Abstract: SA-OR031
The Renal Na-Cl and Na-K-2Cl Cotransporters Are Increased in Urinary Exosomes of Patients with Severe Preeclampsia
Session Information
- Fluids and Electrolytes: Clinical, Translational, and Acid-Base
October 27, 2018 | Location: 23A, San Diego Convention Center
Abstract Time: 04:30 PM - 04:42 PM
Category: Fluid and Electrolytes
- 902 Fluid and Electrolytes: Clinical
Authors
- Medina, Elba O., Hospital General de México Dr. Eduardo Liceaga, México, Mexico
- Perez-Navarro, L. Monserrat, Hospital General de México Dr. Eduardo Liceaga, México, Mexico
- Briones, Jesús C., Hospital General de México Dr. Eduardo Liceaga, México, Mexico
- Hurtado, Ivonne, INCMNSZ, Mexico, Mexico
- Gallardo, Fabiola, INCMNSZ, Mexico, Mexico
- Valdez-Ortiz, Rafael, Hospital General de México Dr. Eduardo Liceaga, México, Mexico
- Rojas, Lorena Leonor, INCMNSZ, Mexico, Mexico
- Gamba, Gerardo, INCMNSZ, Mexico, Mexico
Background
Arterial hypertension (AH) in preeclampsia (PE) is in part due to increased sodium reabsorption in the kidney. One of the major pathways for salt reabsorption is the Na-Cl cotransporter (NCC), whose expression and activity is modulated by female hormones (AJP Renal, 2015). Here we assessed the presence of NCC and NKCC2 in urinary exosomes of women with PE as compared with women with healthy pregnant (HP).
Methods
We included ten women diagnosed with severe PE (ACOG 2013; SBP ≥160mmHg or DBP ≥ 110mmHg, protein/creatinine ratio > than 0.3mg/dl), which were matched with a HP patients by age and gestation weeks. The urine sample was taken at the time of detection of arterial hypertension with criteria of severity. Urinary exosomes were used for Western Blot analysis for total and phosphorylated NCC, NKCC2 and the kinase SPAK. Serum and urinary electrolytes were measured.
Results
Mean age (years), gestation (weeks) and mean blood pressure (mmHg) were 28 ± 4.6, 36 ± 3.7 and 123 ± 11 for PE group and 25 ± 6.7, 37 ± 3.9 and 83 ± 8.5 in HP, respectively. A remarkable increase in the expression of NCC was found in PE group vs HP, 3.0 ± 0.77 vs 1.0 ± 0.7321 (p<0.01, Fig 1). There was no difference in the expression of NKCC2, but a significant increase in the phosphorylated form was observed in PE group (2.56 ± 1.11 vs 1.00 ± 0.15, p=0.015, Fig. 1) . Additionally, increase in the expression and activation of SPAK/OSR1 were observed in the PE group. Serum K+ was similar between PE and HP groups (p=NS).
Conclusion
Our data revealed increased expression/activation of NCC and NKCC2 in PE, suggesting the participation of these cotransporters in the development of AH. The increased phosphorylation of SPAK/OSR1 suggests that these kinases are responsible for NCC and NKCC2 activation.
Figure 1. Total and phosphorylated NCC and NKCC2 in five PE and HP patients
Funding
- Government Support - Non-U.S.