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Lithium Nephrogenic Diabetes Insipidus

Lithium And Chronic Kidney Disease

Lithium And Chronic Kidney Disease

What is lithium? Lithium is a common medicine used to help calm mood for treating people with mental disorders. Since such disorders need lifelong treatment, long-term use of lithium may be harmful to organs, such as the kidneys. How does lithium cause kidney damage? Lithium may cause problems with kidney health. Kidney damage due to lithium may include acute (sudden) or chronic (long-term) kidney disease and kidney cysts. The amount of kidney damage depends on how long you have been taking lithium. It is possible to reverse kidney damage caused by lithium early in treatment, but the damage may become permanent over time. What is nephrogenic diabetes insipidus? The most common problem from taking lithium is a form of diabetes due to kidney damage called nephrogenic diabetes insipidus. This type of diabetes is different than diabetes mellitus caused by high blood sugar. In nephrogenic diabetes insipidus, the kidneys cannot respond to anti-diuretic hormone (ADH), a chemical messenger that controls fluid balance. This results in greater than normal urine out-put and excessive thirst. It can be hard to treat nephrogenic diabetes insipidus. What are the signs and symptoms of kidney damage and nephrogenic diabetes insipidus due to lithium? When the kidneys are not able to control fluid balance you may notice: Greater than normal urine out-put (polyuria), along with greater than normal fluid intake (polydipsia) due to excessive thirst Getting up at night to urinate (nocturia) can be a sign of polyuria Signs of modest dehydration Low blood pressure while standing (orthostatic hypertension) Very fast heart beat (tachycardia) Dry mouth Signs of severe dehydration High blood sodium level (hypernatremia) Change in mental status Too much fluid loss can cause electrolyte imbalance. E Continue reading >>

Lithium Intoxication And Nephrogenic Diabetes Insipidus: A Case Report And Review Of Literature

Lithium Intoxication And Nephrogenic Diabetes Insipidus: A Case Report And Review Of Literature

Lithium intoxication and nephrogenic diabetes insipidus: a case report and review of literature Kayseri Training and Research Hospital, Internal Medicine Department, Kayseri, Turkey Correspondence: Samet Karahan, Hastane caddesi, Kayseri Egitim Aratirma Hastanesi, 9 Blok 3 Kat Hastaliklari Servisi, Kocasinan, Kayseri, Trkiye, Tel +90 50 6302 0036, Email [email protected] Author information Copyright and License information Disclaimer Copyright 2013 Erden et al, publisher and licensee Dove Medical Press Ltd This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited. This article has been cited by other articles in PMC. Lithium is one of the drugs used widely in the treatment of mood disorders. However, it has a very narrow therapeutic index and side effects can be seen in many organ systems, one of which affects the kidneys. We can see varying degrees of renal damage associated with acute or chronic lithium use. Lithium intoxication is diagnosed by a rise in the serum lithium concentration, but it must be remembered that serum levels and clinical findings do not always overlap. Treatment of lithium intoxication varies according to the clinical findings. There are various ways of treating lithium intoxication, but there is no specific antidote. The purpose of treatment is to remove the toxin from the body. Here we report a patient who was treated for lithium intoxication and developed diabetes insipidus during follow-up, and discuss the relevant literature. Keywords: diabetes insipidus, intoxication, lithium Lithium salts have been used in clinical practice since the 1970s. Widely used in the treatment and prophylaxis of bipolar disorder, lithium has a very narrow therapeutic index and toxicity is common Continue reading >>

Lithium Induced Nephrogenic Diabetes Insipidus

Lithium Induced Nephrogenic Diabetes Insipidus

SDN members see fewer ads and full resolution images. Join our non-profit community! Lithium Induced Nephrogenic Diabetes Insipidus So i've been looking at a couple books and can't seem to get any sort of consensus. For Lithium Induced Nephrogenic Diabetes Insipidus, is the current to give the patient a Thiazide Diuretic or Amiloride? I was under the impression that thiazides would decrease the secretion of lithium in the kidneys; but it seems like it is used according to certain sources (e.g. emedicine) but certain texts refer to the use of amiloride as a treatment (e.g. Lippencott's). Anyone have an idea as to whether one is more "ideal" than the other? So i've been looking at a couple books and can't seem to get any sort of consensus. For Lithium Induced Nephrogenic Diabetes Insipidus, is the current to give the patient a Thiazide Diuretic or Amiloride? I was under the impression that thiazides would decrease the secretion of lithium in the kidneys; but it seems like it is used according to certain sources (e.g. emedicine) but certain texts refer to the use of amiloride as a treatment (e.g. Lippencott's). Anyone have an idea as to whether one is more "ideal" than the other? From what I understand, both Thiazides and Amiloride are used for Lithium Induced Diabetes Insipidus. Remember, Amiloride is a K+ sparing agent, so they are used along with other diuertics. So, in the case of Lithium induced diabetes inspidus, both could be used. I'm not which one is the "ideal" one. If I am wrong, someone please correct me. From the looks of the abstract, nobody completely understands the renal physiology of lithium. I will venture the following hypotheses of treatment of lithium toxicity: 1. Amiloride: according to that article, the amiloride sensitive Na+ channel in the distal Continue reading >>

Nephrogenic Diabetes Insipidus

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 >>

Lithium-induced Nephrogenic Diabetes Insipidus

Lithium-induced Nephrogenic Diabetes Insipidus

March, 2005 >> Syed Khalid Imam, Asim Hasan, Syed Khurram Shahid ( Department of Internal Medicine/Endocrinology, Liaquat National Hospital, Karachi ) Read PDF Abstract We report a case of a 43 year-old female who presented with lithium-induced nephrogenic diabetes insipidus. This patient had history of bipolar disorder for which she had been taking lithium carbonate for last 16 years. Appropriate work up was done and she was diagnosed with nephrogenic diabetes insipidus, secondary to lithium toxicity, and was managed accordingly. Introduction Diabetes insipidus is a disorder resulting from deficient anti-diuretic hormone (ADH) action and is characterized by the passage of copious amounts of very dilute urine. This disorder must be differentiated from other polyuric states such as primary polydipsia, osmotic diuresis, and diabetes mellitus. Nephrogenic diabetes insipidus results when kidneys fail to respond to circulating ADH. This causes cellular and extra-cellular dehydration, which stimulates thirst and results in polydipsia.1 As many as 20 to 40 % of patients taking lithium have had symptoms related to a concentrating defect, and 12 percent have frank nephrogenic diabetes insipidus.2 Case Report The presented patient was a 43 year-old female, with a history of bipolar disorder for 16 years and was treated with lithium carbonate 1200 mg per day, risperidone Table 1. Serum Na+ 169 mmol/l Serum K+ 4.6 mmol/l Serum Cl- 105 mmol/l Serum HCO3- 26 mmol/l Serum Urea 70 mg/dl Serum Creatinine 2.0 mg/dl Blood Glucose Random 120 mg/dl Serum Ca++ 8.45 mg /dl Serum Osmolality 345 mosm/kg Urine Osmolality 158 mosm/kg Thyroid Stimulating Hormone 0.74 mu/ml (0.4-4.0 mu/ml) Serum Lithium 3.2 ng/dl ( 0.5-1.2 ng/dl) and carbamazepine. She had symptoms of compulsive water drinking and Continue reading >>

(pdf) Lithium-induced Nephrogenic Diabetes Insipidus: New Clinical And Experimental Findings

(pdf) Lithium-induced Nephrogenic Diabetes Insipidus: New Clinical And Experimental Findings

2010 Societ Italiana di Nefrologia - ISSN 1121-8428 Lithium (Li+) salts are the rst-line therapy for bipolar mood disorders (1). Li+ has been widely used for mood disorders since 1970. The development of novel narcoleptics has decreased the use of Li+ salts. Today a new potential ef- cacy of lithium in lowering the progression of amyotrophic lateral sclerosis (2) and Alzheimers disease (3) is attract- ing the attention of clinicians and researchers. About 50% of patients under lithium treatment experi- ence urinary concentration defects (4). Therefore, it has been reported that long-term lithium therapy (more than 10-20 years) can induce chronic kidney failure promot- ing a tubulointerstitial nephritis with a slow progression to end-stage renal disease (5). This condition is irreversible. Other reports showed an incomplete form of renal tubular Several experimental models showed that dysregulation of aquaporins in the collecting duct (CD) is a crucial mecha- nism for the development of Li+-dependent nephrogenic di- abetes insipidus (NDI). Li+ affects many regulatory pathways counteracting the vasopressin-dependent cellular signaling and also rearranging the entire cellular structure of the CD. Although Li+ is a very efcacious drug for psychiatrics, re- nal adverse effects are a limiting problem. This manuscript reviews the latest clinical and experimental studies on the Li+-induced urinary concentration impairment. re n a l h a n d l I n g o f l I t h I u m Li+ is a monovalent cation that shares some features with more abundant cations present in the body (Na+ and Mg++). Li+ can take the place of Mg++, competitively, inhibiting the activity of GSK3 (7). In addition, in vitro evidence shows that Li+ can compete with Na+ for the amiloride-sensitive epithelial Na+ channel Continue reading >>

Perioperative Prolonged Lithium-induced Nephrogenic Diabetes Insipidus

Perioperative Prolonged Lithium-induced Nephrogenic Diabetes Insipidus

Perioperative prolonged lithium-induced nephrogenic diabetes insipidus Mfon Ewang, Rahat Chaudry, Dennis Barnes, Peter Goulden, A Turner & Jesse Kumar Department of Endocrinology and ITU, Maidstone and Tunbridge Wells NHS Trust, Maidstone, Kent, UK. Introduction: Lithium-induced nephrogenic diabetes insipidus (NDI) occurs in approximately 20% of patients on chronic lithium therapy, and additionally 30% of patients have impaired concentrating ability of urine. Perioperative precipitation of NDI is an uncommon phenomenon complicating fluid management in a surgical patient and masking signs of renal hypoperfusion. Case: A 70-year-old man on chronic lithium therapy for bipolar disorder presented with 24 h history of chest pain after eating. Oesophageal rupture was diagnosed after imaging and surgically repaired. Serum electrolytes, glucose, calcium, lithium levels and urine output were normal on admission. Despite profound sepsis and hypotension, significant polyuria was observed with urine volumes greater than 300 ml/h and up to 9 l/day. There was a gradual elevation in serum sodium to 170 mmol/l and creatinine to 167 mcmol/l with other electrolytes remaining normal. Serum osmolarity was 350 mosm/l with an inappropriately dilute urine osmolality (309421 mosm/l) despite desmopressin challenge. NDI was diagnosed lithium was stopped and desmopressin commenced at 400 mcg/day in addition to chlorthalidone, indomethacin and amiloride. Serum sodium normalised with urine output improving to 3 l/day. He has remained on the above treatment for 6 months with periodic recurrence of hypernatraemia and hyperosmolarity when drugs are withdrawn. Discussion: Lithium-induced NDI is a common problem which often resolves after cessation of lithium. The pathogenesis is attributed to adenyl cy Continue reading >>

Use Of Acetazolamide In Lithium-induced Nephrogenic Diabetes Insipidus: A Case Report - Edm Case Reports

Use Of Acetazolamide In Lithium-induced Nephrogenic Diabetes Insipidus: A Case Report - Edm Case Reports

Use of acetazolamide in lithium-induced nephrogenic diabetes insipidus: a case report Ricardo A Macau 1, * , Tiago Nunes da Silva 2, * , Joana Rego Silva 1 , Ana Gonalves Ferreira 2 and Pedro Bravo 1 [1] Nephrology DepartmentHospital Garcia de Orta[2] Endocrinology DepartmentHospital Garcia de Orta, Almada, Portugal Endocrinology, Diabetes & Metabolism Case Reports, 02 2018, EDM-17-0154, 10.1530/EDM-17-0154 . Lithium-induced nephrogenic diabetes insipidus (Li-NDI) is a rare and difficult-to-treat condition. A study in mice and two recent papers describe the use of acetazolamide in Li-NDI in 7 patients (a case report and a 6 patient series). We describe the case of a 63-year-old woman with bipolar disorder treated with lithium and no previous history of diabetes insipidus. She was hospitalized due to a bowel obstruction and developed severe dehydration after surgery when she was water deprived. After desmopressin administration and unsuccessful thiazide and amiloride treatment, acetazolamide was administrated to control polyuria and hydroelectrolytic disorders without significant side effects. To our knowledge, this is the third publication on acetazolamide use in Li-NDI patients. Treatment of lithium-induced nephrogenic diabetes insipidus might be challenging. Vasopressin, amiloride and thiazide diuretics have been used in lithium-induced nephrogenic diabetes insipidus treatment. Acetazolamide might be an option to treat lithium-induced nephrogenic diabetes insipidus patients who fail to respond to standard treatment. The use of acetazolamide in lithium-induced nephrogenic diabetes insipidus must be monitored, including its effects on glomerular filtration rate. Diabetes insipidus (DI) is a rare condition in which patients excrete large quantities of diluted urine (up Continue reading >>

Atorvastatin For The Treatment Of Lithium-induced Nephrogenic Diabetes Insipidus

Atorvastatin For The Treatment Of Lithium-induced Nephrogenic Diabetes Insipidus

Lithium remains the gold-standard treatment for bipolar disorder, with 30-40% of patients with responding preferentially to this medication. Additionally, lithium is commonly used in treatment-resistant depression, and other psychiatric disorders (e.g. schizoaffective disorder). Lithium is especially valuable considering the great difficulty in achieving and maintaining symptomatic remission, the high rates of disability, as well as tremendous personal, family, and societal costs associated with bipolar disorder and treatment-resistant depression. Despite this, clinicians are increasingly avoiding lithium, largely due to fear of irreversible chronic kidney disease (CKD), particularly in North America. It is well known that lithium exposure, even when dosed safely (<1.0mmol/L in adults 11 and <0.8mmol/L in geriatric patients 12,13), can increase the risk of CKD by 3 times, in large part through Nephrogenic Diabetes Insipidus (NDI) 14-19. NDI itself has also been associated with acute kidney injury 20, and life-threatening hypernatremia, which is an electrolyte imbalance characterized by high levels of blood sodium. Aside from hypertension, diabetes mellitus, aging, and other nonspecific CKD risk factors. NDI is characterized by excessive thirst (polydipsia) due to increased production of dilute urine (polyuria). In NDI, lithium is believed to interact with the inositol monophosphate and protein kinase C pathways, thereby affecting calcium-related intracellular signaling, cyclic AMP (cAMP), inhibition of Glycogen Synthase Kinase-3 Beta (GSK3Beta), activation of MAP Kinase and many other pathways. NDI occurs commonly in lithium users: 50% of chronic lithium users have urinary concentrating difficulties, with 12-19% have decreased urine osmolality (UOsm) <300mOsm/Kg). To da Continue reading >>

Lithium Induced Diabetes Insipidus: Symptoms & Treatment

Lithium Induced Diabetes Insipidus: Symptoms & Treatment

This lesson goes over a relatively complex situation involving one drug and two completely different medical conditions. You'll learn how bipolar disorder, lithium, and diabetes insipidus are all tied together. One Disorder After Another The last thing you want or need when you're sick is another disease or disorder, right? And the last thing you'd expect is that the new disease is caused by the treatment for the first. Unfortunately, this is a possibility in some cases. You'll learn how this is the case in this lesson on lithium-induced diabetes insipidus. What Is Lithium-Induced Diabetes Insipidus? Bipolar disorder, also called bipolar affective disorder or manic-depressive illness, is a type of mental illness characterized by a period of extreme depression followed by a period of elevated or irritable mood called mania. One possible treatment option is a medication called lithium. The problem is lithium has the potential to be nephrotoxic, or poisonous to the kidneys. The kidneys are responsible for regulating the water balance in your body. They do so, in part, by responding to a hormone called antidiuretic hormone (ADH). This hormone is produced in your brain. Once it reaches the kidneys, ADH tells the kidneys to stop making urine and to start preserving water within the body. If the lithium ends up damaging the kidneys, they may no longer respond to ADH as well as they should. This disorder is called nephrogenic diabetes insipidus, or diabetes insipidus whose genesis ('-genic') is a problem in the kidneys ('nephro-'). Symptoms Diabetes insipidus, of any cause, is characterized by two main signs and symptoms: Polyuria - which is production of an excessive volume of urine Polydipsia - which refers to an excessive feeling of thirst and thus the consumption of abnorma Continue reading >>

Lithium Induced Diabetes Insipidus

Lithium Induced Diabetes Insipidus

For those diagnosed with a mental illness or disorder, one of the most effective medications used for treatment is lithium. It is particularly useful when treating conditions such as bipolar disorder. It controls moods effectively, keeps people stable and active, and generally allows for a good quality of life. Over time, however, lithium can also create an unwanted side effect: diabetes insipidus. Lithium induced diabetes insipidus will typically first be discovered on a routine checkup or walk-in appointment, either at the doctor’s office or with the individual’s psychiatrist. The most common complaint is an increased level of thirst, but there may also be unusual daytime fatigue, problems sleeping at night, and even muscle tremors. Why Does Lithium Cause Diabetes Insipidus? Medical science doesn’t actually know why lithium will sometimes cause diabetes insipidus to form. What is known is that lithium works in some way as a counter-agent to the hormone Vasopressin, which acts as an anti-diuretic hormone [ADH]. When lithium is used for an extended period of time, it will desensitize or reduce the ability of the kidney to respond to the ADH that is being produced by the body. This means the kidneys stop listening to the hormones, which is a trademark sign of nephrogenic diabetes insipidus. This creates the need to get up frequently at night to go to the bathroom, which creates insomnia and daytime fatigue. Lithium induced diabetes insipidus is rather common. For those who are receiving long-term lithium therapies, the incidence rate of diabetes insipidus is 40%. How Is Lithium Induced Diabetes Insipidus Diagnosed? Upon presentation, the individual with DI will have an interview that examines their entire medical history. If the disease is supsected, then a water r Continue reading >>

Lithium-induced Nephrogenic Diabetes Insipidus: Renal Effects Of Amiloride

Lithium-induced Nephrogenic Diabetes Insipidus: Renal Effects Of Amiloride

Lithium-induced Nephrogenic Diabetes Insipidus: Renal Effects of Amiloride Jennifer J. Bedford ,* Susan Weggery ,* Gaye Ellis ,* Fiona J. McDonald , Peter R. Joyce , John P. Leader ,* and Robert J. Walker * Departments of *Medical and Surgical Sciences and Physiology, University of Otago, Dunedin, New Zealand; and Department of Psychological Medicine, University of Otago, Christchurch, New Zealand Departments of *Medical and Surgical Sciences and Physiology, University of Otago, Dunedin, New Zealand; and Department of Psychological Medicine, University of Otago, Christchurch, New Zealand Departments of *Medical and Surgical Sciences and Physiology, University of Otago, Dunedin, New Zealand; and Department of Psychological Medicine, University of Otago, Christchurch, New Zealand Departments of *Medical and Surgical Sciences and Physiology, University of Otago, Dunedin, New Zealand; and Department of Psychological Medicine, University of Otago, Christchurch, New Zealand Departments of *Medical and Surgical Sciences and Physiology, University of Otago, Dunedin, New Zealand; and Department of Psychological Medicine, University of Otago, Christchurch, New Zealand Departments of *Medical and Surgical Sciences and Physiology, University of Otago, Dunedin, New Zealand; and Department of Psychological Medicine, University of Otago, Christchurch, New Zealand Departments of *Medical and Surgical Sciences and Physiology, University of Otago, Dunedin, New Zealand; and Department of Psychological Medicine, University of Otago, Christchurch, New Zealand Departments of *Medical and Surgical Sciences and Physiology, University of Otago, Dunedin, New Zealand; and Department of Psychological Medicine, University of Otago, Christchurch, New Zealand Correspondence: Prof. Robert J. Walker, Continue reading >>

Lithium Carbonate-induced Nephrogenic Diabetes Insipidus And Glucose Intolerance

Lithium Carbonate-induced Nephrogenic Diabetes Insipidus And Glucose Intolerance

Lithium Carbonate-Induced Nephrogenic Diabetes Insipidus and Glucose Intolerance The use of lithium carbonate in manic-depressive disorders appears to be of definite therapeutic value.1-3 Because of potential toxic reactions, frequent measurements to assure that lithium plasma levels remain between 1.5 and 2.0 mEq/liter are required. Common side effects of lithium carbonate treatment are abnormal electrolyte metabolism and changes in renal function.4-7 Recently, a syndrome of nephrogenic diabetes insipidus has been described in some patients receiving lithium carbonate therapy.8-11 The present report is that of a man in whom nephrogenic diabetes insipidus resulted from lithium carbonate treatment. In addition, despite absence of previous evidence of diabetes mellitus, glucose intolerance developed. Patient Summary A 52-year-old white man suffering from chronic schizophrenia had been treated with lithium carbonate since 1967 because of episodic mania resistant to phenothiazine therapy. The severity of his psychotic disorder fluctuated while receiving lithium carbonate doses ranging from 2.4 to 3.4 gm daily. Monthly determinations Continue reading >>

Jci Insight -role Of Adenylyl Cyclase 6 In The Development Of Lithium-induced Nephrogenic Diabetes Insipidus

Jci Insight -role Of Adenylyl Cyclase 6 In The Development Of Lithium-induced Nephrogenic Diabetes Insipidus

Body weight and plasma [Li+] in AC6/ mice versus WT mice and AC6loxloxCre mice versus AC6loxlox mice under baseline conditions and Li+ administration AC6loxloxCre mice have greater water intake and lower urine osmolality under baseline conditions. AC6 expression is heterogeneous in the kidney tubule ( 21 ), and we have previously demonstrated roles of AC6 in cells of the proximal tubule, thick ascending limb, and distal convoluted tubule ( 22 , 23 ). Therefore, to isolate a potential role of AC6 in kidney and CD PCs, the main target cell for Li+ effects ( 24 ), we generated a conditional mouse model with AC6 deletion controlled by AQP2-dependent Cre recombinase expression ( 25 ). After several attempts with antibodies from various commercial sources, we identified an antibody that, in cortex homogenates from WT mice, detected AC6 as a smear centered at 150 kDa ( 26 , 27 ). No signal was detectable in AC6/ mice, demonstrating for the first time to our knowledge specificity of an AC6 antibody in Western blots ( Figure 2A ). In AC6loxloxCre mice under baseline conditions, AC6 protein was approximately 50% reduced in IM homogenate compared with AC6loxlox mice ( Figure 2B, P < 0.05), a finding consistent and indicative of efficient AC6 knockout in PCs. No significant differences were detected in AC6 levels in the cortex and outer medulla/cortex (OM/cortex) homogenates ( Figure 2B ), presumably due to AC6 expression remaining in non-AQP2-expressing cells, which compose the vast majority of the cortex/outer stripe OM. Although labeling of AC6, using IHC, was unsuccessful (our unpublished observations), clear nuclear IHC labeling of Cre recombinase in both cortical, OM and IM collecting ducts in AC6loxloxCre mice suggested successful deletion of AC6 in AQP2-expressing cells th Continue reading >>

Acetazolamide In Lithium-induced Nephrogenic Diabetes Insipidus

Acetazolamide In Lithium-induced Nephrogenic Diabetes Insipidus

To the Editor: The most common cause of acquired nephrogenic diabetes insipidus is long-term lithium treatment. The management of lithium-induced nephrogenic diabetes insipidus is challenging, even when the drug is discontinued and therapy is changed to thiazide diuretics, amiloride, and reduced sodium intake. Amiloride inhibits lithium entry into renal collecting-duct cells through the epithelial sodium channel. Thiazide diuretics and a low-sodium diet result in hypovolemia-induced activation of the renin–angiotensin–aldosterone system, which stimulates proximal tubule sodium and water reabsorption, resulting in less volume delivery to the distal nephron.1 Recent data from animal models of lithium-induced nephrogenic diabetes insipidus showed that hydrochlorothiazide reduces polyuria in mice lacking the thiazide-sensitive sodium–chloride cotransporter, which suggests that the mechanism of action of the drug may be mediated by carbonic anhydrase inhibition.2 Acetazolamide monotherapy was as effective as the combination of hydrochlorothiazide and amiloride in reducing polyuria in an animal model of lithium-induced nephrogenic diabetes insipidus but had fewer side effects.3 Acetazolamide reduces the glomerular filtration rate by means of tubuloglomerular feedback and reduces renal prostaglandin secretion; both effects attenuate polyuria induced by nephrogenic diabetes insipidus. Encouraged by these findings, we administered acetazolamide to a patient with severe lithium-induced nephrogenic diabetes insipidus that was resistant to hydrochlorothiazide treatment and other measures. Here we report our findings on the efficacy, safety, and rapid response to such an intervention. A 49-year-old man with bipolar disorder requiring long-term lithium therapy was admitted for Continue reading >>

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