No abstract available.
Diabetes Insipidus, Nephrogenic*

No abstract available.
Diabetes Insipidus, Nephrogenic* ; Urinary Bladder*

No abstract available.
Diabetes Insipidus, Nephrogenic* ; Humans ; Siblings*

No abstract available.
Diabetes Insipidus, Nephrogenic* ; Urinary Tract Infections ; Vesico-Ureteral Reflux*

Nephrogenic diabetes insipidus(DI) is characterized by insensitivity of the distal nephron to vasopressin(ADH) and the inability to concentrate urine, which leads to excreting excessive quantities of urine. Upper tract dilation secondary to polyuria was previously shown to be associated with nephrogenic DI. We report here on 3 males with nephrogenic DI that caused voiding difficulty as well as massive nonobstructive dilation of the urinary tract.
Diabetes Insipidus ; Diabetes Insipidus, Nephrogenic ; Humans ; Male ; Nephrons ; Polyuria ; Urinary Tract

We describe a case of congenital nephrogenic diabetes insipidus with severe dilatation of bilateral urinary tracts without anatomical obstructions. Functional obstruction can be occurred when polyuria surpasses the transporting ability of urine in the urinary tract. The patient was admitted to our hospital due to decreased mentality developed after traffic accident. On radiologic study, bilateral hydronephrosis and hydroureter were noted. Because the patient excreted copious dilute urine, we performed water deprivation test and the result was consistent with nephrogenic diabetes insipidus. We are presenting this case in an attempt to describe strong association between congenital diabetes insipidus and nonobstructive hydronephrosis in which polyuria is responsible for the hydronephrosis.
Accidents, Traffic ; Diabetes Insipidus ; Diabetes Insipidus, Nephrogenic* ; Dilatation ; Humans ; Hydronephrosis* ; Polyuria ; Urinary Tract ; Water Deprivation

This study aimed to examine whether the expression of major prostaglandin E2 (PGE2) synthesis enzyme, cyclooxygenase-2 (COX-2), is changed in the kidneys of the rats with lithium-induced nephrogenic diabetes insipidus (Li-NDI). Sprague- Dawley rats treated with lithium for 4 weeks were used as the NDI model and expression of renal COX-2 was determined by immunoblotting and immunohistochemistry. In Li-NDI where urine output was markedly increased and urine osmolality was significantly decreased, COX-2 expression in the inner medulla was decreased (28% of control), while it increased 18-fold in the cortex and outer medulla. Consistent with this, labeling intensity of COX-2 in macula densa region was increased, whereas it was decreased in the interstitial cells in the inner medulla, indicating a differential regulation of COX-2 between the cortex and inner medulla in Li-NDI. Accordingly, urinary PGE2 excretion was significantly increased in Li-NDI. In conclusion, there is a differential regulation of COX-2 between cortex and inner medulla in Li- NDI and urinary PGE2 excretion is increased in Li-NDI, possibly due to an increased renal production. This may suggest that increased renal production of PGE2 could play a role in modulating water reabsorption in the renal collecting duct in Li-NDI.
Animals ; Aquaporins ; Cyclooxygenase 2* ; Diabetes Insipidus, Nephrogenic* ; Dinoprostone ; Immunoblotting ; Immunohistochemistry ; Kidney ; Lithium ; Osmolar Concentration ; Prostaglandins ; Rats*

Nephrogenic diabetes insipidus is a rare genetic renal disease characterized by insensitivity of the kidney to the anti-diuretic effect of vasopressin in spite of elevated serum anti-diuretic hormone (ADH). Failure of the kidney to respond to ADH results in impaired osmoregulation and water reabsorption of the kidney, therefore, nephrogenic diabetes insipidus presents with a large amount of hypotonic polyuria, polydipsia, and dehydration. We report our experience of two familial cases of nephrogenic diabetes insipidus in brothers both having c.910+1delG in intron 2 of the AVPR2 gene with the brief review of related literatures.
Dehydration ; Diabetes Insipidus, Nephrogenic ; Humans ; Introns ; Kidney ; Polydipsia ; Polyuria ; Siblings ; Vasopressins ; Water ; Water-Electrolyte Balance

The most common form of genetic nephrogenic diabetes insipidus(NDI), a rare inherited disorder, is congenital and is transmitted in an X-linked recessive mode. It is refractory to the antidiuretic effect of normal to moderately increased levels of plasma arginine vasopressin(AVP) but, in some cases, may respond to high levels of the hormone or its analogue, deamino-D-arginine vasopressin(DDAVP). X-linked congenital NDI has now been linked to over 128 different mutations in diverse coding regions of the AVP receptor 2(AVPR2) gene. The functional effects of these mutations vary from complete loss of responsiveness to a simple shift to the right in the dose response curve. We report a case of congenital partial NDI, with transversion of A to G at codon 280 of the AVPR2 gene, resulting in a subsequent change of amino acid from tyrosine to cysteine, and that has been effective with hydrochlorothiazide and high dose of DDAVP.
Antidiuretic Agents ; Arginine ; Clinical Coding ; Codon ; Cysteine ; Deamino Arginine Vasopressin ; Diabetes Insipidus, Nephrogenic* ; Hydrochlorothiazide ; Plasma ; Tyrosine

Nephrogenic diabetes insipidus is a rare hereditary disorder characterized by insensitivity of the renal tubule to vasopressin. We report a case of nephrogenic diabetes insipidus associated with severe hydronephrosis in a 18 year old male, which was improved in urine volume, urine osmolarity and urine specific gravity with chlorothiazide therapy.
Adolescent ; Chlorothiazide ; Diabetes Insipidus, Nephrogenic* ; Humans ; Hydronephrosis* ; Male ; Osmolar Concentration ; Specific Gravity ; Vasopressins