Literature data and original experience of the authors with 6890 cases of respiratory sarcoidosis (stage I-III) suggest that diabetes ipsipidus in respiratory sarcoidosis (RS) can present as hypothalamic-hypophysial form (observed at the stage I-II by physicians since 1935) and a new form--nephrogenic (vasopressin-resistant) at stage II of pulmonary sarcoidosis. The latter form is little known. It was found that in stage III sarcoidosis patients who have severe fibrosis of the lungs and a long history of corticosteroid hormone treatment the nephrogenic form of the pathogenesis is caused by defects in calcium metabolism leading to nephrocalcinosis with low sensitivity of renal tubular receptors to ADH. Adiurecrine treatment is unefficient. It is recommended to use chlorpropamide which raises sensitivity of the tubules to ADH.
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