MARATTO

article · Zenodo (CERN European Organization for Nuclear Research)

Heterogeneity Of Renal Pathogenicity On The Background Of Asymptomatic Hyperuricemia In Patients With Dual Metabolic Syndrome Diseases (Essential Hypertensive Disease and Type 2 Diabetes Mellitus)

202320 citationsOpen access

In plain language

This study examined how asymptomatic hyperuricemia affects kidney function in individuals with both essential hypertensive disease and type 2 diabetes mellitus. Researchers evaluated 105 patients divided into three clinical groups alongside 15 healthy volunteers. The clinical cohorts comprised individuals with hypertension alone, type 2 diabetes alone, or both conditions simultaneously. Participants were tested for blood uric acid, lipid profiles, inflammatory markers such as tumour necrosis factor alpha and high-sensitivity C-reactive protein, and urine neutrophil gelatinase-associated lipocalin. High blood uric acid occurred in 55.7 percent of patients suffering from both conditions, compared to lower rates in those with only hypertension or diabetes. Increased uric acid levels correlated significantly with higher urine albumin, reduced glomerular filtration rates, elevated urinary biomarkers of kidney injury, and heightened inflammatory markers, demonstrating compounded renal vulnerability in patients with dual metabolic diseases.

Key takeaways

  • Asymptomatic hyperuricemia was most prevalent in patients experiencing both hypertension and type 2 diabetes, affecting 55.7 percent of that group.
  • Elevated uric acid levels correlated directly with indicators of kidney impairment, including decreased glomerular filtration rates and elevated urine neutrophil gelatinase-associated lipocalin.
  • High uric acid also correlated positively with higher systolic blood pressure, glycated haemoglobin, dyslipidaemia, and inflammatory markers.
  • The findings demonstrate diverse mechanisms of renal damage and suggest an increased cardiovascular risk for patients managing both conditions simultaneously.

Why it matters

Hypertension and type 2 diabetes frequently occur together and substantially increase the danger of kidney disease. Demonstrating that high uric acid without gout symptoms correlates with worsening renal function and systemic inflammation highlights an important metric for clinicians. Identifying these relationships helps medical teams recognise heightened risks of organ damage and cardiovascular complications earlier in patients living with multiple metabolic conditions.

Commercialisation angle

This is early-stage clinical research establishing biomarker correlations rather than a direct commercial product. The findings could inform future diagnostic algorithms, risk stratification panels, or clinical monitoring protocols used by healthcare providers and diagnostic laboratories managing metabolic syndrome. Real-world application depends on further translational research and clinical validation to confirm whether targeting asymptomatic hyperuricemia improves patient outcomes.

AI-generated from the published abstract. Always read the original work before citing.

Abstract

ABSTRACT Asymptomatic hyperuricemia is believed to be more severe and more common in patients with dual metabolic syndrome diseases (essential hypertensive disease (EHD) and type 2 diabetes mellitus (T2DM)) and comparatively less severe and less common in patients with either of these dual metabolic syndrome diseases. To determine the heterogeneity of renal pathogenicity on the background of asymptomatic hyperuricemia in the clinical course of EHD combined with T2DM using correlations between uric acid levels in the blood, systolic blood pressure levels, glycated hemoglobin, dyslipidemia, inflammatory processes, kidney damage, etc. The research included 105 patients (50 males and 55 females), aged 41-70 years, average age being (54.2±4.0) years. Patients were divided into 3 groups: Group I (GI) consisted of 25 patients with treatment-compensated EHD, 1-2 degree, stage II; Group ІІ (GII) was made up of 25 patients with subcompensated T2DM (glycated hemoglobin (HbA<sub>1</sub>C) - from 7.0 to 11.0%); Group III (GIII) had 55 patients with EHD, 1-2 degree, stage ІІ combined with subcompensated T2DM. Control group consisted of 15 practically healthy volunteers, 10 (66.7%) females and 5 (33.3%) males, aged (54.6±4.2) years. Groups were randomized according to age, sex, BMI, duration of EHD and T2DM. In addition to general clinical examination conducted; blood levels of uric acid (UA), lipids, tumour necrosis factor alpha (TNF-α), high-sensitivity C-reactive protein (hs-CRP) were determined. Urine levels of neutrophil gelatinase-associated lipocalin (NGAL) was also determined using immuno-fermentation methods. Asymptomatic hyperuricemia characterized by an increase in blood uric acid level of more than 410 μmol/l was observed in 34.6% of GI patients, in 21.8% of GII patients and most commonly in 55.7% of GIII patients with EHD combined with T2DM. Correlations between blood uric acid level with albuminuria was found (r=+0.42; p&lt;0.05); with decrease in GFR (r=-0.51; p&lt;0.05); with increase in NGAL level in urine (r=+0.56; p&lt;0.05), which indicate an adverse effect of asymptomatic hyperuricemia on the functional state of the kidneys in patients with EHD and concomitant T2DM. Positive correlative relationships exist between asymptomatic hyperuricemia, increased albuminuria and a decrease in GFR, dyslipidemia, SBP, HbA<sub>1</sub>C, inflammatory processes and kidney damage, which indicate the heterogeneity of renal pathogenicity in patients with EHD combined with T2DM and a higher risk of cardiovascular disease in such patients. <strong>Keywords</strong><strong>:</strong> Heterogeneity, renal pathogenicity, asymptomatic hyperuricemia, metabolic syndrome diseases, essential hypertensive disease, type 2 diabetes mellitus

Research topics

  • Gout, Hyperuricemia, Uric Acid
  • Healthcare Systems and Public Health

Sustainable Development Goals

Read the original research

This page summarises published work. The authoritative version sits with the publisher.

DOI: 10.5281/zenodo.7690636

Is something wrong with this record? Report it or request removal.

Discussion

Discuss this research

Have you built on this work, tried to replicate it, or seen it applied in practice? Share what you know. Verified researchers and MARATTO™ domain experts can open a discussion, and any member can reply. Contributions are reviewed before they appear.

No discussion yet. Open the first thread.