Bartter's and Gitelman's Flashcards
What features do Bartter’s and Gitelman’s have in common?
In both disorders, there is impaired sodium and chloride reabsorption and this leads to volume depletion and activation of the RAAS. The combination of increased circulating aldosterone and delivery of sodium chloride to the distal tubule results in enhanced urinary excretion of potassium and hydrogen ions (hypokalaemia and metabolic alkalosis). The diluting capacity of the kidney is reduced in both disorders because to form maximally dilute urine you require a functioning TAL and DCT.
What features might differentiate Barrter’s from Gitelman’s syndrome?
Bartter’s patients have no or a blunted response to loops while patients with Gitelman’s syndrome have a blunted response to thiazides. The ability to produce concentrated urine is impaired in Bartter’s but not in Gitelman’s. To produce a maximally concentrated urine, you require a functioning TAL and ADH. Patient’s with Bartter’s have a normal or high urinary calcium excretion while those with Gitelman’s have low urinary calcium excretion. Hypomagnesaemia is more prominent in Gitelman’s syndrome.
Explain the mechanism by which hypovolaemia leads to to activations of the RAAS.
Hypovolaemia results in reduced glomerular filtration and a reduction in the delivery of chloride to the distal tubule. This is sensed by the cells of the macula densa. The cells of the JGA release active renin into the circulation. Renin cleaves angiotensinogen, which is predominantly synthesised in the liver, to produce angiotensin 2. Angiotensin 2 increases sodium and water reabsorption in the proximal tubules and, indirectly, leads to increased Na+ reabsorption in the distal tubules by leading to increased circulating levels of aldosterone. Both of these effects result in an increase in the effective circulating volume and correct (hopefully) the stimulus that resulted in renin release in the first instance.
Why do thiazide diuretics but not loops lead to hyponatraemia?
Firstly, the mechanism of diuresis with loop diuretics is as follows:
How do loop diuretics cause a diuresis?
They block the reabsorption of Na+, K+, and Cl- at the level of the NaK2Cl co-transporter in the thick ascending limb of the loop of Henle. This ultimately results in failure to generate high levels of tonicity in the medulla.
