Nephrogenic Diabetes Insipidus

Abstract

3.2 Introduction 96 3.3 Materials and Methods 97 3.4 Results 3.5 Discussion 105 3.6 References 108 Chapter 4 Three-point linkage analysis using multiple DNA polymorphic markers in families with X-linked Nephrogenic Diabetes Insipidus 4.1 Abstract 4.2 Introduction 4.3 Materials and Methods 4.4 Results and Discussion 4.5 References Chapter 5 Fibrinolytic responses to l-desamino-8-D-arginine vasopressin in patients with congenital Nephrogenic Diabetes Insipidus

Hereditary Nephrogenic Diabetes insipidus and Bilateral Nonobstructive Hydronephrosis

“…I n the absence of dehydration, renal function is said to be normal [46]. However, our 2 patients had mild compromise of glomerular filtration rate and hypertension, which have been described in several of these patients in previous reports [4,7,8,11,16,42], but the exact incidence of decline of renal function in this condition remains unknown.…”

Demeclocycline in the treatment of the syndrome of inappropriate antidiuretic hormone release: with measurement of plasma ADH

“…It has been claimed that while tetracyclines in general (Shils, 1963) and outdated tetracyclines in particular (Gross, 1963) can be nephrotoxic the renal effects of demeclocycline are confined to an impairment of concentrating ability (Wilson et al, 1973). Castell and Sparks (1965) were the first to describe this peculiar property of demeclocycline, and their initial observations have since been confirmed (Singer and Rotenberg, 1973;Wilson et al, 1973;Maxon and Rutsky, 1973; Hayek and Ramirez, Miller and Palo, 1974). The mode of action of demeclocycline in producing nephrogenic diabetes insipidus is complex as both ADH- (Singer and Rotenberg, 1973;Feldman and Singer, 1974) and cyclic AMP- (Singer and Rotenberg, 1973;Dousa and Wilson, 1974) mediated effects on water transport can be separately affected.…”

“…The initial dose of 1200 mg was chosen for the present case as this has been shown to be invariably effective in normal subjects (Singer and Rotenberg, 1973). Although the time of onset of response to demeclocycline is variable ranging from as little as 6-8 hr (Maxon and Rutsky, 1973) to as long as 4 weeks (Miller and Palo, 1974), the dose was increased after one week in order to ensure a response within the time of the study. In retrospect, it is clear that 2400 mg/24 hr was an excessive dose because, although the patient rapidly corrected all biochemical abnormalities (large volumes of dilute urine were passed, sodium was retained, serum sodium rose to high normal values and weight was lost), renal failure ensued.…”