The Cl(-)/anion exchanger pendrin (SLC26A4) is expressed on the apical side of renal non-type A intercalated cells. The abundance of pendrin is reduced during metabolic acidosis induced by oral NH(4)Cl loading. More recently, it has been shown that pendrin expression is increased during conditions associated with decreased urinary Cl(-) excretion and decreased upon Cl(-) loading. Hence, it is unclear if pendrin regulation during NH(4)Cl-induced acidosis is primarily due the Cl(-) load or acidosis. Therefore, we treated mice to increase urinary acidification, induce metabolic acidosis, or provide an oral Cl(-) load and examined the systemic acid-base status, urinary acidification, urinary Cl(-) excretion, and pendrin abundance in the kidney. NaCl or NH(4)Cl increased urinary Cl(-) excretion, whereas (NH(4))(2)SO(4), Na(2)SO(4), and acetazolamide treatments decreased urinary Cl(-) excretion. NH(4)Cl, (NH(4))(2)SO(4), and acetazolamide caused metabolic acidosis and stimulated urinary net acid excretion. Pendrin expression was reduced under NaCl, NH(4)Cl, and (NH(4))(2)SO(4) loading and increased with the other treatments. (NH(4))(2)SO(4) and acetazolamide treatments reduced the relative number of pendrin-expressing cells in the collecting duct. In a second series, animals were kept for 1 and 2 wk on a low-protein (20%) diet or a high-protein (50%) diet. The high-protein diet slightly increased urinary Cl(-) excretion and strongly stimulated net acid excretion but did not alter pendrin expression. Thus, pendrin expression is primarily correlated with urinary Cl(-) excretion but not blood Cl(-). However, metabolic acidosis caused by acetazolamide or (NH(4))(2)SO(4) loading prevented the increase or even reduced pendrin expression despite low urinary Cl(-) excretion, suggesting an independent regulation by acid-base status.

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Bariatric surgery represents the elective treatment of severe obesity (BMI≥40Kg/m2) since it results in better control of cardiovascular risk factors and comorbidities typically associated with obesity, like diabetes, hypertension and dyslipidemia. Obesity is a recognized independent risk factor for chronic kidney disease and for progression of renal insufficiency. Pathomechanisms are still incompletely known. Obesity is associated with hyper-filtration, microalbuminuria and proteinuria all of which favor renal disease and its progression. This narrative review reports on the available evidence linking bariatric surgery and renal function since this surgery may affect proteinuria, hyper-filtration and glomerular filtration rate. Although available data are limited in particular in cases with more advanced stages of renal failure, bariatric surgery associates with improved filtration and lower proteinuria in patients with mild to moderate renal insufficiency. In patients with more advanced stages of renal failure, surgery should be considered if obesity represents a relative contraindication to transplantation. Surgery seems to improve graft survival. Further, nephrologists should be informed on the metabolic and nutritional changes associated with bariatric surgery, which could be responsible for untoward effects requiring early identification and treatment. Bariatric surgery could be a valid therapeutic option in renal patients to improve the negative clinical outcomes of obese subjects.