Related Experiment Video
Updated: Jun 8, 2026
Implementing Patch Clamp and Live Fluorescence Microscopy to Monitor Functional Properties of Freshly Isolated PKD Epithelium
Published on: September 1, 2015
Inflammation, oxidative stress, and insulin resistance in polycystic kidney disease
Vandana Menon1, Darya Rudym, Priya Chandra
1Division of Nephrology, Tufts Medical Center, Boston, Massachusetts, USA. Vandana.menon@gmail.com
Insights
Inflammation and oxidative stress are early indicators of cardiovascular disease risk in autosomal dominant polycystic kidney disease (ADPKD), even with preserved kidney function. These processes may offer targets for future therapeutic interventions to mitigate cardiovascular disease risk.
Area of Science:
- Nephrology
- Cardiology
- Biomarkers
Background:
- Cardiovascular disease (CVD) is the leading cause of mortality in autosomal dominant polycystic kidney disease (ADPKD).
- Novel biomarkers for CVD risk require examination across different stages of ADPKD.
Purpose of the Study:
- To investigate novel cardiovascular disease (CVD) biomarkers in patients with autosomal dominant polycystic kidney disease (ADPKD).
- To assess markers of inflammation, oxidative stress, and insulin resistance in relation to kidney function and hypertension in ADPKD.
Main Methods:
- Recruited 50 hypertensive ADPKD patients (eGFR >60), 52 hypertensive ADPKD patients (eGFR 25-60), 42 normotensive ADPKD patients (eGFR >60), and 50 healthy controls.
- Assayed serum C-reactive protein (CRP) and IL-6 for inflammation, plasma 8-epi-prostaglandin F(2α) (8-epi-PGF2α) and superoxide dismutase (SOD) for oxidative stress, and HOMA for insulin resistance.
Main Results:
- Hypertensive ADPKD patients (eGFR 25-60) showed higher C-reactive protein and IL-6 levels compared to controls and other ADPKD groups.
- All ADPKD groups exhibited elevated 8-epi-PGF2α and reduced SOD compared to controls, indicating increased oxidative stress.
- No significant differences in HOMA (insulin resistance) were observed between any groups.
Conclusions:
- Inflammation and oxidative stress are present early in ADPKD, even with preserved kidney function.
- Inflammation correlates with kidney function decline, while oxidative stress shows a threshold effect.
- These inflammatory and oxidative pathways represent potential therapeutic targets for reducing CVD risk in ADPKD.
Background And Objectives:
Most deaths in autosomal dominant polycystic kidney disease (ADPKD) are attributable to cardiovascular disease (CVD). We examined novel CVD biomarkers in different stages of ADPKD.
Design, Setting, Participants, & Measurements:
We recruited 50 hypertensive subjects with ADPKD with estimated GFR (eGFR) of >60 ml/min per 1.73 m(2); 52 hypertensive subjects with ADPKD with eGFR of 25 to 60 ml/min per 1.73 m(2); 42 normotensive subjects with ADPKD and eGFR of >60 ml/min per 1.73 m(2); and 50 healthy controls. We assayed serum C-reactive protein and IL-6 as markers of inflammation; plasma 8-epi-prostaglandin F(2α (8-epi-PGF2α)) and superoxide dismutase (SOD) as markers of oxidative stress; and homeostasis model assessment (HOMA) as a measure of insulin resistance.
Results:
The hypertensive ADPKD eGFR of 25 to 60 group had higher levels of C-reactive protein and IL-6 than controls, normotensive ADPKD with eGFR of >60, and hypertensive ADPKD with eGFR of >60. The normotensive ADPKD eGFR >60, hypertensive ADPKD eGFR >60, and hypertensive ADPKD eGFR 25 to 60 groups had higher 8-epi-PGF(2α) and lower SOD than controls, with no difference between the ADPKD groups. There was no difference in HOMA levels between any of the groups. Adjustment for age, race, gender, and body mass index did not alter these relationships.
Conclusions:
Inflammation and oxidative stress are evident early in ADPKD even with preserved kidney function. Inflammation exhibits a graded relationship with levels of kidney function, whereas oxidative stress demonstrates a threshold effect. These pathways may be therapeutic targets for CVD risk mitigation.
Related Concept Videos
01:25Chronic Kidney Disease I: Introduction
01:28Diabetic Nephropathy
01:24Chronic Kidney Disease II: Clinical Manifestations
01:21Chronic Pancreatitis II: Pathophysiology
01:10Nephrons
01:24Type II Diabetes II: Pathophysiology