NDLI: Relationship of urinary endothelin-1 with estimated glomerular filtration rate in autosomal dominant polycystic kidney disease: a pilot cross-sectional analysis

Content Provider	Springer Nature : BioMed Central
Author	Raina, Rupesh Lou, Linda Berger, Bruce Vogt, Beth Do, Angelique Sao-Mai Cunningham, Robert Vasavada, Pauravi Herrmann, Karin Dell, Katherine Simonson, Michael
Abstract	Background The pathogenesis of progressive renal insufficiency in autosomal dominant polycystic kidney disease (ADPKD) is unclear. Evidence from experimental models of ADPKD suggests that elevated endothelin-1 (ET-1) drives cyst growth, renal fibrosis and loss of renal function, but whether ET-1 is elevated in humans with ADPKD is uncertain. Methods In a cross-sectional study of ADPKD we measured urinary ET-1, a surrogate for ET-1 in kidney cortex, in spot collections corrected for creatinine. The volume of each kidney was measured using MRI-based stereology. The relationship of urine ET-1 with MDRD eGFR and kidney volume was modeled by multiple linear regression with adjustment for clinical covariates. Results Patients with ADPKD were ages 18 to 53 with eGFRs (median, interquartile range) of 63.2 (43.5–80.2) ml/min/1.73 m2 and albumin/creatinine ratios (ACR) of 115.0 (7.5–58.5) μg/mg. Urine ET-1 was inversely associated with eGFR (r = −0.480, P < 0.05) and positively (r = 0.407, P = 0.066) with ACR independent of age and female sex (P < 0.01). ET-1 appeared to be positively associated with total kidney volume (r = 0.426, P = 0.100), with a test for trend across urine ET-1 quartiles yielding z = 1.83, P = 0.068. ET-1 strongly correlated with NAGase (r = 0. 687, P = 0.001), a marker of tubular damage and a surrogate marker of renal disease progression in ADPKD. Of note, ET-1 levels in urine were not correlated with hypertension. Conclusions In a translational study of patients with ADPKD, urinary ET-1 was inversely associated with eGFR and positively correlated with total kidney volume. Taken together with results from experimental models, these findings suggest that the role of ET-1 in ADPKD warrants further investigation.
Related Links	https://bmcnephrol.biomedcentral.com/counter/pdf/10.1186/s12882-016-0232-8.pdf
Ending Page	6
Page Count	6
Starting Page	1
File Format	HTM / HTML
ISSN	14712369
DOI	10.1186/s12882-016-0232-8
Journal	BMC Nephrology
Issue Number	1
Volume Number	17
Language	English
Publisher	BioMed Central
Publisher Date	2016-02-29
Access Restriction	Open
Subject Keyword	Nephrology Internal Medicine Autosomal dominant polycystic kidney disease Endothelin-1 Cyst growth Hypertension Kidney volume
Content Type	Text
Resource Type	Article
Subject	Nephrology
Journal Impact Factor	2.2/2023
5-Year Journal Impact Factor	2.6/2023

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