An observational study in CKD Progression, sponsored by Assiut University. Not yet recruiting. Open to participants aged 18 Years and older, including healthy volunteers. Per ClinicalTrials.gov, last updated 2025-09-30.
Sponsored by Assiut University · Observational
Chronic kidney disease (CKD) is a major global health problem, and hyperuricemia has emerged as both a consequence and a potential driver of its progression. Elevated uric acid contributes to renal impairment through oxidative stress, endothelial dysfunction, inflammasome activation, and crystal deposition. Epidemiological studies show that hyperuricemia often precedes CKD and serves as an independent predictor, with prevalence reaching up to 38% among CKD patients.
Prediabetes, another growing health concern, is associated with higher serum uric acid levels and increased risk of developing both diabetes and CKD. Factors such as obesity, fatty liver, and dyslipidemia mediate this link. Clinically, higher uric acid levels are correlated with faster eGFR decline and higher risk of ESRD, with the uric acid/HDL ratio proposed as a novel risk marker.
Although debate persists about whether hyperuricemia directly causes CKD, emerging genetic and epidemiological evidence supports its independent role. Given the rising prevalence of prediabetes and hyperuricemia, identifying hyperuricemia as a modifiable early predictor of CKD progression in prediabetic patients could help improve prevention, risk stratification, and management
Chronic kidney disease (CKD) is a global health concern, characterized by a gradual loss of kidney function, and is associated with increased morbidity and mortality. Hyperuricemia, defined as elevated serum uric acid levels, has been identified as both a consequence and a potential contributor to CKD progression. Recent studies have shown that hyperuricemia can aggravate renal impairment through mechanisms such as direct nephrotoxicity, activation of the inflammasome, increased oxidative stress, and endothelial dysfunction.
Epidemiological evidence indicates that hyperuricemia often precedes the development of CKD and may serve as an independent predictor of its onset and progression, even after adjusting for traditional risk factors like hypertension, proteinuria, and dyslipidemia. The prevalence of hyperuricemia is notably higher among CKD patients, reaching up to 38% in some populations. Furthermore, hyperuricemia is implicated in the pathogenesis of several metabolic disorders, including hypertension, obesity, and metabolic syndrome, all of which are risk factors for CKD.
Prediabetes, a state of impaired glucose metabolism, is increasingly recognized as a risk factor for both cardiovascular disease and CKD. Studies have found that individuals with prediabetes exhibit higher serum uric acid levels compared to normoglycemic individuals, and that elevated uric acid is associated with increased risk of progression to diabetes and CKD. The relationship between hyperuricemia and prediabetes appears to be mediated by factors such as fatty liver, dyslipidemia, and body mass index, highlighting the complex interplay between metabolic health and kidney function.
Clinical research has demonstrated that higher serum uric acid levels are associated with a more rapid decline in estimated glomerular filtration rate (eGFR) and an increased risk of progression to end-stage renal disease (ESRD). For example, a baseline uric acid level of ≥7.5 mg/dL has been shown to significantly increase the risk of renal function decline in hypertensive and non-diabetic populations. Additionally, the serum uric acid to high-density lipoprotein (HDL) cholesterol ratio has emerged as a novel marker for predicting CKD risk, reflecting the balance between pro-inflammatory and anti-inflammatory processes.
Despite these associations, the causality of hyperuricemia in CKD progression remains a topic of debate, as some clinical trials have yielded conflicting results regarding the benefits of uric acid-lowering therapy in slowing CKD progression. However, recent genetic and epidemiological studies suggest that hyperuricemia represents a significant risk factor for CKD, independent of genetic predisposition and other comorbidities. The mechanisms by which uric acid may induce kidney injury include crystal deposition, oxidative stress, activation of the renin-angiotensin-aldosterone system, and impairment of endothelial function.The burden of CKD in prediabetic individuals is of particular concern, as early identification of modifiable risk factors such as hyperuricemia could facilitate timely interventions to prevent or delay CKD progression. Given the increasing prevalence of both prediabetes and hyperuricemia worldwide, understanding their interplay is crucial for developing effective preventive strategies.
Despite growing evidence linking hyperuricemia to CKD progression, particularly in at-risk populations such as prediabetic patients, the predictive value of elevated serum uric acid for CKD progression in this group remains underexplored. This study aims to clarify whether hyperuricemia can serve as an early and independent predictor of CKD progression in prediabetic patients, thereby informing clinical practice and guiding risk stratification and management in this vulnerable population
918 studies on the registry are indexed under Prediabetic State; 232 are open to participants now.
This study's planned enrollment of 150 is below the median of 224 across 129 observational studies indexed under Prediabetic State.
Browse Prediabetic State studies →Assiut University is the lead sponsor of 5,078 studies on the registry; 2,178 are open to participants now.
Of its 14 completed or terminated interventional studies of FDA-regulated products, 0 (0%) have results posted.
Counted across the registry records on this site, refreshed daily.
The study population divided into three groups:
The first group includes individuals at high risk of chronic kidney disease (prediabetic patient s) The second group comprises individuals diagnosed with early ckd stage A1,A2,A3 The third group serves as the control group and includes participants with normal renal function
Go through the criteria one by one — yes, no or not sure — and take the list to your doctor or the study team. Kept in this browser only.
Exclusion criteria:
Underlined terms in the criteria open these too. Explained by clinicaltrials.gg, not part of the registry record. The study team decides who can take part.
A blood test of average blood sugar over the past two to three months, given as a percentage or in mmol/mol. 6.5% (48 mmol/mol) or more is the usual threshold for diabetes, normally confirmed by a second test.
GFR (glomerular filtration rate) is how much blood the kidneys filter each minute. It is usually estimated from a blood test — eGFR, by formulas such as CKD-EPI or MDRD — and some studies ask for it to be measured directly instead. Usually given in mL/min/1.73 m².
Check the method, the units and the minimum the study states. A value of 90 or above is in the normal-or-high range, but kidney damage can show in other tests too.
Before you join, the study team explains what taking part involves — its purpose, what happens, the risks and possible benefits — and answers your questions, so you can decide freely. Consent is usually recorded on a form (the informed consent form, ICF) signed by you or, where the law allows, by someone legally authorised to decide for you.
You can keep asking questions during the study, you are told of new information that matters, and you can choose to leave at any time.
Malignancy means cancer. Criteria about another or earlier malignancy ask whether you have had a different cancer, usually within a set number of years.
Some are commonly allowed, such as treated skin cancers other than melanoma and early cancers removed completely — check the exceptions this study lists.
HbA1c
A blood test of average blood sugar over the past two to three months, given as a percentage or in mmol/mol. 6.5% (48 mmol/mol) or more is the usual threshold for diabetes, normally confirmed by a second test.
Explained by clinicaltrials.gg, not part of the registry record. The study team decides who can take part.
GFR and eGFR (kidney filtering)
GFR (glomerular filtration rate) is how much blood the kidneys filter each minute. It is usually estimated from a blood test — eGFR, by formulas such as CKD-EPI or MDRD — and some studies ask for it to be measured directly instead. Usually given in mL/min/1.73 m².
Check the method, the units and the minimum the study states. A value of 90 or above is in the normal-or-high range, but kidney damage can show in other tests too.
Explained by clinicaltrials.gg, not part of the registry record. The study team decides who can take part.
Informed consent
Before you join, the study team explains what taking part involves — its purpose, what happens, the risks and possible benefits — and answers your questions, so you can decide freely. Consent is usually recorded on a form (the informed consent form, ICF) signed by you or, where the law allows, by someone legally authorised to decide for you.
You can keep asking questions during the study, you are told of new information that matters, and you can choose to leave at any time.
Explained by clinicaltrials.gg, not part of the registry record. The study team decides who can take part.
Cancer (malignancy)
Malignancy means cancer. Criteria about another or earlier malignancy ask whether you have had a different cancer, usually within a set number of years.
Some are commonly allowed, such as treated skin cancers other than melanoma and early cancers removed completely — check the exceptions this study lists.
Explained by clinicaltrials.gg, not part of the registry record. The study team decides who can take part.
includes individuals at high risk of chronic kidney disease (prediabetic patient s)
individuals diagnosed with early ckd stage A1,A2,A3
serves as the control group and includes participants with normal renal function.
CKD progression in prediabetics
Progression of CKD, defined as a sustained reduction in eGFR of ≥25% from baseline or advancement to a higher CKD stage (KDIGO classification) during the follow-up period.
Time frame: 1 year
No study locations are listed for this record.
This study is not yet recruiting, as verified in Sep 2025. You cannot join it, but the record below documents what was studied.
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