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Hypertriglyceridemia accompanied by increased serum complement component 3 and proteinuria in non-nephrotic chronic
Kentaro Kohagura1, Masako Kochi, Tsuyoshi Miyagi
1Department of Cardiovascular Medicine, Nephrology and Neurology, University of the Ryukyus School of Medicine, 207 Uehara, Nishihara-cho, Okinawa, 903-0215, Japan, kohagura@med.u-ryukyu.ac.jp.
Insights
High triglycerides (hTG) combined with high complement component 3 (hC3) levels are linked to increased proteinuria in chronic kidney disease (CKD). Arteriolopathy may play a role in this association, warranting further investigation.
Area of Science:
- Nephrology
- Endocrinology
- Immunology
Background:
- Hypertriglyceridemia (hTG) is a known risk factor for chronic kidney disease (CKD) progression.
- The role of adipocytokine complement component 3 (C3) in the hTG-CKD association is unclear.
Purpose of the Study:
- To investigate the association between hypertriglyceridemia (hTG) and proteinuria in non-nephrotic chronic kidney disease (CKD).
- To determine if elevated complement component 3 (C3) levels modify this association.
Main Methods:
- Cross-sectional study of 138 non-nephrotic CKD patients with renal biopsy.
- Assessed proteinuria, hTG, and high C3 levels (hC3, ≥ median).
- Analyzed associations using logistic regression, adjusting for confounders and arteriolopathy.
Main Results:
- Patients with hTG showed significantly higher urine protein levels.
- High C3 (hC3+) alone was associated with increased proteinuria (OR 2.98).
- The combination of hTG and hC3 (hTG+/hC3+) was strongly associated with proteinuria (adjusted OR 5.32), an association reduced by arteriolopathy.
Conclusions:
- Hypertriglyceridemia (hTG) in the presence of high complement component 3 (hC3) is associated with proteinuria in non-nephrotic CKD.
- Renal arteriolopathy may mediate this association.
- Prospective studies are needed to confirm the predictive value for CKD progression.
Background:
Hypertriglyceridemia (hTG) is a risk factor for progression of chronic kidney disease (CKD); however, it remains unknown whether the adipocytokine complement component 3 (C3) is involved in the association between hTG and CKD.
Methods:
The study included 138 patients (54 % male) with non-nephrotic (serum albumin ≥3 g/dl) CKD who had undergone a renal biopsy and did not have hypocomplementemic disease. Renal arteriolopathy was assessed semi-quantitatively. We examined the cross-sectional associations between proteinuria and hTG with or without a higher serum C3 level (hC3), defined as equal or above the median value.
Results:
The mean (SD) age of the patients was 42 (±17) years and urine protein was 1.2 (±1.2) g/gCr. Patients with hTG had a significantly higher urine protein than those without hTG. Subgroup analysis showed that the hTG+/hC3+ group had higher grade arteriolopathy and urine protein levels. Multiple logistic regression analysis adjusted for age, sex, and diabetes mellitus showed that hC3+ alone was associated significantly with higher levels of urine protein [odds ratio (OR), 2.98; 95 % confidence interval (CI) 1.19-7.46, p = 0.02]; however, hTG alone showed no such association. hTG+/hC3+ was a significant factor when hTG-/hC3- was used as the reference (adjusted OR 5.32; 95 % CI 1.40-20.17, p = 0.01), with this OR being decreased by adjustment for arteriolopathy.
Conclusions:
hTG accompanied by hC3 was associated with proteinuria in non-nephrotic CKD. Arteriolopathy may influence this association. A prospective study is needed to determine the predictive value of this association in CKD progression.
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