congenital anomalies of genital organs and urinary system [structural

genitourinary abnormality or recurrent urinary tract infection]



Page 15 of 21

Measurement of donor-derived cell-free DNA of transplant:

CPT codes not covered for indications listed in the CPB:

Measurement of donor-derived cell-free DNA of transplant - no specific code:

ICD-10 codes not covered for indications listed in the CPB:

T86.11

T86.890

Z94.0

Z94.83

The above policy is based on the following references:

1. Humar A, Ramcharan T, Kandaswamy R, et al. Pancreas after kidney

transplants. Am J Surg. 2001;182(2):155-161.

2. Israni AK. Quality of life after transplantation for patients with diabetes

and renal dysfunction. Transplantation. 2001;72(5):969-970.

3. Kaufman DB, Leventhal JR, Elliott MD, et al. Pancreas transplantation at

Northwestern University. Clin Transpl. 2000;239-246.

4. Philosophe B, Farney AC, Schweitzer EJ, et al. Simultaneous pancreas-

kidney (SPK) and pancreas living-donor kidney (SPLK) transplantation at

the University of Maryland. Clin Transpl. 2000;211-216.

5. Elliott MD, Kapoor A, Parker MA, et al. Improvement in hypertension in

patients with diabetes mellitus after kidney/pancreas transplantation.

Circulation. 2001;104(5):563-569.

6. Sutherland DE, Gruessner RW, Gruessner AC. Pancreas transplantation for

treatment of diabetes mellitus. World J Surg. 2001;25(4):487-496.

7. Koznarova R, Saudek F, Hrachovinova T, et al. The quality of life of

pancreas recipients with type-1 diabetes. Transplant Proc. 2001;33

(1-2):1890.



Page 16 of 21

8. Ojo AO, Meier-Kriesche HU, Arndorfer JA, et al. Long-term benefit of

kidney-pancreas transplants in type 1 diabetics. Transplant Proc. 2001;33

(1-2):1670-1672.

9. Stratta RJ, Shokouh-Amiri MH, Egidi MF, et al. Simultaneous kidney-

pancreas transplant with systemic-enteric versus portal-enteric drainage.

Transplant Proc. 2001;33(1-2):1661-1662.

10. Reddy KS, Stablein D, Taranto S, et al. Long-term survival following

simultaneous kidney-pancreas transplantation versus kidney

transplantation alone in patients with type 1 diabetes mellitus and renal

failure. Transplant Proc. 2001;33(1-2):1659-1660.

11. Kahl A, Bechstein WO, Frei U. Trends and perspectives in pancreas and

simultaneous pancreas and kidney transplantation. Curr Opin Urol.

2001;11(2):165-174.

12. Friedman AL. Appropriateness and timing of kidney and/or pancreas

transplants in type 1 and type 2 diabetes. Adv Ren Replace Ther. 2001;8

(1):70-82.

13. Farney AC, Cho E, Schweitzer EJ, et al. Simultaneous cadaver pancreas

living-donor kidney transplantation: A new approach for the type 1

diabetic uremic patient. Ann Surg. 2000;232(5):696-703.

14. Humar A, Sutherland DE, Ramcharan T, et al. Optimal timing for a

pancreas transplant after a successful kidney transplant. Transplantation.

2000;70(8):1247-1250.

15. Elkhammas EA, Demirag A, Henry ML. Simultaneous pancreas-kidney

transplantation at the Ohio State University Medical Center. Clin Transpl.

1999;211-215.

16. Pirson Y, Vandeleene B, Squifflet JP. Kidney and kidney-pancreas

transplantation in diabetic recipients. Diabetes Metab. 2000;26 Suppl 4:86

89.

17. Hricik DE. Kidney-pancreas transplantation for diabetic nephropathy.

Semin Nephrol. 2000;20(2):188-198.

18. Rayhill SC, D'Alessandro AM, Odorico JS, et al. Simultaneous pancreas-kidney transplantation and living related donor renal transplantation in

patients with diabetes: Is there a difference in survival? Ann Surg.

2000;231(3):417-423.

19. Sudan D, Sudan R, Stratta R. Long-term outcome of simultaneous kidney-

pancreas transplantation: Analysis of 61 patients with more than 5 years

follow-up. Transplantation. 2000;69(4):550-555.



Page 17 of 21

20. Cicalese L, Giacomoni A, Rastellini C, Benedetti E. Pancreatic

transplantation: A review. Int Surg. 1999;84(4):305-312.

21. Robertson RP, Davis C, Larsen J, et al. Pancreas and islet transplantation

for patients with diabetes (Technical Review). Diabetes Care. 2000;23:112

116.

22. Holohan T. Simultaneous pancreas-kidney and sequential pancreas-after

kidney transplantation. Health Technology Assessment No. 4. AHCPR Pub.

No. 95-0065. Bethesda, MD: Agency for Healthcare Research and Quality

(AHRQ); August 1995.

23. Health Council of the Netherlands Gezondheidsraad (GR). Kidney-

pancreas transplantation. Rijswijk, The Netherlands: Health Council of the

Netherlands Gezondheidsraad (GR); 1997.

24. American Diabetes Association. Pancreas transplantation for patients with

type 1 diabetes (Position Statement). Diabetes Care. 2003;26(Suppl

1):S120.

25. Pox C, Ritzel R, Busing M, et al. Combined pancreas and kidney

transplantation in a lean type 2 diabetic patient. Effects on insulin

secretion and sensitivity. Exp Clin Endocrinol Diabetes. 2002;110(8):420

424.

26. Kronson JW, Gillingham KJ, Sutherland DE, Matas AJ. Renal transplantation

for type II diabetic patients compared with type I diabetic patients and

patients over 50 years old: a single-center experience. Clin Transplant.

2000;14(3):226-234.

27. Cantarovich D, Murat A, Krempf M, et al. Simultaneous pancreas and

kidney transplantation in a type II (non-insulin-dependent) diabetic uremic

patient requiring pregraft insulin therapy. Transplant Proc. 1990;22(2):662.

28. Belmonte AA. Transplant strategies for diabetic renal patients. EDTNA

ERCA J. 2004;30(3):157-162.

29. Palmer S, McGregor DO, Strippoli GF. Interventions for preventing bone

disease in kidney transplant recipients. Cochrane Database Syst Rev. 2007;

(3):CD005015.

30. Institute for Clinical Systems Improvement (ICSI). Pancreas transplant for

insulin-dependent diabetes. Technology Assessment Report No. 4.

Bloomington, MN: ICSI; October 2003.

31. Elkhammas EA, Demirag A, Henry ML. Simultaneous pancreas-kidney

transplantation at Ohio State University Medical Center. Clinical

Transplantation 1999, JM Cecka, PI Teraski, eds. Los Angeles, CA: UCLA



Page 18 of 21

Immunogenetics Center; 2000:211-215 (cited in Institute for Clinical

Systems Improvement (ICSI). Pancreas transplant for insulin-dependent

diabetes. Technology Assessment Report No. 4. Bloomington, MN: ICSI;

October 2003).

32. Nath DS, Gruessner AC, Kandaswamy R, et al. Outcomes of pancreas

transplants for patients with type 2 diabetes mellitus. Clin Transplant.

2005;19(6):792-797.

33. Light JA, Barhyte DY. Simultaneous pancreas-kidney transplants in type I

and type II diabetic patients with end-stage renal disease: Similar 10-year

outcomes. Transplant Proc. 2005;37(2):1283-1284.

34. Pox C, Ritzel R, Busing M, et al. Combined pancreas and kidney

transplantation in a lean type 2 diabetic patient. Effects on insulin

secretion and sensitivity. Exp Clin Endocrinol Diabetes. 2002;110(8):420

424.

35. Friedman AL, Friedman EA. Pancreas transplantation for type 2 diabetes at

U.S. transplant centers. Diabetes Care. 2002;25(10):1896.

36. Cantarovich D, Murat A, Krempf M, et al. Simultaneous pancreas and

kidney transplantation in a type II (non-insulin-dependent) diabetic uremic

patient requiring pregraft insulin therapy. Transplant Proc. 1990;22(2):662.

37. National Health Service (NHS), UKT Kidney and Pancreas Advisory Group.

National protocol for assessment of kidney and pancreas transplant

patients. Bristol, UK: UK Transplant; September 2003.

38. Ming CS, Chen ZH. Progress in pancreas transplantation and combined

pancreas-kidney transplantation. Hepatobiliary Pancreat Dis Int. 2007;6

(1):17-23.

39. Cohen DJ, Sung RS. Simultaneous kidney-pancreas transplantation.

Minerva Urol Nefrol. 2007;59(3):379-393.

40. Gerber PA, Pavlicek V, Demartines N, et al. Simultaneous islet-kidney vs

pancreas-kidney transplantation in type 1 diabetes mellitus: A 5 year

single centre follow-up. Diabetologia. 2008;51(1):110-119.

41. Diakoff E. Glucose metabolism after pancreas-kidney transplantation. Curr

Diab Rep. 2008;8(4):310-316.

42. Lerner SM. Kidney and pancreas transplantation in type 1 diabetes

mellitus. Mt Sinai J Med. 2008;75(4):372-384.

43. White SA, Shaw JA, Sutherland DE. Pancreas transplantation. Lancet.

2009;373(9677):1808-1817..



Page 19 of 21

44. Farney AC, Doares W, Rogers J, et al. A randomized trial of alemtuzumab

versus antithymocyte globulin induction in renal and pancreas

transplantation. Transplantation. 2009;88(6):810-819.

45. Wiseman AC. Simultaneous pancreas kidney transplantation: A critical

appraisal of the risks and benefits compared with other treatment

alternatives. Adv Chronic Kidney Dis. 2009;16(4):278-287.

46. Morath C, Schmied B, Mehrabi A, et al. Simultaneous pancreas-kidney

transplantation in type 1 diabetes. Clin Transplant. 2009;23 Suppl 21:115

120.

47. Pavlakis M, Khwaja K, Mandelbrot D, et al. Renal allograft failure predictors

after PAK transplantation: Results from the New England Collaborative

Association of Pancreas Programs. Transplantation. 2010;89(11):1347

1353.

48. Andres A. Indications and contraindications of living-donor kidney

transplantation. Nefrologia. 2010;30 Suppl 2:30-38.

49. Fiorina P, Vezzulli P, Bassi R, et al. Near normalization of metabolic and

functional features of the central nervous system in type 1 diabetic

patients with end-stage renal disease after kidney-pancreas

transplantation. Diabetes Care. 2012;35(2):367-374.

50. Margreiter C, Pratschke J, Margreiter R. Immunological monitoring after

pancreas transplantation. Curr Opin Organ Transplant. 2013;18(1):71-75.

51. Kobayashi T, Gruessner AC, Wakai T, Sutherland DE. Three types of

simultaneous pancreas and kidney transplantation. Transplant Proc.

2014;46(3):948-953.

52. Schulz T, Pries A, Caliebe A, Kapischke M. Long-term survival after

simultaneous pancreas-kidney transplantation with primary function of at

least one year -- a single-center experience. Ann Transplant. 2014;19:106

111.

53. Klein CL, Robertson RP. Patient selection for and immunologic issues

relating to kidney-pancreas transplantation in diabetes mellitus. UpToDate

[online serial]. Waltham, MA: UpToDate; reviewed April 2014.

54. Montero N, Webster AC, Royuela A, et al. Steroid avoidance or withdrawal

for pancreas and pancreas with kidney transplant recipients. Cochrane

Database Syst Rev. 2014;9:CD007669.

55. Lehmann R, Graziano J, Brockmann J, et al. Glycemic control in

simultaneous islet-kidney versus pancreas-kidney transplantation in type



Page 20 of 21

1 diabetes: A prospective 13-year follow-up. Diabetes Care. 2015;38

(5):752-759.

56. Chan CM, Chim TM, Leung KC, et al. Simultaneous pancreas and kidney

transplantation as the standard surgical treatment for diabetes mellitus

patients with end-stage renal disease. Hong Kong Med J. 2016;22(1):62-69.

57. Barlow AD, Saeb-Parsy K, Watson CJ. An analysis of the survival outcomes

of simultaneous pancreas and kidney transplantation compared to live

donor kidney transplantation in patients with type 1 diabetes: A UK

Transplant Registry study. Transpl Int. 2017;30(9):884-892.

58. MacCraith E, Davis NF, Browne C, et al. Simultaneous pancreas and kidney

transplantation: Incidence and risk factors for amputation after 10-year

follow-up. Clin Transplant. 58. 2017;31(6).

59. Gruessner AC, Laftavi MR, Pankewycz O, Gruessner RWG. Simultaneous

pancreas and kidney transplantation - Is it a treatment option for patients

with type 2 diabetes mellitus? An analysis of the International Pancreas

Transplant Registry. Curr Diab Rep. 2017;17(6):44.

60. Ziaja J, Kowalik AP, Kolonko A, et al. Type 1 diabetic patients have better

endothelial function after simultaneous pancreas-kidney transplantation

than after kidney transplantation with continued insulin therapy. Diab

Vasc Dis Res. 2018;15(2):122-130.

61. Arjona-Sanchez A, Rodríguez-Ortiz L, Sanchez-Hidalgo JM, et al.

Intraoperative heparinization during simultaneous pancreas-kidney

transplantation: Is it really necessary? Transplant Proc. 2018;50(2):673-675.

62. Knight RJ, Graviss EA, Nguyen DT, et al. Conversion from tacrolimus

mycophenolate mofetil to tacrolimus-mTOR immunosuppression after

kidney-pancreas transplantation reduces the incidence of both BK and

CMV viremia. Clin Transplant. 2018;32(6):e13265.

63. Marcacuzco A, Jimenez-Romero C, Manrique A, et al. Outcome of patients

with hemodialysis or peritoneal dialysis undergoing simultaneous

pancreas-kidney transplantation. Comparative study. Clin Transplant.

2018;32(6):e13268.

64. Knight SR, Thorne A, Lo Faro ML. Donor-specific cell-free DNA as a

biomarker in solid organ transplantation. A systematic review.

Transplantation. 2019;103(2):273-283.


Page 21 of 21

Copyright Aetna Inc. All rights reserved. Clinical Policy Bulletins are developed by Aetna to assist in administering plan

benefits and constitute neither offers of coverage nor medical advice. This Clinical Policy Bulletin contains only a partial,

general description of plan or program benefits and does not constitute a contract. Aetna does not provide health care

services and, therefore, cannot guarantee any results or outcomes. Participating providers are independent contractors in

private practice and are neither employees nor agents of Aetna or its affiliates. Treating providers are solely responsible

for medical advice and treatment of members. This Clinical Policy Bulletin may be updated and therefore is subject to

change.

Copyright © 2001-2019 Aetna Inc.



AETNA BETTER HEALTH® OF PENNSYLVANIA

Amendment to Aetna Clinical Policy Bulletin Number: 0587 Pancreas

Kidney Transplantation

The Pennsylvania Medical Assistance Program considers HIV infection to be poorly controlled if any of the following is present:

• Member does not have sustained virologic response (SVR) with low levels of viremia; or • Member does not have a non-detectable viral load; or • Member has not been on stable anti-viral therapy for at least 3 months; or • Member has opportunistic infections or neoplasms; or • Member's CD4 count has not been 200 cells/mm3 or greater for at least 6 months.

The Pennsylvania Medical Assistance Program considers a “viral load of zero” to mean the viral load is undetectable.

www.aetnabetterhealth.com/pennsylvania revised 08/15/2019

http://www.aetnabetterhealth.com/pennsylvania

Date post:	10-Aug-2020
Category:	Documents
Upload:	others
View:	9 times
Download:	0 times

0587 Pancreas Kidney Transplantation - Aetna · 11/10/2017 · The American Diabetes Association...

Documents