What is Bartter’s Syndrome?

Bartter’s Syndrome is an inherited defect in the renal tubules that causes low potassium levels, low chloride levels, which in turn causes metabolic alkalosis. Bartter Syndrome, is not a single disorder but rather a set of closely related disorders. These Bartter-like syndromes share many of the same physiologic derangements, but differ with regard to the age of onset, the presenting symptoms, the magnitude of urinary potassium (K) and prostaglandin excretion, and the extent of urinary calcium excretion.

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What is Antenatal Bartter Syndrome ?

In contrast to Classic Bartter Syndrome and Gitelman Syndrome, the Antenatal variant of Bartter Syndrome has both the features of metabolic alkalosis (from the low potassium), as well as profound systemic manifestations. Out of all of the variants this form is the most severe.

Antenatal Bartter Syndrome is characterized by polyhydraminos (Increased water in the uterus) due to polyuria in utero (Which means the fetus has urinated so much it has led to an increase in the fluid in the uterus. For this reason the infant is usually born premature.

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What is Gitelman’s Syndrome ?

Gitelman’s syndrome is a rare inherited defect in the renal tubule of the kidneys.  This defect causes the kidney to waste magnesium, sodium, potassium and chloride in the urine, instead of reabsorbing it back into the bloodstream.   Urine calcium levels are lower than normal, despite normal serum values.   This syndrome does not cause kidney failure nor does it cause the kidneys to function abnormally.  The kidneys are normal.  The problem is the reabsorption of important electrolytes and minerals.

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Don’t Eat Liquorice, if you have Bartter’s or Gitelman’s

Don’t eat liquorice !!!

Liqourice is a diuretic that causes potassium loss. You can lose potassium and raise your blood pressure.

Read more about it at Wikipedia, or just don’t eat it.

Diagnosing Electrolyte Disorders

Algorithms for Diagnosing Some Electrolyte Disorders


From the Department of Medicine, Albert Einstein College of Medicine, and Jacobi Medical Center, Bronx, NY.
The differential diagnosis of electrolyte disorders has traditionally been framed in terms of pathophysiology, and analysis of clinical problems has usually proceeded in the same way. However, easier access to rapid-response laboratory analysis has prompted physicians who encounter patients with serious electrolyte abnormalities to try to establish the cause by quickly obtaining further simple tests. In that vein, this article and the algorithms that are presented are intended to assist the preliminary laboratory differential diagnosis of low and high serum levels of sodium, potassium, and calcium.
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Antenatal Bartter Syndrome, Information for Healthcare Workers

In contrast to Classic Bartter Syndrome and Gitelman Syndrome, the Antenatal variant of Bartter Syndrome has both the features of renal tubular hypokalemic alkalosis as well as profound systemic manifestations. Antenatal Bartter Syndrome is characterized by polyhydraminos due to intrauterine polyuria, and premature delivery is common. After birth, life-threatening episodes of fever and dehydration occur secondary to profound polyuria, vomiting, and diarrhea.

Severe electrolyte imbalances and marked growth retardation are typical. The majority of these infants also have severe hypercalciuria with associated nephrocalcinosis and osteopenia. Biochemically, these patients are distinguished by marked stimulation of renal and systemic prostaglandin E2 production. Cyclooxygenase inhibitors,eg, Indomethacin, have been shown to reverse all the clinical and laboratory derangements, save for those related to calcium homeostasis.

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Gitelman Syndrome, Information for Healthcare Workers


Gitelman’s Syndrome was discovered in 1966 by Dr Hillel Gitelman. It was discovered that some patients with Bartter’s showed a different myriad of symptoms. Gitelman’s syndrome is also a renal salt wasting disorder but the defective tubule is in the thiazide-sensitive Na-Cl cotransporter in the distal convoluted tubule(DCT). Both disorders are associated with hypokalemia, renal potassium wasting, activation of the renin-angiotensin-aldosterone axis, and normal blood pressure. Unlike patients with Bartters, patients with Gitelman’s syndrome have hypomagnesemia, increased urinary magnesium, and decreased calcium excretion.

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Hypokalemic Periodic Paralysis

Pediatrics in Review

Volume 18 Number 10 October 1997
Copyright 1997 American Academy of Pediatrics

This section of Pediatrics in Review reminds clinicians of those conditions that can present in a misleading fashion and require suspicion for early diagnosis. Emphasis has been placed on conditions in which early diagnosis is important and that the general pediatrician might be expected to encounter, at least once in a while.

Case 3 Presentation

A 16 year-old boy is referred to the emergency department for evaluation of generalized weakness. He reports that 2 days ago, following 2 days of “flu-like” symptoms, he became weak while climbing stairs. His weakness progressed rapidly; soon he was unable to move his extremities or sit up. His mother has helped him eat, drink, and urinate. He uses no medications, alcohol, or illicit drugs. He has no history of ingestions, fever, dyspnea, dysphagia, or paresthesias. He had a similar episode of weakness 4 years ago that was less severe and resolved spontaneously within 2 days. His grandmother has had similar episodes.

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Stress and Magnesium Levels

Adrenergic control of plasma magnesium in man.
Whyte KF, Addis GJ, Whitesmith R, Reid JL

Regulation of magnesium balance is poorly understood. However, hypomagnesaemia has been reported in patients in clinical situations where circulating catecholamines are raised including myocardial infarction, cardiac surgery and insulin-induced hypoglycaemia stress tests. The effects of L-adrenaline infusions, sufficient to achieve pathophysiological levels of adrenaline, and of therapeutic intravenous infusions of salbutamol, a beta 2-agonist, on plasma magnesium, plasma potassium, plasma glucose and plasma insulin levels were studied in a placebo-controlled design in eight normal subjects. Plasma magnesium levels fell significantly during the adrenaline infusion and also during the salbutamol infusion, though more slowly. In a 1 h period of observation after cessation of the infusions no recovery of plasma magnesium levels was seen. Significant falls in plasma potassium levels were also observed during both infusions with spontaneous recovery within 30 min after the infusions. No significant changes in plasma insulin levels occurred with either salbutamol or L-adrenaline compared with control. Plasma glucose levels rose significantly during the adrenaline infusion. The study suggests that both L-adrenaline and salbutamol cause shifts in plasma magnesium which are not mediated by insulin. We propose that intracellular shifts of magnesium occur as a result of beta-adrenergic stimulation.

Publication Types: Clinical trial Randomized controlled trial

Clin Sci (Colch) 1987 Jan;72(1):135-8
PMID: 3542342, UI: 87103979

Effects of Adrenaline and Exercise on Magnesium Levels

Effects of exogenous catecholamines and exercise on plasma magnesium concentrations.
Joborn H, Akerstrom G, Ljunghall S

Catecholamines and physical exercise are known to influence the metabolism of several minerals in man, but the effects on magnesium (Mg) have been scarcely investigated. In the present study, infusion of adrenaline (5 micrograms/min for 30 min followed by 10 micrograms/min for 30 minutes) significantly reduced the plasma Mg levels in healthy males. This effect was abolished by simultaneous infusion of propranolol. Noradrenaline had no such effect. In order to stimulate endogenous catecholamine release healthy males carried out physical exercise in four different ways: ergometer bicycling at maximum load until exhaustion with and without oral beta-blockade, ergometer bicycling with stepwise increasing load until exhaustion, isokinetic maximal exercise with one leg, with blood sampling both from the venous effluent of the exercising leg and the opposite resting arm and long-term (60 min) steady state ergometer bicycling at approximately 65% of estimated maximum capacity. During short-term (less than 20 min) intense exercise (i.e. experiments 1-3) the plasma Mg concentrations were increased. This was probably due to a reduction of plasma volume and to an influx of Mg to the vascular pool. During long-term steady state exercise (experiment 4) the Mg levels were not significantly affected but decreased during the first hour of recovery. These results suggest that both the beta-adrenergic system and muscular activity by itself affect Mg homeostasis.

1 : Clin Endocrinol (Oxf) 1985 Sep;23(3):219-26
PMID: 4075536, UI: 86080100