Albuminuria in Patients with Morbid Obesity and the Effect of Weight Loss Following Bariatric Surgery.


Journal

Obesity surgery
ISSN: 1708-0428
Titre abrégé: Obes Surg
Pays: United States
ID NLM: 9106714

Informations de publication

Date de publication:
11 2019
Historique:
pubmed: 27 6 2019
medline: 25 6 2020
entrez: 27 6 2019
Statut: ppublish

Résumé

Patients with morbid obesity are at an increased risk for cardiovascular and renal complications, which are not only linked to traditional cardiovascular risk factors. Thus, we evaluated (a) the prevalence of albuminuria in non-diabetic and diabetic morbidly obese patients and (b) the effect of weight loss following bariatric surgery. We included 1307 patients (77% women, mean age 40 ± 12 years, BMI 45.6 ± 6.6 kg/m In the cross-sectional study, the prevalence of microalbuminuria was 16.0% (n = 209), of macroalbuminuria 3.1% (n = 41). The chi-square for the association of albuminuria and diabetes was 31.937 (p < 0.001). Of all patients with albuminuria, 42.0% exhibited normal glucose tolerance. In a multivariate regression analysis, systolic blood pressure (beta = 0.236; p < 0.001), log fasting insulin (beta = 0.309; p < 0.001) and log 2-h postprandial insulin (beta = - 0.173; p = 0.033) were predictive risk factors for albuminuria. Longitudinally, albumin excretion decreased significantly from 11.1 (6.4, 18.4 mg/24 h) to 7.8 mg/24 h (4.9, 13.0 mg/24 h; p < 0.001). In the group with albuminuria preoperatively, albumin excretion decreased from 65.7 (38.2, 147.1 mg/24 h) to 13.5 mg/24 h (8.4, 36.8 mg/24 h; p < 0.001). After adjusting for age, sex and baseline albuminuria, patients with lower creatinine clearance showed a smaller decrease of albuminuria (beta = 0.117; p = 0.021). A substantial portion of patients with morbid obesity exhibits microalbuminuria, nearly half of those present with normal glucose tolerance. After weight loss, we found a significant decrease of albuminuria, potentially indicating or even contributing to the known reduction of cardiovascular mortality after bariatric surgery.

Sections du résumé

BACKGROUND AND OBJECTIVES
Patients with morbid obesity are at an increased risk for cardiovascular and renal complications, which are not only linked to traditional cardiovascular risk factors. Thus, we evaluated (a) the prevalence of albuminuria in non-diabetic and diabetic morbidly obese patients and (b) the effect of weight loss following bariatric surgery.
MATERIAL AND METHODS
We included 1307 patients (77% women, mean age 40 ± 12 years, BMI 45.6 ± 6.6 kg/m
RESULTS
In the cross-sectional study, the prevalence of microalbuminuria was 16.0% (n = 209), of macroalbuminuria 3.1% (n = 41). The chi-square for the association of albuminuria and diabetes was 31.937 (p < 0.001). Of all patients with albuminuria, 42.0% exhibited normal glucose tolerance. In a multivariate regression analysis, systolic blood pressure (beta = 0.236; p < 0.001), log fasting insulin (beta = 0.309; p < 0.001) and log 2-h postprandial insulin (beta = - 0.173; p = 0.033) were predictive risk factors for albuminuria. Longitudinally, albumin excretion decreased significantly from 11.1 (6.4, 18.4 mg/24 h) to 7.8 mg/24 h (4.9, 13.0 mg/24 h; p < 0.001). In the group with albuminuria preoperatively, albumin excretion decreased from 65.7 (38.2, 147.1 mg/24 h) to 13.5 mg/24 h (8.4, 36.8 mg/24 h; p < 0.001). After adjusting for age, sex and baseline albuminuria, patients with lower creatinine clearance showed a smaller decrease of albuminuria (beta = 0.117; p = 0.021).
CONCLUSION
A substantial portion of patients with morbid obesity exhibits microalbuminuria, nearly half of those present with normal glucose tolerance. After weight loss, we found a significant decrease of albuminuria, potentially indicating or even contributing to the known reduction of cardiovascular mortality after bariatric surgery.

Identifiants

pubmed: 31240536
doi: 10.1007/s11695-019-04036-7
pii: 10.1007/s11695-019-04036-7
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

3581-3588

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Auteurs

Johanna Maria Brix (JM)

Department of Medicine I, Rudolfstiftung Hospital, Juchgasse 25, 1030, Vienna, Austria.
Karl Landsteiner Institute for Obesity and Metabolic Disorders, Vienna, Austria.

Carsten Thilo Herz (CT)

Department of Medicine III, Division of Endocrinology, Medical University of Vienna, Vienna, Austria.

Hans Peter Kopp (HP)

Department of Medicine I, Rudolfstiftung Hospital, Juchgasse 25, 1030, Vienna, Austria.
Karl Landsteiner Institute for Obesity and Metabolic Disorders, Vienna, Austria.

Astrid Feder (A)

Department of Medicine I, Rudolfstiftung Hospital, Juchgasse 25, 1030, Vienna, Austria.
Karl Landsteiner Institute for Obesity and Metabolic Disorders, Vienna, Austria.

Eva-Christina Krzizek (EC)

Department of Medicine I, Rudolfstiftung Hospital, Juchgasse 25, 1030, Vienna, Austria.
Karl Landsteiner Institute for Obesity and Metabolic Disorders, Vienna, Austria.

Christoph Sperker (C)

Department of Surgery, Rudolfstiftung Hospital, Vienna, Austria.

Gerit-Holger Schernthaner (GH)

Department of Medicine II, Division of Angiology, Medical University of Vienna, Vienna, Austria.

Guntram Schernthaner (G)

Department of Medicine I, Rudolfstiftung Hospital, Juchgasse 25, 1030, Vienna, Austria.

Bernhard Ludvik (B)

Department of Medicine I, Rudolfstiftung Hospital, Juchgasse 25, 1030, Vienna, Austria. bernhard.ludvik@wienkav.at.
Karl Landsteiner Institute for Obesity and Metabolic Disorders, Vienna, Austria. bernhard.ludvik@wienkav.at.

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