diabetestalk.net

Diabetes Insipidus Hypokalemia

Annals Of Internal Medicine: Paul Epstein, Md, Series Editor

Annals Of Internal Medicine: Paul Epstein, Md, Series Editor

PHYSIOLOGY IN MEDICINE: A SERIES OF ARTICLES LINKING MEDICINE WITH SCIENCE Physiology in Medicine: Dennis A. Ausiello, MD, Editor; Dale J. Benos, PhD, Deputy Editor; Francois Abboud, MD, Associate Editor; William J. Koopman, MD, Associate Editor Nephrogenic Diabetes Insipidus Jeff M. Sands, MD, and Daniel G. Bichet, MD Diabetes insipidus is a condition in which patients pro-duce large quantities of dilute urine. Central or neu- rogenic diabetes insipidus results from the failure of the posterior pituitary to make or secrete vasopressin (also called antidiuretic hormone [ADH]). Nephrogenic diabe- tes insipidus (NDI), which can be congenital or acquired, results from failure of the kidney to respond to vasopressin. Most adults with NDI have an acquired abnormality, with the most common causes being lithium therapy, hypercal- cemia, hypokalemia, protein malnutrition, and release of ureteral obstruction. However, internists will be seeing more adult patients with congenital NDI because genetic screening of newborns in families with a history of this disorder has resulted in improved therapy for these chil- dren, and most are now surviving into adulthood. The standard method for diagnosing diabetes insipi- dus is a water deprivation test. Figure 1 shows the typical changes in urine osmolality in response to water depriva- tion and to the administration of exogenous vasopressin in healthy individuals and in patients with diabetes insipidus. This test, which also distinguishes between persons with complete versus partial versions of each type of diabetes Ann Intern Med. 2006;144:186-194. For author affiliations, see end of text. See also: Web-Only CME quiz Conversion of figures into slides Clinical Principles Patients with diabetes insipidus produce large quantities of dilute Continue reading >>

Central Diabetes Insipidus

Central Diabetes Insipidus

Diabetes insipidus (DI) results from a deficiency of vasopressin (ADH) due to a hypothalamic-pituitary disorder (central DI [CDI]) or from resistance of the kidneys to vasopressin (nephrogenic DI [NDI]). Polyuria and polydipsia develop. Diagnosis is by water deprivation test showing failure to maximally concentrate urine; vasopressin levels and response to exogenous vasopressin help distinguish CDI from NDI. Treatment is with desmopressin or lypressin. Nonhormonal treatment includes use of diuretics (mainly thiazides) and vasopressin-releasing drugs, such as chlorpropamide. The posterior lobe of the pituitary is the primary site of vasopressin storage and release, but vasopressin is synthesized within the hypothalamus. Newly synthesized hormone can still be released into the circulation as long as the hypothalamic nuclei and part of the neurohypophyseal tract are intact. Only about 10% of neurosecretory neurons must remain intact to avoid central diabetes insipidus. The pathology of central diabetes insipidus thus always involves the supraoptic and paraventricular nuclei of the hypothalamus or a major portion of the pituitary stalk. Onset of central diabetes insipidus may be insidious or abrupt, occurring at any age. The only symptoms in primary central diabetes insipidus are polydipsia and polyuria. In secondary central diabetes insipidus, symptoms and signs of the associated lesions are also present. Enormous quantities of fluid may be ingested, and large volumes (3 to 30 L/day) of very dilute urine (specific gravity usually < 1.005 and osmolality < 200 mOsm/L) are excreted. Nocturia almost always occurs. Dehydration and hypovolemia may develop rapidly if urinary losses are not continuously replaced. Central diabetes insipidus must be differentiated from other causes Continue reading >>

Diabetes Insipidus

Diabetes Insipidus

Diabetes insipidus (DI) is a condition characterized by large amounts of dilute urine and increased thirst.[1] The amount of urine produced can be nearly 20 liters per day.[1] Reduction of fluid has little effect on the concentration of the urine.[1] Complications may include dehydration or seizures.[1] There are four types of DI, each with a different set of causes.[1] Central DI (CDI) is due to a lack of the hormone vasopressin (antidiuretic hormone).[1] This can be due to damage to the hypothalamus or pituitary gland or genetics.[1] Nephrogenic diabetes insipidus (NDI) occurs when the kidneys do not respond properly to vasopressin.[1] Dipsogenic DI is due to abnormal thirst mechanisms in the hypothalamus while gestational DI occurs only during pregnancy.[1] Diagnosis is often based on urine tests, blood tests, and the fluid deprivation test.[1] Diabetes mellitus is a separate condition with an unrelated mechanism, though both can result in the production of large amounts of urine.[1] Treatment involves drinking sufficient fluids to prevent dehydration.[1] Other treatments depend on the type.[1] In central and gestational disease treated is with desmopressin.[1] Nephrogenic disease may be treated by addressing the underlying cause or the use of a thiazide, aspirin, or ibuprofen.[1] The number of new cases of diabetes insipidus each year is 3 in 100,000.[4] Central DI usually starts between the ages of 10 and 20 and occurs in males and females equally.[2] Nephrogenic DI can begin at any age.[3] The term "diabetes" is derived from the Greek word meaning siphon.[5] Signs and symptoms[edit] Excessive urination and extreme thirst and increased fluid intake (especially for cold water and sometimes ice or ice water) are typical for DI.[6] The symptoms of excessive urination Continue reading >>

Hypokalemia & Nephrogenic Diabetes Insipidus: Causes & Diagnoses | Symptoma.com

Hypokalemia & Nephrogenic Diabetes Insipidus: Causes & Diagnoses | Symptoma.com

"Nephrogenic Diabetes Insipidus" . [en.wikipedia.org] , NDI - Nephrogen diab insipidus , nephrogenic diabetes insipidus (diagnosis) , nephrogenic diabetes insipidus , Diabetes insipidus nephrogenic , Nephrogenic diabetes insipidus [fpnotebook.com] [] this condition Nephrogenic Diabetes Insipidus 2: It is very rare and certain other abnormal genes are responsible for this condition Who gets Nephrogenic Diabetes Insipidus [dovemed.com] Nephrogenic diabetes insipidus (also known as renal diabetes insipidus ) is a form of diabetes insipidus primarily due to pathology of the kidney . [en.wikipedia.org] nephrogenic , Nephrogenic diabetes insipidus , NDI - Nephrogenic diabetes insipidus , Nephrogenic diabetes insipidus (disorder) , diabetes; insipidus, nephrogenic , nephrogenic [fpnotebook.com] [] causes nephrogenic diabetes insipidus Hypokalemia and Metabolic alkalosis ------- Bartter, Gitelman & Liddle's syndrome Bartter & Gitelman ----- Normal/dec BP Liddle's -- [usmleforum.com] Nephrogenic diabetes insipidus with dilataion of bilateral renal pelvis, ureter and bladder. [sjkdt.org] Continuing The Conversation Diseases and conditions like diabetic ketoacidosis, alkalosis, abnormally high aldosterone levels, Bartter syndrome, kidney failure, and certain [bblc.tv] [] and aldosterone are high causes chloride resistant metabolic alkalosis treat with potassium supplementation clinically it may present with polyuria and polydipsia because hypokalemia [usmleforum.com] Otherwise, there was no difference regarding the degree of hyponatremia, hypochloremia and hypokalemia among the three patterns. [sjkdt.org] [] symptoms: fatigue muscle weakness and cramping headaches palpitations polyuria and polydipsia (hypokalemia induced nephrogenic diabetes insipidus) signs: metabolic alkalosis Continue reading >>

Autophagic Degradation Of Aquaporin-2 Is An Early Event In Hypokalemia-induced Nephrogenic Diabetes Insipidus

Autophagic Degradation Of Aquaporin-2 Is An Early Event In Hypokalemia-induced Nephrogenic Diabetes Insipidus

Autophagic degradation of aquaporin-2 is an early event in hypokalemia-induced nephrogenic diabetes insipidus Scientific Reports volume 5, Articlenumber:18311 (2015) Hypokalemia (low serum potassium level) is a common electrolyte imbalance that can cause a defect in urinary concentrating ability, i.e., nephrogenic diabetes insipidus (NDI), but the molecular mechanism is unknown. We employed proteomic analysis of inner medullary collecting ducts (IMCD) from rats fed with a potassium-free diet for 1 day. IMCD protein quantification was performed by mass spectrometry using a label-free methodology. A total of 131 proteins, including the water channel AQP2, exhibited significant changes in abundance, most of which were decreased. Bioinformatic analysis revealed that many of the down-regulated proteins were associated with the biological processes of generation of precursor metabolites and energy, actin cytoskeleton organization, and cell-cell adhesion. Targeted LC-MS/MS and immunoblotting studies further confirmed the down regulation of 18 selected proteins. Electron microscopy showed autophagosomes/autophagolysosomes in the IMCD cells of rats deprived of potassium for only 1 day. An increased number of autophagosomes was also confirmed by immunofluorescence, demonstrating co-localization of LC3 and Lamp1 with AQP2 and several other down-regulated proteins in IMCD cells. AQP2 was also detected in autophagosomes in IMCD cells of potassium-deprived rats by immunogold electron microscopy. Thus, enhanced autophagic degradation of proteins, most notably including AQP2, is an early event in hypokalemia-induced NDI. Hypokalemia (low serum potassium level) is a very common electrolyte imbalance encountered in clinical medicine, occurring as a result of poor nutritional status, gas Continue reading >>

Bartter Syndrome Type 1 Presenting As Nephrogenic Diabetes Insipidus

Bartter Syndrome Type 1 Presenting As Nephrogenic Diabetes Insipidus

Bartter Syndrome Type 1 Presenting as Nephrogenic Diabetes Insipidus 1Department of Pediatrics, Infermi Hospital, Rimini, Italy 2Medical Genetics Laboratory, Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, Milan, Italy Correspondence should be addressed to Gianluca Vergine ; [email protected] Received 8 August 2017; Accepted 14 December 2017; Published 21 February 2018 Copyright 2018 Gianluca Vergine 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. Bartter syndrome (BS) type 1 (OMIM #601678) is a hereditary salt-losing renal tubular disorder characterized by hypokalemic metabolic alkalosis, hypercalciuria, nephrocalcinosis, polyuria, recurrent vomiting, and growth retardation. It is caused by loss-of-function mutations of the SLC12A1 gene, encoding the furosemide-sensitive Na-K-Cl cotransporter. Recently, a phenotypic variability has been observed in patients with genetically determined BS, including absence of nephrocalcinosis, hypokalemia, and/or metabolic alkalosis in the first year of life as well as persistent metabolic acidosis mimicking distal renal tubular acidosis. We report the case of a child with a genetically determined diagnosis of Bartter syndrome type 1 who presented with a phenotype of nephrogenic diabetes insipidus, with severe hypernatremia and urinary concentrating defect. In these atypical cases, molecular analysis is mandatory to define the diagnosis, in order to establish the correct clinical and therapeutic management. Bartter syndrome is a hereditary salt-losing renal tubular disorder characterized by hypokalemic metabolic alkalosis, hypercalciuria, Continue reading >>

Diabetes Insipidus: Practice Essentials, Background, Etiology

Diabetes Insipidus: Practice Essentials, Background, Etiology

Diabetes insipidus (DI) is defined as the passage of large volumes (>3 L/24 hr) of dilute urine (< 300 mOsm/kg). It has the following 2 major forms: Central (neurogenic, pituitary, or neurohypophyseal) DI, characterized by decreased secretion of antidiuretic hormone (ADH; also referred to as arginine vasopressin [AVP]) Nephrogenic DI, characterized by decreased ability to concentrate urine because of resistance to ADH action in the kidney [ 1 ] Two other forms are gestational DI and primary polydipsia (dipsogenic DI); both are caused by deficiencies in AVP, but the deficiencies do not result from a defect in the neurohypophysis or kidneys. The predominant manifestations of DI are as follows: Polyuria: The daily urine volume is relatively constant for each patient but is highly variable between patients (3-20 L) The most common form is central DI after trauma or surgery to the region of the pituitary and hypothalamus, which may exhibit 1 of the following 3 patterns: Earley LE, Orloff J. The mechanism of antidiuresis associated with the administration of hydrochlorothiazide to patients with vasopressin-resistant diabetes insipidus. J Clin Invest. Nov 1962;41(11):1988-97. Babey M, Kopp P, Robertson GL. Familial forms of diabetes insipidus: clinical and molecular characteristics. Nat Rev Endocrinol. 2011 Jul 5. 7(12):701-14. [Medline] . Bockenhauer D, van't Hoff W, Dattani M, Lehnhardt A, Subtirelu M, Hildebrandt F, et al. Secondary nephrogenic diabetes insipidus as a complication of inherited renal diseases. Nephron Physiol. 2010. 116(4):p23-9. [Medline] . Los EL, Deen PM, Robben JH. Potential of nonpeptide (ant)agonists to rescue vasopressin V2 receptor mutants for the treatment of X-linked nephrogenic diabetes insipidus. J Neuroendocrinol. 2010 May. 22(5):393-9. [Medlin Continue reading >>

Payperview: Hydrochlorothiazide-amiloride In The Treatment Of Congenital Nephrogenic Diabetes Insipidus - Karger Publishers

Payperview: Hydrochlorothiazide-amiloride In The Treatment Of Congenital Nephrogenic Diabetes Insipidus - Karger Publishers

I have read the Karger Terms and Conditions and agree. The effects of treatment with hydrochlorothiazide combined with amiloride were compared to hydrochlorothiazide treatment alone in 2 brothers with congenital nephrogenic diabetes insipidus. Whereas both modalities of treatment resulted in reduction in voiding frequency and urine volume, decrease in daily fluid intake and increase in urine osmolality, the two-drug combination was found to be superior to hydrochlorothiazide alone by preventing urinary potassium losses, hypokalemia, and alkalosis. It was also found that amiloride had a certain additive effect to the thiazide in terms of increasing initial urinary sodium excretion, reducing urine volume and free water clearance, and lowering serum sodium concentration and osmolality. Similar comparison of the hydrochlorothiazide-amiloride regimen to treatment with the hydrochlorothiazide-tolmetin combination in 1 of the patients revealed that the effectiveness of both diuretic modalities was close with slight advantage of the former. Treatment of the 2 patients for 10 months with hydrochlorothiazide and amiloride showed no adverse effects and consistent reduction in fluid intake and urine volume. It is concluded that the hydrochlorothiazide-amiloride regimen is superior to hydrochlorothiazide alone and can be a satisfactory alternative to the hydrochlorothiazide-prostaglandin synthetase inhibitor combination in the treatment of congenital nephrogenic diabetes insipidus. Continue reading >>

Diabetes Insipidus: Causes, Symptoms And Treatment

Diabetes Insipidus: Causes, Symptoms And Treatment

Diabetes insipidus is a condition where the body loses too much fluid through urination, causing a significant risk of dangerous dehydration as well as a range of illnesses and conditions. There are two forms of the disease: nephrogenic diabetes insipidus and central diabetes insipidus (also known as neurogenic diabetes insipidus). A number of factors have been linked to the development of diabetes insipidus, which may also occur in pregnancy or with the use of certain medications. Establishing the cause of the problem can help determine the most appropriate treatment to support the regulation of water balance in the body. Diabetes insipidus is a condition that can be managed successfully. Contents of this article: What is diabetes insipidus? An uncommon condition, diabetes insipidus is a disorder affecting the regulation of body fluid levels. Two key symptoms resemble those of the more common forms of diabetes that affect blood sugar levels (diabetes mellitus types 1 and 2).1-5 People with diabetes insipidus produce excessive amounts of urine (polyuria), resulting in frequent urination and, in turn, thirst (polydipsia). However, the underlying cause of these two symptoms is quite different from the causes in types 1 and 2 diabetes. In diabetes mellitus, elevated blood sugar prompts the production of large volumes of urine to help remove the excess sugar from the body. In diabetes insipidus, it is the body's water balance system itself that is not working properly. Here are some key points about diabetes insipidus. More detail and supporting information is in the body of this article. Diabetes insipidus is a condition where the body fails to properly control water balance, resulting in excessive urination. Diabetes insipidus can be caused by low or absent secretion of t Continue reading >>

Impairment Of Avp Regulation In 17-hydroxylase Deficiency, A Unique Form Of Adrenal Insufficiency

Impairment Of Avp Regulation In 17-hydroxylase Deficiency, A Unique Form Of Adrenal Insufficiency

, Volume 25, Issue7 , pp 635638 | Cite as Impairment of AVP regulation in 17-hydroxylase deficiency, a unique form of adrenal insufficiency 17-hydroxylase deficiency (17- OHDS) results in decreased production of cortisol and sex steroids and hypokalemia secondary to excess mineralocorticoids. It has long been known that glucocorticoid deficiency is associated with impaired urinary dilution and increased secretion of vasopressin (AVP). On the other hand, chronic hypokalemia is a well-established cause of nephrogenic diabetes insipidus. We evaluated the status of AVP secretion in a patient with 17-OHDS and in 8 normokalaemic control subjects during hypertonic saline infusion (5% NaCl 0.06 ml.kg.min.120 min). The patient was evaluated on 3 separate occasions: pre-treatment (PT), and daily treatment with 0.375 mg (T1) and 0.5 mg (T2) dexamethasone. Blood was collected for AVP, corticosterone (B), plasma osmolality (pOsm) and electrolyte determination. In the control group plasma AVP levels increased from 0.80.1 to 4.10.6 pmol/l and pOsm increased from 2822 to 3021.5 mosmol/kg. In the patient, plasma AVP levels increased from 9.3 to 12.3; 4.5 to 6.2; and 2.5 to 6.2 pmol/l, and pOsm increased from 282 to 302, from 290 to 307, and from 291 to 311 mosmol/kg during the PT, T1 and T2 conditions, respectively. Serum potassium levels were low (2.6 mmol/l) during PT and reached normal values after treatment. There was a significant negative correlation between plasma AVP and serum potassium levels (r=0.71; p<0.001). The results originally indicate that high plasma AVP levels may be found in 17-OHDS, suggesting an effect of F deficiency per se. In addition, a concealed partial nephrogenic diabetes insipidus secondary to chronic hypokalemia cannot be excluded. AVP17-hydroxylase defic Continue reading >>

Central Diabetes Insipidus

Central Diabetes Insipidus

In CDI, symptoms may develop over time or abruptly and may affect individuals of any age. CDI is characterized by excessive thirst (polydipsia) and excessive urination (polyuria), even at night (nocturia). The severity and progression of CDI varies from case to case. Some individuals may have a severe form of the disorder (complete CDI) with little or no vasopressin activity. Others may have a mild form of the disorder (partial CDI) with residual vasopressin activity. Without appropriate AVP secretion, individuals with central diabetes insipidus are unable to concentrate the urine by reabsorbing water in the kidneys. This results in obligatory excessive urine output of dilute urine. Consequently, individuals must drink excessively to prevent dehydration. In response to thirst, affected individuals may drink several gallons of water a day. If affected individuals are deprived of water for an extended period of time, rapid dehydration will occur. Thirst cravings can be strong enough to awaken people from sleep. In infants, additional symptoms may occur including irritability, lethargy, vomiting, constipation and fever. If left untreated, repeated episodes of dehydration can potentially result in seizures, brain damage, developmental delays, and physical and mental retardation. However, with proper diagnosis and prompt treatment intelligence and development is usually normal unless more global problems in development of the brain are associated. Affected children may develop bedwetting (enuresis), fatigue, weight loss, and growth retardation. Individuals with CDI are at risk of developing dehydration and cardiovascular symptoms including irregular heartbeats, fever, dry skin and mucous membranes, confusion, seizures, change in consciousness, and potentially coma. Affected Continue reading >>

Nephrogenic Diabetes And Hypokalemia

Nephrogenic Diabetes And Hypokalemia

SDN members see fewer ads and full resolution images. Join our non-profit community! Does anyone know how a decrease in potassium can cause nephrogenic diabetes insipidus? Does anyone know how a decrease in potassium can cause nephrogenic diabetes insipidus? decr aldosterone secondary to hypokalemia, but to the extent of diabetes insipidus...? It's because of decreased responsiveness of the collecting tubules to ADH, which is possibly due to decreased aquaporin 2 expression and/or decreased activity of the Na-K-Cl pump in the TAL (which would diminish the corticopapillary gradient necessary for free water absorption). The entire mechanism is not completely understood. I've never heard of hypokalaemia directly causing nephrogenic DI. Where did you read that? Are you referring to the 8th edition? Which page? (It's not that I don't believe you. But it's important that I read up on it.) It's because of decreased responsiveness of the collecting tubules to ADH, which is possibly due to decreased aquaporin 2 expression and/or decreased activity of the Na-K-Cl pump in the TAL (which would diminish the corticopapillary gradient necessary for free water absorption). The entire mechanism is not completely understood. You're right about the kidney not being responsive to high levels of ADH but my question is what triggers the release of ADH in the first place? I know that hypokalemic patients eventually develop hypertension (must be a chronic imbalance). I just can't connect the dots... Continue reading >>

Clinical Manifestations And Causes Of Nephrogenic Diabetes Insipidus

Clinical Manifestations And Causes Of Nephrogenic Diabetes Insipidus

INTRODUCTION Nephrogenic diabetes insipidus (DI) refers to a decrease in urinary concentrating ability that results from resistance to the action of antidiuretic hormone (ADH). This problem can reflect resistance at the ADH site of action in the collecting tubules, or interference with the countercurrent mechanism due, for example, to medullary injury or to decreased sodium chloride reabsorption in the medullary aspect of the thick ascending limb of the loop of Henle (figure 1) [1]. (See "Diagnosis of polyuria and diabetes insipidus".) Nephrogenic DI, in its mild form, is relatively common since almost all patients who are elderly, sick, or have acute or chronic kidney disease have a reduction in maximum concentrating ability [1]. As an example, the maximum urine osmolality that can be achieved may fall from the normal value of 800 to 1200 mosmol/kg down to 350 to 600 mosmol/kg in these settings [1]. In chronic kidney disease, this defect is due in part to increased solute excretion per functioning nephron and to decreased expression of mRNA for the V2 vasopressin receptor [1,2]. The clinical manifestations and causes of nephrogenic DI will be reviewed here. The treatment of nephrogenic DI, the diagnostic approach to polyuria and diabetes insipidus, and the clinical manifestations and causes of central DI are discussed separately. (See "Treatment of nephrogenic diabetes insipidus" and "Diagnosis of polyuria and diabetes insipidus" and "Clinical manifestations and causes of central diabetes insipidus".) CLINICAL MANIFESTATIONS Patients with moderate to severe nephrogenic or central DI typically present with polyuria, nocturia, and polydipsia. Polyuria is arbitrarily defined as a urine output exceeding 3 L/day in adults or 2 L/m2 in children. Causes of polyuria other than Continue reading >>

Nephrogenic Diabetes Insipidus: Essential Insights Into The Molecular Background And Potential Therapies For Treatment

Nephrogenic Diabetes Insipidus: Essential Insights Into The Molecular Background And Potential Therapies For Treatment

WARNING: RISK OF THYROID C-CELL TUMORS Liraglutide causes dose-dependent and treatment-duration-dependent thyroid C-cell tumors at clinically relevant exposures in both genders of rats and mice. It is unknown whether Victoza® causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans, as the human relevance of liraglutide-induced rodent thyroid C-cell tumors has not been determined. Victoza® is contraindicated in patients with a personal or family history of MTC and in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2). Counsel patients regarding the potential risk for MTC with the use of Victoza® and inform them of symptoms of thyroid tumors (eg, a mass in the neck, dysphagia, dyspnea, persistent hoarseness). Routine monitoring of serum calcitonin or using thyroid ultrasound is of uncertain value for early detection of MTC in patients treated with Victoza®. Risk of Thyroid C-cell Tumors: Patients should be referred to an endocrinologist for further evaluation if serum calcitonin is measured and found to be elevated or thyroid nodules are noted on physical examination or neck imaging. Pancreatitis: Acute pancreatitis, including fatal and nonfatal hemorrhagic or necrotizing pancreatitis, has been observed in patients treated with Victoza® postmarketing. Observe patients carefully for signs and symptoms of pancreatitis (persistent severe abdominal pain, sometimes radiating to the back with or without vomiting). If pancreatitis is suspected, discontinue Victoza® promptly and if pancreatitis is confirmed, do not restart. Victoza® has been studied in a limited number of patients with a history of pancreatitis. It is unknown if patients with a history of pancreatitis are at a higher risk for development of pancreatitis on Victo Continue reading >>

A Case Of Hypokalemic Paralysis In A Patient With Neurogenic Diabetes Insipidus

A Case Of Hypokalemic Paralysis In A Patient With Neurogenic Diabetes Insipidus

Acute hypokalemic paralysis is characterized by muscle weakness or paralysis secondary to low serum potassium levels. Neurogenic diabetes insipidus (DI) is a condition where the patient excretes large volume of dilute urine due to low levels of antidiuretic hormone. Here, we describe a patient with neurogenic DI who developed hypokalemic paralysis without a prior history of periodic paralysis. A 30-year-old right-handed Hispanic male was admitted for refractory seizures and acute DI after developing a dental abscess. He had a history of pituitary adenoma resection at the age of 13 with subsequent pan-hypopituitarism and was noncompliant with hormonal supplementation. On hospital day 3, he developed sudden onset of quadriplegia with motor strength of 0 of 5 in the upper extremities bilaterally and 1 of 5 in both lower extremities with absent deep tendon reflexes. His routine laboratory studies revealed severe hypokalemia of 1.6 mEq/dL. Nerve Conduction Study (NCS) revealed absent compound motor action potentials (CMAPs) with normal sensory potentials. Electromyography (EMG) did not reveal any abnormal insertional or spontaneous activity. He regained full strength within 36 hours following aggressive correction of the hypokalemia. Repeat NCS showed return of CMAPs in all nerves tested and EMG revealed normal motor units and normal recruitment without myotonic discharges. In patients with central DI with polyuria, hypokalemia can result in sudden paralysis. Hypokalemic paralysis remains an important differential in an acute case of paralysis and early recognition and appropriate management is key. The snippet could not be located in the article text. This may be because the snippet appears in a figure legend, contains special characters or spans different sections of the Continue reading >>

More in diabetes