diabetestalk.net

Masked Diabetes Insipidus

A Case Of Pituitary Abscess With Masked Diabetes Insipidus Following Bacterial Meningitis

A Case Of Pituitary Abscess With Masked Diabetes Insipidus Following Bacterial Meningitis

A Case of Pituitary Abscess with Masked Diabetes Insipidus following Bacterial Meningitis Third Department of Internal Medicine, Mie University School of Medicine Third Department of Internal Medicine, Mie University School of Medicine Third Department of Internal Medicine, Mie University School of Medicine Third Department of Internal Medicine, Mie University School of Medicine Third Department of Internal Medicine, Mie University School of Medicine Third Department of Internal Medicine, Mie University School of Medicine Third Department of Internal Medicine, Mie University School of Medicine Third Department of Internal Medicine, Mie University School of Medicine Third Department of Internal Medicine, Mie University School of Medicine DOI Published: July 20, 1996 Received: August 02, 1995 Released: September 24, 2012 Accepted: October 04, 1995 [Advance Publication] Released: - Revised: - A 37-year-old woman was admitted to our institution because of bacterial meningitis with hyponatremia (121mEq/L). Brain magnetic resonance imaging disclosed a cystic mass extending from the intra sellar to suprasellar regions in a T1 weighted image. Basal plasma levels of LH, FSH, ACTH and cortisol were lower than normal range. The plasma levels of ACTH and cortisol were relatively low during the insulin-stress test. During the intravenous administration of LH-RH and CRH, while ACTH and cortisol increased within the normal range, those of LH and FSH did not. Treatment with hydrocortisone produced a rapid normalization of the serum levels of sodium. However, this treatment led to polyuria with hyposthenuria. Saline (5%) infusion and water loading tests were carried out with or without the administration of oral hydrocortisone (60mg/day). The plasma ADH did not decrease during the wate Continue reading >>

A Copeptin-based Approach In The Diagnosis Of Diabetes Insipidus

A Copeptin-based Approach In The Diagnosis Of Diabetes Insipidus

A Copeptin-Based Approach in the Diagnosis of Diabetes Insipidus Antnio Ribeiro-Oliveira, Jr., M.D., Ph.D., The indirect water-deprivation test is the current reference standard for the diagnosis of diabetes insipidus. However, it is technically cumbersome to administer, and the results are often inaccurate. The current study compared the indirect water-deprivation test with direct detection of plasma copeptin, a precursor-derived surrogate of arginine vasopressin. From 2013 to 2017, we recruited 156 patients with hypotonic polyuria at 11 medical centers to undergo both water-deprivation and hypertonic saline infusion tests. In the latter test, plasma copeptin was measured when the plasma sodium level had increased to at least 150 mmol per liter after infusion of hypertonic saline. The primary outcome was the overall diagnostic accuracy of each test as compared with the final reference diagnosis, which was determined on the basis of medical history, test results, and treatment response, with copeptin levels masked. A total of 144 patients underwent both tests. The final diagnosis was primary polydipsia in 82 patients (57%), central diabetes insipidus in 59 (41%), and nephrogenic diabetes insipidus in 3 (2%). Overall, among the 141 patients included in the analysis, the indirect water-deprivation test determined the correct diagnosis in 108 patients (diagnostic accuracy, 76.6%; 95% confidence interval [CI], 68.9 to 83.2), and the hypertonic saline infusion test (with a copeptin cutoff level of >4.9 pmol per liter) determined the correct diagnosis in 136 patients (96.5%; 95% CI, 92.1 to 98.6; P<0.001). The indirect water-deprivation test correctly distinguished primary polydipsia from partial central diabetes insipidus in 77 of 105 patients (73.3%; 95% CI, 63.9 to 81.2), Continue reading >>

Hipofiz Tutulumu Ile Seyreden Akut Monositik Lsemi Olgusu

Hipofiz Tutulumu Ile Seyreden Akut Monositik Lsemi Olgusu

Acute Monocytic Leukemia with Pituitary Involvement: A Case Report Central nervous system involvement is rare in acute myeloid leukemia (AML) cases. Pituitary involvement is much more rarely seen with unknown frequency (1) and if left untreated, may result in death. Although rarely seen, leukemic infiltration of the pituitary gland should be evaluated in leukemic patients with visual disturbance, hypopituitarism or central diabetes insipidus (CDI) (2). To date, AML presenting with CDI has been reported in over 80 patients (3). The presence of both anterior and posterior pituitary deficiency is even rarer with unknown prevalence. Here, we present a patient with AML-M5 (French-American-British (FAB) classification), panhypopituitarism and CDI. A 29-year-old male patient was admitted to our hematology clinic with visual disturbance and poor performance status. His medical history revealed allogeneic hematopoietic stem cell transplantation performed in 2010 after chemotherapy with the diagnosis of acute monocytic leukemia. During follow-up in remission, the patient had visual disturbance in left eye and poor performance status. Central facial paralysis and visual loss was found in physical examination and relapsed leukemia was diagnosed. Leukemic infiltration of the pituitary gland, infundibulum, optic chiasm and brain parencyhma was seen on cranial magnetic resonance imaging (MRI) (Figure 1 a,b). Chemo-radiotherapy and dexamethasone therapy were planned. Endocrine assessment revealed the following; fasting blood glucose: 98 mg/dl (70-109), sodium: 146 mmol/L (136-145); potassium: 4.48 mmol/L (3.5-5.1). Liver and renal function tests were within normal limits. Blood examination revealed leucopenia (WBC: 2800 K/uL), platelet count was slightly elevated (420.000/l) and haemo Continue reading >>

Central Adrenal Insufficiency And Diabetes Insipidus Misdiagnosed As Severe Depression

Central Adrenal Insufficiency And Diabetes Insipidus Misdiagnosed As Severe Depression

Central Adrenal Insufficiency and Diabetes Insipidus Misdiagnosed as Severe Depression 1 Department of Diabetes and Endocrinology, Saiseikai Yokohamashi-Tobu Hospital, Yokohama, Kanagawa, Japan 2 Division of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine (Omori), Faculty of Medicine, Toho University, Tokyo, Japan 1 Department of Diabetes and Endocrinology, Saiseikai Yokohamashi-Tobu Hospital, Yokohama, Kanagawa, Japan 2 Division of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine (Omori), Faculty of Medicine, Toho University, Tokyo, Japan 2 Division of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine (Omori), Faculty of Medicine, Toho University, Tokyo, Japan 2 Division of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine (Omori), Faculty of Medicine, Toho University, Tokyo, Japan 1 Department of Diabetes and Endocrinology, Saiseikai Yokohamashi-Tobu Hospital, Yokohama, Kanagawa, Japan 2 Division of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine (Omori), Faculty of Medicine, Toho University, Tokyo, Japan Corresponding author email: [email protected] Author information Copyright and License information Disclaimer Copyright 2010 the author(s), publisher and licensee Libertas Academica Ltd. This is an open access article. Unrestricted non-commercial use is permitted provided the original work is properly cited. This article has been cited by other articles in PMC. A 68 year-old Japanese man, who had been suffering from immobilization and disuse syndrome, was admitted to our hospital for evaluation of polyuria with polyposia, hyponatremia and low blood pressure. His plasma osmolality was greater than that of his urine. His endocrinological examinatio Continue reading >>

[masked Diabetes Insipidus]

[masked Diabetes Insipidus]

A transition of G to A at nucleotide position 279 in exon 1 of the vasopressin gene has been identified in patients with familial central diabetes insipidus. The mutation predicts an amino acid substitution of Thr (ACG) for Ala (GCG) at the COOH terminus of the signal peptide in preprovasopression (preproVP). Translation in vitro of wild-type and mutant mRNAs produced 19-kD preproVPs. When ... [Show full abstract] translated in the presence of canine pancreatic rough microsomes, wild-type preproVP was converted to a 21-kD protein, whereas the mutant mRNA produced proteins of 21 kD and 23 kD. NH2-terminal amino acid sequence analysis revealed that the 21-kD proteins from the wild-type and the mutants were proVPs generated by the proteolytic cleavage of the 19-residue signal peptide and the addition of carbohydrate. Accordingly, mutant preproVP was cleaved at the correct site after Thr-19, but the efficiency of cleavage by signal peptidase was < 25% that observed for the wild-type preproVP, resulting in the formation of a predominant glycosylated but uncleaved 23-kD product. These data suggest that inefficient processing of preproVP produced by the mutant allele is possibly involved in the pathogenesis of diabetes insipidus in the affected individuals. To evaluate posterior pituitary function without any provocative examination, vasopressin (AVP) concentrations of random urine were measured by high-sensitive radioimmunoassay (AVP-RIA Kit, Mitsubishi Petrochemical Co., Ltd.). No apparent interference for the AVP measurement in unextracted urine was seen after appropriate dilution of urine sample. Urinary AVP did not degenerate at least for 24 hr ... [Show full abstract] at room temperature. AVP concentration of random urine was significantly correlated with AVP excretion Continue reading >>

2016 Endocrine Society Guidelines: Central Adrenal Insufficiency

2016 Endocrine Society Guidelines: Central Adrenal Insufficiency

We suggest measuring serum cortisol levels at 89 am as the first-line test for diagnosing central adrenal insufficiency. We recommend against using a random cortisol level to diagnose AI. We suggest that a cortisol level <3 g/dL is indicative of adrenal insufficiency and a cortisol level >15 g/dL likely excludes an AI diagnosis. We suggest performing a corticotropin stimulation test when morning cortisol values are between 3-15 g/dL to diagnose AI. Peak cortisol levels <18.1 g/dL at 30 or 60 minutes indicate AI. We suggest that clinicians perform biochemical testing for the hypothalamic-pituitary-adrenal (HPA) axis at least 1824 hours after the last hydrocortisone (HC) dose or longer for synthetic glucocorticoids (GC). We recommend using hydrocortisone, usually 1520 mg total daily dose in single or divided doses. Patients using divided doses should take the highest dose in the morning at awakening and the second in the afternoon (two-dose regime) or the second and third at lunch and late afternoon, respectively (three-dose regime). We suggest using longer-acting glucocorticoids in selected cases (eg, non-availability, poor compliance, convenience). We recommend that clinicians teach all patients with adrenal insufficiency regarding stress-dose and emergency GC administration and instruct them to obtain an emergency card/bracelet/necklace regarding AI and an emergency kit containing injectable high-dose GC. We recommend against using fludrocortisone in patients with central adrenal insufficiency. We recommend that clinicians treat patients with suspected adrenal crisis (AC) due to secondary AI with an immediate parenteral injection of 50100 mg hydrocortisone. We suggest evaluating central hypothyroid patients for adrenal insufficiency before starting LT4 therapy. If thi Continue reading >>

Arginine Vasopressin-independent Mechanism Of Impaired Water Excretion In A Patient With Sarcoidosis Complicated By Central Diabetes Insipidus And Glucocorticoid Deficiency

Arginine Vasopressin-independent Mechanism Of Impaired Water Excretion In A Patient With Sarcoidosis Complicated By Central Diabetes Insipidus And Glucocorticoid Deficiency

Arginine Vasopressin-Independent Mechanism of Impaired Water Excretion in a Patient with Sarcoidosis Complicated by Central Diabetes Insipidus and Glucocorticoid Deficiency 1Department of Internal Medicine, Osaka City Sumiyoshi Hospital, 1-2-16, Higashikagaya, Suminoeku, Osaka City, Osaka 559-0012, Japan 2Department of Internal Medicine, Osaka City Juso Hospital, Osaka 532-0034, Japan 3Department of Endocrinology and Metabolism, Osaka City General Hospital, Osaka 534-0021, Japan 4Department of Pathology, Osaka City General Hospital, Osaka 534-0021, Japan Received 13 February 2011; Accepted 7 June 2011 Copyright 2011 Katsunobu Yoshioka et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. A 28-year-old man was admitted to our hospital because of reduced livido and increased fatigability. Four months before admission, he noticed polyuria, which was gradually relieved by admission. Magnetic resonance imaging revealed enhancing lesion centrally in the pituitary stalk. Biopsy from the skin revealed noncaseating granuloma composed of epithelioid cells, and a diagnosis of sarcoidosis was made. Although plasma arginine vasopressin (AVP) was undetectable after administration of hypertonic saline, urinary output was within normal range (1.5 to 2.2 L/day). The urine osmolality became above plasma levels during the hypertonic saline test. Hormonal provocative tests revealed partial glucocorticoid deficiency. Soon after the glucocorticoid therapy was begun, moderate polyuria (from 3.54.0 liters daily) occurred. At this time, plasma AVP was undetectable, and urine osmolality was consistently below plasma levels durin Continue reading >>

Diabetes Insipidus – Diagnosis And Management

Diabetes Insipidus – Diagnosis And Management

Abstract Central diabetes insipidus (CDI) is the end result of a number of conditions that affect the hypothalamic-neurohypophyseal system. The known causes include germinoma/craniopharyngioma, Langerhans cell histiocytosis (LCH), local inflammatory, autoimmune or vascular diseases, trauma resulting from surgery or an accident, sarcoidosis, metastases and midline cerebral and cranial malformations. In rare cases, the underlying cause can be genetic defects in vasopressin synthesis that are inherited as autosomal dominant, autosomal recessive or X-linked recessive traits. The diagnosis of the underlying condition is challenging and raises several concerns for patients and parents as it requires long-term follow-up. Proper etiological diagnosis can be achieved via a series of steps that start with clinical observations and then progress to more sophisticated tools. Specifically, MRI identification of pituitary hyperintensity in the posterior part of the sella, now considered a clear marker of neurohypophyseal functional integrity, together with the careful analysis of pituitary stalk shape and size, have provided the most striking findings contributing to the diagnosis and understanding of some forms of ‘idiopathic’ CDI. MRI STIR (short-inversion-time inversion recovery sequencing) is a promising technology for the early identification of LCH-dependent CDI. © 2012 S. Karger AG, Basel Definition/Classification Diabetes insipidus is a disease in which large volumes of dilute urine (polyuria) are excreted due to vasopressin (AVP) deficiency [central diabetes insipidus (CDI)], AVP resistance [nephrogenic diabetes insipidus (NDI)], or excessive water intake (primary polydipsia). Polyuria is characterized by a urine volume in excess of 2 l/m2/24 h or approximately 150 ml/k Continue reading >>

Neurosarcoidosis-associated Central Diabetes Insipidus Masked By Adrenal Insufficiency.

Neurosarcoidosis-associated Central Diabetes Insipidus Masked By Adrenal Insufficiency.

BMJ Case Rep. 2015 Jan 22;2015. pii: bcr2014206390. doi: 10.1136/bcr-2014-206390. Neurosarcoidosis-associated central diabetes insipidus masked by adrenal insufficiency. Department of Medicine, Albert Einstein Medical Center, Philadelphia, Pennsylvania, USA. Department of Endocrinology, Albert Einstein Medical Center, Elkins Park, Pennsylvania, USA. Central diabetes insipidus (CDI) is an infrequent complication of neurosarcoidosis (NS). Its presentation may be masked by adrenal insufficiency (AI) and uncovered by subsequent steroid replacement. A 45-year-old woman with a history of NS presented 2 weeks after abrupt cessation of prednisone with nausea, vomiting, decreased oral intake and confusion. She was diagnosed with secondary AI and intravenous hydrocortisone was promptly begun. Over the next few days, however, the patient developed severe thirst and polyuria exceeding 6 L of urine per day, accompanied by hypernatraemia and hypo-osmolar urine. She was presumed to have CDI due to NS, and intranasal desmopressin was administered. This eventually normalised her urine output and serum sodium. The patient was discharged improved on intranasal desmopressin and oral prednisone. AI may mask the manifestation of CDI because low serum cortisol impairs renal-free water clearance. Steroid replacement reverses this process and unmasks an underlying CDI. Continue reading >>

Unmasking Of Diabetes Insipidus With Steroid Treatment

Unmasking Of Diabetes Insipidus With Steroid Treatment

Unmasking of diabetes insipidus with steroid treatment Adeel Ghaffar, Barbara McGowan, George Tharakan, Nehal Narayan, Rebecca Cox, Emma Hatfield & Karim Meeran Endocrine Unit, Department of Investigative Medicine, Imperial College Healthcare trust, 6th floor, Commonwealth Building, Hammersmith Hospital, London, UK. A 36-year-old man was referred to the neurologists for leg weakness and pain, fatigue and lethargy for 2 years. Sarcoidosis was diagnosed 6 years previously, on the basis of uveitis, lower motor neurone facial palsy, hilar lymphadenopathy and transbronchial biopsy. Prednisolone had been discontinued 3 years prior to his current presentation. His blood pressure was 99/71. Examination was otherwise unremarkable. His ACE was 109 U/l (1070). His TSH was 1.29 mU/l., with a free T4 of 5.9 pmol/l. Cortisol was 56 nmol/l. Prolactin was 818 mU/l (75375 mU/l). LH and FSH were undetectable. Testosterone was very low at 0.3 nmol/l. GH was 0.5 U/l. IGF-1 was 9 nmol/l (1364). Other bloods, and an LP were unremarkable. MRI of brain and spine showed thickening and contrast enhancement around the pituitary infundibulum and hypothalamus. Peak cortisol on SST was 450 nmol/l. He was commenced on hydrocortisone 10 mg, 5 mg, 5 mg, and thyroxine 50 mcg. He was given 1 g methylprednisolone daily for 3 days. He complained of polyuria and polydipsia. His serum osmolality was 302 mOsmol/kg. Concurrent urinary osmolality was 119 mOsmol/kg. A formal water deprivation test was performed. Continue reading >>

Diagnosing Diabetes Insipidus Subtypes: Copeptin Or Water-deprivation

Diagnosing Diabetes Insipidus Subtypes: Copeptin Or Water-deprivation

For Professionals Research Updates Endocrinology Diagnosing Diabetes Insipidus Subtypes: Copeptin or Water-Deprivation Might blood testing for copeptin offer an easier diagnostic method than the customary water-deprivation in assessing for diabetes insipidus? The researchers recommend copeptin as the new gold standard but longtime experts express caution. With Gary Robertson, MD, and Mirjam Christ-Crain, MD An alternative to the indirect water-deprivation testthe current reference standardmay be more accurate for diagnosing the rare disorder of diabetes insipidus, 1 according to findings published in the New England Journal of Medicine. Mirjam Christ-Crain, MD, of University Hospital Basel in Switzerland and her team performed both the copeptin test and the water deprivation test on 144 patients to evaluate the accuracy of these diagnostic approaches.1 All patients had confirmed hypotonia polyuria and were receiving care across 11 medical centers. The primary outcome of this study was to compare the overall diagnostic accuracy of each test compared with the final reference diagnosis.1 The participants were given both water- and hypertonic saline infusion tests. In the latter, the plasma copeptin was measured when the plasma sodium level had increased to at least 150 mmol per liter after infusion of hypertonic saline. Standard of care for diagnosing diabetes Insipidus remains the indirect deprivation test over copeptin, which is not ready for general use, says leading expert. Photo: 123RF "The most important finding is that a new test, the hypertonic saline infusion copeptin measurement, has a much higher diagnostic accuracy than the classical water deprivation test in the differential diagnosis of polyuria polydipsia syndrome, and is also well received by the patients, Continue reading >>

Diabetes Insipidus As A Presenting Manifestation Of Rathke's Cleft Cyst Kumar M, Dutta D, Shivaprasad K S, Jain R, Sen A, Biswas D, Mukhopadhyay M, Ghosh S, Mukhopadhyay S, Chowdhury S - Indian J Endocr Metab

Diabetes Insipidus As A Presenting Manifestation Of Rathke's Cleft Cyst Kumar M, Dutta D, Shivaprasad K S, Jain R, Sen A, Biswas D, Mukhopadhyay M, Ghosh S, Mukhopadhyay S, Chowdhury S - Indian J Endocr Metab

The anterior and intermediate lobes of the pituitary gland arise embryologically from Rathke's pouch. Inadequate pouch obliteration results in cysts or cystic remnants at the interface between the anterior and posterior pituitary lobes, found in about 20% of pituitary glands at autopsy. [1] Rathke's cleft cysts (RCC) are usually asymptomatic, but can present with symptoms related to mass effects such as headache, visual impairment, vomitings, features of panhypopituitarism and hypothalamic dysfunction. [1] , [2] A 68-year-old Indian male patient presented with the complaints of generalized malaise, poor appetite, weight loss, headache and polyuria for last 2 months. He had a chronic ill-looking appearance, a dehydrated tongue and dry skin. Urine output was 5000-5500 mL/day with a history of nocturia and craving for cold fluids. No history of head injury, tubercular meningitis, central nervous system infections or chronic drug intake. His physical findings on admission were height 156 cm; body weight, 44.5 kg and body mass index, 18.3. Blood pressure was 100/64 mmHg without postural change and pulse rate, 68/min with a regular rhythm. No edema was noted in his legs or feet. He had scant axillary and pubichair. Neurologic examination including visual field was found to be normal. Laboratory findings were as follows: White blood cell count 6400/mm 3 (neutrophils 51%, lymphocyte 42%, monocyte 5%, eosinophils 2%, basophils 0%); hemoglobin, 13.4 g/dL; hematocrit, 35.5%; red blood cell count, 3.4 10 6 /mm 3 ; and platelets, 3.3 10 5 /mm 3 Serum sodium was 137 mmol/L; potassium, 3.9 mmol/L; and chloride, 103 mmol/L. Blood urea nitrogen was 12 mg/dL; serum creatinine, 0.8 mg/dL; and uric acid, 6.1 mg/dL. Fasting plasma glucose was74 mg/dL; hemoglobin A1c, 4.9% and serum calcium Continue reading >>

The Clinical Course And Pathophysiological Investigation Of Adolescent Gestational Diabetes Insipidus: A Case Report

The Clinical Course And Pathophysiological Investigation Of Adolescent Gestational Diabetes Insipidus: A Case Report

The clinical course and pathophysiological investigation of adolescent gestational diabetes insipidus: a case report BMC Endocrine DisordersBMC series open, inclusive and trusted2018 Gestational diabetes insipidus (GDI) is a rare endocrine complication during pregnancy that is associated with vasopressinase overproduction from the placenta. Although increased vasopressinase is associated with placental volume, the regulation of placental growth in the later stage of pregnancy is not well known. A 16-year-old pregnant woman was urgently transferred to our hospital because of threatened premature labor when the Kumamoto earthquakes hit the area where she lived. During her hospitalization, she complained of gradually increasing symptoms of polyuria and polydipsia. The serum level of arginine vasopressin (AVP) was 1.7pg/mL, which is inconsistent with central DI. The challenge of diagnostic treatment using oral 1-deamino-8-D-AVP (DDAVP) successfully controlled her urine and allowed for normal delivery. DDAVP tablets were not necessary to control her polyuria thereafter. Based on these observations, clinical diagnosis of GDI was confirmed. Pathophysiological analyses revealed that vasopressinase expression was more abundant in the GDI patients syncytiotrophoblast in placenta compared with that in a control subject. Serum vasopressinase was also observed during gestation and disappeared soon after delivery. Vasopressinase is reportedly identical to oxytocinase or insulin regulated aminopeptidase (IRAP), which is an abundant cargo protein associated with the glucose transporter 4 (GLUT4) storage vesicle. Interestingly, the expression and subcellular localization of GLUT4 appeared to occur in a vasopressinase (IRAP)-dependent manner. Because placental volume may be associated w Continue reading >>

Internet Scientific Publications

Internet Scientific Publications

D Kujubu, J Agarwal, N Gandhi, J Sim, M Idroos, S Rasgon acute renal failure, aneurysm, diabetes insipidus, obstructive nephropathy D Kujubu, J Agarwal, N Gandhi, J Sim, M Idroos, S Rasgon. A Case of Aneurysm Induced Obstructive Nephropathy Masked. The Internet Journal of Neurology. 2005 Volume 5 Number 2. Although rare, obstructive nephropathy secondary to iliac artery aneurysms have been reported to occur. We describe a case of a patient admitted for non-cardiac chest pain and found to be in non-oligoanuric acute renal failure. A renal ultrasound revealed aortic and bilateral iliac aneurysms with minimal evidence of hydronephrosis. Clinically, the patient had a normal to high urine output requiring continuous volume repletion. Urine studies repeatedly showed low osmolarity without other derangements. Only after progressive deterioration of renal function did obstruction surface as a plausible etiology Bilateral ureteral stent placement and subsequent resolution of renal failure eventually confirmed the diagnosis of obstructive uropathy. This presentation illustrates a case of bilateral ureteral obstruction and obstructive nephropathy that was masked by high urinary output from water diuresis likely due to nephrogenic diabetes insipidus (DI). The DI masked the clinical signs of obstruction, specifically oligoanuria. Arterial aneurysms within the abdominal cavity have been shown to directly cause urinary tract obstruction.1,2,3,4 The majority of these cases involve inflammatory aortic aneurysms associated with perianeurysmal fibrosis that ultimately result in structural compromise of the urinary tract. Indeed ureteral obstruction has been reported to occur in up to 30% of all inflammatory aneursyms.5,6 Inflammatory iliac artery aneurysms are less common but can occur i Continue reading >>

Diabetes Insipidus Classification

Diabetes Insipidus Classification

There are four types of diabetes insipidus including: Central or cranial diabetes insipidus, also called neurogenic diabetes insipidus Nephrogenic diabetes insipidus Dipsogenic diabetes insipidus due to malfunction of the thirst mechanism Gestational diabetes insipidus which occurs during pregnancy Central or cranial diabetes insipidus This occurs if there is a low level of vasopressin or antidiuretic hormone (ADH) in the body. The deficiency means the kidneys are not prevented from excreting large amounts of urine and instead large volumes of dilute urine are expelled, even when the body has become dehydrated. This also causes blood to lose water and become more concentrated and higher in salt. This results in dehydration and stimulation of the thirst centre in the hypothalamus of the brain which causes a person to drink more. This is the most common type of diabetes insipidus and it is mainly caused by disease, infection or injury to the pituitary gland or the hypothalamus gland. Causes The causes of cranial diabetes insipidus include: Genetic inheritance The condition may be cause by an inherited mutation in the vasopressin gene, AVP-NPII which is transmitted to offspring in an autosomal fashion. Acquired disease may have the following causes: Tumours of the pituitary gland (pituitary adenoma), craniopharyngiomas and spread of cancer to the brain (in around 20% of cases). Granuloma formation in the pituitary gland may be another cause. Head injuries (in around 17%) Brain surgery (in around 9%) Meningitis and encephalitis may cause a small number of cases Sheehan's syndrome and haemochromotosis or deposition of iron in pituitary/hypothalamic tissue Blood vessel complications such as those during pregnancy where the blood supply to the hypothalamus and the pituitary gl Continue reading >>

More in diabetes