Nephrol Dial Transplant (2000) 15: 1903-1905
© 2000 European Renal Association-European Dialysis and Transplant Association
Editorial Comments
New insights into the paradoxical effect of thiazides in diabetes insipidus therapy
Hospital das Clínicas da Fac. de Medicina da Univ. de São Paulo, São Paulo, Brazil
Introduction
One of the great advances in the therapy of renal disease occurred in the 1930s and was the synthesis of orally administered diuretic compounds. In 1937 suphanilamides had been introduced as antimicrobiological agents. In patients treated with suphanilamides, metabolic acidosis with alkaline urine was observed. Pursuance of this phenomenon led to the accidental discovery of the diuretic effect of suphanilamides. In 1940 it was found that some suphanilamides inhibited carboanhydrase. An intensive search for suphanilamides without carboanhydrase inhibition led to the synthesis of benzothiazide by Novello and Sprague [1]. Subsequently, numerous congeners were synthesized which are widely used today.
Action of thiazide diuretics
The principal site of thiazide action is the distal convoluted tubule, where they inhibit the NaCl cotransporter in the luminal membrane, thus decreasing the Cl- and Na+ reabsorption. In 1990 Tran et al. [2] studied metolazone, a thiazide type diuretic and suggested that thiazides occupy the
The clinical use of thiazides in nephrogenic diabetes insipidus
Proposed mechanisms of action
Microperfusion studies on the inner medullary collecting duct (IMCD)
Some practical points
Notes
References
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