Effect of Acetazolamide on Obesity-Induced Glomerular Hyperfiltration: A Randomized Controlled Trial
| Autor: | Uzi Gafter, Yaacov Ori, Sarit Bar Sheshet Itach, Arie Erman, Avry Chagnac, Michal Herman-Edelstein, Boris Zingerman, Benaya Rozen-Zvi |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: |
Adult
Male medicine.medical_specialty medicine.drug_class Renal function lcsh:Medicine urologic and male genital diseases Furosemide Internal medicine medicine Humans Carbonic anhydrase inhibitor Obesity Carbonic Anhydrase Inhibitors Diuretics lcsh:Science Tubuloglomerular feedback Multidisciplinary Reabsorption business.industry urogenital system lcsh:R Middle Aged medicine.disease Acetazolamide Endocrinology medicine.anatomical_structure Macula densa Kidney Diseases lcsh:Q business Glomerular hyperfiltration Glomerular Filtration Rate Research Article medicine.drug Kidney disease |
| Zdroj: | PLoS ONE, Vol 10, Iss 9, p e0137163 (2015) PLoS ONE |
| ISSN: | 1932-6203 |
| Popis: | Aims Obesity is an important risk factor for the development of chronic kidney disease. One of the major factors involved in the pathogenesis of obesity-associated kidney disease is glomerular hyperfiltration. Increasing salt-delivery to the macula densa is expected to decrease glomerular filtration rate (GFR) by activating tubuloglomerular feedback. Acetazolamide, a carbonic anhydrase inhibitor which inhibits salt reabsorption in the proximal tubule, increases distal salt delivery. Its effects on obesity-related glomerular hyperfiltration have not previously been studied. The aim of this investigation was to evaluate whether administration of acetazolamide to obese non diabetic subjects reduces glomerular hyperfiltration. Materials and Methods The study was performed using a randomized double-blind crossover design. Obese non-diabetic men with glomerular hyperfiltration were randomized to receive intravenously either acetazolamide or furosemide at equipotent doses. Twelve subjects received the allocated medications. Two weeks later, the same subjects received the drug which they had not received during the first study. Inulin clearance, p-aminohippuric acid clearance and fractional lithium excretion were measured before and after medications administration. The primary end point was a decrease in GFR, measured as inulin clearance. Results GFR decreased by 21% following acetazolamide and did not decrease following furosemide. Renal vascular resistance increased by 12% following acetazolamide, while it remained unchanged following furosemide administration. Natriuresis increased similarly following acetazolamide and furosemide administration. Sodium balance was similar in both groups. Conclusions Intravenous acetazolamide decreased GFR in obese non-diabetic men with glomerular hyperfiltration. Furosemide, administered at equipotent dose, did not affect GFR, suggesting that acetazolamide reduced glomerular hyperfiltration by activating tubuloglomerular feedback. Trial Registration ClinicalTrials.gov NCT01146288 |
| Databáze: | OpenAIRE |
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