scholarly journals Association of serum sodium concentration with coronary atherosclerosis in China: follow-up study

2009 ◽  
Vol 30 (4) ◽  
pp. 494-500
Author(s):  
En-zhi Jia ◽  
Zhen-xia Xu ◽  
Zhi-jian Yang ◽  
Tie-bing Zhu ◽  
Lian-sheng Wang ◽  
...  
Keyword(s):  
Serum Sodium ◽  
Coronary Atherosclerosis ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Follow Up Study

Serum Disaccharides and Osmolality in Ccpd Patients Using Icodextrin Or Glucose as Daytime Dwell

1997 ◽  
Vol 17 (6) ◽  
pp. 602-607 ◽  
Author(s):  
Nynke Pasthuma ◽  
Pieter M. Ter Wee ◽  
Ab J.M. Danker ◽  
Po L. Oe ◽  
Wim Van Dorp ◽  
...  
Keyword(s):  
Peritoneal Dialysis ◽  
Serum Sodium ◽  
Sodium Concentration ◽  
Average Concentration ◽  
Serum Sodium Concentration ◽  
Dialysis Fluid ◽  
Total Carbohydrate ◽  
Initial Decrease ◽  
Osmolal Gap

Objective To evaluate the safety, efficacy, and biocompatibility of icodextrin and glucose-containing dialysis fluid during continuous cycling peritoneal dialysis (CCPD), patients were treated for 2 years with either icodextrin or glucose-containing dialysis fluid for their daytime dwell (14 -15 hours). Prior to entry into the study, all patients used a standard glucose solution (Dianeal 1.36%,2.27%, or 3.86%, Baxter, Utrecht, The Netherlands). Design Open, randomized, prospective, two-center study. Setting University hospital and teaching hospital. Patients Both established and patients new to CCPD were included. A life expectancy of more than 2 years, a stable clinical condition, and written informed consent were necessary before entry. Patients aged under 18, those with peritonitis in the previous month, and women of childbearing potential, unless taking adequate contraceptive precautions, were excluded. Thirty-eight patients entered the study, and 25 (13 glucose, 12 icodextrin) had a follow-up period of 12 months or longer in December 1996. Main Outcome Measures Serum icodextrin metabolites: one to five glucose units (G1–G5), a high molecular weight fraction (G > 10), and total carbohydrate level, as well as a biochemical profile were determined every 3 months in combination with all other study variables. Results In icodextrin-treated patients, serum disaccharide (maltose) concentrations increased from 0.05 ± 0.01 (mean±SEM) at baseline, to an average concentration in the follow-up visits of 1.14 ± 0.13 mg/mL (p < 0.001). All icodextrin metabolites increased significantly from baseline, as illustrated by the serum total carbohydrate minus glucose levels: from 0.42 ± 0.05 mg/mL to an average concentration in the follow-up visits of 5.04 ± 0.49 mg/mL (p < 0.001). At the same time, serum sodium levels decreased from 138.1 ± 0.7 mmol/L to an average concentration in the follow-up visits of 135.4 ± 0.8 mmol/L (p < 0.05). However, after 12 months the serum sodium concentration increased nonsignificantly (NS) from base line to 136.6 ± 0.9 mmol/L, after an initial decrease. Serum osmolality increased significantly from baseline in icodextrin users at 9 and 12 months, but did not differ significantly from glucose users in any visit. In icodextrintreated patients, the calculated serum osmolal gap increased significantly from 4.1 ± 1.4 mOsm/kg to an average of 11.8 ± 1.7 mOsm/kg (p < 0.01). The sum of the serum icodextrin metabolites in millimoles/liter equaled the increase in osmolal gap. Body weight increased in icodextrin users (71.9 ± 2.7 kg to 77.8 ± 3.0 kg; NS). Clinical adverse effects did not accompany these findings. Residual renal function remained stable during follow-up. Conclusions The serum icodextrin metabolite levels in the present study increased markedly and were the same as those found previously in continuous ambulatory peritoneal dialysis patients treated with icodextrin, despite thelonger dwell time for CCPDpatients (14 -16 hr versus 8 -12 hr). The initial decrease in serum sodium concentration was followed by an increase to a concentration not different from baseline at 12 months. The pathophysiology of this finding is speculated. Calculated osmolal gap in icodextrin patients increased significantly (p < 0.01) at every follow-up visit, and could be explained by the serum icodextrin metabolite increase. We encountered no clinical side effects of the observed levels of icodextrin metabolites.

scholarly journals Serum sodium concentration is significantly associated with the angiographic characteristics of coronary atherosclerosis

2007 ◽  
Vol 28 (8) ◽  
pp. 1136-1142 ◽  
Author(s):  
En-zhi JIA ◽  
Zhi-jian YANG ◽  
Tie-bing ZHU ◽  
Lian-sheng WANG ◽  
Bo CHEN ◽  
...  
Keyword(s):  
Serum Sodium ◽  
Coronary Atherosclerosis ◽  
Sodium Concentration ◽  
Serum Sodium Concentration

Risk factors for hepatic encephalopathy in patients with cirrhosis and refractory ascites: relevance of serum sodium concentration

2010 ◽  
Vol 30 (8) ◽  
pp. 1137-1142 ◽  
Author(s):  
Mónica Guevara ◽  
María E. Baccaro ◽  
Jose Ríos ◽  
Marta Martín-Llahí ◽  
Juan Uriz ◽  
...  
Keyword(s):  
Risk Factors ◽  
Hepatic Encephalopathy ◽  
Serum Sodium ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Refractory Ascites

Serum Sodium Concentration Changes Are Related to Fluid Balance and Sweat Sodium Loss

2010 ◽  
Vol 42 (9) ◽  
pp. 1669-1674 ◽  
Author(s):  
MATTHEW D. PAHNKE ◽  
JOEL D. TRINITY ◽  
JEFFREY J. ZACHWIEJA ◽  
JOHN R. STOFAN ◽  
W. DOUGLAS HILLER ◽  
...  
Keyword(s):  
Fluid Balance ◽  
Serum Sodium ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Concentration Changes ◽  
Sodium Loss ◽  
Sweat Sodium

Disorders of Water Balance

2017 ◽  
Author(s):  
Richard H Sterns ◽  
Stephen M. Silver ◽  
John K. Hix ◽  
Jonathan W. Bress
Keyword(s):  
Water Balance ◽  
Water Intake ◽  
Serum Sodium ◽  
Water Conservation ◽  
Free Water ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Water Losses ◽  
Water Excretion ◽  
Impaired Water

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.

scholarly journals Hyperosmolar Non-Ketotic Diabetic Coma — Less Sodium in Therapy?

1980 ◽  
Vol 8 (3) ◽  
pp. 349-352 ◽  
Author(s):  
Luen Bik To ◽  
P. J. Phillips
Keyword(s):  
Older Women ◽  
Water Deficit ◽  
Serum Sodium ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Diabetic Coma ◽  
Factors Affecting ◽  
Serum Osmolarity

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.

scholarly journals Syndrome of Inappropriate Secretion of Antidiuretic Hormone due to Selective Serotonin Reuptake Inhibitors After Pancreaticoduodenectomy for Carcinoma of the Ampulla of Vater: Case Report

2013 ◽  
Vol 98 (4) ◽  
pp. 289-291
Author(s):  
Ryota Iwase ◽  
Hiroaki Shiba ◽  
Takeshi Gocho ◽  
Yasuro Futagawa ◽  
Shigeki Wakiyama ◽  
...  
Keyword(s):  
Antidiuretic Hormone ◽  
Serum Sodium ◽  
Serotonin Reuptake ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Plasma Osmolality ◽  
Sodium Concentration ◽  
Ampulla Of Vater ◽  
Serum Sodium Concentration ◽  
Selective Serotonin ◽  
Inappropriate Secretion

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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