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Type 2 diabetic patients with treatment‐resistant hypertension display urine plasmin excretion that correlate with blood pressure and activate ENaC current
Author(s) -
Friis Ulla Glenert,
Buhl Kristian Bergholt,
Oxlund Christina Stolzenburg,
Svenningsen Per,
Bistrup Claus,
Abildgaard Ib,
Jensen Boye L
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.905.3
Subject(s) - plasmin , urine , proteinuria , medicine , endocrinology , blood pressure , diabetes mellitus , excretion , type 2 diabetes , creatinine , urinary system , chemistry , biochemistry , kidney , enzyme
Background It was hypothesized that urine samples from patients with proteinuria (see below) would be able to activate EnaC through plasmin. Materials A cross sectional study design was applied to type 2 diabetic patients diagnosed with treatment resistant hypertension (RHTN). Urine samples were analyzed for albumin, creatinine, plasmin(ogen) and ability to activate inward currents in single collecting duct cells. Results Albuminuric T2DM patients with RHTN displayed significantly elevated levels of urinary plasmin(ogen) (844 ± 297 plg/crea, n=5) compared to normoalbuminuric‐T2DM‐RHTN patients (1.24 ± 0.9 plg/crea, n=5, P=0.011). The CCD cell line M1 showed significantly increased inward current when superfused with urine from albuminuric T2DM‐RHTN (58.8% ± 14%, n=5) compared to normoalbuminuric T2DM‐RHTN (16.2% ± 5.8%, n=5, P=0.0121). Conclusion A significant proportion of patients with type‐2 diabetes and treatment‐resistant hypertension excrete plasminogen proportional to albumin in urine which confers the ability of urine samples to evoke ENaC currents in vitro. The findings are in agreement with the notion that plasmin in the pre‐urine potentially aggravates hypertension trough inappropriate ENaC stimulation in type 2 diabetic treatment‐resistant hypertensive patients.