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Bartter's syndrome.

The Urologic Clinics of North America

|June 1, 1977

Summary

This summary is machine-generated.

This study identifies a rare genetic disorder causing juxtaglomerular hyperplasia, leading to electrolyte imbalances and high renin. Prostaglandin E plays a key role in this syndrome.

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Area of Science:

Nephrology
Endocrinology
Genetics

Background:

Familial juxtaglomerular hyperplasia can cause hypokalemic, hypochloremic alkalosis, aldosteronism, and hyperreninemia with normal blood pressure.
This syndrome is likely inherited as a recessive trait.

Purpose of the Study:

To investigate the role of prostaglandin E in the pathogenesis of juxtaglomerular hyperplasia syndrome.
To differentiate this syndrome from salt-losing chronic glomerulonephritis.

Main Methods:

Histologic examination of kidneys.
Assessment of sodium handling with low-sodium intake.
Measurement of urinary prostaglandin E levels.
Evaluation of plasma renin and aldosterone levels before and after prostaglandin synthetase inhibitor administration.

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Main Results:

Increased urinary prostaglandin E in untreated patients.
Prostaglandin synthetase inhibitors reduced plasma renin and aldosterone, and increased plasma potassium.
Kidney histology and absence of sodium leak distinguished it from glomerulonephritis.

Conclusions:

Prostaglandin E partially controls renin secretion and is a key feature of juxtaglomerular hyperplasia syndrome.
Prostaglandin E may be a primary cause of the syndrome's manifestations.