CClinicalTrials.gg
Not yet recruitingNCT07651397Updated Jun 26, 2026

Dietary Modulation of Urinary MCP-1 in ADPKD

An interventional study of Carbohydrate Restricted, Plant Dominant Diet and usual diet in Autosomal Dominant Polycystic Kidney Disease (ADPKD), sponsored by Assaf-Harofeh Medical Center. Not yet recruiting. Open to participants aged 18 Years and older. Per ClinicalTrials.gov, last updated 2026-06-26.

Sponsored by Assaf-Harofeh Medical Center · Not applicable, Interventional, and Basic science

Phase
Not applicable
Study type
Interventional
Enrollment
36
Allocation
Randomized
Ages
18 Years and older
Sex
All
01

Study summary

Autosomal dominant polycystic kidney disease (ADPKD) is characterized by progressive cyst growth and declining kidney function. Inflammatory pathways, including those mediated by monocyte chemoattractant protein-1 (MCP-1), are increasingly recognized as contributors to disease progression. Metabolic alterations in cystic epithelial cells may influence inflammatory signaling, suggesting a potential role for dietary interventions targeting metabolic pathways.

This study is a prospective, randomized, open-label crossover trial designed to evaluate the effect of a carbohydrate restricted, plant dominant dietary intervention on urinary MCP-1 levels in adults with ADPKD. Participants will be randomized to one of two sequences: dietary intervention followed by usual diet, or usual diet followed by dietary intervention, with a washout period between study phases. Each study period will last 12 weeks.

The primary objective is to assess within subject differences in urinary MCP-1/creatinine ratio between the dietary intervention and usual diet conditions. Secondary outcomes include measures of metabolic parameters, insulin resistance, dietary adherence, and safety.

This study aims to explore whether a structured dietary approach may influence intrarenal inflammatory activity in ADPKD and provide preliminary data to inform future interventional studies.

02

Conditions studied

  • Autosomal Dominant Polycystic Kidney Disease (ADPKD)
03

Who can participate

Ages eligible
18 Years and older
Sexes eligible
All
Accepts healthy volunteers
No

Inclusion criteria

  1. Age ≥18
  2. Diagnosis of ADPKD based on established clinical or genetic criteria (PKD 1/PKD2)
  3. Estimated glomerular filtration rate (eGFR) between 45 and 90 mL/min/1.73 m²
  4. Mayo Imaging Classification class 1C-1E based on MRI-derived height-adjusted total kidney volume.
  5. Stable kidney function, defined as no acute kidney injury and no decline in eGFR >20% within the preceding 3 months
  6. Stable antihypertensive and chronic medications for at least 4 weeks prior to enrollment
  7. Ability and willingness to adhere to the prescribed dietary intervention
  8. Ability to provide written informed consent

Exclusion criteria

Exclusion Criteria:

  1. eGFR \<45 mL/min/1.73 m² or requirement for dialysis
  2. History of kidney transplantation
  3. Significant albuminuria, defined as urine albumin to creatinine ratio (UACR) >300 mg/g
  4. Poorly controlled or unstable diabetes mellitus (e.g., HbA1c >8% or clinically significant glycemic variability or frequent hypoglycemia)
  5. Use of Tolvaptan at the time of screening or within the study period
  6. Current adherence to a ketogenic or carbohydrate restricted diet
  7. Unintentional weight loss >5% within the preceding 3 months
  8. Active infection, inflammatory disease, or malignancy that may influence inflammatory markers
  9. Current use of systemic corticosteroids or immunosuppressive therapy
  10. Active or symptomatic nephrolithiasis
  11. Serum bicarbonate \<20 mmol/L
  12. Pregnancy or breastfeeding
  13. Known eating disorder or condition limiting adherence to dietary interventions
  14. Participation in another interventional study within the previous 3 months
  15. Any condition that, in the opinion of the investigators, would interfere with study participation or interpretation of results
04

Study design

Phase
Not applicable
Primary purpose
Basic science
Allocation
Randomized
Intervention model
Crossover assignment
Masking
Single (Investigator)
Enrollment
36 participants (estimated)

Study arms

  • Experimental
    Sequence A: Dietary Intervention → Usual Diet

    Participants receive a carbohydrate restricted, plant dominant diet for 12 weeks, followed by a washout period and then usual diet for 12 weeks.

    Behavioral: Carbohydrate Restricted, Plant Dominant Diet · Behavioral: usual diet

  • Experimental
    Sequence B: Usual Diet → Dietary Intervention

    Participants follow their usual diet for 12 weeks, followed by a washout period and then the dietary intervention for 12 weeks.

    Behavioral: Carbohydrate Restricted, Plant Dominant Diet · Behavioral: usual diet

Interventions

  • BehavioralCarbohydrate Restricted, Plant Dominant Diet

    A structured dietary intervention targeting approximately 20% of total daily energy intake from carbohydrates (range 15-25%), with a plant dominant composition. Energy and protein intake are prescribed based on adjusted body weight. The intervention is not ketogenic and is not intended to induce nutritional ketosis. Participants receive individualized dietary counseling and ongoing support from a registered dietitian.

  • Behavioralusual diet

    Participants continue their habitual diet without specific dietary intervention or structured nutritional guidance.

05

What researchers measure

Primary outcomes

  1. Change in Urinary MCP-1/Creatinine Ratio

    Urinary MCP-1 levels will be measured in first morning urine samples and normalized to urine creatinine (MCP-1/creatinine ratio). For each study period, two samples will be collected within the final week (2-5 days apart), and the mean value will be used. The primary outcome is the within subject difference in MCP-1/creatinine ratio between the dietary intervention and usual diet conditions.

    Time frame: Baseline and End of each 12-week study period (weeks 0,12, 18 and 30)

Secondary outcomes

  1. Association Between Carbohydrate Intake and MCP-1

    Mean carbohydrate intake during each study period will be calculated from repeated dietary assessments. The association between carbohydrate intake and urinary MCP-1/creatinine ratio will be evaluated to explore a potential dose response relationship.

    Time frame: Baseline and End of each 12-week study period (weeks 0,12, 18 and 30)

  2. Association Between Change in HOMA-IR and MCP-1

    The association between changes in insulin resistance (HOMA-IR) and changes in urinary MCP-1/creatinine ratio will be evaluated within individuals across study conditions.

    Time frame: Baseline and End of each 12-week study period (weeks 0,12, 18 and 30)

  3. Dietary Adherence and MCP-1 Response

    Dietary adherence will be defined as the proportion of dietary assessments in which carbohydrate intake falls within the target range (15-25% of total energy intake). The association between adherence and urinary MCP-1/creatinine ratio will be evaluated.

    Time frame: Baseline and End of each 12-week study period (weeks 0,12, 18 and 30)

  4. Change in Metabolic and Biochemical Parameters (Safety Outcomes)

    Changes in selected metabolic and biochemical parameters, including serum bicarbonate, LDL cholesterol, and estimated glomerular filtration rate (eGFR), will be assessed between study conditions to evaluate the safety of the dietary intervention.

    Time frame: Baseline and End of each 12-week study period (weeks 0,12, 18 and 30)

Other outcomes

  1. Mediation Analysis of Insulin Resistance and MCP-1

    Exploratory analysis to evaluate whether changes in insulin resistance (HOMA-IR) mediate the relationship between dietary intervention and urinary MCP-1/creatinine ratio using regression based mediation models.

    Time frame: Baseline and End of each 12-week study period (weeks 0,12, 18 and 30)

  2. Gene Expression of CPT1A and ACOX1

    Pre-specified exploratory analysis of gene expression of CPT1A and ACOX1, key regulators of fatty acid oxidation pathways, measured in peripheral blood samples. Expression levels will be evaluated in relation to dietary intervention and changes in urinary MCP-1/creatinine ratio.

    Time frame: Baseline and End of each 12-week study period (weeks 0,12, 18 and 30)

  3. Exploratory Analysis of the Gut Microbiome

    Exploratory analyses will evaluate changes in gut microbial composition associated with the dietary intervention. Stool samples collected at baseline and at the end of each study period will undergo microbiome analysis. Changes in microbial diversity and taxonomic composition will be explored and correlated with dietary adherence, urinary MCP-1 levels, and metabolic parameters. Given the exploratory nature of these analyses and the limited sample size, findings will be considered hypothesis-generating.

    Time frame: Baseline and End of each 12-week study period (weeks 0,12, 18 and 30)

  4. Health-Related Quality of Life (SF-36)

    Pre-specified exploratory assessment of health-related quality of life using the Short Form-36 (SF-36) questionnaire.

    Time frame: Baseline and end of each 12-week study period (Weeks 0, 12, 18, and 30)

06

Study locations

No study locations are listed for this record.

07

References and documents

Publications

  • Maroni BJ, Steinman TI, Mitch WE. A method for estimating nitrogen intake of patients with chronic renal failure. Kidney Int. 1985 Jan;27(1):58-65. doi: 10.1038/ki.1985.10. PubMed 3981873 ↗
  • D'Alessandro C, Torreggiani M, Lippi F, Avesani C, Cupisti A, Piccoli GB. A Requiem for a Standardized Calculation of Ideal Body Weight in Chronic Kidney Disease? J Ren Nutr. 2026 May;36(3):373-380. doi: 10.1053/j.jrn.2025.12.007. Epub 2026 Jan 15. PubMed 41547473 ↗
  • Bouillanne O, Morineau G, Dupont C, Coulombel I, Vincent JP, Nicolis I, Benazeth S, Cynober L, Aussel C. Geriatric Nutritional Risk Index: a new index for evaluating at-risk elderly medical patients. Am J Clin Nutr. 2005 Oct;82(4):777-83. doi: 10.1093/ajcn/82.4.777. PubMed 16210706 ↗
  • Ryu H, Park HC, Kim H, Heo J, Kang E, Hwang YH, Cho JY, Lee KB, Oh YK, Oh KH, Ahn C. Bioelectrical impedance analysis as a nutritional assessment tool in Autosomal Dominant Polycystic Kidney Disease. PLoS One. 2019 Apr 4;14(4):e0214912. doi: 10.1371/journal.pone.0214912. eCollection 2019. PubMed 30947248 ↗
  • Cederholm T, Jensen GL, Correia MITD, Gonzalez MC, Fukushima R, Higashiguchi T, Baptista G, Barazzoni R, Blaauw R, Coats A, Crivelli A, Evans DC, Gramlich L, Fuchs-Tarlovsky V, Keller H, Llido L, Malone A, Mogensen KM, Morley JE, Muscaritoli M, Nyulasi I, Pirlich M, Pisprasert V, de van der Schueren MAE, Siltharm S, Singer P, Tappenden K, Velasco N, Waitzberg D, Yamwong P, Yu J, Van Gossum A, Compher C; GLIM Core Leadership Committee; GLIM Working Group. GLIM criteria for the diagnosis of malnutrition - A consensus report from the global clinical nutrition community. Clin Nutr. 2019 Feb;38(1):1-9. doi: 10.1016/j.clnu.2018.08.002. Epub 2018 Sep 3. PubMed 30181091 ↗
  • Irazabal MV, Rangel LJ, Bergstralh EJ, Osborn SL, Harmon AJ, Sundsbak JL, Bae KT, Chapman AB, Grantham JJ, Mrug M, Hogan MC, El-Zoghby ZM, Harris PC, Erickson BJ, King BF, Torres VE; CRISP Investigators. Imaging classification of autosomal dominant polycystic kidney disease: a simple model for selecting patients for clinical trials. J Am Soc Nephrol. 2015 Jan;26(1):160-72. doi: 10.1681/ASN.2013101138. Epub 2014 Jun 5. PubMed 24904092 ↗
  • Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985 Jul;28(7):412-9. doi: 10.1007/BF00280883. PubMed 3899825 ↗
  • Charles K, Lewis MJ, Montgomery E, Reid M. The 2021 Chronic Kidney Disease Epidemiology Collaboration Race-Free Estimated Glomerular Filtration Rate Equations in Kidney Disease: Leading the Way in Ending Disparities. Health Equity. 2024 Jan 12;8(1):39-45. doi: 10.1089/heq.2023.0038. eCollection 2024. PubMed 38250300 ↗
  • Ludwig DS, Willett WC, Putt ME. Wash-in and washout effects: mitigating bias in short term dietary and other trials. BMJ. 2025 Apr 22;389:e082963. doi: 10.1136/bmj-2024-082963. PubMed 40262831 ↗
  • Passey C. Reducing the Dietary Acid Load: How a More Alkaline Diet Benefits Patients With Chronic Kidney Disease. J Ren Nutr. 2017 May;27(3):151-160. doi: 10.1053/j.jrn.2016.11.006. Epub 2017 Jan 20. PubMed 28117137 ↗
  • Kim H, Caulfield LE, Garcia-Larsen V, Steffen LM, Grams ME, Coresh J, Rebholz CM. Plant-Based Diets and Incident CKD and Kidney Function. Clin J Am Soc Nephrol. 2019 May 7;14(5):682-691. doi: 10.2215/CJN.12391018. Epub 2019 Apr 25. PubMed 31023928 ↗
  • Karihaloo A, Koraishy F, Huen SC, Lee Y, Merrick D, Caplan MJ, Somlo S, Cantley LG. Macrophages promote cyst growth in polycystic kidney disease. J Am Soc Nephrol. 2011 Oct;22(10):1809-14. doi: 10.1681/ASN.2011010084. Epub 2011 Sep 15. PubMed 21921140 ↗
  • Messchendorp AL, Meijer E, Boertien WE, Engels GE, Casteleijn NF, Spithoven EM, Losekoot M, Burgerhof JGM, Peters DJM, Gansevoort RT; DIPAK Consortium. Urinary Biomarkers to Identify Autosomal Dominant Polycystic Kidney Disease Patients With a High Likelihood of Disease Progression. Kidney Int Rep. 2017 Oct 14;3(2):291-301. doi: 10.1016/j.ekir.2017.10.004. eCollection 2018 Mar. PubMed 29725632 ↗
  • Zheng D, Wolfe M, Cowley BD Jr, Wallace DP, Yamaguchi T, Grantham JJ. Urinary excretion of monocyte chemoattractant protein-1 in autosomal dominant polycystic kidney disease. J Am Soc Nephrol. 2003 Oct;14(10):2588-95. doi: 10.1097/01.asn.0000088720.61783.19. PubMed 14514736 ↗
  • Deshmane SL, Kremlev S, Amini S, Sawaya BE. Monocyte chemoattractant protein-1 (MCP-1): an overview. J Interferon Cytokine Res. 2009 Jun;29(6):313-26. doi: 10.1089/jir.2008.0027. PubMed 19441883 ↗
  • Donadelli R, Abbate M, Zanchi C, Corna D, Tomasoni S, Benigni A, Remuzzi G, Zoja C. Protein traffic activates NF-kB gene signaling and promotes MCP-1-dependent interstitial inflammation. Am J Kidney Dis. 2000 Dec;36(6):1226-41. doi: 10.1053/ajkd.2000.19838. PubMed 11096048 ↗
  • Burke SJ, Collier JJ. Transcriptional regulation of chemokine genes: a link to pancreatic islet inflammation? Biomolecules. 2015 May 26;5(2):1020-34. doi: 10.3390/biom5021020. PubMed 26018641 ↗
  • Saxton RA, Sabatini DM. mTOR Signaling in Growth, Metabolism, and Disease. Cell. 2017 Mar 9;168(6):960-976. doi: 10.1016/j.cell.2017.02.004. PubMed 28283069 ↗
  • Shillingford JM, Murcia NS, Larson CH, Low SH, Hedgepeth R, Brown N, Flask CA, Novick AC, Goldfarb DA, Kramer-Zucker A, Walz G, Piontek KB, Germino GG, Weimbs T. The mTOR pathway is regulated by polycystin-1, and its inhibition reverses renal cystogenesis in polycystic kidney disease. Proc Natl Acad Sci U S A. 2006 Apr 4;103(14):5466-71. doi: 10.1073/pnas.0509694103. Epub 2006 Mar 27. PubMed 16567633 ↗
  • Torres JA, Kruger SL, Broderick C, Amarlkhagva T, Agrawal S, Dodam JR, Mrug M, Lyons LA, Weimbs T. Ketosis Ameliorates Renal Cyst Growth in Polycystic Kidney Disease. Cell Metab. 2019 Dec 3;30(6):1007-1023.e5. doi: 10.1016/j.cmet.2019.09.012. Epub 2019 Oct 17. PubMed 31631001 ↗
  • Rowe I, Chiaravalli M, Mannella V, Ulisse V, Quilici G, Pema M, Song XW, Xu H, Mari S, Qian F, Pei Y, Musco G, Boletta A. Defective glucose metabolism in polycystic kidney disease identifies a new therapeutic strategy. Nat Med. 2013 Apr;19(4):488-93. doi: 10.1038/nm.3092. Epub 2013 Mar 24. PubMed 23524344 ↗
  • Torres VE, Chapman AB, Devuyst O, Gansevoort RT, Grantham JJ, Higashihara E, Perrone RD, Krasa HB, Ouyang J, Czerwiec FS; TEMPO 3:4 Trial Investigators. Tolvaptan in patients with autosomal dominant polycystic kidney disease. N Engl J Med. 2012 Dec 20;367(25):2407-18. doi: 10.1056/NEJMoa1205511. Epub 2012 Nov 3. PubMed 23121377 ↗
  • Torres VE, Harris PC, Pirson Y. Autosomal dominant polycystic kidney disease. Lancet. 2007 Apr 14;369(9569):1287-1301. doi: 10.1016/S0140-6736(07)60601-1. PubMed 17434405 ↗

Individual participant data

Plan to share: Undecided

08

Registry details

Key details

Study ID
NCT07651397
Lead sponsor
Assaf-Harofeh Medical Center
Responsible party
Elad Nizri (MEDICAL DOCTOR, NEPHROLOGIST, Assaf-Harofeh Medical Center) — Principal investigator
First posted
Jun 16, 2026
Start date
Jul 10, 2026 (estimated)
Primary completion
Jan 1, 2029 (estimated)
Completion
Jan 1, 2029 (estimated)
Last update
Jun 26, 2026

Study contacts

ELAD NIZRI, MD
Contact
nizrielad@gmail.com
972-502932222

Oversight

FDA-regulated drug
No
FDA-regulated device
No
View the source record on ClinicalTrials.gov ↗

Not currently enrolling

This study is not yet recruiting, as verified in Apr 2026. You cannot join it, but the record below documents what was studied.

Follow this study

Get an email when the registry record changes — status, dates, results — or when someone posts here.

Sign in to follow

Discussion

Questions and observations about this study, from anyone following it. Not medical advice, and not a channel to the study team — their contact details are on the registry record.

Sign in to join the discussion. Reading takes no account; posting does. You choose a display name, and a pseudonym is the default.

Nothing here yet. If you are running this trial, taking part in it, or weighing whether to, this is the place to say so.

Start the discussion