Page last updated: 2024-10-20

uric acid and ADPKD

uric acid has been researched along with ADPKD in 22 studies

Uric Acid: An oxidation product, via XANTHINE OXIDASE, of oxypurines such as XANTHINE and HYPOXANTHINE. It is the final oxidation product of purine catabolism in humans and primates, whereas in most other mammals URATE OXIDASE further oxidizes it to ALLANTOIN.
uric acid : An oxopurine that is the final oxidation product of purine metabolism.
6-hydroxy-1H-purine-2,8(7H,9H)-dione : A tautomer of uric acid having oxo groups at C-2 and C-8 and a hydroxy group at C-6.
7,9-dihydro-1H-purine-2,6,8(3H)-trione : An oxopurine in which the purine ring is substituted by oxo groups at positions 2, 6, and 8.

Research Excerpts

ExcerptRelevanceReference
"Patients treated with ALA at T1 and T2 showed a significant reduction in serum glucose, insulin, homeostatic model assessment-insulin resistance, and serum uric acid (P = 0."5.34α-lipoic acid in patients with autosomal dominant polycystic kidney disease. ( Amabile, MI; Ansuini, M; Carta, M; Cianci, R; D'Ambrosio, V; Galani, A; Lai, S; Letizia, C; Mazzaferro, S; Mitterhofer, AP; Molfino, A; Muscaritoli, M; Pasquali, M; Petramala, L; Ramaccini, C, 2020)
" Specific significant metabolites, including pseudo-uridine, indole-3-lactate, uric acid, isothreonic acid, and creatinine, have been previously shown to accumulate in plasma and/or urine in both diabetic and cystic renal diseases with advanced renal insufficiency."5.30Plasma metabolites and lipids associate with kidney function and kidney volume in hypertensive ADPKD patients early in the disease course. ( Chapman, A; Gao, G; Kim, K; Trott, JF; Weiss, RH, 2019)
"Among the 44 patients with ADPKD, the serum uric acid (SUA) was 7."5.29A study of uric acid metabolism and gouty arthritis in patients with polycystic kidney. ( Hosoya, T; Ichida, K; Sakai, O; Tabe, A, 1993)
"ADPKD patients with higher serum uric acid levels had a higher asymmetric dimethylarginine (ADMA) level (1."5.17Serum uric acid levels and endothelial dysfunction in patients with autosomal dominant polycystic kidney disease. ( Axelsson, J; Eroglu, E; Kalay, N; Kocyigit, I; Orscelik, O; Oymak, O; Sipahioglu, MH; Tokgoz, B; Unal, A; Yilmaz, MI, 2013)
"Elevated serum uric acid is not an independent risk factor for disease progression in ADPKD."4.02Serum Uric Acid and Progression of Autosomal Dominant Polycystic Kidney Disease: Results from the HALT PKD Trials. ( Brosnahan, GM; Chonchol, M; Gitomer, BY; Wang, W; You, Z, 2021)
" As a potentially modifiable risk factor, we examined whether serum uric acid levels correlate with early hypertension, kidney volume and progression to end-stage renal disease (ESRD) in autosomal-dominant polycystic kidney disease (ADPKD)."3.79Serum uric acid, kidney volume and progression in autosomal-dominant polycystic kidney disease. ( Fick-Brosnahan, GM; Helal, I; McFann, K; Reed, B; Schrier, RW; Yan, XD, 2013)
"Forty-seven nephrolithiasis patients without ADPKD (N) and 48 healthy controls (HC) were selected as control groups."1.91Assessment of metabolic risk factors for nephrolithiasis in patients with autosomal dominant polycystic kidney disease: a cross-sectional study. ( Artan, AS; Chasan, O; Elcioglu, OC; Gursu, M; Kazancioglu, R; Mirioglu, S, 2023)
"Hypocitraturia is not specific of ADPKD but it is also present in all tested nephropathies and is related with renal impairment and not with serum bicarbonate."1.72Hypocitraturia is present when renal function is impaired in diverse nephropathies and is not related with serum bicarbonate levels. ( Borrego Utiel, FJ; García Cortés, MJ; Herrera Contreras, I; Merino García, E; Moriana Domínguez, C; Ocaña Pérez, E, 2022)
"The study included ADPKD patients and control group, who carried out uroflowmetry, an assessment of renal function, metabolic and nutritional parameters and an evaluation of endothelial dysfunction and atherosclerotic markers, such as Renal Resistive Index (RRI), Intima-Media Thickness (IMT) and Flow-Mediated Dilation (FMD)."1.51Uroflowmetry alterations in patients with autosomal dominant polycystic kidney disease. ( Cianci, R; Ciccariello, M; Lai, S; Mastroluca, D; Mazzaferro, S; Mittherhofer, AP; Ricciuti, GP; Riviello, L; Salciccia, S; Vocaturi, M; Von Heland, M, 2019)
"Twenty-five ADPKD patients without hypertension and 25 healthy controls were studied cross-sectionally."1.40Pentraxin 3 as a novel bio-marker of inflammation and endothelial dysfunction in autosomal dominant polycystic kidney disease. ( Eroglu, E; Gungor, O; Imamoglu, H; Karakukcu, C; Kocyigit, I; Orscelik, O; Oymak, O; Ozturk, F; Sipahioglu, MH; Tokgoz, B; Unal, A, 2014)
"Patients with ADPKD and normal renal function showed plasma urate levels within normal range and normal renal urate handling."1.31Urate homeostasis in polycystic kidney disease: comparison with chronic glomerulonephritic kidney. ( Magoula, I; Mavromatidis, K; Tsapas, G, 2002)
"Among the 44 patients with ADPKD, the serum uric acid (SUA) was 7."1.29A study of uric acid metabolism and gouty arthritis in patients with polycystic kidney. ( Hosoya, T; Ichida, K; Sakai, O; Tabe, A, 1993)
"The occurrence of pancreatic cysts was significantly associated with liver cysts."1.28Clinical aspects of polycystic kidney disease. ( Aso, Y; Higashihara, E; Ito, H; Koiso, K; Sakai, O; Shimazaki, J, 1992)

Research

Studies (22)

TimeframeStudies, this research(%)All Research%
pre-19900 (0.00)18.7374
1990's3 (13.64)18.2507
2000's3 (13.64)29.6817
2010's10 (45.45)24.3611
2020's6 (27.27)2.80

Authors

AuthorsStudies
Borrego Utiel, FJ1
Herrera Contreras, I1
Merino García, E1
Moriana Domínguez, C1
Ocaña Pérez, E1
García Cortés, MJ1
Chasan, O1
Mirioglu, S1
Artan, AS1
Gursu, M1
Kazancioglu, R1
Elcioglu, OC1
Lai, S2
Petramala, L1
Muscaritoli, M1
Cianci, R2
Mazzaferro, S2
Mitterhofer, AP1
Pasquali, M1
D'Ambrosio, V1
Carta, M1
Ansuini, M1
Ramaccini, C1
Galani, A1
Amabile, MI1
Molfino, A1
Letizia, C1
Wang, GQ1
Rui, HL1
Dong, HR1
Sun, LJ1
Yang, M1
Wang, YY1
Ye, N1
Zhao, ZR1
Liu, XJ1
Xu, XY1
Chen, YP1
Cheng, H1
Brosnahan, GM1
You, Z1
Wang, W1
Gitomer, BY1
Chonchol, M1
Uchiyama, K1
Mochizuki, T1
Shimada, Y1
Nishio, S1
Kataoka, H1
Mitobe, M1
Tsuchiya, K1
Hanaoka, K1
Ubara, Y1
Suwabe, T1
Sekine, A1
Nutahara, K1
Tsuruya, K1
Ishimura, E1
Nakatani, S1
Sofue, T1
Tanaka, S1
Narita, I1
Maruyama, S1
Horie, S1
Muto, S1
Kim, K1
Trott, JF1
Gao, G1
Chapman, A1
Weiss, RH1
Mittherhofer, AP1
Riviello, L1
Vocaturi, M1
Mastroluca, D1
Ciccariello, M1
Von Heland, M1
Ricciuti, GP1
Salciccia, S1
Kocyigit, I2
Yilmaz, MI1
Orscelik, O2
Sipahioglu, MH2
Unal, A2
Eroglu, E2
Kalay, N1
Tokgoz, B2
Axelsson, J1
Oymak, O2
Gungor, O1
Ozturk, F1
Karakukcu, C1
Imamoglu, H1
Stiburkova, B1
Stekrova, J1
Nakamura, M1
Ichida, K2
Venkat-Raman, G1
Gast, C1
Marinaki, A1
Fairbanks, L1
Mir, S1
Yavascan, O1
Mutlubas, F1
Berdeli, A1
Sen, S1
Irazabal, MV1
Torres, VE1
Hogan, MC1
Glockner, J1
King, BF1
Ofstie, TG1
Krasa, HB1
Ouyang, J1
Czerwiec, FS1
Bollée, G1
Dahan, K1
Flamant, M1
Morinière, V1
Pawtowski, A1
Heidet, L1
Lacombe, D1
Devuyst, O1
Pirson, Y1
Antignac, C2
Knebelmann, B1
Helal, I1
McFann, K1
Reed, B1
Yan, XD1
Schrier, RW1
Fick-Brosnahan, GM1
Mavromatidis, K1
Magoula, I1
Tsapas, G1
Cameron, JS1
Simmonds, HA1
Kudo, E1
Itakura, M1
Hosoya, T1
Tabe, A1
Sakai, O2
Stavrou, C1
Pierides, A1
Zouvani, I1
Kyriacou, K1
Neophytou, P1
Christodoulou, K1
Deltas, CC1
Higashihara, E1
Aso, Y1
Shimazaki, J1
Ito, H1
Koiso, K1

Clinical Trials (3)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
HALT Progression of Polycystic Kidney Disease Study A[NCT00283686]Phase 3558 participants (Actual)Interventional2006-01-31Completed
Endothelial Dysfunction in Patients With Polycystic Kidney Disease[NCT01589705]150 participants (Actual)Observational2012-01-31Terminated (stopped due to Patients recruitment and analysis were terminated)
Longitudinal Efficacy and Safety Study of Tolvaptan on Autosomal Dominant Polycystic Kidney Disease Patients (LET-PKD Study)[NCT02729662]118 participants (Actual)Interventional2016-10-01Active, not recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Albuminuria

Urine albumin excretion, centrally processed from 24 hour urine collection (NCT00283686)
Timeframe: Up to 96 months (assessed annually)

Interventionannual percent change in mg/24 hr (Mean)
ACE-I + ARB-1.1
ACE-I Alone-0.4
Low Blood Pressure Group-3.8
Standard Blood Pressure Group2.4

Aldosterone

Urinary aldosterone excretion, centrally processed, 24 hour urine collection (NCT00283686)
Timeframe: Up to 96 months (assessed annually)

Interventionannual % change micrograms per 24 hr (Mean)
ACE-I + ARB-8.5
ACE-I Alone-7.3
Low Blood Pressure Group-8.5
Standard Blood Pressure Group-7.3

All-Cause Hospitalizations

(NCT00283686)
Timeframe: Up to 96 months

Interventionevents (Number)
ACE-I + ARB85
ACE-I Alone128
Low Blood Pressure Group93
Standard Blood Pressure Group120

Kidney Function (eGFR)

The estimated GFR was calculated by means of the Chronic Kidney Disease Epidemiology Collaboration equation with the use of central serum creatinine measurements. (NCT00283686)
Timeframe: Up to 96 months (6 month assessments)

Interventionml/min/1.73/m2/yr (Mean)
ACE-I + ARB-3.0
ACE-I Alone-2.9
Low Blood Pressure Group-2.9
Standard Blood Pressure Group-3.0

Left Ventricular Mass Index

Left ventricular mass index (g/m^2) measured by MRI, centrally reviewed and measured (NCT00283686)
Timeframe: 0, 24 months, 48 months, 60 months

Interventionannual change in g/m^2 (Mean)
ACE-I + ARB-0.91
ACE-I Alone-0.83
Low Blood Pressure Group-1.17
Standard Blood Pressure Group-0.57

Quality of Life Mental Component Summary

Short Form-36 Quality of LIfe Mental Component Summary ranges from 0 (worst possible outcome) to 100 (best possible outcome) (NCT00283686)
Timeframe: baseline, 12, 24, 36, 48, 60, 72, 84, and 96 months (assessed annually)

Interventionannual change in units on a scale (Mean)
ACE-I + ARB0.19
ACE-I Alone-0.06
Low Blood Pressure Group-0.05
Standard Blood Pressure Group0.18

Quality of Life Physical Component Summary

Short Form-36 Quality of Life Physical Component Summary ranges from 0 (worst possible outcome) to 100 (best possible outcome) (NCT00283686)
Timeframe: baseline, 12, 24, 36, 48, 60, 72, 84, and 96 months (assessed annually)

Interventionannual change in units on a scale (Mean)
ACE-I + ARB-0.24
ACE-I Alone-.23
Low Blood Pressure Group-0.17
Standard Blood Pressure Group-0.30

Renal Blood Flow

renal blood flow (mL/min/1.73 m^2) from MRI, centrally reviewed and measured. This outcome was more difficult to measure resulting in more missing data than other MRI outcomes such as total kidney volume (TKV) and left ventricular mass index (LVMI). (NCT00283686)
Timeframe: 0, 24 months, 48 months, 60 months

Interventionannual change in mL/min/1.73 m^2 (Mean)
ACE-I + ARB-6.6
ACE-I Alone-9.5
Low Blood Pressure Group-7.6
Standard Blood Pressure Group-8.5

Study A: Percent Annual Change in Total Kidney Volume

Annual percentage change in total kidney volume as assessed by abdominal magnetic resonance imaging (MRI) at baseline, 2 years, 4 years, and 5 years follow-up. (NCT00283686)
Timeframe: Baseline and 2-, 4- and 5-year follow-up

Interventionpercentage of Total Kidney Volume (Mean)
ACE-I + ARB6.0
ACE-I Alone6.2
Low Blood Pressure Group5.6
Standard Blood Pressure Group6.6

Reviews

3 reviews available for uric acid and ADPKD

ArticleYear
From juvenile hyperuricaemia to dysfunctional uromodulin: an ongoing metamorphosis.
    Pediatric nephrology (Berlin, Germany), 2016, Volume: 31, Issue:11

    Topics: Adolescent; Chromosomes, Human, Pair 16; DNA Mutational Analysis; Exons; Gout; Hepatocyte Nuclear Fa

2016
Hereditary hyperuricemia and renal disease.
    Seminars in nephrology, 2005, Volume: 25, Issue:1

    Topics: Genetic Predisposition to Disease; Humans; Hyperuricemia; Hypoxanthine Phosphoribosyltransferase; Ki

2005
[Uromodulin mutation and hyperuricemia].
    Nihon rinsho. Japanese journal of clinical medicine, 2008, Volume: 66, Issue:4

    Topics: Animals; Humans; Hyperuricemia; Kidney Failure, Chronic; Kidney Tubules, Proximal; Mucoproteins; Mut

2008

Trials

4 trials available for uric acid and ADPKD

ArticleYear
α-lipoic acid in patients with autosomal dominant polycystic kidney disease.
    Nutrition (Burbank, Los Angeles County, Calif.), 2020, Volume: 71

    Topics: Adult; Anti-Inflammatory Agents; Antioxidants; Biomarkers; Blood Glucose; C-Reactive Protein; Caroti

2020
Plasma metabolites and lipids associate with kidney function and kidney volume in hypertensive ADPKD patients early in the disease course.
    BMC nephrology, 2019, 02-25, Volume: 20, Issue:1

    Topics: Adult; Creatinine; Disease Progression; Female; Humans; Indoles; Kidney; Kidney Function Tests; Long

2019
Serum uric acid levels and endothelial dysfunction in patients with autosomal dominant polycystic kidney disease.
    Nephron. Clinical practice, 2013, Volume: 123, Issue:3-4

    Topics: Adult; Arginine; C-Reactive Protein; Cross-Sectional Studies; Endothelium, Vascular; Glomerular Filt

2013
Short-term effects of tolvaptan on renal function and volume in patients with autosomal dominant polycystic kidney disease.
    Kidney international, 2011, Volume: 80, Issue:3

    Topics: Adult; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Biomarkers; Contrast Media; Creatini

2011

Other Studies

15 other studies available for uric acid and ADPKD

ArticleYear
Hypocitraturia is present when renal function is impaired in diverse nephropathies and is not related with serum bicarbonate levels.
    International urology and nephrology, 2022, Volume: 54, Issue:6

    Topics: Bicarbonates; Biomarkers; Citrates; Citric Acid; Female; Glomerular Filtration Rate; Humans; Kidney;

2022
Assessment of metabolic risk factors for nephrolithiasis in patients with autosomal dominant polycystic kidney disease: a cross-sectional study.
    Clinical and experimental nephrology, 2023, Volume: 27, Issue:11

    Topics: Adult; Cross-Sectional Studies; Humans; Kidney Calculi; Polycystic Kidney, Autosomal Dominant; Risk

2023
SMRT sequencing revealed to be an effective method for ADTKD-MUC1 diagnosis through follow-up analysis of a Chinese family.
    Scientific reports, 2020, 05-25, Volume: 10, Issue:1

    Topics: Adult; Aged; Asian People; Case-Control Studies; China; Exome Sequencing; Female; Frameshift Mutatio

2020
Serum Uric Acid and Progression of Autosomal Dominant Polycystic Kidney Disease: Results from the HALT PKD Trials.
    Current hypertension reviews, 2021, Volume: 17, Issue:3

    Topics: Disease Progression; Female; Glomerular Filtration Rate; Humans; Kidney; Male; Polycystic Kidney, Au

2021
Factors predicting decline in renal function and kidney volume growth in autosomal dominant polycystic kidney disease: a prospective cohort study (Japanese Polycystic Kidney Disease registry: J-PKD).
    Clinical and experimental nephrology, 2021, Volume: 25, Issue:9

    Topics: Adult; Age Factors; Blood Glucose; Cholesterol, HDL; Disease Progression; Fasting; Female; Follow-Up

2021
Uroflowmetry alterations in patients with autosomal dominant polycystic kidney disease.
    European review for medical and pharmacological sciences, 2019, Volume: 23, Issue:7

    Topics: Adult; Aged; Atherosclerosis; Biomarkers; Cardiovascular Diseases; Carotid Intima-Media Thickness; C

2019
Pentraxin 3 as a novel bio-marker of inflammation and endothelial dysfunction in autosomal dominant polycystic kidney disease.
    Journal of nephrology, 2014, Volume: 27, Issue:2

    Topics: Adult; Biomarkers; C-Reactive Protein; Case-Control Studies; Cross-Sectional Studies; Endothelium, V

2014
Hereditary Renal Hypouricemia Type 1 and Autosomal Dominant Polycystic Kidney Disease.
    The American journal of the medical sciences, 2015, Volume: 350, Issue:4

    Topics: Adult; Aged; Alleles; Animals; Czech Republic; DNA Mutational Analysis; Family Health; Female; Gene

2015
A rare cause of chronic renal failure in a girl with elevated serum uric acid level.
    Pediatric nephrology (Berlin, Germany), 2010, Volume: 25, Issue:1

    Topics: Adolescent; Diagnosis, Differential; DNA Mutational Analysis; Family Health; Female; Humans; Hyperur

2010
Phenotype and outcome in hereditary tubulointerstitial nephritis secondary to UMOD mutations.
    Clinical journal of the American Society of Nephrology : CJASN, 2011, Volume: 6, Issue:10

    Topics: Adult; Belgium; Biomarkers; Central Nervous System Diseases; Chi-Square Distribution; Dental Enamel;

2011
Serum uric acid, kidney volume and progression in autosomal-dominant polycystic kidney disease.
    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2013, Volume: 28, Issue:2

    Topics: Adult; Cohort Studies; Disease Progression; Female; Humans; Hypertension; Hyperuricemia; Kidney; Kid

2013
Urate homeostasis in polycystic kidney disease: comparison with chronic glomerulonephritic kidney.
    Renal failure, 2002, Volume: 24, Issue:4

    Topics: Chronic Disease; Female; Glomerulonephritis; Homeostasis; Humans; Kidney; Kidney Failure, Chronic; M

2002
A study of uric acid metabolism and gouty arthritis in patients with polycystic kidney.
    Nihon Jinzo Gakkai shi, 1993, Volume: 35, Issue:1

    Topics: Adult; Arthritis, Gouty; Female; Humans; Male; Middle Aged; Polycystic Kidney, Autosomal Dominant; U

1993
Medullary cystic kidney disease with hyperuricemia and gout in a large Cypriot family: no allelism with nephronophthisis type 1.
    American journal of medical genetics, 1998, May-01, Volume: 77, Issue:2

    Topics: Adult; Age of Onset; Aged; Cyprus; Female; Genes, Dominant; Genetic Linkage; Gout; Humans; Hypertens

1998
Clinical aspects of polycystic kidney disease.
    The Journal of urology, 1992, Volume: 147, Issue:2

    Topics: Adult; Blood Pressure; Cysts; Female; Humans; Kidney; Kidney Calculi; Male; Middle Aged; Polycystic

1992