scholarly journals Association between pre hemodialysis serum sodium concentration and blood pressure: results from a retrospective analysis from the international monitoring dialysis outcomes (MONDO) initiative

2015 ◽  
Vol 30 (7) ◽  
pp. 442-448 ◽  
Author(s):  
J G Raimann ◽  
◽  
B Canaud ◽  
M Etter ◽  
J P Kooman ◽  
...  
2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Natasha Eftimovska-Otovikj ◽  
Natasha Petkovikj ◽  
Elizabeta Poposka ◽  
Olivera Stojceva-Taneva

Abstract Background and Aims The dialysate sodium prescription remain unclear as an important component of sodium balance in HD patients Pre-hemodialysis (pre-HD) serum sodium levels can vary among different patients, therefore, a single dialysate sodium prescription may not be appropriate for all patients. Dialysate sodium is one of the most easy changeable parameter which can influence hemodynamic stability. The aim of the study was to investigate whether dialysis patients will have some beneficial effects of prescription of different models of dialysate sodium Method 77 nondiabetic subjects (41 men; 36 women) performed 12 months hemodialysis (HD) sessions with dialysate sodium concentration set up at 138 mmol/L, followed by additional 3 models of dialysate sodium (each model performed 2 months sessions with 2 months standard dialysate sodium between each model) wherein dialysate sodium was set up: model 1: according to pre-HD serum sodium concentration, model 2: according to sodium concentration in UF fluid, model 3: sodium profiling ( from 144 to 136 mmol/L). Blood pressure (BP), interdialytic weight gain (IDWG), thirst score, sodium gradient were analysed. After the standard dialysate sodium hemodialyses, the subjects were divided into 3 groups: normotensive (N=58), hypertensive (N= 14) and hypotensive (N=5) based on the average pre-HD systolic BP during the standard dialysate sodium hemodialyses. Results Model 1: resulted in significantly lower blood pressure (133,61±11.88 versus 153.60±14.26 mmHg; p=0.000) and IDWG (2.21±0.93 versus 1.87±0.92 kg; p=0.018) in hypertensive patients, whereas normotensive patients showed only significant decrease in IDWG (2.21±0.72 versus 2.06±0.65, p=0,004). Hypertensive patients had significant highest sodium gradient compared to other patients (p<0.05), followed by significant increase of 0,6% IDWG confirmed with univariate regression analysis. Thirst score was significantly lower in all patients with individualized-sodium HD and the use of antihypertensive drugs significantly reduced in hypertensive patients during the individualized phase. Model 2: resulted in significantly lower BP in normotensive and hypertensive patients (126.92±9.71 versus 124.08±8.71 mmHg; p=0.000; 153.60±14.26 versus 138.91±8.48 mmHg, accordingly), with no influence on IDWG, thirst score compared to standard dialysate sodium. Model 3: significantly higher BP and IDWG in all 3 groups (normotensive 126.92±9.71 versus 130.20±9.5 mmHg; p=0.001; IDWG 2.21±0.72 versus 2.34±0.82 kg, p=0,005; hypertensive 153.60±14.26 versus 157.58±5.0 mmHg; IDWG 2.21±0.93 versus 2.39±0.74 kg; p=0.005; hipotensive 79.81±11.78 versus 91.09±24.98 mmHg, IDWG 2.53±0.57 versus 2.73±0.15 kg, p=0.005) and significantly higher thirst score in normotensive and hypotensive patients, with no influence in hypertensive patients. Conclusion A reduction of the dialysate sodium concentration based on the pre HD serum sodium level of the patient, reduced the BP, IDWG, thirst score and use of antihypertensive drug compare to dialysate sodium according to sodium concentration in UF or sodium profiling. We recommend prescription of dialysate sodium according to pre HD serum sodium concentration.


2010 ◽  
Vol 30 (8) ◽  
pp. 1137-1142 ◽  
Author(s):  
Mónica Guevara ◽  
María E. Baccaro ◽  
Jose Ríos ◽  
Marta Martín-Llahí ◽  
Juan Uriz ◽  
...  

2010 ◽  
Vol 42 (9) ◽  
pp. 1669-1674 ◽  
Author(s):  
MATTHEW D. PAHNKE ◽  
JOEL D. TRINITY ◽  
JEFFREY J. ZACHWIEJA ◽  
JOHN R. STOFAN ◽  
W. DOUGLAS HILLER ◽  
...  

2017 ◽  
Author(s):  
Richard H Sterns ◽  
Stephen M. Silver ◽  
John K. Hix ◽  
Jonathan W. Bress

Guided by the hypothalamic antidiuretic hormone vasopressin, the kidney’s ability to conserve electrolyte–free water when it is needed and to excrete large volumes of water when there is too much of it normally prevents the serum sodium concentration from straying outside its normal range. The serum sodium concentration determines plasma tonicity and affects cell volume: a low concentration makes cells swell, and a high concentration makes them shrink. An extremely large water intake, impaired water excretion, or both can cause hyponatremia. A combination of too little water intake with too much salt, impaired water conservation, or excess extrarenal water losses will result in hypernatremia. Because sodium does not readily cross the blood-brain barrier, an abnormal serum sodium concentration alters brain water content and composition and can cause serious neurologic complications. Because bone is a reservoir for much of the body’s sodium, prolonged hyponatremia can also result in severe osteoporosis and fractures. An understanding of the physiologic mechanisms that control water balance will help the clinician determine the cause of impaired water conservation or excretion; it will also guide appropriate therapy that can avoid the life-threatening consequences of hyponatremia and hypernatremia.


1980 ◽  
Vol 8 (3) ◽  
pp. 349-352 ◽  
Author(s):  
Luen Bik To ◽  
P. J. Phillips

Eighteen patients with hyperosmolar non-ketotic diabetic coma were studied retrospectively to identify factors affecting prognosis and to review treatment. This condition affected older women two-thirds of whom were unrecognised diabetics. Eight (44%) died. Mortality correlated with age above 60, uraemia and hyperosmolarity, but not with the degree or rate of fall of hyperglycaemia. Hyperglycaemia responded to rehydration and insulin, but in all patients serum osmolarity remained high for several days. In 14 patients (78%) the serum sodium concentration initially increased and in four (22 %) serum osmolarity increased. This persistence or worsening of the hyperosmolar state can be avoided without the risk of cerebal oedema by replacing the fluid and electrolyte deficits over 48 hours and using 5% dextrose for the water deficit.


2013 ◽  
Vol 98 (4) ◽  
pp. 289-291
Author(s):  
Ryota Iwase ◽  
Hiroaki Shiba ◽  
Takeshi Gocho ◽  
Yasuro Futagawa ◽  
Shigeki Wakiyama ◽  
...  

Abstract A 68-year-old man underwent pancreaticoduodenectomy with lymph nodes dissection for carcinoma of the ampulla of Vater. The patient had anxiety neurosis and had been treated with a selective serotonin reuptake inhibitor (SSRI). Postoperatively, SSRI was resumed on postoperative day 2. His serum sodium concentration gradually decreased, and the patient was given a sodium supplement. However, 11 days after the operation, laboratory findings included serum sodium concentration of 117 mEq/L, serum vasopressin of 2.0 pg/mL, plasma osmolality of 238 mOsm/kg, urine osmolality of 645 mOsm/kg, urine sodium concentration of 66 mEq/L, serum creatinine concentration of 0.54 mg/dL, and serum cortisol concentration of 29.1 μg/dL. With a diagnosis of syndrome of inappropriate secretion of antidiuretic hormone (SIADH), the antianxiety neurosis medication was changed from the SSRI to another type of drug. After switching the medication, the patient made a satisfactory recovery with normalization of serum sodium by postoperative day 20.


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