Isolated acquired hypoaldosteronism as a cause of hypovolemic hyponatremia with urinary sodium loss

2020 ◽  
Author(s):  
Sánchez Jorge Gabriel Ruiz ◽  
M Cuesta ◽  
Miguel P De ◽  
X Perez ◽  
I Moraga ◽  
...  
Keyword(s):  
Urinary Sodium ◽  
Sodium Loss

Curt Richter and regulatory physiology

2000 ◽  
Vol 279 (2) ◽  
pp. R357-R363 ◽  
Author(s):  
Timothy H. Moran ◽  
Jay Schulkin
Keyword(s):  
Behavioral Responses ◽  
Urinary Sodium ◽  
Research Focus ◽  
Internal Milieu ◽  
Sodium Ingestion ◽  
Sodium Loss ◽  
And Behavior ◽  
Molecular Bases ◽  
Active Investigation ◽  
Experimental Challenge

Curt Richter made seminal contributions to our understanding of a number of issues regarding the relationships between physiology and behavior. He was the first to conceptualize behavior as an aspect of regulatory physiology. These ideas developed from his work on behavioral responses to a variety of physiological perturbations. The classic example is Richter's demonstration of the development of avid sodium ingestion in response to urinary sodium loss after adrenalectomy. Some of Richter's ideas on the nature and underlying physiology of specific appetites maintain their influence and continue to stimulate active investigation. Others, focused on abilities to self-select balanced diets, have not borne the test of time or experimental challenge. As current research takes a more molecular focus, Richter's ideas on behavior in the service of the internal milieu maintain their currency, and the search for the molecular bases for these relationships should serve as a research focus.

scholarly journals Moderate/severe Hypovolemic Hyponatremia with urinary sodium loss secondary to Hypoaldosteronism: analysis of 28 cases

2016 ◽  
Author(s):  
Rona Penso ◽  
Ana Ortola ◽  
Angela Amengual ◽  
Irene Crespo ◽  
Teresa Ruiz-Gracia ◽  
...  
Keyword(s):  
Urinary Sodium ◽  
Sodium Loss

scholarly journals Urinary Sodium Loss following Hypertonic Saline Administration Curtails its Superior Osmolar Effect in Comparison to Mannitol in Severe Traumatic Brain Injury: A Secondary Analysis of a Randomized Controlled Trial

2018 ◽  
Vol 05 (03) ◽  
pp. 164-167 ◽  
Author(s):  
Aniruddha Tekkatte Jagannatha ◽  
Kamath Sriganesh ◽  
Bhagavatula Indira Devi ◽  
Ganne Sesha Umamaheswara Rao
Keyword(s):  
Traumatic Brain Injury ◽  
Randomized Controlled Trial ◽  
Brain Injury ◽  
Controlled Trial ◽  
Urinary Sodium ◽  
Urine Osmolarity ◽  
Post Hoc Analysis ◽  
Randomized Controlled ◽  
Sodium Loss ◽  
Post Hoc

Abstract Background Mannitol and hypertonic saline (HTS) are used as boluses during episodes of raised intracranial pressure (ICP) in severe traumatic brain injury (TBI). We recently demonstrated that ICP reduction and neurological outcomes are similar with mannitol and HTS in TBI. In the current post hoc analysis, we hypothesized that this lack of difference between mannitol and HTS is due to increased urinary sodium losses after HTS. Methods In this post hoc analysis of our earlier randomized controlled trial, we analyzed serum and urine osmolarity and sodium levels in 38 patients with severe TBI over 6 days. Equiosmolar boluses of mannitol and HTS were administered whenever ICP increased above 20 mm Hg. Seven hundred sixty samples each of serum sodium, urine sodium, serum osmolarity, and urine osmolarity were analyzed during this period. Results Three hundred and one and 187 boluses of mannitol and HTS, respectively, were required to maintain ICP below 20 mm Hg. The urinary osmolarity was similar between mannitol and HTS groups (p = 0.63). The urinary sodium excretion was significantly higher in HTS group compared with mannitol group (p = 0.002). Serum sodium and osmolarity values were similar between mannitol and HTS groups (p = 0.16 and 0.31, respectively). There was no difference in the mean ICP between the groups (p = 0.31). Conclusion Increased urinary sodium loss after HTS contributes to its lack of superiority over mannitol in controlling raised ICP.

Low Urinary Sodium Is Associated With Greater Risk of Myocardial Infarction Among Treated Hypertensive Men

Hypertension ◽  
1995 ◽  
Vol 25 (6) ◽  
pp. 1144-1152 ◽  
Author(s):  
Michael H. Alderman ◽  
Shantha Madhavan ◽  
Hillel Cohen ◽  
Jean E. Sealey ◽  
John H. Laragh
Keyword(s):  
Myocardial Infarction ◽  
Urinary Sodium

scholarly journals Albuminuria intensifies the link between urinary sodium excretion and central pulse pressure in the general population: the Wakuya study

2021 ◽  
Author(s):  
Kaname Tagawa ◽  
Yusuke Tsuru ◽  
Katsumi Yokoi ◽  
Takanori Aonuma ◽  
Junichiro Hashimoto
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Pulse Pressure ◽  
Augmentation Index ◽  
Sodium Intake ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Pressure Amplitude ◽  
Excess Sodium ◽  
Central Pulse Pressure

Abstract Background Central pulse pressure is responsible for the hemodynamics of vital organs, and monitoring this parameter is important for cardiovascular disease prevention. Excess sodium intake and (micro)albuminuria (a manifestation of renal microvascular damage) are known to be strong predictors of cardiovascular disease. We sought to investigate the cross-sectional relationships among dietary sodium intake, albuminuria, and central pulse pressure in a general population cohort. Methods The subjects were 933 apparently healthy adults (mean age, 56 ± 10 years). Radial pressure waveforms were recorded with applanation tonometry to estimate mean arterial pressure, central pulse pressure, forward and backward pressure amplitudes, and augmentation index. The urinary sodium/creatinine and albumin/creatinine ratios were measured in spot urine samples. Results Both the urinary sodium/creatinine and albumin/creatinine ratios were positively correlated with central pulse pressure, even after adjusting for mean arterial pressure (P < 0.001). Moreover, both ratios had a synergistic influence on increasing the central pulse pressure independent of age, sex, estimated glomerular filtration rate, hyperlipidemia, and diabetes (interaction P = 0.04). A similar synergistic influence was found on the forward pressure amplitude, but not on the backward pressure amplitude or augmentation index. The overall results were not altered when the urinary albumin/creatinine ratio was replaced with the existence of chronic kidney disease. Conclusion (Micro)albuminuria strengthens the positive association between urinary sodium excretion and central pulse pressure and systolic forward pressure. Excess sodium intake may magnify the cardiovascular risk by widening the aortic pulsatile pressure, particularly in the presence of concomitant chronic kidney disease.

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