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
| Excerpt | Relevance | Reference |
|---|---|---|
| "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." | 5.34 | α-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." | 5.30 | Plasma 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." | 5.29 | A 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." | 5.17 | Serum 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." | 4.02 | Serum 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)." | 3.79 | Serum 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." | 1.91 | Assessment 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." | 1.72 | Hypocitraturia 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)." | 1.51 | Uroflowmetry 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." | 1.40 | Pentraxin 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." | 1.31 | Urate 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." | 1.29 | A 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." | 1.28 | Clinical aspects of polycystic kidney disease. ( Aso, Y; Higashihara, E; Ito, H; Koiso, K; Sakai, O; Shimazaki, J, 1992) |
Research
Studies (22)
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 3 (13.64) | 18.2507 |
| 2000's | 3 (13.64) | 29.6817 |
| 2010's | 10 (45.45) | 24.3611 |
| 2020's | 6 (27.27) | 2.80 |
Authors
| Authors | Studies |
|---|---|
| Borrego Utiel, FJ | 1 |
| Herrera Contreras, I | 1 |
| Merino García, E | 1 |
| Moriana Domínguez, C | 1 |
| Ocaña Pérez, E | 1 |
| García Cortés, MJ | 1 |
| Chasan, O | 1 |
| Mirioglu, S | 1 |
| Artan, AS | 1 |
| Gursu, M | 1 |
| Kazancioglu, R | 1 |
| Elcioglu, OC | 1 |
| Lai, S | 2 |
| Petramala, L | 1 |
| Muscaritoli, M | 1 |
| Cianci, R | 2 |
| Mazzaferro, S | 2 |
| Mitterhofer, AP | 1 |
| Pasquali, M | 1 |
| D'Ambrosio, V | 1 |
| Carta, M | 1 |
| Ansuini, M | 1 |
| Ramaccini, C | 1 |
| Galani, A | 1 |
| Amabile, MI | 1 |
| Molfino, A | 1 |
| Letizia, C | 1 |
| Wang, GQ | 1 |
| Rui, HL | 1 |
| Dong, HR | 1 |
| Sun, LJ | 1 |
| Yang, M | 1 |
| Wang, YY | 1 |
| Ye, N | 1 |
| Zhao, ZR | 1 |
| Liu, XJ | 1 |
| Xu, XY | 1 |
| Chen, YP | 1 |
| Cheng, H | 1 |
| Brosnahan, GM | 1 |
| You, Z | 1 |
| Wang, W | 1 |
| Gitomer, BY | 1 |
| Chonchol, M | 1 |
| Uchiyama, K | 1 |
| Mochizuki, T | 1 |
| Shimada, Y | 1 |
| Nishio, S | 1 |
| Kataoka, H | 1 |
| Mitobe, M | 1 |
| Tsuchiya, K | 1 |
| Hanaoka, K | 1 |
| Ubara, Y | 1 |
| Suwabe, T | 1 |
| Sekine, A | 1 |
| Nutahara, K | 1 |
| Tsuruya, K | 1 |
| Ishimura, E | 1 |
| Nakatani, S | 1 |
| Sofue, T | 1 |
| Tanaka, S | 1 |
| Narita, I | 1 |
| Maruyama, S | 1 |
| Horie, S | 1 |
| Muto, S | 1 |
| Kim, K | 1 |
| Trott, JF | 1 |
| Gao, G | 1 |
| Chapman, A | 1 |
| Weiss, RH | 1 |
| Mittherhofer, AP | 1 |
| Riviello, L | 1 |
| Vocaturi, M | 1 |
| Mastroluca, D | 1 |
| Ciccariello, M | 1 |
| Von Heland, M | 1 |
| Ricciuti, GP | 1 |
| Salciccia, S | 1 |
| Kocyigit, I | 2 |
| Yilmaz, MI | 1 |
| Orscelik, O | 2 |
| Sipahioglu, MH | 2 |
| Unal, A | 2 |
| Eroglu, E | 2 |
| Kalay, N | 1 |
| Tokgoz, B | 2 |
| Axelsson, J | 1 |
| Oymak, O | 2 |
| Gungor, O | 1 |
| Ozturk, F | 1 |
| Karakukcu, C | 1 |
| Imamoglu, H | 1 |
| Stiburkova, B | 1 |
| Stekrova, J | 1 |
| Nakamura, M | 1 |
| Ichida, K | 2 |
| Venkat-Raman, G | 1 |
| Gast, C | 1 |
| Marinaki, A | 1 |
| Fairbanks, L | 1 |
| Mir, S | 1 |
| Yavascan, O | 1 |
| Mutlubas, F | 1 |
| Berdeli, A | 1 |
| Sen, S | 1 |
| Irazabal, MV | 1 |
| Torres, VE | 1 |
| Hogan, MC | 1 |
| Glockner, J | 1 |
| King, BF | 1 |
| Ofstie, TG | 1 |
| Krasa, HB | 1 |
| Ouyang, J | 1 |
| Czerwiec, FS | 1 |
| Bollée, G | 1 |
| Dahan, K | 1 |
| Flamant, M | 1 |
| Morinière, V | 1 |
| Pawtowski, A | 1 |
| Heidet, L | 1 |
| Lacombe, D | 1 |
| Devuyst, O | 1 |
| Pirson, Y | 1 |
| Antignac, C | 2 |
| Knebelmann, B | 1 |
| Helal, I | 1 |
| McFann, K | 1 |
| Reed, B | 1 |
| Yan, XD | 1 |
| Schrier, RW | 1 |
| Fick-Brosnahan, GM | 1 |
| Mavromatidis, K | 1 |
| Magoula, I | 1 |
| Tsapas, G | 1 |
| Cameron, JS | 1 |
| Simmonds, HA | 1 |
| Kudo, E | 1 |
| Itakura, M | 1 |
| Hosoya, T | 1 |
| Tabe, A | 1 |
| Sakai, O | 2 |
| Stavrou, C | 1 |
| Pierides, A | 1 |
| Zouvani, I | 1 |
| Kyriacou, K | 1 |
| Neophytou, P | 1 |
| Christodoulou, K | 1 |
| Deltas, CC | 1 |
| Higashihara, E | 1 |
| Aso, Y | 1 |
| Shimazaki, J | 1 |
| Ito, H | 1 |
| Koiso, K | 1 |
Clinical Trials (3)
Trial Overview
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| HALT Progression of Polycystic Kidney Disease Study A[NCT00283686] | Phase 3 | 558 participants (Actual) | Interventional | 2006-01-31 | Completed | ||
| Endothelial Dysfunction in Patients With Polycystic Kidney Disease[NCT01589705] | 150 participants (Actual) | Observational | 2012-01-31 | Terminated (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) | Interventional | 2016-10-01 | Active, 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)
| Intervention | annual 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 Group | 2.4 |
Aldosterone
Urinary aldosterone excretion, centrally processed, 24 hour urine collection (NCT00283686)
Timeframe: Up to 96 months (assessed annually)
| Intervention | annual % 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
| Intervention | events (Number) |
|---|---|
| ACE-I + ARB | 85 |
| ACE-I Alone | 128 |
| Low Blood Pressure Group | 93 |
| Standard Blood Pressure Group | 120 |
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)
| Intervention | ml/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
| Intervention | annual 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)
| Intervention | annual change in units on a scale (Mean) |
|---|---|
| ACE-I + ARB | 0.19 |
| ACE-I Alone | -0.06 |
| Low Blood Pressure Group | -0.05 |
| Standard Blood Pressure Group | 0.18 |
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)
| Intervention | annual 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
| Intervention | annual 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
| Intervention | percentage of Total Kidney Volume (Mean) |
|---|---|
| ACE-I + ARB | 6.0 |
| ACE-I Alone | 6.2 |
| Low Blood Pressure Group | 5.6 |
| Standard Blood Pressure Group | 6.6 |
Reviews
3 reviews available for uric acid and ADPKD
| Article | Year |
|---|---|
From juvenile hyperuricaemia to dysfunctional uromodulin: an ongoing metamorphosis.
Topics: Adolescent; Chromosomes, Human, Pair 16; DNA Mutational Analysis; Exons; Gout; Hepatocyte Nuclear Fa | 2016 |
Hereditary hyperuricemia and renal disease.
Topics: Genetic Predisposition to Disease; Humans; Hyperuricemia; Hypoxanthine Phosphoribosyltransferase; Ki | 2005 |
[Uromodulin mutation and hyperuricemia].
Topics: Animals; Humans; Hyperuricemia; Kidney Failure, Chronic; Kidney Tubules, Proximal; Mucoproteins; Mut | 2008 |
Trials
4 trials available for uric acid and ADPKD
| Article | Year |
|---|---|
α-lipoic acid in patients with autosomal dominant polycystic kidney disease.
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.
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.
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.
Topics: Adult; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Biomarkers; Contrast Media; Creatini | 2011 |
Other Studies
15 other studies available for uric acid and ADPKD
| Article | Year |
|---|---|
Hypocitraturia is present when renal function is impaired in diverse nephropathies and is not related with serum bicarbonate levels.
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.
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.
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.
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).
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.
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.
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.
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.
Topics: Adolescent; Diagnosis, Differential; DNA Mutational Analysis; Family Health; Female; Humans; Hyperur | 2010 |
Phenotype and outcome in hereditary tubulointerstitial nephritis secondary to UMOD mutations.
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.
Topics: Adult; Cohort Studies; Disease Progression; Female; Humans; Hypertension; Hyperuricemia; Kidney; Kid | 2013 |
Urate homeostasis in polycystic kidney disease: comparison with chronic glomerulonephritic kidney.
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.
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.
Topics: Adult; Age of Onset; Aged; Cyprus; Female; Genes, Dominant; Genetic Linkage; Gout; Humans; Hypertens | 1998 |
Clinical aspects of polycystic kidney disease.
Topics: Adult; Blood Pressure; Cysts; Female; Humans; Kidney; Kidney Calculi; Male; Middle Aged; Polycystic | 1992 |