Diagnosis Of Diabetes Insipidus Research Articles

Langerhans cell histiocytosis presenting spinal cord compression after diabetes insipidus diagnosis: a case report

Langerhans cell histiocytosis presenting spinal cord compression after diabetes insipidus diagnosis: a case report

The 3% hypertonic saline infusion test for the differential diagnosis of diabetes insipidus and primary polydipsia: assessment of diagnostic accuracy

AIM: assessment of the diagnostic accuracy of a 3% hypertonic saline infusion test in relation to a set of clinical and laboratory data (including a water deprivation test and MRI data) for differential diagnoses of diabetes insipidus (DI) and primary polydipsia (PP).METHODS: An interventional cross-sectional study was carried out at Endocrinology Research Centre From September 2021 to September 2023 ninety patients with polyuria-polydipsia syndrome were included. In order to assess the diagnostic characteristics, all the subjects underwent two tests with osmotic stimulation: a 3% hypertonic saline infusion test and a water deprivation test. Adverse events were assessed.RESULTS: Based on the results of clinical, anamnestic, laboratory and instrumental data, and the results of a water deprivation test, a final diagnosis of DI was made in 48 (53%) patients and PP in 42 (47%) patients. The agreement between the two samples is significant — Kappa = 0.823, 95% CI (0.707, 0.939). The operational parameters of the 3% hypertonic saline infusion test are: sensitivity 98% (95% CI: 89%; 100%); specificity 98% (95% CI: 87%; 100%), positive and negative predictive values 98% (95% CI: 89%–100%) and 98% (95% CI: 87%–100%). Respectively. Chills occurred significantly more often (31% vs. 12%), and dizziness and headache were more pronounced during the 3% hypertonic saline infusion test. The median duration of the water deprivation test in patients was 11 hours, and median duration of 3% hypertonic saline infusion test was 1.5 hour (P<0.001).CONCLUSION: The 3% hypertonic saline infusion test has a high overall diagnostic accuracy 98%; 95% CI 92% to 100%)) in relation to the classical set of clinical, laboratory and instrumental data of patients (including a water deprivation test), However, it is important the advantage of the latter is its short duration and, as a consequence, better tolerability and probably better compliance, while no significant differences in adverse events frequencies during the tests were identified.

Langerhans cell histiocytosis: Central nervous system findings

A 4-year-old boy was admitted for polyuria and polydipsia syndrome for which the diagnosis of diabetes insipidus was retained after doing a hydrous restriction test with the Minirin test.

Diabetes Insipidus: Types, Diagnosis and Management

Diabetes insipidus (DI) is an acquired or hereditary water imbalance disorder characterized by polydipsia and polyuria. It is a condition that involves the excretion of dilute urine in large volumes. The illness can strike at any age, with males and females have identical rates of occurrence of the disease. The two main mechanisms responsible for diabetes insipidus are either insufficient release or production of ADH (antidiuretic hormone) from the hypothalamus (central diabetes insipidus) or ADH resistance in which the kidneys are unable to respond to ADH (nephrogenic diabetes insipidus). Another form of DI is transient diabetes insipidus commonly known as gestational diabetes insipidus that occurs in the second/third trimester of pregnancy due to increased levels of placental vasopressinase that occurs progressively during pregnancy and increases metabolic clearance of vasopressin. The fourth type of DI is primary polydipsia, characterized by elevated levels of water intake that physiologically lower vasopressin and may be psychogenic, iatrogenic or dipsogenic. Signs and symptoms of DI often include water electrolyte-imbalance, excessive or severe thirst, frequent and excessive urination, fatigue, dehydration, and weight loss. Diabetes insipidus (DI) should be distinguished from primary polydipsia, and whether it is caused by a central, nephrogenic, or gestational cause. This distinction is critical since incorrect treatment can result in serious repercussions. Diagnosis of DI includes measurement of plasma sodium and osmolality, baseline copeptin, hypertonic saline stimulation and arginine stimulation test. The treatment for DI includes the use of drugs such as desmopressin, thiazide diuretics, indomethacin and amiloride.

FRI349 Atypical Timing: Transient Diabetes Insipidus After Pituitary Apoplexy

Abstract Disclosure: I.A. Rivera Nazario: None. A.M. Santiago Carrion: None. M.T. Torres: None. A. Figueroa Cruz: None. Y. Ortiz: None. A. Aponte Velez: None. A. Vazquez: None. E.J. Sola Sanchez: None. M.M. Mangual Garcia: None. Pituitary apoplexy results from acute hemorrhage or infarction of the pituitary gland. Also, an adenoma that can develop transient or permanent pituitary hormone deficiency. Posterior pituitary function is nearly always preserved due to alternate blood supply. Most cases presenting among the fifth or sixth decade. Few cases of transient Diabetes Insipidus (DI) have been described in literature, approximately 4% of patients, making this an uncommon complication of this condition. Hereby, we describe a young male with sudden onset headache due to pituitary apoplexy with transient DI. A 33-year-old man without past medical history, presented to the emergency room with the chief complain of sudden severe headache. Physical examination without altered consciousness, visual impairment or meningeal irritation. Initial head CT was negative, except for findings of muscle spasms. Patient was discharged home with muscle relaxant and NSAIDs. Ten days later, patient continued with worsening headache, not responding to medical therapy. On reevaluation, brain MRI identified a pituitary macroadenoma, measuring 2.2 cm, with mass effect, suprasellar extension impinging the pituitary stalk, prechiasmatic optic nerves and cavernous sinus extension. Blood tests showed Na 139 mEq/L, K 4.1 mmol/L and adequate renal function. Pituitary function test consistent for hypopituitarism with free T4 0.39 ng/dL, TSH 0.084 mIU/mL, cortisol 0.19 mcg/dL, ACTH 9.39 ng/mL, GH <0.1 ng/mL, IGF-1 22.8 ng/mL and prolactin 1.52 ng/mL; except normal FSH, LH and testosterone levels. After four months of apoplectic episode, he developed polyuria and polydipsia. Brain MRI with residual sellar mass of 1.2 cm with resolution of mass effect. Visual field charting was normal. Blood tests showed Na 139 mEq/L, K 4.1 mmol/L and adequate renal function. Started on hydrocortisone and levothyroxine replacement. Diagnosis of DI was suspected, but he refused water deprivation test or DDAVP therapy. During follow-up, patient was found with serum osmolality 288 mOsm/kg, urine osmolality 202 mOsm/kg and 4.6 L 24-hour urine collection. Three months later serum osmolality was 294 mOsm/kg, urine osmolality of 383 mOsm/kg with resolution of polyuria and polydipsia. This case presents a delayed onset of transient DI treated in a conservative way. In documented cases average onset was a period of 2 weeks with resolution in 2 months. Etiology most likely due to compression or destruction of the pituitary gland or stalk impeding transit of ADH from hypothalamus to the neurohypophysis. Transient impairment of the ADH secretion is rare in pituitary apoplexy deserving evaluation in this clinical scenario. When seen, it has been related to glucocorticoid use. This is an example of an atypical pituitary disorder requiring prompt recognition to prevent further complications. Presentation: Friday, June 16, 2023

The laboratory investigation of diabetes insipidus: A review.

Diabetes insipidus (DI) is a group of disorders that lead to inappropriate production of large volumes of dilute urine. The three main forms are central DI (CDI), nephrogenic DI (NDI) and primary polydipsia (PP). Differentiating CDI/NDI from PP is important as patients with true DI are at risk of severe dehydration without treatment. Biochemical testing is key in the diagnosis of DI. The indirect water deprivation test (WDT) is commonly used in the investigation of DI but has drawbacks including being cumbersome and sometimes producing equivocal results. Direct measurement of AVP has theoretical advantages but has generally only been used in specialist centres. Disadvantages include the requirement to measure AVP under hypertonic stimulation and pre-analytical/analytical challenges. Copeptin (CT-proAVP) is a proxy marker for AVP that is more stable, easier to measure and has been studied more widely in recent years. Historically, the evidence supporting the diagnostic performance of these tests has been relatively poor, being based on a few small, usually single-centre studies. However more recent, well-designed prospective studies are improving the evidence base for investigation of DI. These studies have focused on the utility of copeptin measurements during stimulation tests. There is evidence that measurement of copeptin under stimulation offers improved diagnostic performance compared to the WDT. There is currently a lack of systematic, evidence-based guidelines on the diagnosis of DI, but as the quality of the evidence defining the diagnostic performance of tests for DI continues to improve, a clearer consensus on the optimal approach should become achievable.

Transient diabetes insipidus in critically ill COVID19 patients

PurposeVasopressin has become an important vasopressor drug while treating a critically ill patient to maintain adequate mean arterial pressure. Diabetes insipidus (DI) is a rare syndrome characterized by the excretion of a large volume of diluted urine, inappropriate for water homeostasis. We noticed that several COVID19 patients developed excessive polyuria suggestive of DI, with a concomitant plasma sodium-level increase and/or low urine osmolality. We noticed a temporal relationship between vasopressin treatment cessation and polyuria periods. We reviewed those cases to better describe this phenomenon. MethodsWe retrospectively collected COVID19 ECMO patients' (from July 6, 2020, to November 30, 2021) data from the electronic medical records. By examining urine output, urine osmolality (if applicable), plasma sodium level, and plasma osmolality, we set DI diagnosis. We described the clinical course of DI episodes and compared baseline characteristics between patients who developed DI and those who did not. ResultsOut of 37 patients, 12 had 18 episodes of DI. These patients were 7 years younger and had lower severity scores (APACHE-II and SOFA). Mortality difference was not seen between groups. 17 episodes occurred after vasopressin discontinuation; 14 episodes were treated with vasopressin reinstitution. DI lasted for a median of 21 h, with a median increase of 14 mEq/L of sodium. ConclusionsTemporary DI prevalence after vasopressin discontinuation in COVID19 ECMO patients might be higher than previously described for vasopressin-treated patients.

Changing the Name of Diabetes Insipidus: A Position Statement of the Working Group for Renaming Diabetes Insipidus.

Recent data show that patients with a diagnosis of diabetes insipidus (DI) are coming to harm. Here we give the rationale for a name change to arginine vasopressin deficiency and resistance for central and nephrogenic DI, respectively.

Multiorgan sarcoidosis as a diabetes insipidus mask.

Sarcoidosis is an inflammatory, multisystem disease with an undetermined etiology. The presence of noncaseating granulomas in involved organs is a characteristic pathomorphological feature. Sarcoidosis, like a chameleon, can mimic different medical conditions. Although the lungs are most commonly involved, extrapulmonary manifestations can influence any system. The clinical course of the disease may differ. Immediate initiation of glucocorticosteroid therapy is important when critical organs are impaired. A case of a patient with sarcoidosis whose first clinical symptoms were related to diabetes insipidus (DI) was presented. The diagnosis of multiple organ sarcoidosis was delayed because of an adequate response to treatment with vasopressin. The multidisciplinary diagnostic approach validated the involvement of the pituitary gland, lungs, lymph nodes, bones, and subcutaneous tissue. The presented case emphasizes the critical importance of the multifaceted differential diagnosis of patients with DI. Sarcoidosis usually affects the lung but can also be a multisystemic disease. The assessment of the extension of sarcoidosis remains complex. A multidisciplinary approach must identify all-organ involvement and initiate appropriate sarcoidosis treatment. Diabetes insipidus (DI) can be the first symptom of a systemic granulomatous disorder. In the differential diagnosis of DI, a comprehensive assessment of rare causes of endocrine disorders, including extrapulmonary sarcoidosis, should be considered.

Diabetes Insipidus after Vasopressin Withdrawal: A Scoping Review.

The objective of this study is to synthesize the current literature about the relationship between the occurrence of diabetes insipidus (DI), its diagnosis criteria, and management after withdrawal of vasopressin (VP) in critically ill. This scoping review followed the recommendations of Preferred Reporting Items for Systematic Review and Meta-Analyses for Scoping Review (PRISMA-ScR). The search literature was conducted in MEDLINE and EMBASE databases, until March 2022. A manual search was also conducted in order to include articles that were not identified in the initial search performed in the databases. The selection of studies and extraction of data were carried out in a paired and independent manner. There was no restriction regarding the language of publication of the included manuscripts. The analysis included 17 studies (16 case reports and one retrospective cohort). All studies used VP, with a median time of drug infusion of 48 hours (IQR: 16-72) and DI incidence of 1.53%. The diagnosis of DI was based on diuresis output and concomitant hypernatremia or changes in serum sodium concentration, with median time to symptoms onset after discontinuation of VP of 5 hours (IQR: 3-10). The treatment of DI consisted mainly of fluid management and the use of desmopressin. DI after VP withdrawal was present in 51 patients described in 17 studies, but diagnosis and management varied among each report. Using the available data, we propose a diagnosis suggestion and a flowchart for managing patients with DI after withdrawal of VP in the Intensive Care Unit. Multicentric collaborative research is urgently needed to obtain more quality data on this topic. Pérsico RS, Viana MV, Viana LV. Diabetes Insipidus after Vasopressin Withdrawal: A Scoping Review. Indian J Crit Care Med 2022;26(7):846-852.

Usefulness of non-stimulated copeptin in the diagnosis of diabetes insipidus after pituitary surgery.

Usefulness of non-stimulated copeptin in the diagnosis of diabetes insipidus after pituitary surgery.

The Emerging Role of Copeptin.

Direct measurement of the nonapeptide vasopressin has been limited by analyte instability ex vivo and in vivo rapid degradation, low serum concentrations requiring a sensitive assay and inherent secretory pulsatility. Copeptin is a 39 amino acid glycopeptide cleavage product of vasopressin synthesis with high stability, providing a marker of vasopressin secretion. Copeptin measurement has applications in diagnosis of diabetes insipidus and other diseases with altered vasopressin secretion. This review summarises our current understanding of serum copeptin measurement in diabetes insipidus and possible future applications of copeptin assays. As vasopressin is a stress hormone, there is emerging evidence on the use of copeptin for diagnosis and prognostication of disorders such as syndrome of inappropriate anti-diuretic hormone secretion, diabetes mellitus, critical illness, stroke, cardiovascular disease, respiratory disease, renal disease and thermal stress. Copeptin concentration measurement is likely to improve the diagnostic reliability of diabetes insipidus and, as a marker of stress, may have diagnostic or prognostic utility in specific clinical circumstances. Further studies are needed to determine if goal-directed therapy using plasma copeptin concentrations may improve patient outcomes.

Arginine-stimulated copeptin measurements in the differential diagnosis of diabetes insipidus: A prospective diagnostic study

Summary Background Differential diagnosis of diabetes insipidus is challenging. The most reliable approach is hypertonic saline-stimulated copeptin measurements. However, this test is based on the induction of hypernatraemia and requires close monitoring of plasma sodium concentrations. Arginine-stimulated copeptin measurements might provide an alternative, simple, and safe test. Methods In this prospective diagnostic study, we recruited a development cohort from University Hospital Basel, Basel, Switzerland, and a validation cohort from five centres in Basel, Aarau, Luzern, Bern, and St Gallen, Switzerland, and the University Hospital Wurzburg, Wurzburg, Germany. For both cohorts, patients were eligible for inclusion if they were aged 18 years or older, were newly referred with polyuria (>50 mL/kg bodyweight per day) or had a known diagnosis of central diabetes insipidus or primary polydipsia. We also recruited a comparator cohort of healthy controls in parallel to each cohort, comprising adults (aged 18 years and older, with normal drinking habits, and no history of polyuria) and children who underwent arginine stimulation to diagnose growth hormone deficiency (children were only included in the comparator cohort to the development cohort as proof of concept). Patients and healthy controls underwent arginine stimulation with measurement of plasma copeptin at baseline and 30, 45, 60, 90, and 120 min. The primary objective in the development cohort was to determine the diagnostic accuracy of plasma copeptin concentrations to discriminate between diabetes insipidus and primary polydipsia, and in the validation cohort was to confirm those results. Adverse effects of the test were monitored in all participants, with tolerability of the test rated using a visual analogue scale (VAS) that ranged from no (0) to maximum (10) discomfort. This trial is registered with ClinicalTrials.gov, number NCT00757276. Findings Between May 24, 2013, and Jan 11, 2017, 52 patients were enrolled in the development cohort (12 [23%] with complete diabetes insipidus, nine [17%] with partial diabetes insipidus, and 31 [60%] with primary polydipsia) alongside 20 healthy adults and 42 child controls. Between Oct 24, 2017, and June 27, 2018, 46 patients were enrolled in the validation cohort (12 [26%] with complete diabetes insipidus, seven [15%] with partial diabetes insipidus, and 27 [59%] with primary polydipsia) alongside 30 healthy adult controls (two patients in this cohort were excluded from the main analysis because of early vomiting during the test). In the pooled patient and control datasets, median arginine-stimulated copeptin concentrations increased in healthy adult controls (from 5·2 pM [IQR 3·3–10·9] to a maximum of 9·8 pM [6·4–19·6]) and in participants with primary polydipsia (from 3·6 pM [IQR 2·4–5·7] to a maximum of 7·9 pM [5·1–11·8]), but only minimally in those with diabetes insipidus (2·1 pM [IQR 1·9–2·7] to a maximum of 2·5 pM [1·9–3·1]). In the development cohort, a cutoff of 3·5 pM at 60 min provided the highest diagnostic accuracy of 94% (95% CI 84–98). The accuracy of this cutoff in the validation cohort was 86% (95% CI 73–94). By pooling the data from both cohorts, an optimal accuracy of 93% (95% CI 86–97) was reached at a cutoff of 3·8 pM copeptin at 60 min (sensitivity 93%, 95% CI 86–98; specificity 92%, 95% CI 84–100). The test was safe and well tolerated, with median VAS scores of 3·5 (IQR 2–4) in patients with diabetes insipidus, 3 (2–4) in those with primary polydipsia, 1 (1–3) in healthy adults, and 1 (0–5) in healthy children in the pooled participant dataset. Interpretation Arginine-stimulated copeptin measurements are an innovative test for diabetes insipidus with high diagnostic accuracy, and could be a simplified, novel, and safe diagnostic approach to diabetes insipidus in clinical practice. Funding Swiss National Science Foundation and University Hospital Basel.

MON-270 Diagnostic Value of Copeptin in Central Diabetes Insipidus

Background: The diagnosis of diabetes insipidus (DI) relies on indirect measurement of serum and urine sodium and osmolality. Since the diagnosis can only be made when an inappropriately dilute urine is paired with a significantly concentrated serum, the process is tedious for the clinician and uncomfortable for the patient. Copeptin is the C-terminal portion of the anti-diuretic hormone (ADH) prohormone which correlates with the less stable ADH, therefore providing a direct measurement of posterior pituitary response to hyperosmolar stress. (1,2) Aim: This study aims to assess the diagnostic accuracy of copeptin in patients with central DI compared with subjects who underwent pituitary surgery without developing DI. Methods: Serum samples from subjects with central DI, control subjects post pituitary surgery with no DI (NDI) and control subjects with SIADH were collected and analysed on the BRAHMS KRYPTOR copeptin assay. Groups were compared using unpaired T-test and Levene’s test for equal variance. Results: 56 samples from 22 subjects (13 females, 9 males, mean age 53.9 ± 15.5 y.o.) were analysed. Two subjects had resolved DI (RDI) after copeptin analysis and were successfully weaned off DDAVP and reclassified as NDI. Of the DI subjects, 1 had acute and 5 had chronic DI. Copeptin was lower in DI compared to NDI group (p = 0.013), while serum sodium, osmolality, urine osmolality were similar. Copeptin did not differentiate between the SIADH and NDI groups. After exclusion of NDI samples with serum sodium ≤ 140 mmol/L, the area under the curve was 0.97 (95% CI 0.9 to 1.0), a copeptin cut-off of 2.9 pmol/L predicts DI with a sensitivity of 92% and a specificity of 90%. Conclusion: Copeptin concentration of < 3.0 pmol/L concurrently with serum sodium concentration of > 140mmol/L predicted central DI when using post pituitary surgery subjects without DI as controls.1. Winzeler, B., Zweifel, C., Nigro, N., Arici, B., Bally, M., Schuetz, P., Blum, C., Kelly, C., Berkmann, S., Huber, A., Gentili, F., Zadeh, G., Landolt, H., Mariani, L., Müller, B. and Christ-Crain, M. (2015). Postoperative Copeptin Concentration Predicts Diabetes Insipidus After Pituitary Surgery. The Journal of Clinical Endocrinology & Metabolism, 100(6), pp.2275-2282.2. Fenske, J., Refardt, I., SchnyderI., Winzeler, B., Drummond J., Ribeiro-Oliveira, Jr. A., Drescher, T., Bilz S., Vogt, D.R., Malzahn, U., Kroiss, M., Christ, E., Henzen, C., Fischli S., Tönjes, A., Mueller, B., Schopohl, J., Flitsch, J., Brabant, G., Fassnacht M., Christ-Crain, M. (2018). Copeptin in the Diagnosis of Diabetes Insipidus. New England Journal of Medicine, 379(18), pp.1784-1786.

Incidence and Effect of Diabetes Insipidus in the Acute Care of Patients with Severe Traumatic Brain Injury.

Literature on diabetes insipidus (DI) after severe traumatic brain injury (TBI) is scarce. Some studies have reported varying frequencies of DI and have showed its association with increased mortality, suggesting it as a marker of poor outcome. This knowledge gap in the acute care consequences of DI in severe TBI patients led us to conceive this study, aimed at identifying risk factors and quantifying the effect of DI on short-term functional outcomes and mortality. We assembled a historic cohort of adult patients with severe TBI (Glasgow Coma Scale ≤ 8) admitted to the intensive care unit (ICU) of a tertiary-care university hospital over a 6-year period. Basic demographic characteristics, clinical information, imaging findings, and laboratory results were collected. We used logistic regression models to assess potential risk factors for the development of DI, and the association of this condition with death and unfavorable functional outcomes [modified Rankin scale (mRS)] at hospital discharge. A total of 317 patients were included in the study. The frequency of DI was 14.82%, and it presented at a median of 2days (IQR 1-3) after ICU admission. Severity according to the Abbreviated Injury Scale (AIS) score of the head, intracerebral hemorrhage, subdural hematoma, and skull base fracture was suggested as risk factors for DI. Diagnosis of DI was independently associated death (OR 4.34, CI 95% 1.92-10.11, p = 0.0005) and unfavorable outcome (modified Rankin Scale = 4-6) at discharge (OR 7.38; CI 95% 2.15-37.21, p = 0.0047). Diabetes insipidus is a frequent and early complication in patients with severe TBI in the ICU and is strongly associated with increased mortality and poor short-term outcomes. We provide clinically useful risk factors that will help detect DI early to improve prognosis and therapy of patients with severe TBI.

Central Diabetes Insipidus in a Young Feline

Background: Central diabetes insipidus (CDI) is an endocrine disorder caused by the failure to produce, transport, or release ADH. This disease may show a primary etiology (idiopathic or congenital) or a secondary one (trauma or neoplasms). It is characterized by signs such as polyuria and polydipsia. The definitive diagnosis is obtained by the two-step water deprivation test; the absence of adequate urinary concentration in the first stage confirms the diagnosis of diabetes insipidus and, in the second stage, the response to the application of synthetic desmopressin confirms a central origin. Because CDI is rare in felines, the aim of this study was to report the occurrence of a case of CDI, probably of congenital primary origin, in an 8-month-old kitten.Case: An 8-month-old male feline, castrated, 3.2 kg, was brought to consultation with a report of polydipsia, polyuria, smaller size and weight, and lower activity when compared to his brother, for several months. On physical examination, lethargy, body score 2/5, and mild dehydration were noted, as well as deciduous teeth that should have already been replaced. Abdominal ultrasound and laboratory tests were requested, which ruled out chronic kidney disease (CKD), diabetes mellitus (DM), hyperadrenocorticism (HAC), and hyperthyroidism. Due to the fact that urinalysis evidenced hyposthenuria (urinary density [UD] 1.004), CDI was suspected. The patient underwent a water deprivation test and, after 7.5 h, lost 4.7% of his initial weight, while UD was 1.012, confirming the diagnosis of DI. The investigation then proceeded to the evaluation of the response to synthetic desmopressin by the application of 5 U IM. Two h later, UD was 1.019, confirming the diagnosis of CDI. The prescribed treatment was oral desmopressin at a dose of 100 μg BID. Upon return after 30 days, the feline had gained weight, was well hydrated, and the tutor reported higher activity. A new urinalysis showed a UD of 1.004 and inactive sediment. The tutor was asked to start administering the drug three times a day. However, noting that the patient’s quality of life had significantly improved, and wishing to spare the animal from the stress of taking medication once more a day, she chose not to modify the therapy and not to perform additional tests, due to financial limitation.Discussion: First, CKD, DM, HAC, and hyperthyroidism, more common conditions, were ruled out, and the investigation then proceeded to a water deprivation test. The feline lost 3% to 5% of the initial weight and UD was on the borderlinebetween hypo- and isosthenuria, as described in the literature for the diagnosis of DI. In the second stage of the test, slight urinary concentration was observed after the application of synthetic desmopressin, which confirmed the diagnosis of CDI. The dose of desmopressin prescribed for home treatment, 100 μg BID, was effective to relieve the clinical signs, but urine remained in hyposthenuria in the interval between administrations, suggesting that, for this patient, treatment would be more effective by administering the medication three times a day, in order to maintain an adequate serum concentration. Due to the diagnosis of CDI and the feline being young, the condition’s primary origin is believed to be congenital. It is also suspected that the patient may still have congenital hypothyroidism, due to the clinical signs of late tooth exchange and constant lethargy, in addition to laboratory results of thyroid hormones below reference levels. However, because thyroid tests were made by chemiluminescence, a repetition by radioimmunoassay is indicated. If hypothyroidism is confirmed,it would be possible to assume a common etiological factor between CDI and hypothyroidism, such as hypothalamicpituitary malformation.

Transient Diabetes Insipidus Following Organophosphorus Poisoning.

IntroductionOrganophosphorus poisoning is the most common poison used for suicidal attempt in Nepal. Diabetes insipidus is unusual and rare in this poisoning. This is the second case report of Diabetes insipidus developing in organophosphorus poisoning. Management of diabetes insipidus includes desmopressin and adequate fluid management.Case presentationA 34-year-old female patient accompanied by her father presented at the Emergency department with an alleged history of ingestion of unknown amount of chlorpyrifos, cypermethrin and quinalphos. On admission, she had a Glasgow Coma Scale (GCS) of 7/15. Her blood pressure was 110/60 mm Hg, pulse 54/min, respiratory rate 45/min and saturation 35% on room air, pinpoint pupil reactive to light and bilateral crepitations. She was immediately resuscitated with two litres of normal saline and intubated with a 7 mm endotracheal tube. Atropinisation was done, and pralidoxime was started. She developed a urine output of 250-350 ml per hour with rising sodium and serum osmolality. The urine examination showed low sodium and urine specific gravity. A diagnosis of diabetes insipidus was made. There was no immediate improvement in her GCS. She was managed with 5% dextrose and subcutaneous desmopressin and was transferred out of the intensive care unit on the sixth day and was discharged from hospital on the fifteenth day.ConclusionDiabetes insipidus is a rare transient complication in organophosphorus poisoning that requires careful observation and early management with desmopressin and adequate fluid balance to improve patient outcome.

A Copeptin-based approach in the diagnosis of diabetes insipidus

A Copeptin-based approach in the diagnosis of diabetes insipidus

Diabetes insipidus.

Diabetes insipidus (DI) is a disorder characterized by excretion of large amounts of hypotonic urine. Central DI results from a deficiency of the hormone arginine vasopressin (AVP) inthe pituitary gland or the hypothalamus, whereas nephrogenic DI results from resistance to AVP in the kidneys. Central and nephrogenic DI are usually acquired, but genetic causes must be evaluated, especially if symptoms occur in early childhood. Central or nephrogenic DI must bedifferentiated from primary polydipsia, which involves excessive intake of large amounts of water despite normal AVP secretion and action. Primary polydipsia is most common in psychiatric patients and health enthusiasts but the polydipsia in a small subgroup of patients seems to be dueto an abnormally low thirst threshold, a condition termed dipsogenic DI. Distinguishing between the different types of DI can be challenging and is done either by a water deprivation test or by hypertonic saline stimulation together with copeptin (or AVP) measurement. Furthermore, a detailed medical history, physical examination and imaging studies are needed toensure an accurate DI diagnosis. Treatment of DI or primary polydipsia depends on the underlying aetiology and differs in central DI, nephrogenic DI and primary polydipsia.

Visual Vignette

Case Presentation: A 30-year-old female with no prior comorbidities presented to a nephrology center with polyuria and polydipsia of 2-weeks duration. Her 24-hour urine output was more than 6 L/day, and her serum sodium was 147 mEq/L, serum osmolality 302 mOsm/L, and urine osmolality 108 mOsm/L, consistent with a diagnosis of diabetes insipidus. Her glucose, potassium, and calcium levels were normal. Her thyroid-stimulating hormone was 1.13 mIU/L, thyroxine was 8.7 µg/dL, prolactin 34.6 ng/mL, and an 8 am cortisol was 3 µg/dL. She had two normal pregnancies, with last childbirth 8 years back. Her menstrual cycles were regular. Magnetic resonance imaging (MRI) of the brain showed a thickened stalk and enlarged pituitary gland (Fig. 1). On contrast, there was thickening and abnormal enhancement of the stalk and an enlarged pituitary measuring 15 mm, with abnormal heterogeneous enhancement with a peripheral rim of enhancement and a central nonenhancing area (Fig. 1). A diagnosis of infundibulo-hypophysitis was made, and a detailed set of investigations, including antinuclear antibodies, antineutrophil cytoplasmic autoantibodies (ANCA), IgG4, angiotensin-converting enzyme levels, chest X-ray, and skin tuberculin testing was done, with nonrevealing reports. She was started on intranasal desmopressin and prednisolone 60 mg/day with good resolution of symptoms. Desmopressin was stopped after 3 months; after being on high-dose steroids for 6 months, she presented to our center with weight gain and cushingoid features. A repeat MRI was unchanged. Due to a lack of resolution of the MRI features despite prolonged steroid therapy, a whole-body computed tomography scan with a transnasal biopsy of the pituitary gland was planned. Patient's prednisone dose was reduced to 15 mg/day. Patient presented a month later to the medical emergency with acute hypoxemic respiratory failure and acute renal failure, with serum creatinine of 4.75 mg/dL. Chest X-ray showed “white out” lungs, and urine analysis showed numerous red blood cells. A clinical diagnosis of pulmonary-renal syndrome was made, and the patient was started on high-dose steroids and plasma exchange was attempted. However, the patient succumbed within 48 hours of admission. What is the diagnosis?