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PubMed1975

The mechanism of acute renal failure after uranyl nitrate.

Administration of 25 mg/kg uranyl nitrate (UN) to rats leads to a brief period of polyuria followed by progressive oliguria with death at 5 days. Factors that determine glomerular filtration rate (GFR) were examined in control Munich-Wistar rats (n equals 16) and 2 h after either 15 mg/kg (n equals 8) or 25 mg/kg (n equals 7) of UN (i.v.) utilizing direct measurements of hydrostatic and oncotic pressures and plasma flow. Total kidney GFR was reduced to 47% of control in the low dose group and to 21% in the high dose group. The simultaneous nephron filtration rate (sngfr) was 28.6 plus or minus 0.8 nl/min/g kidney wt in control, 29.1 plus or minus 1.0 in the low dose group, and 18.1 plus or minus 1.2 (P less than 0.001) in the higher dose group. This disparity in UN effect upon GFR and sngfr was due to tubular back-diffusion of solute through damaged epithelia beyond the early proximal tubule as demonstrated by microinjection of inulin and mannitol in the proximal tubule. Inulin "leak" persisted at 6 h after UN when tubular pressure had returned to normal. Comparison of sngfr measured in early vs. late proximal tubule revealed no difference after high dose UN, suggesting no significant leak of inulin from the early proximal tubule, and that the decreased sngfr was due to primary reductions in ultrafiltration. Nephron plasma flow was equal to control at both doses of UN. Also directly measured hydrostatic pressure gradient across the glomerular capillary was not changed. The effective filtration pressure achieved equilibrium in control of animals but became significantly positive at the efferent end of the capillary at both doses of UN and increased. Total glomerular permeability (LpA) was progressively reduced from control (0.089 plus or minus 0.005 nl/s/g kidney wt/mm Hg) at low dose UN (0.047 plus or minus 0.013) and high dose 0.024 plus or minus 0.003 nl/s/g kidney wt/mm Hg). Therefore UN decreases GFR by two mechanisms: (1) tubular damage leading to back-diffusion of solutes and (b) a primary reduction in sngfr due to reduced LpA.

Acute Kidney Injury↗
PubMed1995

Lithium-induced downregulation of aquaporin-2 water channel expression in rat kidney medulla.

Lithium, a widely used treatment for bipolar affective disorders, often causes nephrogenic diabetes insipidus. The effect of chronic lithium therapy on the expression of the vasopressin-regulated water channel Aquaporin-2 (AQP2) in rat kidney was examined. Membranes were prepared from inner medulla of one kidney from each rat, while the contralateral one was fixed for immunofluorescence and immunoelectronmicroscopy. Immunoblotting revealed that lithium treatment reduced AQP2 expression dramatically, to 31 +/- 8% after 10 d and to 4 +/- 1% after 25 d, coincident with development of severe polyuria. Immunofluorescence and immunogold quantitation confirmed the lithium-induced decrease in AQP2 expression (from 11.2 +/- 1.0 to 1.1 +/- 0.2 particles/microns 2). The downregulation was only partly reversed by return to lithium-free diet for 1 wk (40 +/- 8% of control). Furthermore, immunoblotting and immunogold quantitation revealed that 2 d of thirsting or 7 d of dDAVP treatment, in the continued presence of lithium, increased AQP2 expression by six- and threefold, respectively, coincident with increased urinary osmolality. Thirsting increased AQP2 immunolabeling mainly of vesicles, whereas dDAVP caused accumulation of AQP2 predominantly in the subapical region and plasma membrane. Thus, lithium causes marked downregulation of AQP2 expression, only partially reversed by cessation of therapy, thirsting or dDAVP treatment, consistent with clinical observations of slow recovery from lithium-induced urinary concentrating defects.

Animals↗
PubMed1991

Less frequent lithium administration and lower urine volume.

OBJECTIVE: This study was designed to determine whether patients maintained on a regimen of lithium on a once-per-day schedule have lower urine volumes than do patients receiving multiple doses per day. METHOD: This was a cross-sectional study of 85 patients from a lithium clinic who received different dose schedules. Patients were admitted to the hospital for measurement of lithium level, creatinine clearance, urine volume, and maximum osmolality. RESULTS: Multiple daily doses of lithium were associated with higher urine volumes. The dosing schedule, duration of lithium treatment, and daily dose of lithium did not affect maximum osmolality or creatinine clearance. CONCLUSIONS: Urine volume can be reduced by giving lithium once daily and/or by lowering the total daily dose. Lithium-induced polyuria seems to be related to extrarenal as well as to renal effects.

Depressive Disorder↗
PubMed1986

Familial juvenile nephronophthisis. A review and differential diagnosis.

Familial juvenile nephronophthisis (FJN) is a frequent cause of chronic renal failure in children and adolescents. Typically it presents after 6 years of age through adolescence, but may become apparent in early childhood. The clinical presentation is insidious, and the early symptoms of polyuria and polydipsia are often overlooked in the presence of a relatively normal urinalysis and in the absence of proteinuria, azotemia, and hypertension. Thus most patients are not diagnosed until after the onset of renal failure. These children are excellent candidates for properly selected transplantation.

Abnormalities, Multiple↗
PubMed1994

Compulsive water drinking in infants and young children.

The management and follow-up of five patients with asymptomatic compulsive water drinking is described. Three out of the five patients were female and two were male. The age range was 6 to 20 months. All the patients presented with polyuria or polydipsia and urine osmolalities of 39 to 112 mOsm/L. The daily fluid intake ranged from 3.5 to 5 L, and the urine output was 11 to 14 mL/kg/hr. Significant improvement was noticed after a gradual weaning process. As fluid intake returned to normal, urine osmolalities reached values between 210 and 500 mOsm/L after 4 weeks, and between 630 and 800 mOsm/L after 8 weeks. No relapse was noted during the 6- to 24-month follow-up period. Pediatricians should be aware of this potentially dangerous--yet not uncommon--habit.

Drinking↗
PubMed1984

A double-blind multicentre study of piretanide and hydrochlorothiazide in patients with essential hypertension.

In a randomized double-blind parallel group study conducted in three centres the hypotensive activity of piretanide 6 mg b.i.d. was compared with that of hydrochlorothiazide (HCT) 25 mg b.i.d. and HCT 50 mg b.i.d. Ninety-three patients entered the study and sixty-one completed a 16-week trial period. All three treatments produced a significant reduction in supine diastolic and systolic blood pressure after only 2 weeks of active treatment and this was maintained for the duration of the study. The mean maximal reduction in supine diastolic blood pressure was 18% in the piretanide group, 18.8% in the HCT 25 mg b.i.d. group, and 20% in the HCT 50 mg b.i.d. group. The corresponding figures for the percentage of patients attaining a supine diastolic pressure below 95 mm Hg were 83%, 62% and 89%. There were no significant differences between the three groups. Side-effects were generally mild and transient, except for polyuria which was noted in all three groups but more commonly in the piretanide group. Two patients were withdrawn because of side-effects: one patient in the high dose HCT group developed severe postural symptoms; and one patient in the low dose HCT group was withdrawn because of restlessness, nausea, weakness, dizziness and somnolence. All three treatments caused a significant increase in serum uric acid concentrations. Four patients in each of the HCT groups developed hypokalaemia, but no patients in the piretanide group did so.

Adult↗
PubMed1980

Long-term lithium treatment and the kidney. Interim report on fifty patients.

This is a report on the first part of our study of the effects of long-term lithium treatment on the kidney. Creatinine clearance, maximum urinary osmolality and 24 hour urine volume have been tested in 50 affectively ill patients who have been on long-term lithium for more than one year. These findings have been compared with norms and with values of the same tests from screening prior to lithium, available for most of our patients. No evidence was found for any reduction of glomerular filtration during lithium treatment. Low clearance values found in several patients could be accounted for by their age and their pre-lithium values. Urinary concentration defect appeared frequent but the extent of the impairment is difficult to assess because of the uncertainty about the norms applicable to this group of patients. The concentration defect appeared reversible, at least in part. Polyuria above 3 litres/24 hours was found in 10% of patients. An attempt is made to draw practical conclusions from the preliminary findings.

Adult↗
PubMed1985

The medical and psychological investigation of psychogenic polydipsia: a case study.

The case of a 17 year-old female with psychogenic polydipsia is reported; 13 out of 18 members of her maternal family were known to have had polydipsia and polyuria, but only two had undergone endocrine investigations--one had diabetes insipidus and one also had psychogenic polydipsia. There are probable contributions of non-genetic family factors including imitation and identification to the development of this patient's condition. Detailed family and developmental histories may be of particular assistance in the understanding of the psychogenesis of the disorder in some patients.

Adolescent↗
PubMed2004

A novel mutation in the preprovasopressin gene identified in a kindred with autosomal dominant neurohypophyseal diabetes insipidus.

Autosomal dominant neurohypophyseal diabetes insipidus (ADNDI) is a defect in free water conservation caused by mutations in the single gene that encodes both vasopressin (VP) and its binding protein, neurophysin II (NP II). Most of the human mutations in this gene have been in the portion encoding the NP molecule; the resultant abnormal gene products are believed to cause cellular toxicity as improperly folded precursor molecules accumulate in the endoplasmic reticulum. We identified a new American kindred with ADNDI and found a novel mutation in the VP molecule. A 78-yr-old man was noted to have hypotonic polyuria and plasma hyperosmolarity; the urinary concentration defect was reversed by administration of VP. His symptomatology dated to childhood, and his family history was consistent with autosomal transmission of the polyuric syndrome, with affected members in three generations, including several females. Affected individuals were found to be heterozygous for a 3-bp deletion in exon 1 of arginine VP (AVP)-NP II, predicting a deletion of phenylalanine 3 (known to be critical for receptor binding) in the VP nonapeptide. Neuro 2A cells stably transfected with the mutant AVP-NP construct showed increased rates of apoptosis as assessed by flow cytometric methods. These observations support the concept that cellular toxicity of abnormal AVP-NP gene products underlies the development of ADNDI, and the data further demonstrate that mutations affecting the AVP moiety can result in initiation of these pathological processes.

Aged↗
PubMed1990

Atrial natriuretic peptide in patients with the syndrome of inappropriate antidiuretic hormone secretion and with diabetes insipidus.

To examine a possible role for atrial natriuretic peptide (ANP) in water and sodium metabolism disturbances associated with abnormal vasopressin (AVP) secretion, we measured plasma ANP concentrations in 15 patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) and in 17 patients with central diabetes insipidus (DI). The mean plasma ANP concentration (30.2 +/- 10.4 pmol/L) in SIADH patients who had hyponatremia, plasma hypoosmolality, hyperosmolar urinary compared to plasma sodium levels, and increased plasma AVP levels relative to plasma osmolality was significantly higher than that in normal subjects (12.6 +/- 4.9 pmol/L), although there was a considerable individual variation in plasma ANP ranging from normal to clearly elevated levels (15.1-47.0 pmol/L). When hyponatremia was corrected by water restriction or demeclocycline administration, plasma ANP levels decreased significantly and fell into the normal range (12.5 +/- 4.3 pmol/L). DI patients who complained of polyuria and polydipsia and had hypoosmolar urine, normal or elevated plasma sodium concentrations, and decreased plasma AVP levels relative to plasma osmolality, on the other hand, had a significantly lower mean plasma ANP level (7.6 +/- 2.9 pmol/L) than normal subjects. There was, again, a considerable overlap between plasma ANP levels in individual DI patients (4.2-13.9 pmol/L) and those in normal subjects. Treatment with 1-desamino-8-D-arginine vasopressin resulted in a significant increase in the mean plasma ANP level (18.6 +/- 8.0 pmol/L). There were no significant correlations between plasma ANP and AVP levels in either group of patients. The results indicate that ANP secretion is modulated by changes in plasma volume consequent to abnormal AVP secretion, which may have a pathophysiological significance in maintaining volume homeostasis.

Adolescent↗
PubMed1996

The influence of polydipsia on water excretion in hyponatremic, polydipsic, schizophrenic patients.

To determine whether polydipsia is responsible for the altered water excretion in the subset of polydipsic schizophrenic patients who develop hyponatremia, the regulation of antidiuretic function was assessed in polydipsic schizophrenic patients with hyponatremia (n = 5), polydipsic schizophrenic patients without hyponatremia (n = 5), nonpolydipsic schizophrenic patients (n = 6), and normal controls (n = 8). The severity and duration of polyuria were similar in the two polydipsic groups. After oral water loading, maximal free water clearance was similar across all four groups. Free water clearance diminished, however, at lower plasma osmolalities in the hyponatremic polydipsics (P < 0.02) and at higher plasma osmolalities in the normonatremic polydipsics (P < 0.05) relative to that in the nonpolydipsic schizophrenics and normal subjects. The increase in plasma vasopressin after osmotic stimulation with hypertonic saline was slightly, but significantly (P < 0.02), blunted in both polydipsic groups. Hyponatremia occurs in some polydipsic schizophrenics because the relationship between free water clearance to plasma osmolality/sodium is shifted to the left. Polydipsia per se is not responsible for this still unexplained shift.

Adult↗
PubMed1996

A new type of familial central diabetes insipidus caused by a single base substitution in the neurophysin II coding region of the vasopressin gene.

We studied the genetic basis of familial neurohypophyseal diabetes insipidus in a Japanese family. The members had polyuria and a deficiency of plasma vasopressin (AVP). Polymerase chain reaction (PCR) amplified exons of the AVP-neurophysin-II gene were subcloned and sequenced. Exons 1 and 3 were normal, but nucleotide 1884 Guanine (G) in exon 2 was substituted with Thymine (T), which induced a substitution of glycine (Gly) for valine (Val). To examine the presence of this mutation in the affected subjects, we designed two mutated primers. One of them induced a new endonuclease restriction site in the PCR fragments from normal, and the other induced a new endonuclease restriction site from patients with the mutation. DNA fragments from two affected members of this family were amplified with this primer, and the PCR products were digested by endonuclease and resolved by electrophoresis. The results indicated that these subjects had both normal and mutant alleles, indicating that the mutation was heterozygous. We concluded that this mutation caused neurohypophyseal diabetes insipidus in this family.

Arginine Vasopressin↗
PubMed1996

Maximal dose glyburide therapy in markedly symptomatic patients with type 2 diabetes: a new use for an old friend.

No consensus exists as to the best approach for treating markedly symptomatic patients with new-onset (or diet-treated) type 2 diabetes. Therefore, based on the experience of one successful case, further studies were undertaken to determine the safety and efficacy of maximal dose glyburide (10 mg, twice daily, in patients < 65 yr of age) or half the dose (10 mg, daily, in patients > or = 65 yr of age) for treating these patients. Fifty-five patients with polyuria, polydipsia, nocturia, involuntary weight loss, and blood glucose concentrations of 300 mg/dL or greater were treated following protocols that used maximal dose ( < 65 yr of age) or half-maximal dose ( > or = 65 yr of age) sulfonylurea agent therapy. Data were collected retrospectively in 30 patients and prospectively in 25. Patients in the prospective group differed only in that more laboratory measurements were obtained, and less strict guidelines for using insulin were adopted. Data were collected in both groups at baseline and 1 week and 4 months after starting the sulfonylurea agent therapy. Patients responded rapidly with a fall in blood glucose levels from 456 +/- 12 mg/dL at baseline to 202 +/- 10 mg/dL at 1 week to 120 +/- 5 mg/dL at 4 months. Glycated hemoglobin levels fell from 18.1 +/- 0.4% at baseline to 8.1 +/- 0.2% ( P < 0.0001) at 4 months. Most patients had symptomatic improvement within 3 days. Seventeen patients had positive (small or larger) urinary ketones, and 5 had positive serum ketones. Insulin to glucose and C peptide to glucose ratios improved maximally at 1 week, indicating rapid reversal of glucotoxicity on the beta-cell. At 4 months, 11 patients were receiving diet therapy alone, 29 were receiving submaximal dose sulfonylurea agent therapy, 6 remained on maximal dose sulfonylurea agent therapy, and only 3 were receiving insulin therapy. Six patients were lost to follow-up. No patient experienced hypoglycemia in the first 2 weeks of treatment. Maximal dose sulfonylurea agent therapy is a safe and effective method for treating patients with markedly symptomatic type 2 diabetes. Patients improve rapidly and are able to avoid the immediate institution of long term insulin therapy.

Adolescent↗
PubMedDate not supplied

A comparison of renal effects and metabolism of sevoflurane and methoxyflurane in enzyme-induced rats.

Twenty-five 5-month-old male Fischer-344 rats were randomly divided into 5 groups: Group I, no anesthesia; Group II, 1.4 precent sevoflurane for 2 hours; Group III, 0.1 percent phenobarbital, ad lib, in drinking water for 7 days; followed by 1.4 percent sevoflurane for 2 hours; Group IV, 0.25 percent methoxyflurane, 1 hour; Group V, phenobarbital in water as in Group III, followed by methoxyflurane as in group IV. Pre- and postanesthetic serum and urinary osmolality, Na+, K+, urea nitrogen (BUN), inorganic fluoride (F-) levels, and 24-hour urine volume were measured. Kidney tissue was obtained for examination by light and electron microscopy. Sevoflurane was metabolized to F- to a lesser extent than was methoxyflurane; treatment with phenobarbital-sevoflurane doubled urinary F- excretion, resulting in a value similar to that seen after methoxyflurane alone. There was no functional or morphologic evidence of renal abnormalities in either group of rats anesthetized with sevoflurane. Methoxyflurane dosage was sufficiently low that renal abnormalities did not occur except in rats treated also with phenobarbital; these animals developed polyuria and the morphologic lesion typically associated with F--induced nephrotoxicity.

Anesthetics↗
PubMed2001

Hyperintensity of posterior pituitary on MR T1WI in a boy with central diabetes insipidus caused by missense mutation of neurophysin II gene.

We present a 10-year old boy with central diabetes insipidus (CDI) showing hyperintensity in a normal-sized posterior pituitary on magnetic resonance (MR) T1-weighted image (T1WI). He complained of nocturnal enuresis and polyuria. Daily urine volume increased to 4 to 5 L, and AVP plasma level was very low. Polymerase chain reaction (PCR)-amplified exons of the arginine vasopressin (AVP)-neurophysin (NP) II gene were sequenced. Nucleotide-1884 guanine in Exon 2 was substituted with thymine, which induced a substitution of glycine for valine at amino acid position 65 in the NP II moiety. However, MR imaging showed hyperintensity in the posterior pituitary on T1WI. These results suggest that the MR findings of the posterior pituitary in CDI may vary.

Child↗
PubMed1988

A short water deprivation test incorporating urinary arginine vasopressin estimations for the investigation of posterior pituitary function in children.

The value of a 7-h water deprivation test incorporating urinary osmolality and urinary arginine vasopressin (AVP) measurements was investigated in 20 children with suspected anterior or posterior pituitary dysfunction (group A) and 11 presenting with polyuria and polydipsia (group B). A control group of 16 healthy children was also studied. Urinary osmolalities in the control subjects after 7 h of water deprivation were 827-1136 mosmol/kg and urinary AVP 114-320 pmol/l. Of the group A patients, 5 had symptomatic diabetes insipidus with urinary osmolalities less than 300 mosmol/kg, and urinary AVP concentrations of less than 10 pmol/l, and 5 had normal urinary concentrating ability. The other 10 patients had varying degrees of partial diabetes insipidus (urinary AVP 6-53 pmol/l) although in 3 urinary concentrating ability was well maintained (osmolality 650-747 mosmol/kg). In group B, a diagnosis of compulsive water drinking was made in 9 patients, 1 had nephrogenic diabetes insipidus (urinary osmolality 68 mosmol/kg, AVP 782 pmol/l), and the final patient had transient diabetes insipidus. The test described was easy to perform and well tolerated even in young children. Using this test alone, it was possible to identify patients with partial defects of posterior pituitary function even when urinary concentrating ability was maintained, as well as those with complete cranial diabetes insipidus, nephrogenic diabetes insipidus, and compulsive water drinking.

Adolescent↗
PubMed2004

Identification of a novel mutation in the arginine vasopressin-neurophysin II gene affecting the sixth intrachain disulfide bridge of the neurophysin II moiety.

OBJECTIVE: Most mutations of the arginine vasopressin-neurophysin II (AVP-NPII) gene cause autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI). Such mutations are predicted to alter the three-dimensional structure of the prohormone, which accumulates in the cell body, ultimately leading to neuronal degeneration and hormonal deficit. In this study we describe the case of a 26-year-old female reporting a long-lasting history of polyuria/polydipsia. The father of the patient was affected by diabetes insipidus and was under desmopressin treatment until the time of his death. Nevertheless, the patient had never been subjected to endocrine evaluation. DESIGN AND METHODS: Clinical and genetic studies were performed. An 8-h fluid deprivation test plus desmopressin challenge and a 5% saline solution test were performed, in order to confirm the diagnosis. DNA was extracted from peripheral blood lymphocytes and subjected to direct sequencing of the entire coding region of the AVP-NPII gene. RESULTS AND CONCLUSIONS: Clinical assessment of the patient confirmed the diagnosis of neurohypophyseal diabetes insipidus. Desmopressin treatment was started, which effectively reversed the polyuria/ polydipsia syndrome. Genetic analysis revealed a novel mutation (1665T>A) in exon 2 of the AVP-NPII gene, disrupting one of the disulfide bonds present in the NPII moiety which play a fundamental role in determining the proper folding of the molecule. In summary, in the present study we have described a novel mutation of the AVP-NPII gene, which is consistent with the malfolding/toxicity hypothesis underlying the pathogenesis of adFNDI.

Adult↗