prior authorization review panel mco policy submission...dhar and denstedt (2009) stated that...

Prior Authorization Review Panel MCO Policy Submission

A separate copy of this form must accompany each policy submitted for review. Policies submitted without this form will not be considered for review.

Plan: Aetna Better Health Submission Date:09/01/2019

Policy Number: 0392 Effective Date: Revision Date: 07/15/2011

Policy Name: Metabolic and Environmental Profiling and Imaging for Kidney Stone Risk

Type of Submission – Check all that apply:

New PolicyRevised Policy* Annual Review – No Revisions Statewide PDL

*All revisions to the policy must be highlighted using track changes throughout the document.

Please prov ide a ny clarifying information for the p olicy below:

CPB 0392 Metabolic and Environmental Profiling and Imaging for Kidney Stone Risk

Clinical content was last revised on 07/15/2011 . Additional non-clinical updates were made by Corporate since the last PARP submission, as documented below.

Update History since the last PARP Submission:

07/16/2019- This CPB has been updated with additional background information and 1 reference.

Name of Authorized Individual (Please t ype or print):

Dr. Bernard Lewin, M.D.

Signature of Authorized Individual:

Revised July 22, 2019

http://www.aetna.com/cpb/medical/data/300_399/0392.html

Page 1 of 12

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

Metabolic and Environmental Profiling and Imaging for KidneyStone Risk

Clinical Policy Bulletins Medical Clinical Policy Bulletins

Policy History Last

Review

07/16/2019

Effective: 03/06/2000

Next Review:

04/10/2020

Review History

Definitions

Additional

Number: 0392

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

Aetna considers metabolic and environmental profiling for assessing kidney stone

risk experimental and investigational because these studies have not been

demonstrated in the peer-reviewed medical literature to improve health outcomes of

individuals with kidney stones.

Aetna considers the use of computed tomography (CT) or magnetic resonance

imaging (MRI) for urolithiasis screening of asymptomatic persons experimental and

investigational because there is a lack of clinical evidence regarding their use for

this indication.

Aetna considers the use of calcifying nanoparticles for assessing kidney stone risk

experimental and investigational because its effectiveness has not been

established.

Aetna considers the use of genetic/molecular analysis for assessing kidney stone

risk experimental and investigational because its effectiveness has not been

established.

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https://www.aetna.com/


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Background

Nephrolithiasis (also known as urolithiasis, renal calculi, or kidney stones) is

exceeded in frequency as a urinary tract disorder only by infections and prostatic

disease. Calcium salts, uric acid, cystine, and struvite are the basic components of

most kidney stones in the Western Hemisphere. Calcium stones constitute more

than 70 % of all kidney stones. It has been suggested that there are metabolic as

well as environmental risk factors that render urine more conducive to

crystallization, thus resulting in an increase risk of stone formation. Metabolic and

environmental profiling involves studies used to ascertain these risk factors of

nephrolithiasis. These clinical and laboratory tests usually entail measurements of

a number of blood and urine parameters, including estimates of urine state of

saturation with calcium and uric acid salts, net gastro-intestinal alkali absorption,

renal threshold of phosphate and other renal clearances, as well as net acid and

total nitrogen excretions.

Although there are published studies on metabolic and environmental profiling, the

value of these tests in the management of patients with kidney stones is still

questionable. Additionally, there are factors other than urine composition that may

play a role in stone formation. Furthermore, there is a lack of data to show that

metabolic and environmental profiling improves the health outcomes of patients

with kidney stones. Although guidelines on urolithiasis from the European

Association of Urology (Tiselius et al, 2006) include metabolic profiling, they state

that there is "no absolute consensus that a selective treatment is better than a non-

selective treatment for recurrence prevention in idiopathic calcium stone disease",

and note that an analysis of data from the literature has suggested only a slight

difference in favor of treatment directed towards individual biochemical

abnormalities.

Guidelines from the American College of Physicians (2014) on prevention of kidney

stones recommends monotherapy with thiazide diuretics, potassium citrate and

allopurinol in patients with active disease in which increased fluid intake fails to

reduce the formation of stones. The evidence for this recommendation came

primarily from calcium stone formers. According to ACP, although biochemistry and

some observational data on stone recurrence suggest that the choice of treatment

could be based on the type of metabolic abnormality, evidence from randomized,

controlled trials is lacking to correlate the drug of choice and stone type to the

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prevention of stone recurrence. Most patients have calcium stones, notes ACP, and

evidence showed that thiazide diuretics, citrates, and allopurinol all effectively

reduced recurrence of this stone type.

The significance of urolithiasis screening is controversial. In a review on the clinical

and cost effectiveness of CT and MRI for selected clinical disorders, the Canadian

Agency for Drugs and Technologies in Health (CADTH) reported that no clinical or

economic evidence was found on the use of CT and MRI for screening urolithiasis.

CADTH concluded that the use of CT or MRI for this indication should be

considered investigational (Murtagh et al, 2006).

Dhar and Denstedt (2009) stated that imaging has an essential role in the

diagnosis, management, and follow-up of patients with stone disease. A variety of

imaging modalities are available to urologists, including conventional radiography

(KUB), intravenous urography (IVU), ultrasound (US), magnetic resonance

urography, and CT scans, each with its advantages and limitations. Traditionally,

IVU was considered the gold standard for diagnosing renal calculi, but this modality

has largely been replaced by un-enhanced spiral CT scans at most centers. Renal

US is recommended as the initial imaging modality for suspected renal colic in

pregnant women and children, but recent literature suggests that a low-dose CT

scan may be safe in pregnancy. Intra-operative imaging by fluoroscopy or US

plays a large part in assisting urologists with the surgical intervention chosen for the

individual stone patient. Post-treatment imaging of stone patients is recommended

to ensure complete fragmentation and stone clearance. Plain radiography is

suggested for the follow-up of radiopaque stones, with US and limited IVU reserved

for the follow-up of radiolucent stones to minimize cumulative radiation exposure

from repeated CT scans. Patients with asymptomatic calyceal stones who prefer

an observational approach should have a yearly KUB to monitor progression of

stone burden.

Shiekh and associates (2009) noted that although much has been learned

regarding the pathogenesis of kidney stones, the reason(s) why some individuals

form stones while others do not remains unclear. Nanoparticles, which have been

observed in geological samples, have also been isolated from biological

specimens, including kidney stones. These nanoparticles have certain properties

that are consistent with a novel life form, including in vitro self-replication, and

contain lipids, DNA and proteins. Thus, it has been hypothesized that

nanoparticles may represent a type of infective agent that initiates stone formation

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in some patients. Despite a large body of suggestive evidence, the true biological

nature of these entities has been elusive, and controversy remains as to whether

these nano-sized particles are analogous to other recently described unusual and

novel microorganisms, or a transmissible, yet inert nanoparticle. Although unique

DNA or RNA has yet to be identified, a proteomic biosignature is beginning to

emerge that may allow more definitive clinical investigation. The authors stated

that there is need for additional research to further elucidate the role, if any, of

calcifying nanoparticles in the formation of kidney stones.

Sayer (2011) stated that nephrolithiasis may be the manifestation of rare single

gene disorders or part of more common idiopathic renal stone-forming diseases.

Molecular genetics has allowed significant progress to be made in the

understanding of certain stone-forming conditions. The molecular defect underlying

single gene disorders often contributes to a significant metabolic risk factor for

stone formation. In contrast, idiopathic renal stone formation relates to the interplay

of environmental, dietary and genetic factors, with hypercalciuria being the most

commonly found metabolic risk factor. Candidate genes for idiopathic stone

formers have been identified using numerous approaches, some of which are

outlined here. Despite this, the genetic basis underlying familial hypercalciuria and

calcium stone formation remains elusive. The molecular basis of other metabolic

risk factors such as hyperuricosuria, hyperoxaluria and hypocitraturia is being

unraveled and is allowing new insights into renal stone pathogenesis. The author

concluded that the discovery of both rare and common molecular defects leading to

renal stones will hopefully increase the understanding of the disease pathogenesis.

Such knowledge will allow screening for genetic defects and the use of specific

drug therapies in order to prevent renal stone formation.

Tang et al (2012) stated that the role of vitamin D in kidney stone disease is

controversial. Current evidence is inconsistent and existing studies were limited by

small sample populations. These investigators used the 3rd National Health and

Nutrition Examination Survey (NHANES III), a large US population-based cross-

sectional study, to determine the independent association between serum 25

hydroxyvitamin D [25(OH)D] concentration and prevalent kidney stone disease in a

sample of 16,286 men and women aged 18 years or older. A prevalent kidney

stone was defined as self-report of any previous episode of kidney stones. Among

16,286 adult participants, 759 subjects reported a history of previous kidney stones.

Concentrations of serum 25(OH)D were not different between stone formers and non-

stone formers (mean of 29.28 versus 29.55 ng/ml, p = 0.57). Higher 25(OH)D

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concentration was not associated with increased odds ratio (OR) for previous

kidney stones [OR = 0.99; 95 % confidence interval (CI): 0.99 to 1.01] after

adjustment for age, sex, race, history of hypertension, diabetes, body mass index,

diuretic use and serum calcium. Furthermore, after these researchers divided 25

(OH)D concentrations into quartiles, or into groups using clinically significant cut

offs (e.g., 40 and 50 ng/ml), still no significant differences were found in stone

formation in group comparisons. The authors concluded that high serum 25(OH)D

concentrations were not associated with prevalent kidney stone disease in

NHANES III participants. They stated that prospective studies are needed to clarify

the relationship between vitamin D and kidney stone formation, and whether

nutritional vitamin D supplementation will increase risk of stone recurrence.

Nguyen et al (2014) noted that increasing 25(OH)D serum levels can prevent a

wide range of diseases. There is a concern about increasing kidney stone risk with

vitamin D supplementation. These investigators used GrassrootsHealth data to

examine the relationship between vitamin D status and kidney stone incidence.

The study included 2,012 participants followed prospectively for a median of 19

months; 13 individuals self-reported kidney stones during the study period. Multi

variate logistic regression was applied to assess the association between vitamin D

status and kidney stones. These researchers found no statistically significant

association between serum 25(OH)D and kidney stones (p = 0.42). Body mass

index was significantly associated with kidney stone risk (OR = 3.5; 95 % CI: 1.1 to

11.3). The authors concluded that a serum 25(OH)D level of 20 to 100 ng/ml has

no significant association with kidney stone incidence.

Dasgupta and colleagues (2014) stated that compound heterozygous and

homozygous (comp/hom) mutations in solute carrier family 34, member 3

(SLC34A3), the gene encoding the sodium (Na(+))-dependent phosphate co-

transporter 2c (NPT2c), cause hereditary hypophosphatemic rickets with

hypercalciuria (HHRH), a disorder characterized by renal phosphate wasting

resulting in hypophosphatemia, correspondingly elevated 1,25(OH)2 vitamin D

levels, hypercalciuria, and rickets/osteomalacia. Similar, albeit less severe,

biochemical changes are observed in heterozygous (het) carriers and

indistinguishable from those changes encountered in idiopathic hypercalciuria (IH).

These investigators reported a review of clinical and laboratory records of 133

individuals from 27 kindreds, including 5 previously unreported HHRH kindreds and

2 cases with IH, in which known and novel SLC34A3 mutations (c.1357delTTC

[p.F453del]; c.G1369A [p.G457S]; c.367delC) were identified. Individuals with

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mutations affecting both SLC34A3 alleles had a significantly increased risk of

kidney stone formation or medullary nephrocalcinosis, namely 46 % compared with

6 % observed in healthy family members carrying only the wild-type SLC34A3 allele

(p = 0.005) or 5.64 % in the general population (p < 0.001). Renal calcifications

were also more frequent in het carriers (16 %; p = 0.003 compared with the general

population) and were more likely to occur in comp/hom and het individuals with

decreased serum phosphate (OR, 0.75, 95 % CI: 0.59 to 0.96; p = 0.02), decreased

tubular reabsorption of phosphate (OR, 0.41; 95 % CI: 0.23 to 0.72; p = 0.002), and

increased serum 1,25(OH)2 vitamin D (OR, 1.22; 95 % CI: 1.05 to 1.41; p = 0.008).

The authors concluded that additional studies are needed to examine if these

biochemical parameters are independent of genotype and can guide therapy to

prevent nephrocalcinosis, nephrolithiasis, and potentially, chronic kidney disease.

Rai et al (2014) examined the fate of indeterminate lesions incidentally found on non-

contrast computed tomography (NCCT) for suspected urolithiasis. These

investigators performed a retrospective review of 404 consecutive cases of

suspected urolithiasis between May 2010 and April 2011. Data were collected for

patient demographics, presence of calculus disease, and additional urologic or non

urologic pathologies and their clinical relevance. The indeterminate or suspicious

lesions were followed-up and the data were reviewed in September 2012. In total,

404 patients underwent NCCT for renal colic (mean age of 50 years [range of 13 to

91 years]; 165 females). Minimum follow-up period was 15 months; 58 patients (14

%) had ureteric, 85 (21 %) had renal, and 39 patients (10 %) had combined ureteric

and renal stones. Non-calculus pathologies were found in 107 patients (26 %).

Sixty patients (15 %) had indeterminate lesions. Of these patients, 6 required

operative intervention, 35 had a benign diagnosis after further imaging and multi

disciplinary team meeting, and 13 remained under surveillance after 1 year.

Indeterminate pulmonary lesions (8 of 16) were the commonest lesions to remain

under surveillance. The authors concluded that NCCT is vital for the diagnosis of

urolithiasis with a pick up rate of 45 % and remains the standard of care. However,

with incidental detection of potential malignant lesions, a significant minority will

need close monitoring, intervention, or both. In this study, approximately 1/3 of

these lesions either remained under surveillance or had intervention.

An UpToDate review on “Diagnosis and acute management of suspected

nephrolithiasis in adults” (Curhan et al, 2015) states that “The diagnosis of

nephrolithiasis is initially suspected by the clinical presentation. Helical non-

contrast computerized tomography (CT) or ultrasonography can be used initially to

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visualize and confirm the presence of a stone …. Radiological tests that are less

frequently used include plain X-ray, intravenous pyelography, and magnetic

resonance imaging. Some of these tests are used in the initial diagnosis of

nephrolithiasis only if CT is unavailable …. Magnetic resonance imaging is rarely

used during the management of stone disease, except in the evaluation of pregnant

patients, because this modality is not optimal for identifying stones. Thus, this

modality can be utilized if there is a specific indication to reduce radiation

exposure”.

Wang and colleagues (2016) stated that many epidemiological studies have been

conducted to evaluate the association between serum vitamin D levels and the risk

of kidney stone. These investigators summarized the evidence from

epidemiological studies. Pertinent studies were identified by a search of PubMed,

Embase, the Cochrane Library, China National Knowledge Infrastructure (CNKI)

and China Biology Medical literature up to July 2015. Standardized mean

difference (SMD) was conducted to combine the results. Random-effect model was

used. Publication bias was estimated using Egger's regression asymmetry test. A

total of 7 articles involving 451 kidney stone cases and 482 controls were included

in this meta-analysis. The pooled results suggested that kidney stone patients had

a significantly higher serum vitamin D level compared with controls [summary SMD

= 0.65, 95 % CI: 0.51 to 0.79, I(2) = 97.0 %]. The associations were also significant

both in Europe [SMD = 0.35, 95 % CI: 0.17 to 0.53] and in Asia [SMD = 1.00, 95 %

CI: 0.76 to 1.25]. No publication bias was found. The authors concluded that the

findings of this analysis indicated that serum vitamin D level in kidney stone

patients was significantly higher than that in non-kidney stone controls, both in

Europe and Asia populations.

This study had several drawbacks: (i) 6 of 7 studies were of case-control design

and only 1 study was of randomized controlled trial design, (ii) as a meta-

analysis of epidemiologic studies, the authors could not rule out that individual

studies may have failed to control for potential confounders, which may

introduce bias in an unpredictable direction, (iii) for the subgroups of

geographic locations, the associations were significant both in Europe and in

Asia between serum vitamin D levels and kidney stone risk. Only 1 study was

conducted from United States. Thus, these researchers did not combine the

results for other populations. Due to this limitation, the results are applicable

to Europe and Asia, but cannot be extended to other populations. More

studies originating in other countries are needed to investigate the association

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between serum vitamin D levels and kidney stone risk, and (iv) between-study

heterogeneity was high in the pooled analysis, but the heterogeneity was not

successfully explained by the subgroup analysis and meta-regression. However,

other environment variables, as well as their possible interaction may be potential

contributors to this disease-effect unconformity.

Ticinesi and colleagues (2018) stated that the involvement of the gut microbiota in

the pathogenesis of calcium (Ca) nephrolithiasis has been hypothesized since the

discovery of the oxalate-degrading activity of oxalobacter formigenes, but never

comprehensively studied with metagenomics. In a case-control study, these

researchers compared the fecal microbiota composition and functionality between

recurrent idiopathic Ca stone formers (SFs) and controls. Fecal samples were

collected from 52 SFs and 48 controls (mean age of 48 ± 11 years). The

microbiota composition was analyzed via 16S rRNA microbial profiling approach;

10 samples (5 SFs, 5 controls) were also analyzed with deep shotgun

metagenomics sequencing, with focus on oxalate-degrading microbial metabolic

pathways. Dietary habits, assessed via a food-frequency questionnaire, and 24

hour urinary excretion of pro-lithogenic and anti-lithogenic factors, including Ca and

oxalate, were compared between SFs and controls, and considered as co-variates

in the comparison of microbiota profiles. SFs exhibited lower fecal microbial

diversity than controls (Chao1 index 1,460 ± 363 versus 1,658 ± 297, fully adjusted

p = 0.02 with step-wise backward regression analysis). At multi-variate analyses, 3

taxa (fecalibacterium, enterobacter, dorea) were significantly less represented in

fecal samples of SFs. The oxalobacter abundance was not different between

groups. Fecal samples from SFs exhibited a significantly lower bacterial

representation of genes involved in oxalate degradation, with inverse correlation

with 24-hour oxalate excretion (r = -0.87, p = 0.002). The oxalate-degrading genes

were represented in several bacterial species, whose cumulative abundance was

inversely correlated with oxaluria (r = -0.85, p = 0.02). The authors concluded that

idiopathic Ca SFs exhibited altered gut microbiota composition and functionality

that could contribute to nephrolithiasis physiopathology.

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 "+":

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Metabolic and environmental profiling for assessment of kidney stone risk:

CPT codes not covered for indications listed in the CPB:

72192 Computed tomography, pelvis; without contrast material

72193 with contrast material(s)

72194 without contrast material(s) followed by contrast material(s) and

further sections

72195 Magnetic resonance (e.g., proton) imaging, pelvis; without contrast

material(s)

72196 with contrast material(s)

72197 without contrast material(s), followed by contrast material(s) and

further sequences

Other CPT c odes related to this CPB:

82340 Calcium; urine quantitative, timed specimen

82507 Citrate

82570 Creatinine; other source

82615 Cystine and homocystine, urine, qualitative

83945 Oxalate

83986 pH, body fluid, except blood

84105 Phosphorus inorganic (phosphate); urine

84540 Urea nitrogen, urine

84545 Urea nitrogen, clearance

84560 Uric acid; other source

ICD-10 codes coverd if selection criteria are met :

R82.998

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

N20.0

Z87.442

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Metabolic and Environmental Profiling and Imaging for Kidney Stone Risk - Medical ... Page 10 of 12

The above policy is based on the following references:

1. Sutton RA. Causes and prevention of calcium-containing renal calculi. West

J Med. 1991;155(3):249-252.

2. Hobarth K, Hofbauer J. Values of routine analysis and calcium/citrate

ration in calcium urolithiasis. Eur Urol. 1991;19(2):165-168.

3. Hiatt RA, Ettinger B, Caan B, et al. Randomized controlled trial of a low

animal protein, high fiber diet in the prevention of recurrent calcium

oxalate kidney stones. Am J Epidemiol. 1996;144(1):25-33.

4. Asplin JR, Lingeman J, Kahnoski R, et al. Metabolic urinary correlates of

calcium oxalate dihydrate in renal stones. J Urol. 1998;159(3):664-668.

5. van Drongelen J, Kiemeney LA, Debruyne FM, de la Rosette JJ. Impact of

urometabolic evaluation on prevention of urolithiasis: A retrospective

study. Urology. 1998;52(3):384-391.

6. Trinchieri A, Ostini F, Nespoli R, et al. A prospective study of recurrence

rate and risk factors for recurrence after a first renal stone. J Urol.

1999;162(1):27-30.

7. Marangella M, Vitale C, Bagnis C, et al. Idiopathic calcium nephrolithiasis.

Nephron. 1999;81 (Suppl 1):38-44.

8. Tiselius HG, Ackermann D, Alken P, et al. Guidelines on urolithiasis.

Arnhem, The Netherlands: European Association of Urology; 2006.

9. Murtagh J, Foerster V, Warburton RN, et al. Clinical and cost effectiveness

of CT and MRI for selected clinical disorders: Results of two systematic

reviews. Technology Overview No. 22. Ottawa, ON: Canadian Agency for

Drugs and Technologies in Health (CADTH); August 2006.

10. Dhar M, Denstedt JD. Imaging in diagnosis, treatment, and follow-up of

stone patients. Adv Chronic Kidney Dis. 2009;16(1):39-47.

11. Ferrandino MN, Bagrodia A, Pierre SA, et al. Radiation exposure in the

acute and short-term management of urolithiasis at 2 academic centers. J

Urol. 2009;181(2):668-672; discussion 673.

12. Shiekh FA, Miller VM, Lieske JC. Do calcifying nanoparticles promote

nephrolithiasis? A review of the evidence. Clin Nephrol. 2009;71(1):1-8.

13. Sayer JA. Renal stone disease. Nephron Physiol. 2011;118(1):35-44.

14. Tang J, McFann KK, Chonchol MB. Association between serum 25-

hydroxyvitamin D and nephrolithiasis: The National Health and Nutrition

Examination Survey III, 1988-94. Nephrol Dial Transplant. 2012;27

(12):4385-4389.

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15. Nguyen S, Baggerly L, French C, et al. 25-Hydroxyvitamin D in the range of

20 to 100 ng/ml and incidence of kidney stones. Am J Public Health.

2014;104(9):1783-1787.

16. Dasgupta D, Wee MJ, Reyes M, et al. Mutations in SLC34A3/NPT2c are

associated with kidney stones and nephrocalcinosis. J Am Soc Nephrol.

2014;25(10):2366-2375.

17. Rai BP, Ali A, Raslan M, et al. Fate of indeterminate lesions detected on

noncontrast computed tomography scan for suspected urolithiasis: A

retrospective cohort study with a minimum follow-up of 15 months.

Urology. 2014;84(6):1272-1274.

18. Curhan GC, Aronson MD, Preminger GM. Diagnosis and acute

management of suspected nephrolithiasis in adults. UpToDate [online

serial]. Waltham, MA: UpToDate; reviewed February 2015.

19. American College of Physicians (ACP). Dietary and pharmacologic

management to prevent recurrent nephrolithiasis in adults: A clinical

practice guideline from the American College of Physicians. Ann Intern

Med. 2014;161(9):659-667.

20. Wang H, Man L, Li G, et al. Association between serum vitamin D levels and

the risk of kidney stone: Evidence from a meta-analysis. Nutr J. 2016;15:32.

21. Wong Y, Cook P, Roderick P, Somani BK. Metabolic syndrome and kidney

stone disease: A systematic review of literature. J Endourol. 2016;30

(3):246-253.

22. Ticinesi A, Milani C, Guerra A, et al. Understanding the gut-kidney axis in

nephrolithiasis: An analysis of the gut microbiota composition and

functionality of stone formers. Gut. 2018;67(12):2097-2106.

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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.

http://www.aetna.com/cpb/medical/data/300_399/0392.html 08/28/2019


AETNA BETTER HEALTH® OF PENNSYLVANIA

Amendment to Aetna Clinical Policy Bulletin Number: 0392 Metabolic and Environmental Profiling and Imaging for Kidney Stone Risk

There are no amendments for Medicaid.

www.aetnabetterhealth.com/pennsylvania updated 07/16/2019

http://www.aetnabetterhealth.com/pennsylvania

prior authorization review panel mco policy submission...dhar and denstedt (2009) stated that...

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