This was a retrospective observational cohort study of 458 patients with primary IgA nephropathy. The exposure was dyslipidemia, defined as total cholesterol ≥5.2 mmol/L, triglycerides ≥1.7 mmol/L, or LDL-C ≥3.4 mmol/L, compared to patients without dyslipidemia. The primary outcome was renal survival.
Over a mean follow-up of 54.7 months, dyslipidemia was associated with poorer renal survival. In model 1, the hazard ratio was 2.206 (95% CI 1.127–4.317, p=0.021). In model 2, the HR was 2.085 (95% CI 1.059–4.106, p=0.034). Abnormalities in total cholesterol (p=0.016) and triglycerides (p=0.001) were also associated with poorer renal survival. Dyslipidemia was significantly associated with T1–2 tubular atrophy/interstitial fibrosis and arterial intimal fibrosis.
Safety and tolerability data were not reported. Key limitations include the retrospective design and the cohort nature, which may imply a single-center study. The study does not report whether lipid-lowering therapies improved renal survival. The association is reported, not causation, and is based on observational cohort data.
The practice relevance is that dyslipidemia indicates adverse renal outcomes and serves as an independent prognostic predictor in IgA nephropathy. However, clinicians should not overstate these findings, as dyslipidemia is an independent predictor but not necessarily causal.
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Dyslipidemia is common in chronic kidney disease (CKD), including immunoglobulin A (IgA) nephropathy (IgAN), and may be associated with renal prognosis; however, the value of dyslipidemia in IgAN remains insufficiently assessed. The objective of our study was to investigate clinicopathological characteristics and renal outcomes in IgAN patients with dyslipidemia and to evaluate the prognostic value of lipid abnormalities.
This cohort study included 458 primary IgAN patients for a retrospective analysis. The clinicopathological features and renal outcomes were recorded. In univariate and multivariate models, the associations between dyslipidemia and renal outcomes, as well as dyslipidemia-associated pathological features, were analyzed.
Patients with dyslipidemia—defined as a total cholesterol of ≥5.2 mmol/L, triglycerides of ≥1.7 mmol/L, or low-density lipoprotein cholesterol [LDL-C] of ≥3.4 mmol/L—exhibited elevated complement levels and worse clinical characteristics with regard to blood pressure, proteinuria, kidney function, and glomerulosclerosis; tubular atrophy/interstitial fibrosis (T1–2), crescents, and vascular lesions were more common. A multivariate logistic regression revealed that T1–2 and arterial intimal fibrosis were significantly associated with dyslipidemia. After a mean follow-up of 54.7 months, dyslipidemia (p = 0.001), especially abnormalities in total cholesterol (p = 0.016) and triglycerides (p = 0.001), was significantly associated with poorer renal survival, and renal survival was not improved after lipid-lowering therapies. In addition to estimated glomerular filtration rate (eGFR) and arterial intimal fibrosis, dyslipidemia is an independent predictor for renal survival in multivariate Cox analyses (model 1: HR, 2.206; 95% CI, 1.127–4.317; p = 0.021; model 2: HR, 2.085; 95% CI, 1.059–4.106; p = 0.034).
IgAN patients with dyslipidemia exhibited more severe clinicopathological features. Tubular atrophy/interstitial fibrosis and arteriosclerosis/arteriolosclerosis were closely associated with dyslipidemia. Dyslipidemia not only indicates adverse renal outcomes but also serves as an independent prognostic predictor.