[On a case of diabetes insipidus associated with diabetes mellitus].
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Diabetes Complications↗
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Diabetes insipidus in a patient with diabetes mellitus.
The association of Diabetes Mellitus (DM) and Diabetes Insipidus (DI) without any congenital defects is very rare and we report here a case of type 2 diabetes mellitus (NIDDM) whose blood sugar was controlled by insulin, developing central diabetes insipidus 2 years later, which could be successively controlled by synthetic vasopressin.
Diabetes Insipidus↗
[Wegener's disease and central diabetes insipidus].
Vasculitis with central diabetes insipidus is a rare condition which must be recognized for proper management. We report a case of Wegener's granulomatosis with diabetes insipidus and review the literature concerning the clinical and radiological features of this association. We examined the data supporting the efficacy of cyclophosphamide in diabetes insipidus. Diabetes insipidus is inaugural in 46% of cases. Wegener's granulomatosis has no distinctive features when associated with diabetes insipidus. MR imaging reveals an enlargement of the posterior pituitary in 100% of cases. Cyclophosphamide is effective in 80% of cases. In Wegener's granulomatosis, pituitary vasculitis is a rare condition. MR imaging is the most accurate method for pituitary exploration. Cyclophosphamide is effective in the treatment of vasculitis lesions in Wegener's granulomatosis.
Aged↗
The value of urine specific gravity in detecting diabetes insipidus in a patient with uncontrolled diabetes mellitus: urine specific gravity in differential diagnosis.
When a patient with diabetes mellitus presents with worsening polyuria and polydipsia, what is a sensible, cost-effective approach? We report the unique coincidence of type 2 diabetes mellitus and diabetes insipidus. A 46-year-old woman with poorly controlled type 2 diabetes complained of polyuria with a daily output of 5 L. Although urinalysis demonstrated significant glucosuria, diabetes insipidus was suspected owing to a low urine specific gravity (1.008). The low specific gravity persisted during a water deprivation test. Ultimately, diabetes insipidus was confirmed when urine specific gravity and urine osmolality normalized following desmopressin administration. This case emphasizes the importance of accurately interpreting the urine specific gravity in patients with polyuria and diabetes mellitus to detect diabetes insipidus.
Diabetes Insipidus↗
Vasopressin antagonist in early postoperative diabetes insipidus.
23 patients without diabetes insipidus before transfrontal (hypothalamic) or trans-sphenoidal (pituitary) surgery were studied prospectively to investigate the pathogenesis of early postoperative diabetes insipidus. 12 patients who underwent trans-sphenoidal surgery and who did not develop diabetes insipidus were used as controls. All received prophylactic corticosteroid replacement. Blood samples were obtained immediately after operation, at the onset of diabetes insipidus, and 24 h later. Immediately after trans-sphenoidal pituitary surgery, plasma vasopressin (AVP) was raised but had fallen to subnormal concentrations by the onset of diabetes insipidus. After transfrontal hypothalamic surgery diabetes insipidus occurred sooner and was associated with high plasma AVP immunoreactivity--but the plasma showed no antidiuretic bioactivity and greatly attenuated the antidiuretic response to standard AVP. Early diabetes insipidus after hypothalamic surgery is associated with release of a substance, presumably an analogue, from the damaged hypothalamo-neurohypophyseal system, which acts as an antagonist to normal AVP activity; after trans-sphenoidal operations diabetes insipidus seems to be caused by failure of AVP release.
Adolescent↗
Reproduction in Brattleboro rats with diabetes insipidus.
The Brattleboro diabetes insipidus mutant is incapable of synthesizing vasopressin, but is activated in its production and release of oxytocin. In the homozygous female mutant, there were abnormally short and long oestrous cycles and reduced conception rates after mating with mutant males, a shortened gestation length, and a shorter time-course of labour. A better conception rate when mutant females were mated with normal Brattleboro males indicates the involvement of a male factor in the subfertility. The reduced litter size in diabetes insipidus rats appeared neither dependent of the male's genotype, nor due to a decreased viability of diabetes insipidus fetuses.
Animals↗
A case of a novel mutant vasopressin receptor-dependent nephrogenic diabetes insipidus with bilateral non-obstructive hydronephrosis in a middle aged man: differentiation from aquaporin-dependent nephrogenic diabetes insipidus by response of factor VII and von Willebrand factor to 1-diamino-8-arginine vasopressin administration.
We describe a case of a novel mutant vasopressin 2 receptor (V2R)-dependent nephrogenic diabetes insipidus (NDI) with bilateral non-obstructive hydronephrosis in a middle aged man. This could be distinguished from aquaporin 2 (AQP2)-dependent NDI by the response of factor VIII and von Willebrand factor (vWF) to 1-deamino-8-D-arginine vasopressin (DDAVP) administration. A 47-year-old man was admitted to hospital because of polyuria, which had been present from infancy and was suspected of causing non-obstructive hydronephrosis. His mother's father, the older brother of his mother and his second daughter also all had polyuria. Sodium concentration, osmolality and vasopressin in blood were high, while sodium concentration and osmolality in urine were low. There were no changes in urine osmolality, factor VIII and vWF in response to DDAVP infusion. Neither was heart rate, diastolic blood pressure nor facial flushing affected. These findings suggested this case was V2R-dependent NDI rather than AQP2-dependent NDI. Molecular genetic analysis demonstrated that the patient had a V2R missense mutation involving a substitution of cysteine for arginine at position 104 (R104C) located in the first extracellular loop of the V2R. It was also found that the patient's mother and his second daughter were heterozygous for this R104C mutation.
Aquaporin 2↗
Central diabetes insipidus and autoimmunity: relationship between the occurrence of antibodies to arginine vasopressin-secreting cells and clinical, immunological, and radiological features in a large cohort of patients with central diabetes insipidus of known and unknown etiology.
Central diabetes insipidus (CDI) is a rare hypothalamus-pituitary disease due to the deficiency of arginine vasopressin (AVP) synthesis from the hypothalamus and/or secretion from the neurohypophysis. The etiology of CDI is unknown in over one third of cases, classified as idiopathic CDI. The aim of this study was 2-fold: 1) to evaluate the occurrence of circulating autoantibodies to AVP-secreting cells (AVPcAb), and 2) to correlate it to clinical (sex, age of disease onset, disease duration, and degree), immunological (clinical history of autoimmune diseases and presence of related organ-specific autoantibodies), and radiological features (neurohypophyseal bright spot, pituitary stalk thickening, and empty sella) in a large cohort of patients with apparently idiopathic CDI or CDI of known etiology. To this purpose, 150 patients with CDI were studied: 64 idiopathic, 6 familial, 12 associated to granulomatous diseases, and 68 secondary to cranial trauma, tumor, or surgery. AVPcAb were measured by an indirect immunofluorescence method. AVPcAb were found in 23.3% of CDI patients: 21 idiopathic (32.8%) and 14 nonidiopathic (16.3%; chi(2) = 13.1; P < 0.001). AVPcAb were independently associated with age less than 30 yr at disease onset (P = 0.001) in patients with idiopathic CDI and with history of autoimmune diseases (P = 0.006 and P = 0.02, respectively) and radiological evidence of pituitary stalk thickening (P = 0.02 and P = 0.003, respectively) in both idiopathic and nonidiopathic CDI. The likelihood of autoimmunity in one patient with apparently idiopathic CDI with age of disease onset less than 30 yr was 53%, it increased to 91% when history of autoimmune diseases was associated and to 99% when pituitary stalk thickening was further associated. In conclusion, autoimmunity is associated with one third of patients with apparently idiopathic CDI, which should therefore be classified as autoimmune CDI. Autoimmune CDI is highly likely in young patients with a clinical history of autoimmune diseases and radiological evidence of pituitary stalk thickening. Conversely, autoimmunity probably represents an epiphenomenon in patients with nonidiopathic CDI.
Adult↗
[Diabetes insipidus: etiology, diagnosis, and therapy].
Diabetes insipidus is a disorder of the water retaining ability of the organism. It is a polydipsic-polyuric syndrome caused by partial or complete vasopressin deficiency (central diabetes insipidus) or vasopressin resistance of the kidney tubules (nephrogenic diabetes insipidus) or increased water intake due to oversensitivity of the thirst centre (dipsogenic diabetes insipidus = primary polydipsia). The pathogenetic factors may affect the osmoreceptors, the vasopressinergic magnocellular nuclei of the hypothalamus, the median eminence, the pituitary stalk, the vasopressin release from the neurohypophysis, the vasopressin inactivating mechanisms and the renal structures mediating the antidiuretic effect of vasopressin. In the evaluation of the results of the diagnostic procedures, it is to be considered that long-term overhydration of any origin suppresses the vasopressin secretion and the "washout" effect of the long-term water-diuresis decreases the concentration gradient of the renal medulla leading to blunted sensitivity towards vasopressin. This is, why the differential diagnostics of central, nephrogenic and dipsogenic diabetes insipidus seems sometimes to be enigmatic. Central diabetes insipidus can be excluded only on the basis of proportional parallel increase of plasma osmolality and plasma vasopressin level. Similarly, nephrogenic diabetes insipidus will be excluded when plasma vasopressin increases proportionately with the increase of urinary osmolality. In equivocal cases T1-weighted MRI of the pituitary may be of help in the establishment of an exact diagnosis. As far as possible, the therapy is to be focused on the diabetes insipidus evoking basal diseases. In central diabetes insipidus, diuresis can be decreased by vasopressin substitution. The first choice compound for this purpose is 1-desamino-8-D-arginine-vasopressin. The non-vasopressin containing oral antidiuretics have become outdated in the treatment of central diabetes insipidus. There is no specific treatment for nephrogenic and dipsogenic diabetes insipidus, so far. Nephrogenic diabetes insipidus can be influenced by non-steroidal antiinflammatory agents or diuretics. Their combined administration is even more effective, however, still does not exceed a 50-percent mitigation in diuresis.
Deamino Arginine Vasopressin↗
[COMPLETE REVERSIBILITY OF AN INDUCED DIABETES INSIPIDUS AND OF A SEVERE DIABETES MELLITUS IN A POTOMANIC AND POLYPHAGIC MENTALLY DEBILITATED PATIENT].
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Conditioning, Psychological↗
Nephrogenic diabetes insipidus.
In nephrogenic diabetes insipidus, the kidney is unable to concentrate urine despite normal or elevated concentrations of the antidiuretic hormone arginine vasopressin (AVP). In congenital nephrogenic diabetes insipidus (NDI), the obvious clinical manifestations of the disease, that is polyuria and polydipsia, are present at birth and need to be immediately recognized to avoid severe episodes of dehydration. Most (>90%) congenital NDI patients have mutations in the AVPR2 gene, the Xq28 gene coding for the vasopressin V2 (antidiuretic) receptor. In <10% of the families studied, congenital NDI has an autosomal recessive inheritance and mutations of the aquaporin-2 gene (AQP2), ie, the vasopressin-sensitive water channel, have been identified. When studied in vitro, most AVPR2 mutations lead to receptors that are trapped intracellularly and are unable to reach the plasma membrane. A minority of the mutant receptors reach the cell surface but are unable to bind AVP or to trigger an intracellular cyclic adenosine-monophosphate (cAMP) signal. Similarly AQP2 mutant proteins are trapped intracellularly and cannot be expressed at the luminal membrane. The acquired form of NDI is much more common than the congenital form, is almost always less severe, and is associated with downregulation of AQP2. The advances described here are examples of "bedside physiology" and provide diagnostic tools for physicians caring for these patients.
Aquaporins↗
A low affinity vasopressin V2-receptor in inherited nephrogenic diabetes insipidus.
Congenital nephrogenic diabetes insipidus (NDI) is an X-linked inherited disorder characterized by renal resistance to the antidiuretic hormonal action of vasopressin. This study describes the molecular basis of nephrogenic diabetes insipidus in a dog family. Kidney membranes prepared from NDI-affected male huskies were examined for vasopressin binding and response. Compared to membranes from unaffected canines, those from the kidney inner medulla of NDI-dogs possessed normal V2-receptor numbers, but with 10-fold lower affinity for [Arg8] vasopressin (AVP). Adenylate cyclase stimulation by AVP in contrast to that by forskolin or GTP-analogues was similarly reduced in a dose responsive manner. The NDI-affected dogs showed antidiuretic responses to very high doses of V2-specific agonists, consistent with their possessing V2-receptors of lower affinity. Prolonged treatment with V2-agonists, 1-deamino [D-Arg8] VP (dDAVP) and 1-deamino [Val4, Sar7] AVP (dVSAVP), rendered the NDI-affected dogs near normal in terms of water intake and urine osmolality.
Adenylyl Cyclases↗
Mutations in the vasopressin V2 receptor and aquaporin-2 genes in 12 families with congenital nephrogenic diabetes insipidus.
Congenital nephrogenic diabetes insipidus (CNDI) is a rare inherited disorder characterized by renal tubular insensitivity to the antidiuretic effect of arginine vasopressin (AVP). In a large majority of the cases, nephrogenic diabetes insipidus is an X-linked recessive disorder caused by mutations in the AVP V2 receptor gene (AVPR2). In the remaining cases, the disease is autosomal recessive or dominant and, for these patients, mutations in the aquaporin 2 gene (AQP2) have been reported. Fourteen probands belonging to 12 families were analyzed by single-strand conformational polymorphism and direct sequencing of the AVPR2 and AQP2 genes. Ten mutations of the AVPR2 gene (six previously reported mutations and four novel mutations: G107E, W193X, L43P, and 15delC) were identified. Three mutations of the AQP2 gene were also identified in two patients: the first patient is homozygous for the R85X mutation and the second is a compound heterozygote for V168 M and S216P mutations. Extrarenal responses to infusion of the strong V2 agonist 1-desamino-8-D-arginine vasopressin allowed AVPR2- and AQP2-associated forms of CNDI to be distinguished in three patients. This test also identified an unexpectedly high urinary osmolality (614 mosmol/kg) in a patient with a P322S mutation of AVPR2 gene and a mild form of CNDI.
Adult↗
Two novel mutations in the coding region for neurophysin-II associated with familial central diabetes insipidus.
Familial central diabetes insipidus is an autosomal dominant disease caused by a deficiency of arginine vasopressin (AVP). We previously reported three distinct mutations in the AVP gene in Japanese familial central diabetes insipidus pedigrees that result in a substitution of Ser for Gly57 in the neurophysin-II (NPII) moiety of the AVP precursor, a substitution of Thr for Ala at the COOH-terminus of the signal peptide, and a deletion of Glu47 in the NPII moiety. In this study, we analyzed the AVP gene in two pedigrees by direct sequencing of the polymerase chain reaction-amplified DNA and found two novel mutations in exon 2, which encodes the central part of the NPII moiety of the precursor. The mutation in one pedigree was a C to A transition at nucleotide position 1891, which replaces Cys67 (TGC) with stop codon (TGA). As the premature termination eliminates part of the COOH domain of the NPII moiety and the glycoprotein moiety, the conformation of the truncated protein is likely to be markedly different from that of normal precursor. In another pedigree, a G to T transversion was detected at nucleotide position 1874, which substitutes polar Trp (TGG) for hydrophobic Gly62 (GGG). It is possible that mutated NPII molecules, as a consequence of a conformational change, cannot bind AVP or self-associate to form higher oligomer complexes. Interestingly, all mutations we have identified to date, with the exception of the signal peptide mutation, are located in exon 2, suggesting the importance of the highly conserved central part of the NPII molecules and/or the NPII moiety in the precursor for AVP synthesis.
Adolescent↗
Non-hormonal drugs for the treatment of diabetes insipidus.
Patients with diabetes insipidus may be successfully controlled with drugs other than vasopressin. These have the advantage of being effective when administered orally. The most important are the diuretics and the hypoglycemic agent chlorpropamide. The mode of action, indications and side effects of these drugs are reviewed. A third potentially useful agent is clofibrate. Recent experience with this drug has been described but more observations are needed before its possible role in the management of diabetes insipidus can be established.
Chlorothiazide↗
Clinical presentation and follow-up of 30 patients with congenital nephrogenic diabetes insipidus.
Congenital nephrogenic diabetes insipidus is characterized by insensitivity of the distal nephron to arginine vasopressin. Clinical knowledge of this disease is based largely on case reports. For this study, data were collected on clinical presentation and during long-term follow-up of 30 male patients with congenital nephrogenic diabetes insipidus. The majority of patients (87%) were diagnosed within the first 2.5 yr of life. Main symptoms at clinical presentation were vomiting and anorexia, failure to thrive, fever, and constipation. Three older patients were diagnosed as a result of events not directly related to the disease. Except for a possibly milder phenotype in patients with a G185C mutation, no clear relationship between clinical and genetic data could be found. Most patients were on hydrochlorothiazide-amiloride treatment without significant side effects. Two patients suffered from severe hydronephrosis with a small rupture of the urinary tract after a minor trauma, and two patients experienced episodes of acute urine retention. Height SD scores for age remained below the 50th percentile in the majority of patients, whereas weight for height SD scores showed a catch-up after several years of underweight.
Adolescent↗
Identification of mutations of the arginine vasopressin-neurophysin II gene in two kindreds with familial central diabetes insipidus.
Familial central diabetes insipidus is transmitted as an autosomal dominant trait with almost complete penetrance. Twenty-three different mutations of the arginine vasopressin-neurophysin II gene have been reported to date, located within the signal peptide-, the arginine vasopressin-, or the neurophysin II-coding region. In the present study two kindreds with familial central diabetes insipidus were examined. The entire coding region of the arginine vasopressin-neurophysin II gene of one affected subject of each family was amplified by PCR and subcloned into a pUC 18 plasmid, and six positive clones were sequenced. After identification of the mutation, direct sequencing was performed on the respective sequence of family members and 28 healthy control subjects. In family A, a missense mutation (C-->T) at nucleotide position 280 was detected, predicting the substitution of alanine by valine at position -1 of the signal peptide. All affected subjects were heterozygote for the mutation, whereas none of the unaffected family members or control subjects displayed the mutant sequence. In family B, a missense mutation within the neurophysin II-coding sequence was identified (nucleotide 1757, G-->C), predicting the substitution of glycine by arginine at position 23. Again, affected family members were found to be heterozygote for the mutation, which was not observed in unaffected family members or in control subjects. Although the mutation of family A was recently described in 3 other kindreds as well, the mutation within the neurophysin II-coding region represents a novel mutation of the AVP-NP II gene.
Arginine Vasopressin↗
Identification of a novel mutation in the arginine vasopressin-neurophysin II gene in familial central diabetes insipidus.
Familial central diabetes insipidus is an inherited disease of predominant autosomal dominant trait characterized by a deficiency of arginine vasopressin. The arginine vasopressin-neurophysin II ( AVP-NPII) gene consists of three exons and is located on chromosome 20p13 encoding for the precursor protein of AVP. We investigated two Caucasian families with a typical autosomal dominant trait of familial central diabetes insipidus, defined by deficiency of arginine vasopressin. After PCR amplification of exon 1 and exon 2/3, fragments were pooled and purified. Nucleotide sequencing was performed with the Taq DyeDeoxy-terminator cycle sequencing method using nested primers. Two mutations in the coding region of NPII were identified. In family C we found a heterozygous G ==> C missense mutation (AA61) in exon 2 leading to the substitution of cystein with serine. In family D a novel heterozygous nonsense mutation in exon 3 (AA 83, GAG ==> TAG) was indentified, leading to a stop codon instead of glutamine. Both mutations were confirmed by restriction analysis and were found in all affected but not in healthy family members or control subjects. We therefore have identified a missense mutation of the AVP-NPII gene and a novel mutation predicting a truncated protein.
Adult↗