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
Practice Essentials 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: 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. Signs and symptoms The predominant manifestations of DI are as follows: 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: In infants with DI, the most apparent signs may be the following: In children, the following manifestations typically predominate: If the condition that caused DI also damaged the anterior pituitary or hypothalamic centers that produce releasing factors, patients may present with the following: Physical findings vary with the severity and chronicity of DI; they may be entirely normal or may include the following: See Clinical Presentation for more detail. If the clinical presentation suggests DI, laboratory tests must be performed to confirm the diagnosis, as follows: Additional studies that may be indicated include the following: See Workup for more detail. Management Most patients with DI can drink enough fluid to replace their urine losses. When oral intake is inadequate and hypernatremia is present, provide fluid replacement as follows: Give dextrose and water or an intravenous fluid that is hypo-osmolar with respect to the patient’s serum; do not administer sterile water without dextrose IV Administer fluids at a rate no greater than 500-750 mL/hr; aim at reducing serum sodium by approximately 0.5 mmol/L (0.5 mEq/L) every hour Pharmacologic therapeutic options include the follo Continue reading >>
Hypokalemia, Nephrogenic Diabetes Insipidus, Palpitations: 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] Diabetes Insipidus: Nephrogenic Diabetes Insipidus 1: This type is X-chromosome linked, which means that it affects only the male population, while females are carriers of [dovemed.com] Chronic hypokalemia stimulates thirst and can cause nephrogenic diabetes insipidus. [sharinginhealth.ca] Hypertension and hypokalemia can also be seen with a deficiency of the 11-beta-hydroxysteroid dehydrogenase type 2 enzyme which allows cortisols to stimulate aldosterone receptors [en.wikipedia.org] Table 2: Diseases / situations potentially contributing to the pro-arrhythmic risk of hypokalemia. [escardio.org] [] can be vague, and can include: weakness paralysis palpitations abdominal cramping and constipation (ileus) muscle pain cardiac ischemia A careful history, with emphasis on [sharinginhealth.ca] [] include diarrhea , medications like furosemide and steroids , dialysis , diabetes insipidus , hyperaldosteronism , hypomagnesemia , and not enough intake in the diet. [1] [en.wikipedia.org] The pro Continue reading >>
Diabetes Insipidus - Endocrine - Medbullets Step 1
This patient is suffering from diabetes insipidus (DI). In a standard desmopressin test, an increase in urine osmolality of greater than 10% is highly suggestive of a diagnosis of central DI. Central DI is characterized by the failure of the hypothalamic-pituitary axis to produce and secrete sufficient levels of the hormone vasopressin (ADH). A desmopressin test is a highly useful diagnostic tool to differentiate between central (described above) and nephrogenic (resistance to ADH action in the kidneys) DI. The test involves injection of exogenous vasopressin. In central DI, injection of exogenous vasopressin will act to rectify the inappropriately low levels of endogenous ADH, leading to an increase in urine osmolality towards the normal range. In contrast, injection of ADH in the setting of nephrogenic ADH will not have any notable effect, as increasing ADH levels will not overcome the disease mechanism of renal resistance to ADH action. Adam describes the diagnostic protocol of DI in which the desmopressin test can help distinguish neurogenic from nephrogenic cases of DI. The treatment of neurogenic DI may involve nasal administration of desmopressin while nephrogenic DI requires hydration and the administration of thiazides and amiloride. Thompson et al. describe the normal physiological action of ADH, which is to recruit aquaporin channels in the renal distal tubules and collecting ducts, leading to increased reabsorption of water and an improved ability to excrete concentrated urine. Thus, both forms of diabetes insipidus manifest with symptoms of dehydration and inappropriate excretion of excessive volumes of dilute urine. Illustration A depicts urine osmolality and response to water deprivation and desmopressin test in both central and nephrogenic DI. Answer 1 Continue reading >>
Nephrogenic Diabetes Insipidus
Not to be confused with Neurogenic diabetes insipidus. Nephrogenic diabetes insipidus (also known as renal diabetes insipidus) is a form of diabetes insipidus primarily due to pathology of the kidney. This is in contrast to central/neurogenic diabetes insipidus, which is caused by insufficient levels of antidiuretic hormone (ADH, that is, arginine vasopressin or AVP). Nephrogenic diabetes insipidus is caused by an improper response of the kidney to ADH, leading to a decrease in the ability of the kidney to concentrate the urine by removing free water. Signs and symptoms[edit] The clinical manifestation is similar to neurogenic diabetes insipidus, presenting with excessive thirst and excretion of a large amount of dilute urine. Dehydration is common, and incontinence can occur secondary to chronic bladder distension.[1] On investigation, there will be an increased plasma osmolarity and decreased urine osmolarity. As pituitary function is normal, ADH levels are likely to be abnormal or raised. Polyuria will continue as long as the patient is able to drink. If the patient is unable to drink and is still unable to concentrate the urine, then hypernatremia will ensue with its neurologic symptoms.[citation needed] Causes[edit] Acquired[edit] Nephrogenic DI (NDI) is most common in its acquired forms, meaning that the defect was not present at birth. These acquired forms have numerous potential causes. The most obvious cause is a kidney or systemic disorder, including amyloidosis,[2] polycystic kidney disease,[3] electrolyte imbalance,[4][5] or some other kidney defect.[2] The major causes of acquired NDI that produce clinical symptoms (e.g. polyuria) in the adult are lithium toxicity and high blood calcium. Chronic lithium ingestion – appears to affect the tubules by enterin 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 Find articles by Monica Verduzco-Gutierrez 1Department of Neurology, UT Health, University of Texas Medical School, Houston, TX, USA 3Department of Neurosurgery, UT Health, University of Texas Medical School, Houston, TX, USA 1Department of Neurology, UT Health, University of Texas Medical School, Houston, TX, USA 2Department of Physical Medicine and Rehabilitation, UT Health, University of Texas Medical School, Houston, TX, USA 3Department of Neurosurgery, UT Health, University of Texas Medical School, Houston, TX, USA Frederic N. Nguyen, UT Health, University of Texas Medical School at Houston 6431 Fannin, Suite 7.044, Houston, TX 77030, USA. Email: [email protected] 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 norm 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 Department of Biomedicine, Aarhus University, Department of Pediatrics, Aarhus University Hospital, and Center for Interactions of Proteins in Epithelial Transport, Aarhus University, Aarhus 8000, Denmark Address all correspondence and requests for reprints to: Hanne B. Moeller, Department of Biomedicine, Aarhus University, Wilhelm Meyers Alle 3, Building 1234, Aarhus 8000, Denmark., E-mail: [email protected] ; or Robert A. Fenton. E-mail: [email protected] . Received 2012 Jul 11; Accepted 2012 Dec 7. Copyright 2013 by The Endocrine Society This article has been cited by other articles in PMC. The water channel aquaporin-2 (AQP2), expressed in the kidney collecting ducts, plays a pivotal role in maintaining body water balance. The channel is regulated by the peptide hormone arginine vasopressin (AVP), which exerts its effects through the type 2 vasopressin receptor (AVPR2). Disrupted function or regulation of AQP2 or the AVPR2 results in nephrogenic diabetes insipidus (NDI), a common clinical condition of renal origin characterized by polydipsia and polyuria. Over several years, major research efforts have advanced our understanding of NDI at the genetic, cellular, molecular, and biological levels. NDI is commonly characterized as hereditary (congenital) NDI, arising from genetic mutations in the AVPR2 or AQP2; or acquired NDI, due to for exmple medical treatment or electrolyte disturbances. In this article, we provide a comprehensive overview of the genetic, cell biological, and pathophysiological causes of NDI, with emphasis on the congenital forms and the acquired forms arising from lithium and other drug therapies, acute and chronic renal failure, and di Continue reading >>
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 >>
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 >>
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 >>
Diabetes Insipidus: A Challenging Diagnosis With New Drug Therapies
ISRN Nephrology Volume 2013 (2013), Article ID 797620, 7 pages Division of Nephrology, Department of Medicine, Staten Island University Hospital, 475 Seaview Avenue, Staten Island, NY 10305, USA Academic Editors: M. Léone and D. Malhotra Copyright © 2013 Chadi Saifan 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. Abstract Diabetes Insipidus (DI) is either due to deficient secretion of arginine vasopressin (central) or to tubular unresponsiveness (nephrogenic). Drug induced DI is a well-known entity with an extensive list of medications. Polyuria is generally defined as urine output exceeding 3 liters per day in adults. It is crucial to identify the cause of diabetes insipidus and to implement therapy as early as possible to prevent the electrolyte disturbances and the associated mortality and morbidity. It is very rare to have an idiosyncratic effect after a short use of a medication, and physicians should be aware of such a complication to avoid volume depletion. The diagnosis of diabetes insipidus is very challenging because it relies on laboratory values, urine output, and the physical examination of the patient. A high clinical suspicion of diabetes insipidus should be enough to initiate treatment. The complications related to DI are mostly related to the electrolyte imbalance that can affect the normal physiology of different organ systems. 1. Background Though it is a rare disorder, diabetes insipidus was first described in the 18th century [1]. Diabetes insipidus (DI) is either due to deficient secretion of arginine vasopressin (AVP), also known as antidiuretic hormone (ADH) by the pitu Continue reading >>
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 >>
Diabetes Insipidus
Anti-Diuretic Hormone (ADH) from the posterior pituitary stimulates water uptake from the distal convoluted tubule and collecting ducts of the kidney and so conserves water. Release is regulated by osmoreceptors in the hypothalamus and volume receptors in the hypothalamus. A deficiency of ADH is known as Diabetes insipidus. Causes of deficiency may be: Central: Central DI is characterized by decreased secretion of antidiuretic hormone (ADH)—also known as arginine vasopressin (AVP)—which gives rise to polyuria and polydipsia by diminishing the patient’s ability to concentrate urine. Diminished or absent ADH can be the result of a defect in 1 or more sites involving the hypothalamic osmoreceptors, the supraoptic or paraventricular nuclei, or the supraopticohypophyseal tract. Nephrogenic: failure of the nephrons to respond to ADH present in the kidney.Is characterized by a decrease in the ability to concentrate urine due to a resistance to ADH action in the kidney. Nephrogenic DI can be observed in chronic renal insufficiency, lithium toxicity, hypercalcemia, hypokalemia, and tubulointerstitial disease, rarely, diabetes insipidus may be hereditary. Psychogenic diabetes insipidus (psychogenic polydipsia) : It results from a neurological disorder of thirst control or as a result of some behavioral problem that triggers excessive water intake. In either case, the abnormally large volume of excreted urine in animals with psychogenic polydipsia is caused by excessive water intake (polydipsia), rather than by some primary problem with kidney, pituitary or hypothalamic function. Clinical Signs There will be a marked polyuria, 5-20X normal output, often resulting in nocturia and incontinence. There will also be a desperate polydipsia, animal will search for water. Other clin 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 Department of Biomedicine, Aarhus University, Department of Pediatrics, Aarhus University Hospital, and Center for Interactions of Proteins in Epithelial Transport, Aarhus University, Aarhus 8000, Denmark Address all correspondence and requests for reprints to: Hanne B. Moeller, Department of Biomedicine, Aarhus University, Wilhelm Meyers Alle 3, Building 1234, Aarhus 8000, Denmark. Search for other works by this author on: Department of Biomedicine, Aarhus University, Department of Pediatrics, Aarhus University Hospital, and Center for Interactions of Proteins in Epithelial Transport, Aarhus University, Aarhus 8000, Denmark Search for other works by this author on: Department of Biomedicine, Aarhus University, Department of Pediatrics, Aarhus University Hospital, and Center for Interactions of Proteins in Epithelial Transport, Aarhus University, Aarhus 8000, Denmark Search for other works by this author on: Endocrine Reviews, Volume 34, Issue 2, 1 April 2013, Pages 278301, Hanne B. Moeller, Sren Rittig, Robert A. Fenton; Nephrogenic Diabetes Insipidus: Essential Insights into the Molecular Background and Potential Therapies for Treatment, Endocrine Reviews, Volume 34, Issue 2, 1 April 2013, Pages 278301, The water channel aquaporin-2 (AQP2), expressed in the kidney collecting ducts, plays a pivotal role in maintaining body water balance. The channel is regulated by the peptide hormone arginine vasopressin (AVP), which exerts its effects through the type 2 vasopressin receptor (AVPR2). Disrupted function or regulation of AQP2 or the AVPR2 results in nephrogenic diabetes insipidus (NDI), a common clinical condition of renal origin characterized by polyd Continue reading >>
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 >>
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