Metabolic factors and microinflammatory state promote kidney injury in type 2 diabetes mellitus patients.
OBJECTIVE
This study examined the associations among the factors of metabolic syndrome, microinflammatory state, and kidney injury in type 2 diabetes mellitus patients.


METHODS
A retrospective study was conducted on 914 type 2 diabetes mellitus patients from January 2007 to May 2008. We observed the prevalence of chronic kidney disease in different groups of type 2 diabetes mellitus patients, and analyzed the association between metabolic syndrome and chronic kidney disease. We chose 84 cases randomly from this cohort to test their inflammatory biomarkers including tumor necrosis factor alpha, interleukin-6, and C-reactive protein to study the relationship to chronic kidney disease.


RESULTS
The prevalence of chronic kidney disease was 39.17% (358 patients), and patients with metabolic factors had a significantly higher prevalence of chronic kidney disease than without metabolic factors (40.90% vs. 17.65%, p < 0.01). The metabolic factors and microinflammatory biomarkers were significantly higher in patients with chronic kidney disease. Patients who had more abnormal metabolic factors also had higher levels of microinflammatory biomarkers, as well as higher risk of chronic kidney disease. Multiple logistic regression analyses revealed that systolic blood pressure, serum triglyceride, low density lipoprotein, age, and duration of diabetes were independent risk factors of chronic kidney disease in type 2 diabetes mellitus patients.


CONCLUSIONS
The abnormality of metabolic factors in type 2 diabetes mellitus had a close relationship to the microinflammatory state and chronic kidney disease. Hypertension and hyperlipidemia were independent factors of chronic kidney disease in type 2 diabetes mellitus.
Cao
Changchun
C
Department of Nephrology, Nanjing First Hospital Affiliated to Nanjing Medical University, Nanjing, China. caochangchun@medmail.com.cn
Wan
Xin
X
Chen
Yu
Y
Wu
Wenfang
W
D000368:Aged; D001786:Blood Glucose / Q000032:analysis; D002097:C-Reactive Protein / Q000378:metabolism; D016009:Chi-Square Distribution; D015331:Cohort Studies; D015897:Comorbidity; D003924:Diabetes Mellitus, Type 2 / Q000175:diagnosis / Q000453:epidemiology*; D003928:Diabetic Nephropathies / Q000175:diagnosis / Q000453:epidemiology*; D018450:Disease Progression; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D015994:Incidence; D018836:Inflammation Mediators / Q000378:metabolism*; D015850:Interleukin-6 / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000175:diagnosis / Q000453:epidemiology*; D007677:Kidney Function Tests; D008074:Lipoproteins / Q000097:blood; D016015:Logistic Models; D008297:Male; D024821:Metabolic Syndrome / Q000175:diagnosis / Q000453:epidemiology*; D008875:Middle Aged; D015999:Multivariate Analysis; D011336:Probability; D012189:Retrospective Studies; D018570:Risk Assessment; D012720:Severity of Illness Index; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D001786:Blood Glucose; D018836:Inflammation Mediators; D015850:Interleukin-6; D008074:Lipoproteins; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein