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PubMed2005

Diabetic complications in a new animal model (TSOD mouse) of spontaneous NIDDM with obesity.

The TSOD mouse has been established as an inbred strain with spontaneous development of diabetes mellitus as the first clinical signs of diabetes. Polydipsia and polyuria are observed at about 2 months old only in male mice, after which hyperglycemia and hyperinsulinemia are detected. Following these symptoms obesity gradually develops until about 12 months old. In histopathological examination of the pancreas, severe hypertrophy of pancreatic islets was observed due to proliferation and swelling of B cells. In the kidney, thickening of the basement membrane in glomeruli and an increase of the mesangial area were observed at 18 months old. Motor neuropathy in TSOD mice began to appear at 14 months old and most male mice at 17 months old showed weakness of front and hind paws caused by neuron degeneration in the peripheral nerve. In sensory neuropathy, the threshold in the tail pressure test decreased significantly at 12 months old. Light microscopic and electron microscopic examination of sciatic nerves showed a decrease in the density of nerve fibers by the endoneural fibrosis and loss of these fibers. Degenerative changes of myelinated fibers, separation of myelin sheaths with intralamellar edema and remyelination were frequently observed. In the severely affected nerve fibers, the lamellar structure was completely destroyed and macrophages migrated around the myelin sheath or invaded the intramyelin space. Considering these findings similar to non-insulin dependent diabetes mellitus (NIDDM) in humans, the TSOD mouse should be a useful model for the pathogenic study of diabetic complications, especially of peripheral neuropathy.

Animals↗

PubMed2000

T-cell-rich B-cell lymphoma in a ring-tailed lemur (Lemur catta).

A 13-yr-old ring-tailed lemur (Lemur catta) was evaluated for depression, anorexia, polyuria, and polydipsia. The lemur was in poor body condition and was anemic, hypoalbuminemic, and hyponatremic. Cytologic examination of aspirates of the spleen, liver, and bone marrow and histopathologic examination of liver and bone marrow biopsies revealed a disseminated round cell tumor. After euthanasia, necropsy revealed hepatomegaly, splenomegaly, and mesenteric lymphadenomegaly. Neoplastic cells were present within the spleen, liver, kidneys, multiple lymph nodes, bone marrow, lung, small intestine, pancreas, and testicle and were composed of large anaplastic round cells in a background of small well-differentiated lymphocytes. Immunohistochemical analysis revealed that the small well-differentiated lymphocytes labeled for the anti-human T-cell marker, CD3, and the large anaplastic round cells labeled with the anti-human B-cell marker, CD79a. On the basis of the immunohistochemical staining results and morphologic appearance, a diagnosis of a T-cell-rich B-cell lymphoma was made.

Animal Diseases↗

PubMed1998

Central diabetes insipidus associated with a missense mutation in the arginine vasopressin gene that replaces Ala at the carboxyterminus of the signal peptide with Thr.

We report an 18-year-old male with a history of polyuria, polydipsia, and thirst since childhood. In a hypertonic saline infusion test, the patient's plasma vasopressin rose only to 0.28 pg/ml. In a water deprivation test, his urinary osmolality rose only to 189 mosmol/kg and then rose to 538 mosmol/kg by vasopressin administration. A T1-weighted magnetic resonance imaging (MRI) scan revealed a loss of the posterior pituitary bright spot. Sequencing of the vasopressin gene showed a heterozygous point mutation that replaced Ala at the carboxyterminus of the signal peptide with Thr. His father also had similar history, and we therefore diagnosed his illness as familial central diabetes insipidus.

Adolescent↗

PubMed1994

The consulting psychiatrist and the polydipsia-hyponatremia syndrome in schizophrenia.

OBJECTIVE: The authors seek to extend understanding and treatment of hospitalized schizophrenics presenting with complications of polydipsia and dilutional hyponatremia. Attending physicians may ask the consultation/liaison psychiatrist to see schizophrenics with hyponatremically-induced delirium or other psychiatric syndromes. The referring physician may or may not have identified polydipsia and dilutional hyponatremia and their complications. This article will help the consultation/liaison psychiatrist recognize early evidence of water imbalance, describe evaluation, and provide somatic and behavioral treatment approaches to this life-threatening syndrome. METHOD: Over the past ten years, the authors have treated more than 100 patients with the polydipsia-hyponatremia syndrome. The authors discuss their and others' experience with drugs that help and hinder patients suffering from dilutional hyponatremia. They review current key articles from the polydipsia-hyponatremia syndrome literature including articles identified via Medline search 1985-94. RESULTS: Schizophrenics with the polydipsia-hyponatremia syndrome most commonly present with polydipsia, polyuria, urinary incontinence, cognitive, affective, and behavioral changes, seizures, or coma. Quantitating polydipsia, hyponatremia, and diurnal changes in body weight facilitate therapeutic interventions. Treatment include patient and caregiver education, drug therapies to better treat psychosis and better treat osmotic dysregulation, behavioral interventions to interdict polydipsia, and diurnal weight monitoring. CONCLUSIONS: Once recognized, acute, subacute, and chronic complications of the polydipsia-hyponatremia syndrome are readily treatable. Besides treating the patient, consultation/liaison psychiatrists can teach their medical colleagues about this syndrome. In so doing, they will enhance the quality of their patients' lives and help the internist and surgeon feel more comfortable when working with schizophrenics.

Angiotensin II↗

PubMed1976

Metabolic and morphologic studies in intraportal-islet-transplanted rats.

The intraportal injection of 350 to 1,000 isolated islets into streptozotocin-diabetic rats immediately normalized (approximately 24 hours) fasting plasma glucose and insulin levels. Polyuria, polydipsia, and hyperglucagonemia disappeared more gradually over a 2-to-12-week period--the time required for normalization varying with the severity of the diabetes and the number of islets transplanted. In long-term islet-transplanted rats (greater than five months), the hepatic insulin and glucagon reserves averaged 50 per cent and 25 per cent, respectively, of the corresponding normal pancreatic hormone content. Glucagon was increased slightly in the pancreas of streptozotocin-diabetic rats and decreased considerably in transplanted animals. However, total pancreatic glucagon (i.e. pancreatic and hepatic reserves) in transplanted animals was the same as the pancreatic content of normal control rats, indicating the presence of feedback control mechanism(s) in the regulation of pancreatic glucagon reserves. Long-term transplanted islets demonstrated well-granulated A-, B-, and D-cell movement out of the vascular space and the formation of narrow intercellular spaces and junctional complexes with surrounding hepatocytes.

Animals↗

PubMed1976

Diabetes mellitus: incidence, prevalence, survivorship, and causes of death in Rochester, Minnesota, 1945-1970.

The incidence and prevalence of diabetes mellitus in residents of Rochester, Minnesota, for 25 years (1945 to 1970) were determined from available medical records. The over-all incidence rate for diabetes is 133 new cases per 100,000 population per year (age-adjusted to 1970 U.S. white population). The rate increased with age for both men and women and was higher among men over 30 years of age. The average annual incidence rates per five-year period for juvenile-onset diabetes mellitus were low and variable and showed little change. Polyuria, polydipsia, glycosuria, lean habitus, loss of weight, and high levels of fasting hyperglycemia at initial diagnosis occurred more frequently in younger than in older patients. The peak incidence in 1960 through 1964 and the decrease in the following five years may be a reflection of the introduction of the AutoAnalyzer method for blood glucose in 1958. The average annual incidence rates for 1955 through 1959 and 1965 through 1969 were essentially the same. The over-all prevalence for diabetes mellitus is 1.6 per cent, with a higher rate among men than among women over 40 years of age; among school children the rate is 0.1 per cent. Survivorship in the diabetic population is lower than that in the general population. The leading cause of death was coronary heart disease, the death rate from it being higher than for the general population.

Adolescent↗

PubMed1999

Mice transgenic for an expanded CAG repeat in the Huntington's disease gene develop diabetes.

The autosomal dominant neurological syndrome of Huntington's disease has been modeled in transgenic mice by the expression of a portion of the human huntingtin gene together with 140 CAG repeats (the R6/2 strain). The mice develop progressive chorea with onset at approximately 9 weeks of age and with death at approximately 13 weeks. Associated symptoms include weight loss and polyuria in the absence of eating or drinking deficits. We have found that these mice have insulin-responsive diabetes. Fasting glucose was 211 + 19 mg/dl in R6/2 mice compared with 93 + 5 mg/dl in C57/B6 controls (n = 12, both groups; P < 0.01). Administration of insulin intraperitoneally led to a reduction in blood glucose. At 12.5 weeks, animals were killed and pancreas weighed and analyzed for insulin and glucagon. Pancreatic mass in R6/2 mice was the same as controls, and islets appeared normal in morphology without lymphocytic infiltration. Immunohistochemical staining showed dramatic reductions in glucagon in the alpha-cells and in insulin in the beta-cells. Direct tissue assays showed glucagon and insulin content were reduced to only 10 and 15% of controls, respectively. Diabetes has been reported as being more common in Huntington's disease and other triplet repeat disorders. The R6/2 mouse should prove useful for elucidating the mechanism of diabetes in these genetic diseases.

Aging↗

PubMed2002

Results of clinical examinations, laboratory tests, and ultrasonography in dogs with pituitary-dependent hyperadrenocorticism treated with trilostane.

OBJECTIVE: To determine the efficacy of trilostane, a 3beta-hydroxysteroid dehydrogenase inhibitor, in dogs with pituitary-dependent hyperadrenocorticism (PDH). ANIMALS: 11 dogs with PDH. PROCEDURE: The initial dose of trilostane was 30 mg, PO, q 24 h for dogs that weighed < 5 kg and 60 mg, PO, q 24 h for dogs that weighed > or = 5 kg. A CBC count, serum biochemical analyses, urinalysis, ACTH stimulation test, and ultrasonographic evaluation of the adrenal glands were performed in each dog 1, 3 to 4, 6 to 7, 12 to 16, and 24 to 28 weeks after initiation of treatment. RESULTS: All dogs responded well to treatment. All had reductions in polyuria-polydipsia and panting and an increase in activity. Polyphagia decreased in 9 of 10 dogs, and 9 of 11 dogs had improvement of coat quality and skin condition. Concentration of cortisol after ACTH stimulation significantly decreased by 1 week after initiation of treatment. After treatment for 6 months, clinical signs resolved in 9 dogs. In the other 2 dogs, marked clinical improvement was reported for 1 dog, and moderate improvement was reported in the other dog. Ultrasonographically, there was a considerable change in the parenchyma and an increase in size of the adrenal glands. Adverse effects consisted of 1 dog with transient lethargy and 1 dog with anorexia. CONCLUSIONS AND CLINICAL RELEVANCE: Trilostane is an efficacious and safe medication for treatment of dogs with PDH. Additional studies in a larger group of dogs and characterization of progressive changes in adrenal glands are needed.

Adrenocortical Hyperfunction↗

PubMed1997

Disordered water homeostasis in Asian patients with schizophrenia.

OBJECTIVE: The aim of this study was to determine the prevalence of polydipsia-hyponatremia among patients with schizophrenia in an Asian mental hospital. METHOD: Seven hundred and twenty-eight inpatients with schizophrenia were assessed for polydipsia-hyponatremia using case notes reviews, specific gravity of urine, normalised diurnal weight gain, and serum sodium levels. RESULTS: One hundred and three (13.8%) patients had polydipsia, 30 (4.1%) had polydipsia-hyponatremia and 14 (1.9%) had a history of water intoxication. Eight of the 30 patients were receiving carbamazepine, three were on tricyclic antidepressants and two had diabetes mellitus and were on sulfonylureas. CONCLUSION: The prevalence of water intoxication among polydipsic patients was low compared to Western studies. This could be due to different methods of assessing polyuria, or ethnic differences and/or the prohibition of smoking in our patients. Certain medications might have also contributed to hyponatremia.

Adult↗

PubMed1981

Persistent water diuresis in renal amyloidosis. A case report.

A 67-year-old male with previous history of osteomyelitis presented with persistent thirst and polyuria. His urine remained hyposmolar to plasma after overnight fasting and administration of pitressin. Biopsy and postmortem examination revealed renal amyloidosis with involvement of many glomeruli and smaller vessels. Amyloid was also found in the medulla, particularly around the collecting tubules. It is suggested that amyloid interfered directly with diffusion of water through the walls of the collecting tubules.

Aged↗

PubMed1976

Management of diabetes insipidus in neurosurgical patients.

The authors present a brief review of the problem of diabetes insipidus in neurosurgical patients, with particular emphasis on the differential diagnosis of postoperative and posttraumatic polyuria and the management of diabetes insipidus in these periods. A listing of drugs currently used in its treatment is given.

Administration, Intranasal↗

PubMed2005

Pituitary cyst presenting with hyponatremia and increased secretion of brain natriuretic peptide. Case report.

In most cases of pituitary cyst there are no clinical symptoms and the lesions are found incidentally. The authors report the case of a 60-year-old man with a pituitary cyst causing visual disturbance and hyponatremia. The patient presented with appetite loss and general fatigue. On admission, blood workup showed severe hyponatremia (112 mEq/L), and bitemporal hemianopsia was observed on neurological examination. Magnetic resonance imaging revealed an intra- and suprasellar region cystic mass extending to the frontal base and hypothalamic area. The serum level of brain natriuretic peptide (BNP) was elevated (92 pg/ml) with polyuria and excessive Na excretion. Transsphenoidal surgery was performed to drain the cyst. The cyst wall was partially excised and the cystic fluid was aspirated. The secretion of BNP normalized postoperatively, and the hyponatremia and visual symptoms resolved. Histological examination, including an electron microscopy study, confirmed the diagnosis of a simple cyst. This appears to be the first reported case of a pituitary simple cyst associated with hyponatremia and an elevated BNP level.

Cysts↗

PubMed1994

Insulin reverses the protection given by diabetes against gentamicin nephrotoxicity in the rat.

Rats with untreated diabetes mellitus are protected from gentamicin-induced nephrotoxicity. In order to evaluate the role of hyperglycemia, glycosuria, and polyuria in this phenomenon, miniosmotic pumps filled with insulin were implanted for 15 days in seven female Sprague-Dawley rats with streptozotocin-induced diabetes mellitus. Plasma glucose levels were successfully maintained under 126 mg/dl. To serve as the control group, eight age-matched diabetic (plasma glucose > 400 mg/dl) rats had miniosmotic pumps placed delivering only Ringer's solution. Six days after placement of the pumps, gentamicin (40 mg/Kg/day) was administered to all animals for 9 days. The insulin-treated diabetic rats exhibited clear signs of nephrotoxicity by Day 6 of gentamicin, whereas the diabetic control group remained free from any functional or morphological evidence of proximal tubular damage throughout the 9 days of the aminoglycoside administration. At the end of the experiment, the creatinine clearance in the insulin-treated diabetic group was 45% lower than in the untreated diabetic group (P < 0.005). In addition, there was a rise in plasma creatinine (P < 0.02), muramidase appeared in the urine, and mild patchy acute tubular necrosis of the renal cortex was observed by light microscopic examination. The insulin-treated group also accumulated more gentamicin in the renal cortex than the untreated animals (P < 0.005). It is concluded that protection against the nephrotoxic effects of gentamicin is a feature of untreated experimental diabetes mellitus in the rat and that correction of the hyperglycemic state with insulin reverses this resistance.

Animals↗

PubMed2006

Congenital nephrogenic diabetes insipidus presented with bilateral hydronephrosis: genetic analysis of V2R gene mutations.

Most cases of hydronephrosis are caused by urinary tract obstruction. However, excessive polyuric syndrome rarely gives rise to non-obstructive hydronephrosis, megaureter, and a distended bladder. The authors report here on two cases of congenital nephrogenic diabetes insipidus (NDI) with severe bilateral hydronephrosis and megaureter. It is Interesting that the patients were symptomless except for their polyuria, and they both presented with bilateral hydronephrosis. Fluid deprivation testing revealed the presence of AVP resistant NDI. Gene analysis for these patients showed the AVP receptor 2 (V2R) missense mutations (Q225X and S126F), which have previously been reported on in other studies. We made the diagnosis of NDI by using a physiologic test, and we confirmed it by mutation analysis of the V2R gene.

Adult↗

PubMedDate not supplied

Leber's congenital amaurosis with associated nephronophthisis.

The authors present a case of a 15-year-old girl with Leber's congenital amaurosis with associated nephronophthisis. The main findings in this case are: congenital blindness; enophthalmos; photophobia; nystagmus; keratoconus; cataracts; pigmentary degeneration in the fundus of both eyes; progressive uremia with absence of hematuria, proteinuria, pyuria, and glycosuria; low urinary density, normal lipidic profile; osteoporosis; absence of edema; polydipsia; polyuria; and a history of consanguinity between her parents. Tranmission of this entity allows an autosomal recessive pattern.

Adolescent↗

PubMedDate not supplied

Idiopathic neurohypophysial diabetes insipidus: reversibility of structural and functional renal abnormalities after treatment.

OBJECTIVE: To present a case of untreated long-term idiopathic neurohypophysial diabetes insipidus (DI) with structural and functional renal abnormalities that regressed after treatment. METHODS: We describe the clinical course, biochemical data, and imaging findings in a man with idiopathic neurohypophysial DI in whom structural and functional abnormalities involving the urinary tract diminished after treatment. The patient underwent intravenous pyelography, retrograde pyelography, computed tomographic (CT) scanning of the kidneys and abdomen, iodohippurate renal scanning, and voiding cystourethrography. Ultrasonography of the kidneys at presentation and at 8-year followup and serial determinations of serum creatinine for a period of 9 years were also done. RESULTS: A 43-year-old man had polyuria for 30 years attributable to untreated idiopathic neurohypophysial DI. He presented with bilateral flank pain and a high serum creatinine level (156 mmol/L). Ultrasonography, intravenous pyelography, retrograde pyelography, and CT scan of the kidneys demonstrated severe bilateral hydronephrosis, notably dilated and tortuous ureters, a distended bladder, and atrophy of the left renal cortex. Retrograde pyelography and voiding cystourethrography confirmed the absence of mechanical obstruction or urinary reflux. A renal scan study showed bilaterally impaired function. Treatment with intranasally administered desmopressin and clean intermittent straight bladder catheterization resulted in resolution of flank pain, improvement of renal function, normalization of serum creatinine levels, and decreased hydronephrosis during 9 years of follow-up. CONCLUSION: This case provides information about renal abnormalities in the natural history of a long-term polyuric state, idiopathic neurohypophysial DI, before and after treatment. Reversibility of renal structural and functional abnormalities after treatment is documented. Recognition of renal abnormalities associated with untreated neurohypophysial DI is important for prevention and treatment of such complications.

Adult↗

PubMed1976

[Diagnosis and pathophysiology of renal concentration disorders].

Basic physiology and pathophysiological mechanisms of renal concentrating ability and its defects are discussed. Normal urinary concentration depends on the concerted action of a variety of factors. Consequently, many different causes may underly the symptom of polyuria. Clinical tests of concentrating ability (water deprivation, pitressin test) are of diagnostic importance in diabetes insipidus and polydipsia, but have little practical value in the work-up for chronic renal disease. A critical analysis of maximal concentrating capacity (TcH2O) during induced osmotic diuresis is conducted. It is inferred that the height and shape of the normal TcH2O curve results basically from two physiological processes: It is raised by increasing NaCL transport out of the medullary parts of the ascending limbs of Henle's loops and lowered by influx of hypotonic tubular urine into the collecting ducts. Preponderance of hypotonic influx may result in hypotonic final urine in the absence of tubular functional abnormalitiy. It is not appropriate, therefore, to classify renal concentrating defects according to the shape and height of the TcH2O curve. A synopsis and short description of the known renal concentrating defects is given. They are classified into hereditary, metabolic, diuretic-induced, and toxic disturbances, as well as those seen in renal disease of various etiology. Each defect is discussed in terms of the underlying pathophysiological mechanism as far as currently understood. The most important mechanisms are either disturbed NaCL transport in the ascending limb of Henle's loop, or antidiuretic hormone (ADH) dependent or ADH independent decrease in water permeability of the enddistal convolutions and collecting ducts, or osmotic diuresis.

Diabetes Insipidus↗

PubMedDate not supplied

[Effect of lithium chloride on kidney function in rats].

Test staged on rats have brought evidence that lithium chloride acts damagingly on all parts of the nephron, inhibiting, first of all, the processes of filtration and then of secretion and reabsorption. Polyuria arising under the effect of lithium is caused by reduced reabsorption of water in the tubules and anuria--by depression of the glomerular filtration.

Animals↗