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characterization of a calcium-sensing receptor mutation in severe autosomal dominant hypocalcemia with a Bartter-like syndrome. Association between activating mutations of calcium-sensing receptor and Bartter's syndrome. Lifton RP. Bartter's syndrome, hypokalemic alkalosis with hypercalciuria, is caused by mutations in the Na–K–2Cl cotransporter NKCC2. variant of Bartter's syndrome, inherited hypokalemic alkalosis, is caused by mutations in the thiazide-sensitive Na–Cl cotransporter. molecular variants of the Na–K–2Cl cotransporter gene are responsible for antenatal Bartter syndrome. A common NKCC2 mutation in Costa Rican Bartter's syndrome patients: evidence for a founder effect. International collaborative study group for Bartter-like syndromes. Mutations in the gene encoding the inwardly rectifying renal potassium channel, ROMK, cause the antenatal variant of Bartter syndrome: evidence for genetic heterogeneity. et al. Mutations in the chloride channel gene CLCNKB as a cause of classic Bartter syndrome. Clinical presentation of genetically defined patients with hypokalemic salt-losing tubulopathies. et al. Barttin is a Cl – channel beta-subunit crucial for renal Cl – reabsorption and inner ear K þ secretion. In renal atherosclerotic vascular disease there is often no firm randomized trial data to guide clinical practice. Nephrologists often have to interpret trial data from other vascular territories. Vascular protection devices are now an issue in the carotid and cardiac territories. Should they have a role in renal atherosclerotic disease? There is considerable literature on renal athero-embolic disease. The early paper of Thurlbeck and Castleman [1] showed that in post-mortem renal histology analysis after aortic aneurysm repair followed by death there was an incidence of renal atheroembolic

Do protection devices have a role in renal angioplasty and stent placement?