Growth failure and metabolic acidosis due to total body sodium depletion in an infant with an ileostomy

2021 ◽  
Vol 14 (3) ◽  
pp. e241570
Author(s):  
Christina Marie Zarraga ◽  
Stephen Mark Borowitz
Keyword(s):  
Metabolic Acidosis ◽  
Sodium Intake ◽  
Significant Risk ◽  
Growth Failure ◽  
Sodium Depletion ◽  
Body Sodium ◽  
Essential Nutrient ◽  
Sodium Loss ◽  
Total Body ◽  
Renal Tubular

Sodium is an essential nutrient and inadequate sodium intake and/or excessive sodium losses can result in suboptimal growth. Infants with ileostomies are at significant risk of developing growth failure as a result of excessive sodium loss in their ileostomy effluent. Chronic sodium depletion can also limit the kidney’s ability to excrete hydrogen and potassium ions, mimicking electrolyte abnormalities found in type 4 renal tubular acidosis. This report describes an infant with an ileostomy with severe growth failure, hyperkalaemia and metabolic acidosis—all of which promptly resolved with sodium supplementation.

Metabolic Acidosis

2017 ◽  
Author(s):  
Lisa Cohen ◽  
Dipal Savla ◽  
Shuchi Anand
Keyword(s):  
Metabolic Acidosis ◽  
Lactic Acidosis ◽  
The Body ◽  
Anion Gap ◽  
Plasma Sodium ◽  
Toxic Substances ◽  
Disease States ◽  
Common Causes ◽  
Total Body ◽  
Renal Tubular

Metabolic acidosis is a common clinical entity that can arise from a variety of disease states, medications, and toxic ingestions. This review covers the pathophysiology, diagnosis, and management of common presentations of metabolic acidosis. We have differentiated various causes of metabolic acidosis based on the presence of a normal or elevated anion gap (AG), the sum of serum anions unaccounted for by the measurement of plasma sodium, bicarbonate, and chloride levels. Normal AG metabolic acidosis, or non-AG metabolic acidosis, arises when there is excessive loss of bicarbonate from the gastrointestinal tract or in the urine. This review covers the development and diagnosis of non-AG metabolic acidosis, including a discussion of the spectrum of renal tubular acidosis subtypes. The treatment of non-AG metabolic acidosis is reviewed. Metabolic acidosis with an elevated AG, also called AG metabolic acidosis, develops when exogenous or endogenous nonchloride acid accumulates in the body. The most common causes of AG metabolic acidosis are lactic acidosis and ketoacidosis from starvation, heavy alcohol intake, or diabetes with total body insulin depletion. Medications, toxic substances, and uremia can also lead to AG acidosis. The mechanisms and management of these causes of metabolic acidosis with high AG are covered in detail. Key words: anion-gap acidosis, diabetic ketoacidosis, lactic acidosis, non–anion gap acidosis

scholarly journals Lateral parabrachial nucleus serotonergic mechanisms and salt appetite induced by sodium depletion

1998 ◽  
Vol 274 (2) ◽  
pp. R555-R560 ◽  
Author(s):  
José Vanderlei Menani ◽  
Laurival Antonio De Luca ◽  
Alan Kim Johnson
Keyword(s):  
Water Deprivation ◽  
Sodium Intake ◽  
Parabrachial Nucleus ◽  
Salt Appetite ◽  
Sodium Depletion ◽  
Volume Depletion ◽  
Deficient Diet ◽  
Lateral Parabrachial Nucleus ◽  
Sodium Loss ◽  
Ingestive Behaviors

This study investigated the effects of bilateral injections of a serotonin (5-HT) receptor agonist into the lateral parabrachial nucleus (LPBN) on the intake of NaCl and water induced by 24-h water deprivation or by sodium depletion followed by 24 h of sodium deprivation (injection of the diuretic furosemide plus 24 h of sodium-deficient diet). Rats had stainless steel cannulas implanted bilaterally into the LPBN. Bilateral LPBN injections of the serotonergic 5-HT1/2 receptor antagonist methysergide (4 μg/200 nl at each site) increased hypertonic NaCl intake when tested 24 h after sodium depletion and after 24 h of water deprivation. Water intake also increased after bilateral injections of methysergide into the LPBN. In contrast, the intake of a palatable solution (0.06 M sucrose) under body fluid-replete conditions was not changed after bilateral LPBN methysergide injections. The results show that serotonergic mechanisms in the LPBN modulate water and sodium intake induced by volume depletion and sodium loss. The finding that sucrose intake was not affected by LPBN serotonergic blockade suggests that the effects of the methysergide treatment on the intakes of water and NaCl are not due to a mechanism producing a nonspecific enhancement of all ingestive behaviors.

scholarly journals A Study on Electrolyte Imbalance in Asphyxiated Neonates

KYAMC Journal ◽  
2017 ◽  
Vol 7 (2) ◽  
pp. 775-779 ◽  
Author(s):  
Farhana Rahman ◽  
Md Abu Bakar Siddique ◽  
Md Wahidul Hassan ◽  
Md Nasimul Bari ◽  
Firoz Ahmed
Keyword(s):  
Metabolic Acidosis ◽  
Perinatal Asphyxia ◽  
Respiratory Acidosis ◽  
Morbidity And Mortality ◽  
Electrolyte Imbalance ◽  
Tubular Damage ◽  
Developed Country ◽  
Body Sodium ◽  
Less Developed Country ◽  
Renal Tubular

In less developed country like Bangladesh, perinatal asphyxia remains a major cause of death and disability. Disorders of electrolytes are one of the common derangements encountered in critically ill asphyxiated neonates. It may remain unrecognized leading to morbidity and mortality irrespective of the primary problem. Syndrome of inappropriate secretion of ADH (SIADH) causes hyponatraemia in perinatal asphyxia. Metabolic acidosis may further exaggerate hyponatraemia. Where as in hypernatraemia there is an absolute or relative deficit of water in relation to body sodium. Hyponatraemia and hypernatraemia may aggravate the neurological morbidity in asphyxiated infants. Metabolic acidosis may causes hyperkalamia. On the other hand respiratory acidosis may cause hypochloraemia and renal tubular damage in perinatal asphyxia may further cause loss of potassium leading to hypokalaemia. This study has been conducted to find out the pattern of electrolyte abnormalities in asphyxiated neonates. In the study out of 133 asphyxiated babies 40 (30.1%) were hyponatremic. Hypokalaemia observed in 8 (6.0%) asphyxiated babies. Hyperkalaemia was found in 28 (21.1%) asphyxiated neonates in this study. Immediate measurements of serum electrolyte followed by appropriate fluid and electrolytes therapy can reduce the overall morbidity and mortality in asphyxiated neonates.KYAMC Journal Vol. 7, No.-2, Jan 2017, Page 775-779

Effect of adrenocorticotrophic hormone on sodium appetite in mice

1999 ◽  
Vol 277 (4) ◽  
pp. R1033-R1040 ◽  
Author(s):  
D. A. Denton ◽  
J. R. Blair-West ◽  
M. I. McBurnie ◽  
J. A. P. Miller ◽  
R. S. Weisinger ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Sodium Content ◽  
Adrenocorticotrophic Hormone ◽  
Sodium Appetite ◽  
Corticotrophin Releasing Factor ◽  
Intracerebroventricular Infusion ◽  
Thymus Weight ◽  
Body Sodium ◽  
Voluntary Intake ◽  
Total Body

A main vector of the effects of stress is secretion of corticotrophin releasing factor (CRF), adrenocorticotrophin (ACTH), and adrenal steroids. Systemic administration of ACTH (2.8 μg/day sc) for 7 days in BALB/c mice caused a very large increase of voluntary intake of 0.3 M NaCl equivalent to turnover of total body sodium content each day. Intracerebroventricular infusion of ACTH (20 ng/day) had no effect. Intracerebroventricular infusion of ovine CRF (10 ng/h for 7 days) caused an increase of sodium intake. The large sodium appetite-stimulating effect of systemic ACTH was not influenced by concurrent systemic infusion of captopril (2 mg/day). Induction of stress by immobilization of mice on a running wheel caused an increase in Na appetite associated with a 50% decrease of thymus weight, indicative of corticosteroid effects. The present data suggest that stress and the hormone cascade initiated by stress evoke a large sodium appetite in mice, which may be an important survival mechanism in environmental conditions causing stress.

Metabolic Acidosis

2017 ◽  
Author(s):  
Lisa Cohen ◽  
Dipal Savla ◽  
Shuchi Anand
Keyword(s):  
Metabolic Acidosis ◽  
Lactic Acidosis ◽  
The Body ◽  
Anion Gap ◽  
Plasma Sodium ◽  
Toxic Substances ◽  
Disease States ◽  
Common Causes ◽  
Total Body ◽  
Renal Tubular

Metabolic acidosis is a common clinical entity that can arise from a variety of disease states, medications, and toxic ingestions. This review covers the pathophysiology, diagnosis, and management of common presentations of metabolic acidosis. We have differentiated various causes of metabolic acidosis based on the presence of a normal or elevated anion gap (AG), the sum of serum anions unaccounted for by the measurement of plasma sodium, bicarbonate, and chloride levels. Normal AG metabolic acidosis, or non-AG metabolic acidosis, arises when there is excessive loss of bicarbonate from the gastrointestinal tract or in the urine. This review covers the development and diagnosis of non-AG metabolic acidosis, including a discussion of the spectrum of renal tubular acidosis subtypes. The treatment of non-AG metabolic acidosis is reviewed. Metabolic acidosis with an elevated AG, also called AG metabolic acidosis, develops when exogenous or endogenous nonchloride acid accumulates in the body. The most common causes of AG metabolic acidosis are lactic acidosis and ketoacidosis from starvation, heavy alcohol intake, or diabetes with total body insulin depletion. Medications, toxic substances, and uremia can also lead to AG acidosis. The mechanisms and management of these causes of metabolic acidosis with high AG are covered in detail. Key words: anion-gap acidosis, diabetic ketoacidosis, lactic acidosis, non–anion gap acidosis

scholarly journals Total Body Sodium Balance in Chronic Kidney Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Kylie Martin ◽  
Sven-Jean Tan ◽  
Nigel D. Toussaint
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Sodium Intake ◽  
Dynamic Assessment ◽  
Sodium Balance ◽  
Sodium Homeostasis ◽  
Body Sodium ◽  
Clinical Associations ◽  
Total Body ◽  
Tissue Sodium

Excess sodium intake is a leading but modifiable risk factor for mortality, with implications on hypertension, inflammation, cardiovascular disease, and chronic kidney disease (CKD). This review will focus mainly on the limitations of current measurement methods of sodium balance particularly in patients with CKD who have complex sodium physiology. The suboptimal accuracy of sodium intake and excretion measurement is seemingly more marked with the evolving understanding of tissue (skin and muscle) sodium. Tissue sodium represents an extrarenal influence on sodium homeostasis with demonstrated clinical associations of hypertension and inflammation. Measurement of tissue sodium has been largely unexplored in patients with CKD. Development and adoption of more comprehensive and dynamic assessment of body sodium balance is needed to better understand sodium physiology in the human body and explore therapeutic strategies to improve the clinical outcomes in the CKD population.

Pressure-dependent renin release: effects of sodium intake and changes of total body sodium

1999 ◽  
Vol 277 (2) ◽  
pp. R548-R555 ◽  
Author(s):  
Erdmann Seeliger ◽  
Katrin Lohmann ◽  
Benno Nafz ◽  
Pontus B. Persson ◽  
H. Wolfgang Reinhardt
Keyword(s):  
Sodium Intake ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Renin Release ◽  
Response Curves ◽  
Exponential Relationship ◽  
High Sodium ◽  
Body Sodium ◽  
Total Body ◽  
The Impact

The impact of sodium intake and changes in total body sodium (TBS) for the setting of pressure-dependent renin release (PDRR) was studied in freely moving dogs. An aortic cuff allowed servo control of renal perfusion pressure (RPP) at preset values. Protocols were 1) high sodium intake (HSI), 2) low sodium intake (LSI), 3) TBS moderately increased (+3.1 mmol Na/kg body wt) by 20% reduction of RPP for 2–4 days, 4) large increase of TBS (+8.2) by combining protocol 3 with aldosterone infusion, and 5) TBS reduced (−3.1) by peritoneal dialyses. Twenty-four-hour time courses of arterial plasma renin activity (PRA) revealed that LSI increased PRA for the first 10 h only; afterward PRA did not differ between LSI and HSI. Reduced TBS increased PRA constantly, and the large increase of TBS constantly reduced PRA. PDRR stimulus-response curves (assessed 20 h after last sodium intake) revealed an exponential relationship in each protocol. PDRR was not changed by different sodium intake. Conversely, reduced TBS increased PDRR markedly, whereas the large increase of TBS suppressed it. Thus an inverse relationship between TBS and PRA, i.e., a TBS-dependent renin release, was found. This relationship was enhanced by decreasing RPP. This interplay between TBS-dependent renin release and PDRR allows the organism a differentiated reaction to changes in TBS and arterial pressure.

Chronic activation of plasma renin is log-linearly related to dietary sodium and eliminates natriuresis in response to a pulse change in total body sodium

2008 ◽  
Vol 294 (1) ◽  
pp. R17-R25 ◽  
Author(s):  
Mads Kjolby ◽  
Peter Bie
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Dietary Sodium ◽  
Ang Ii ◽  
Low Sodium ◽  
Arterial Blood ◽  
Body Sodium ◽  
Custom Made ◽  
Total Body

Responses to acute sodium loading depend on the load and on the level of chronic sodium intake. To test the hypothesis that an acute step increase in total body sodium (TBS) elicits a natriuretic response, which is dependent on the chronic level of TBS, we measured the effects of a bolus of NaCl during different low-sodium diets spanning a 25-fold change in sodium intake on elements of the renin-angiotensin-aldosterone system (RAAS) and on natriuresis. To custom-made, low-sodium chow (0.003%), NaCl was added to provide four levels of intake, 0.03–0.75 mmol·kg−1·day−1for 7 days. Acute NaCl administration increased PV (+6.3–8.9%) and plasma sodium concentration (∼2%) and decreased plasma protein concentration (−6.4–8.1%). Plasma ANG II and aldosterone concentrations decreased transiently. Potassium excretion increased substantially. Sodium excretion, arterial blood pressure, glomerular filtration rate, urine flow, plasma potassium, and plasma renin activity did not change. The results indicate that sodium excretion is controlled by neurohumoral mechanisms that are quite resistant to acute changes in plasma volume and colloid osmotic pressure and are not down-regulated within 2 h. With previous data, we demonstrate that RAAS variables are log-linearly related to sodium intake over a >250-fold range in sodium intake, defining dietary sodium function lines that are simple measures of the sodium sensitivity of the RAAS. The dietary function line for plasma ANG II concentration increases from theoretical zero at a daily sodium intake of 17 mmol Na/kg (intercept) with a slope of 16 pM increase per decade of decrease in dietary sodium intake.

scholarly journals Tenofovir and Severe Symptomatic Hypophosphatemia

2019 ◽  
Vol 7 ◽  
pp. 232470961984879 ◽  
Author(s):  
Asim Kichloo ◽  
Savneek Singh Chugh ◽  
Sanjeev Gupta ◽  
Jay Panday ◽  
Ghazaleh Goldar
Keyword(s):  
Renal Damage ◽  
Organic Anion ◽  
Significant Risk ◽  
Anion Transporters ◽  
Immunodeficiency Virus ◽  
Tubular Lumen ◽  
Associated Proteins ◽  
Proximal Tubular ◽  
Renal Tubular ◽  
Initial Results

Tenofovir is a broadly used drug used for the treatment of human immunodeficiency virus (HIV). Although the initial results of the clinical trials supported the renal safety of Tenofovir, clinical use of it has caused a low, albeit a significant, risk of renal damage either in the form of AKI or CKD. The pathophysiology has been linked to the effect of this medication on the proximal tubular cell. Although the exact mechanism is unknown, studies have suggested that Tenofovir accumulates in proximal tubular cells which are rich in mitochondria. It is both filtered in the glomerulus and actively secreted in the tubules for elimination and is excreted unchanged in the urine. Studies have shown an active transportation of 20-30% of this drug into the renal proximal tubule (PCT) cells via the organic anion transporters in the baso-lateral membrane (primarily hOAT1, and OAT3 to a lesser extent) and ultimate excretion of the drug into the tubular lumen via the transporters in the proximal tubular apical membrane MRP4 and MRP2 (multidrug resistance-associated proteins 2 & 4). Subsequently, the mitochondrial injury caused by Tenofovir can lead to the development of Fanconi’s syndrome which causes renal tubular acidosis, phosphaturia, aminoaciduria, glucosuria with normoglycemia, and tubular proteinuria. Here we present a case where Tenofovir treatment resulted in severe hypophosphatemia requiring hospitalization for parentral phosphate repletion.

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