scholarly journals Are Sodium Transporters in Urinary Exosomes Reliable Markers of Tubular Sodium Reabsorption in Hypertensive Patients?

2010 ◽  
Vol 114 (3) ◽  
pp. p25-p34 ◽  
Author(s):  
Cristina Esteva-Font ◽  
Xiaoyan Wang ◽  
Elisabet Ars ◽  
Elena Guillén-Gómez ◽  
Laia Sans ◽  
...  
Keyword(s):  
Sodium Reabsorption ◽  
Hypertensive Patients ◽  
Sodium Transporters ◽  
Tubular Sodium Reabsorption ◽  
Urinary Exosomes

Increased Proximal Tubular Sodium Reabsorption in Hypertensive Patients with Type 2 Diabetes

1989 ◽  
Vol 6 (7) ◽  
pp. 614-620 ◽  
Author(s):  
J.-C. Mbanya ◽  
T. H. Thomas ◽  
R. Taylor ◽  
K. G. M. M. Alberti ◽  
R. Wilkinson
Keyword(s):  
Type 2 Diabetes ◽  
Sodium Reabsorption ◽  
Hypertensive Patients ◽  
Tubular Sodium Reabsorption ◽  
Proximal Tubular

scholarly journals Increased phosphorylation of the renal Na+-Cl−cotransporter in male kidney transplant recipient patients with hypertension: a prospective cohort

2015 ◽  
Vol 309 (10) ◽  
pp. F836-F842 ◽  
Author(s):  
Lorena Rojas-Vega ◽  
Aldo R. Jiménez-Vega ◽  
Silvana Bazúa-Valenti ◽  
Isidora Arroyo-Garza ◽  
José Victor Jiménez ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Kidney Transplant ◽  
Prospective Cohort ◽  
Blood Pressure Monitoring ◽  
Kidney Transplant Recipient ◽  
Blood Levels ◽  
Kidney Transplant Recipients ◽  
Hypertensive Patients ◽  
Urinary Exosomes ◽  
Trough Blood

Evidence in rodents suggests that tacrolimus-induced posttransplant hypertension is due to upregulation of the thiazide-sensitive Na+-Cl−cotransporter NCC. Here, we analyzed whether a similar mechanism is involved in posttransplant hypertension in humans. From January 2013 to June 2014, all adult kidney transplant recipients receiving a kidney allograft were enrolled in a prospective cohort study. All patients received tacrolimus as part of the immunosuppressive therapy. Six months after surgery, we assessed general clinical and laboratory variables, tacrolimus trough blood levels, and ambulatory 24-h blood pressure monitoring. Urinary exosomes were extracted to perform Western blot analysis using total and phospho-NCC antibodies. A total of 52 patients, including 17 women and 35 men, were followed. At 6 mo after transplantation, of the 35 men, 17 developed hypertension and 18 remained normotensive, while high blood pressure was observed in only 3 of 17 women. The hypertensive patients were significantly older than the normotensive group; however, there were no significant differences in body weight, history of acute rejection, renal function, and tacrolimus trough levels. In urinary exosomes, hypertensive patients showed higher NCC expression (1.7 ± 0.19) than normotensive (1 ± 0.13) ( P = 0.0096). Also, NCC phosphorylation levels were significantly higher in the hypertensive patients (1.57 ± 0.16 vs. 1 ± 0.07; P = 0.0049). Our data show that there is a positive correlation between NCC expression/phosphorylation in urinary exosomes and the development of hypertension in posttransplant male patients treated with tacrolimus. Our results are consistent with the hypothesis that NCC activation plays a major role in tacrolimus-induced hypertension.

Mechanism of increased renal tubular sodium reabsorption in cirrhosis

1972 ◽  
Vol 52 (2) ◽  
pp. 198-202 ◽  
Author(s):  
C. Chaimovitz ◽  
P. Szylman ◽  
G. Alroy ◽  
O.S. Better
Keyword(s):  
Sodium Reabsorption ◽  
Tubular Sodium Reabsorption ◽  
Renal Tubular

Local and Downstream Actions of Proximal Tubule Angiotensin II Signaling on Sodium Transporters in the Mouse Nephron

2021 ◽  
Author(s):  
Jonathan William Nelson ◽  
Alicia A. McDonough ◽  
Zhidan Xiang ◽  
Donna L. Ralph ◽  
Joshua A Robertson ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Renin Angiotensin System ◽  
Cell Types ◽  
Sodium Reabsorption ◽  
Electrolyte Balance ◽  
Sodium Transporters ◽  
Lower Abundance ◽  
Angiotensin Ii Signaling ◽  
Distinct Cell

The renal nephron consists of a series of distinct cell types which function in concert to maintain fluid and electrolyte balance and blood pressure. The renin angiotensin system (RAS) is central to sodium and volume balance. We aimed to determine how loss of angiotensin II signaling in the proximal tubule (PT), which reabsorbs the bulk of filtered sodium and volume, impacts solute transport throughout the nephron. We hypothesized that proximal tubule (PT) RAS disruption would not only depress PT sodium transporters, but also impact downstream Na+ transporters. Utilizing a mouse model in which the type 1a angiotensin receptor (AT1aR) is deleted specifically within the PT (AT1aR PTKO), we profiled the abundance of sodium transporters, channels, and claudins along the nephron. Absence of PT AT1aR signaling was associated with lower abundance of PT transporters (NHE3, NBCe2 and claudin 2) as well as lower abundance of downstream transporters (total and phosphorylated NKCC2, medullary Na,K-ATPase, phosphorylated NCC and claudin 7) versus controls. However, transport activities of NKCC2 and NCC (assessed with diuretics) were similar between groups in order to maintain electrolyte balance. Together, these results demonstrate the primary impact of angiotensin II regulation on sodium reabsorption in PT at baseline and the associated influence on downstream Na+ transporters, highlighting the ability of the nephron to integrate sodium transport along the nephron to maintain homeostasis.

Sign in / Sign up

Export Citation Format

Share Document