Key result
The metabolically unhealthy and obese phenotype in hypertensive subjects was associated with the highest risk of microalbuminuria (OR 6.0, p<0.0001) and decreased eGFR (OR 5.4, p=0.03).
Why the study?
To explore the individual and combined effects of obesity and metabolic profile on the impairment of glomerular function among hypertensive subjects.
Does the combination of obesity and metabolic disorders increase the risk of glomerular dysfunction in hypertensive subjects?
Cross-Sectional (n=499)
Does the combination of obesity and metabolic disorders increase the risk of glomerular dysfunction in hypertensive subjects?
The co-occurrence of obesity and metabolic disorders synergistically exacerbates the decline of glomerular function in hypertensive patients.
Answers are grounded in this paper and cite their sources.
Metabolic phenotypes may relate to glomerular impairment in hypertension; leaves open independent roles of obesity and metabolic status.
AIM: The aim of this study is to explore the individual and combined effects of obesity and metabolic profile on the impairment of glomerular function among hypertensive subjects. METHODS: This is a cross-sectional study enrolling 499 hypertensive subjects. Based on body mass index values and metabolic profile, they were assigned to one of four metabolic phenotype groups: MHNO: metabolically healthy non-obese, MHO: metabolically healthy but obese, MUHNO: metabolically unhealthy but non-obese, and MUHO: metabolically unhealthy and obese. The effect of the interaction between obesity and metabolic profile was tested on an additive scale, for both microalbuminuria and reduced estimated glomerular filtration rate (eGFR). RESULTS: After adjustment for confounding factors, the highest risk of both microalbuminuria and decreased eGFR was found among patients of the MUHO group (OR = 6.0 [2.13], p < 0.0001, OR = 5.4 [1.26], p = 0.03, respectively). Analysis of the additive interaction indicates that 51% and 53% of the risk of microalbuminuria and its combination with low eGFR respectively is explained by the co-occurrence of obesity and metabolic disorder. The mechanism of this interaction is synergistic (synergy index = 2.6, [1.5.3]). CONCLUSION: The decline of glomerular function in hypertensive subjects is significantly exacerbated by the interaction between obesity and metabolic disorders. The management of such high-risk subjects requires, in addition to the therapeutic regimen, an adequate dietary and physical program in order to preserve glomerular function.
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Bennouar et al. (2021) conducted a cross-sectional in Hypertension (n=499). Metabolically unhealthy and obese (MUHO) phenotype vs. Metabolically healthy non-obese (MHNO) phenotype was evaluated on Microalbuminuria (OR 6.0, p=<0.0001). The metabolically unhealthy and obese phenotype in hypertensive subjects was associated with the highest risk of microalbuminuria (OR 6.0, p<0.0001) and decreased eGFR (OR 5.4, p=0.03).
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