Thiazide Induced Diabetes

Drug-induced Glucose Alterations Part 2: Drug-induced Hyperglycemia

A variety of pharmacological agents A variety of pharmacological agents affect glucose homeostasis resulting in either hypo- or hyperglycemia. Hormones such as insulin, glucagon, catecholamines, growth hormone, and cortisol, among others, contribute to normoglycemia. Drug-induced serum glucose alterations manifested as hyperglycemia or hypoglycemia can have perpetual effects on the body, particularly in patients with diabetes. This article is the second of a two-part series reviewing drug-induced serum glucose alterations. The first article in the series appeared in the previous issue of this journal (Diabetes Spectrum 24:171-177, 2011). In this article, we review select therapies commonly contributing to the development of hyperglycemia. Hyperglycemia is clinically defined as a serum glucose level > 180 mg/dl that persists for more than 2 hours. Unlike hypoglycemia, acute hyperglycemia is often benign and may persist without any clinically significant signs or symptoms; however the development of diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic state (HHS) are hyperglycemic emergencies. Often signs and symptoms of hyperglycemia manifest when serum glucose levels are in the range of 270–360 mg/dl for an extended period and include the classical symptoms of polyphagia, polydipsia, and polyuria (Table 1). Untreated hyperglycemia, when accompanied with excretion of ketones in urine (DKA), is a medical emergency more common in people with type 1 diabetes. It results in the following symptoms: fatigue, weakness, fruity odor of the breath, confusion, lack of concentration, shortness of breath, nausea and vomiting, dry skin, and flushing of the skin. People with type 2 diabetes are more likely to develop HHS, formerly known as hyperosmolar hyperglycemic nonketotic c Continue reading >>

Thiazide-induced Hypokalemia May Mediate Increased Diabetes Risk

Thiazide-Induced Hypokalemia May Mediate Increased Diabetes Risk by Todd Neale Todd Neale, Staff Writer, MedPage Today Explain to interested patients that this study found that hypokalemia associated with thiazide diuretic use appears to mediate the increased risk of diabetes with the drugs. Point out that the researchers said randomized trials are needed to determine whether treating hypokalemia can mitigate the increased diabetes risk with thiazide diuretics. BALTIMORE, Nov. 25 -- Thiazide diuretic-induced decreases in serum potassium levels appear to be at least partially responsible for the link between the hypertension drugs and diabetes, researchers here found. Among older patients participating in a placebo-controlled blood pressure lowering trial with chlorthalidone, each 0.5-mEq/L decrease in serum potassium was associated with a 45% increased risk of diabetes (P<0.001), Tariq Shafi, M.D., of Johns Hopkins, and colleagues reported online in Hypertension: Journal of the American Heart Association. Through the first year of the trial, the increased risk of diabetes in the treatment group was attenuated by 40.7% after controlling for changes in serum potassium, which indicated a significant mediating effect, the researchers said. "This study shows us that as long as physicians monitor and regulate potassium levels, thiazides could be used safely," Dr. Shafi said. "It could be as simple as increasing the consumption of potassium-rich foods like bananas and oranges and/or reducing salt intake, both of which will keep potassium from dropping," he said. However, the researchers noted, the effect of potassium supplementation on diabetes risk needs to be evaluated in randomized trials. Although past studies have shown that the use of thiazide diuretics was associated w Continue reading >>

Thiazide Induced Dysglycemia It's Time To Take Notice

Thiazide Induced Dysglycemia It's Time To Take Notice Rhonda M. Cooper-DeHoff, Division of Cardiovascular Medicine, College of Medicine, University of Florida, Gainesville, Florida. Address for correspondence: Rhonda M. Cooper-DeHoff, PharmD, MS, FAHA, Research Associate Professor, University of Florida College of Medicine, PO Box 100277, Gainesville, FL 32610-0277; Tel: 352-273-8470; FAX: 352-371-0370; [email protected] The publisher's final edited version of this article is available at Expert Rev Cardiovasc Ther See other articles in PMC that cite the published article. Almost a half century ago, Wolff et al wrote, During the course of studies of hypertensive patients, including a double blind study, observations were made concerning the diabetogenic activity of benzothiadiazine derivatives. This activity was observed to occur in nonobese patients without a family history of diabetes as well as in obese hypertensives with such a family history. These observations suggest that benzothiadiazines should not be given to young or middle-aged hypertensives in whom there is a lengthy life expectancy and for whom alternative hypotensive therapy is feasible. [ 1 ] Despite these insightful recommendations, benzothiadiazine derivatives (most often hydrochlorothiazide [HCTZ]) are the first line recommended therapy for hypertension regardless of glycemic status [ 2 ]. Epidemiologic data as well as data from randomized controlled trials have associated a new diagnosis of diabetes with hypertension treatment that contains a thiazide diuretic, including chlorthalidone [ 3 , 4 ], HCTZ [ 5 , 6 ] and bendroflumethiazide [ 7 ]. There is controversy over the long-term significance of diuretic-induced diabetes [ 8 ], primarily related to the benefit of BP lowering vs. the hazard o Continue reading >>

Payperview: Attenuation Of The Lithium-induced Diabetes-insipidus-like Syndrome By Amiloride In Rats - Karger Publishers

I have read the Karger Terms and Conditions and agree. The effect of amiloride on lithium-induced polydipsia and polyuria and on the lithium concentration in the plasma, brain, kidney, thyroid and red blood cells was investigated in rats, chronically treated with LiCl. Amiloride reduced the drinking and urine volume of rats in an acute (6 or 12 h) and a subacute (3 days) experiment. 6 h after the administration of amiloride, a reduction was observed in the lithium content of the renal medulla but not in the other organs studied. At 12 h, all the tissues showed a slight increase in lithium levels. After 3 days of combined treatment, a marked elevation in plasma and tissue lithium levels accompanied a reduction in water intake. In all the experiments, the attenuation of the lithium-induced diabetes-insipidus-like syndrome by amiloride was accompanied by a reduction of the ratio between the lithium concentration in the renal medulla and its levels in the blood and an elevation in the plasma potassium level. It is concluded that acute amiloride administration to lithium-treated patients suffering from polydipsia and polyuria might relieve these patients but prolonged amiloride supplementation would result in elevated lithium levels and might be hazardous. Continue reading >>

Diuretic-related Side Effects: Development And Treatment

Please confirm that you would like to log out of Medscape.If you log out, you will be required to enter your username and password the next time you visit. Log out Cancel Diuretic-Related Side Effects: Development and Treatment Prolonged thiazide diuretic therapy can lead to glucose intolerance and may occasionally precipitate diabetes mellitus.[ 4 , 5 , 54 , 55 ] Short-term metabolic studies, epidemiologic studies, and a variety of clinical trials suggest a connection between ongoing thiazide diuretic use and the development of type 2 diabetes. However, it should be noted that interpretation of these studies is confounded by multiple factors including: differing definitions of new-onset diabetes, small numbers of patients, inadequate comparison groups, relatively limited periods of follow-up, selection criteria that limited the generalizability of the findings, and study designs that prohibited valid comparisons among antihypertensive drug classes.[ 56 ] Moreover, in a review of all the placebo-controlled hypertension trials with diuretics, there was only an approximate 1% increase in new-onset diabetes compared with placebo.[ 57 ] Hyperglycemia and carbohydrate intolerance have been linked to diuretic-induced hypokalemia. K+ deficiency is known to inhibit insulin secretion by cells; however, diuretic-induced changes in glucose metabolism are not conclusively related to altered K+ homeostasis, and impaired glucose tolerance occurs even when thiazide-type diuretics in relatively low doses are combined with K+ -sparing agents. The glucose intolerance seen with diuretic therapy can deteriorate further with an increase in sympathetic nervous system activity, which also decreases peripheral glucose utilization. Diuretic-associated glucose intolerance appears to be dose-rel Continue reading >>

Changes In Serum Potassium Mediate Thiazide-induced Diabetes.

Hypertension. 2008 Dec;52(6):1022-9. doi: 10.1161/HYPERTENSIONAHA.108.119438. Epub 2008 Nov 3. Changes in serum potassium mediate thiazide-induced diabetes. Division of Nephrology, Johns Hopkins University School of Medicine, Baltimore, MD 21224-2780, USA. [email protected] Thiazides, recommended as first-line antihypertensive therapy, are associated with an increased risk of diabetes. Thiazides also lower serum potassium. To determine whether thiazide-induced diabetes is mediated by changes in potassium, we analyzed data from 3790 nondiabetic participants in the Systolic Hypertension in Elderly Program, a randomized clinical trial of isolated systolic hypertension in individuals aged >or=60 years treated with chlorthalidone or placebo. Incident diabetes was defined by self-report, antidiabetic medication use, fasting glucose >or=126 mg/dL, or random glucose >or=200 mg/dL. The mediating variable was change in serum potassium during year 1. Of the 459 incident cases of diabetes during follow-up, 42% occurred during year 1. In year 1, the unadjusted incidence rates of diabetes per 100 person-years were 6.1 and 3.0 in the chlorthalidone and placebo groups, respectively. In year 1, the adjusted diabetes risk (hazard ratio) with chlorthalidone was 2.07 (95% CI: 1.51 to 2.83; P<0.001). After adjustment for change in serum potassium, the risk was significantly reduced (hazard ratio: 1.54; 95% CI: 1.09 to 2.17; P=0.01); the extent of risk attenuation (41%; 95% CI: 34% to 49%) was consistent with a mediating effect. Each 0.5-mEq/L decrease in serum potassium was independently associated with a 45% higher adjusted diabetes risk (95% CI: 24% to 70%; P<0.001). After year 1, chlorthalidone use was not associated with increased diabetes risk. In conclusion, thiazide-induced diabetes o Continue reading >>

Drug-induced Diabetes

Many therapeutic agents can predispose to or precipitate diabetes, especially when pre-existing risk factors are present, and these may cause glucose control to deteriorate if administered to those with existing diabetes. They may act by increasing insulin resistance, by affecting the secretion of insulin, or both. For convenience, these agents may be subdivided into widely used medications that are weakly diabetogenic, and drugs used for special indications that are more strongly diabetogenic. Examples of the former include antihypertensive agents and statins, and examples of the latter include steroids, antipsychotics and a range of immunosuppressive agents. There are also a number of known beta cell poisons including the insecticide Vacor, alloxan and streptozotocin. Introduction A wide range of therapeutic agents may affect glucose tolerance, and the list of known or suspected drugs is lengthy. This entry summarizes evidence concerning the agents most frequently implicated. Widely used medications A number of drugs used to reduce cardiovascular risk also predispose to the development of diabetes. These include the thiazide diuretics, beta-blockers and statins. It should however be appreciated that these are commonly offered to individuals who are at increased risk of diabetes by virtue of risk factors such as obesity and hypertension, and that risk association does not necessarily mean causation. Thiazides: Thiazide diuretics revolutionized the treatment of hypertension in the 1960s, but were soon noted to increase the risk of diabetes[1]. Subsequent experience showed that that this risk is greatly reduced by low-dose therapy, whose benefits therefore outweigh its risks. The thiazides have a weak inhibitory effect upon release of insulin from the beta cell. This eff Continue reading >>

Thiazide-induced Hyperglycemia In A 6 Years Old Girl: A Case Report And Review Of The Literature | Walia | Journal Of Medical Cases

Journal of Medical Cases, ISSN 1923-4155 print, 1923-4163 online, Open Access Article copyright, the authors; Journal compilation copyright, J Med Cases and Elmer Press Inc Volume 7, Number 2, February 2016, pages 49-51 Thiazide-Induced Hyperglycemia in a 6 Years Old Girl: A Case Report and Review of the Literature aDepartment of Anesthesiology & Pain Medicine, Nationwide Childrens Hospital, Columbus, OH, USA bDepartment of Anesthesiology & Pain Medicine, The Ohio State University, Columbus, OH, USA cCorresponding Author: Hina Walia, Department of Anesthesiology & Pain Medicine, Nationwide Childrens Hospital, 700 Childrens Drive, Columbus, OH 43205, USA Manuscript accepted for publication January 07, 2016 Short title: Thiazide-Induced Hyperglycemia Various factors may affect glucose homeostasis in children resulting in rare clinical scenarios. Alterations in glucose regulation and hyperglycemia may result from pharmacologic interventions and the introduction of new medications. Although used most commonly to control fluid balance, an uncommon adverse effect of the thiazide diuretics is hyperglycemia. We present a 6-year-old girl with congenital heart disease who developed clinically significant hyperglycemia when a thiazide diuretic was added to her medication regimen. Previous reports of similar responses are reviewed, physiologic mechanisms are postulated, and treatment strategies are proposed. Keywords: Hyperglycemia; Thiazides; Diazoxide Various factors may be responsible for alterations in glucose homeostasis in children. In rare clinical scenarios, alterations in glucose regulation and hyperglycemia may result from pharmacologic interventions and the introduction of new medications [ 1-5 ]. Although used most commonly to control fluid balance, an uncommon adverse Continue reading >>

Renal Fellow Network: Thiazide-induced Hyperglycemia

In recent years, there has been the suggestion that thiazide diuretics--long considered a front-line therapy for hypertension based on the ALLHAT study and others--may increase the risk of diabetes. Subsequent retrospective analysis of other major historical cohorts by Eric Taylor and others--such as the Nurse's Health Study and Health Professionals Follow-Up Study--seem to indicate that the relative risk of being diagnosed with incident diabetes is somewhere between 1.2 to 1.46 in individuals taking thiazides compared to those not taking thiazides with similar baseline characteristics. What do we think about this data and should it change our clinical practice of prescribing thiazide monotherapy to an individual recently diagnosed with hypertension? Also, why should thiazides result in hyperglycemia? Interestingly, there is data to suggest that the thiazide-induced hyperglycemia effect is a potassium effect: a 2006 review of >50 trials in which thiazides were compared to other blood pressure-lowering medications or placebo , it was found that for every 1 mEq/L decrease in K, there is a 10 mg/dL increase in glucose. Furthermore, normalization of serum potassium in patients on thiazides (with potassium supplements) will lower the serum glucose. From a molecular level, this is perhaps explained by the fact that the pancreatic b-cell secretion of insulin is regulated in large part by ATP-sensitive K channels in the beta-cell membrane. Alterations in the extracellular potassium concentration to which these cells are exposed could potentially lead to decreased insulin secretion. If this mechanism is correct, it would imply that thiazide-induced hyperglycemia occurs by a different mechanism (decreased insulin secretion) than the standard type 2 diabetes (peripheral insulin r Continue reading >>

Impact Of Long-term Potassium Supplementation On Thiazide Diuretic-induced Abnormalities Of Glucose And Uric Acid Metabolisms

Journal of Human Hypertensionvolume32,pages301310 (2018) Treatment of hypertension with thiazide diuretics may trigger hypokalemia, hyperglycemia, and hyperuricemia. Some studies suggest simultaneous potassium supplementation in hypertensive patients using thiazide diuretics. However, few clinical studies have reported the impact of long-term potassium supplementation on thiazide diuretic-induced abnormalities in blood glucose and uric acid (UA) metabolisms. One hundred hypertensive patients meeting the inclusion criteria were equally randomized to two groups: IND group receiving indapamide (1.252.5 mg daily) alone, and IND/KCI group receiving IND (1.252.5 mg daily) plus potassium chloride (40 mmol daily), both for 24 weeks. At the end of 24-week follow-up, serum K+ level in IND group decreased from 4.27 0.28 to 3.98 0.46 mmol/L (P < 0.001), and fasting plasma glucose (FPG) and UA increased from 5.11 0.52 to 5.31 0.57 mmol/L (P < 0.05), and from 0.404 0.078 to 0.433 0.072 mmol/L (P < 0.05), respectively. Serum K+ level in IND/KCl group decreased from 4.27 0.36 to 3.89 0.28 mmol/L (P < 0.001), and FPB and UA increased from 5.10 0.41 to 5.35 0.55 mmol/L (P < 0.01), and from 0.391 0.073 to 0.457 0.128 mmol/L (P < 0.001), respectively. The difference value between the serum K+ level and FPG before and after treatment was not statistically significant between the two groups. However, the difference value in UA in IND/KCl group was significantly higher than that in IND group (0.066 (95% confidence interval (CI): 0.0410.090) mmol/L vs. 0.029 (95% CI: 0.0060.058) mmol/L, P < 0.05). The results showed that long-term routine potassium supplementation could not prevent or attenuate thiazide diuretic-induced abnormalities of glucose metabolism in hypertensive patients; rather, it Continue reading >>

Diuretics May Increase Diabetes Risk By Lowering Blood Potassium Levels

Diuretics may increase diabetes risk by lowering blood potassium levels Posted on Nov 25, 2008, 6 a.m. By Rich Hurd New research suggests that depleted blood potassium levels could help to explain why people prescribed diuretics for the treatment of high blood pressure are at increased risk of type 2 diabetes. New research suggests that depleted blood potassium levels could help to explain why people prescribed diuretics for the treatment of high blood pressure are at increased risk of type 2 diabetes. Tariq Shafi and colleagues examined data from 3,790 non-diabetic participants in the Systolic Hypertension in Elderly Program (SHEP), a study designed to determine the risk versus benefit of treating people age 60 years or older with the thiazide diuretic chlorthalidone. Previous research has shown that treatment with thiazide diuretics causes potassium levels to drop and increases patients' risk of developing type 2 diabetes by as much as 50%, although whether the drop in blood potassium was linked to the increased risk of diabetes was uncertain. Results of this study suggest that the increased risk of type 2 diabetes associated with thiazide diuretics is indeed linked to their action on blood potassium levels. In fact, results showed that for each 0.5 milliequivalent-per-liter (MEq/L) decrease in serum potassium, there was a 45% increased risk of diabetes . Thiazides are effective at treating high blood pressure and are inexpensive, however their association with diabetes has led many doctors to prescribe other, more expensive, drugs. However, according to Dr Shafi, the study findings suggest that thiazides can be used safely as long as doctors monitor and regulate blood potassium levels. The authors speculate that potassium supplement may prevent thiazide-induced diab Continue reading >>

Clinical And Genetic Factors Associated With Thiazide-induced Hyponatremia

Thiazide diuretics are one of the most widely recommended first-line therapies for hypertension. Evidence from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial and other pivotal hypertension studies has suggested that thiazide-type diuretics significantly reduce stroke and cardiovascular events. 13 However, there are concerns that thiazide diuretics may be linked to unfavorable side effects, such as new-onset of diabetes 4,5 and electrolyte imbalance. 610 Hyponatremia is a typical complication after thiazide diuretic treatment 69 and is a potential cause of morbidity and mortality. 1113 This raises the question of what subgroup of patients is more susceptible to the adverse effects of this class of diuretics. The Potassium Channel, Inwardly Rectifying Subfamily J, Member 1 (KCNJ1) gene encodes the renal outer medullary potassium channel (ROMK), which is highly expressed in the apical surface of epithelial cells in the thick ascending limb (TAL) and cortical collecting duct (CCD) of the kidney. 1416 Loss-of-function mutations in the human ROMK cause renal Na+ wasting. 1719 However, whether there is a link between genetic variation of KCNJ1 and thiazide-induced hyponatremia remains unknown. Given the clinical recommendation of thiazide diuretics, especially for elderly hypertensive and resistant hypertensive patients, there should be careful monitoring of the incidence of hyponatremia after thiazide diuretic treatment. However, clinical information concerning which patients are more susceptible to thiazide-induced hyponatremia is not conclusive, and the impact of genetic factors is unknown. For these reasons, this study aimed to investigate potential clinical and genetic predictors of hyponatremia following thiazide diuretic treatment. The Continue reading >>

Paradoxical Antidiuretic Effect Of Thiazides In Diabetes Insipidus: Another Piece In The Puzzle

Diabetes insipidus (DI) is a temporary or chronic disorder characterized by the excretion of excessive quantities of very dilute, but otherwise normal urine. The disease results either from impaired synthesis and secretion of antidiuretic hormone (ADH, vasopressin) by the hypothalamus and posterior pituitary, respectively (central DI), or from an unresponsiveness of the kidneys to the hormone itself (nephrogenic DI) (1–3⇓⇓). The renal water transport defect is located in the collecting system (i.e. the connecting tubule – CNT and the collecting duct – CD) in which vasopressin normally controls the expression and cell surface targeting of the apical water channel aquaporin-2 (AQP2) (4). The CNT and CD are also the site of amiloride-sensitive sodium reabsorption via the epithelial sodium channel (ENaC) (5). Sodium transport across ENaC may osmotically drive transepithelial water reabsorption. Consistently, both AQP2 and ENaC are regulated by vasopressin via V2-receptor-dependent cAMP production (4,5⇓). While exogenous application of vasopressin efficiently corrects the reduced AQP2 expression and the urinary concentration defect in central DI (4), the treatment of nephrogenic DI is usually less obvious and may include different approaches such as dietary sodium restriction, prostaglandin synthesis inhibitors, potassium-sparing diuretics and/or thiazide diuretics (3,6⇓). The use of diuretics for the treatment of a polyuric disease appears paradoxical, but the beneficial effect of thiazides has now been proven for more than 45 yr. In 1959, Crawford and Kennedy showed in a seminal paper that thiazides reduce polyuria and increase urine osmolality in DI (7). Since then, thiazides have become an important component in the therapeutic repertoire for treatment of D Continue reading >>

Jci -phenotypic And Pharmacogenetic Evaluation Of Patients With Thiazide-induced Hyponatremia

1NIHR Biomedical Research Unit in Cardiovascular Disease at Royal Brompton & Harefield, NHS Foundation Trust and Imperial College London, London, United Kingdom. 2National Heart and Lung Institute, Imperial College London, London, United Kingdom. 3Genetic Epidemiology Group, Department of Health Sciences, University of Leicester, Leicester, United Kingdom. 4Division of Therapeutics and Molecular Medicine, University of Nottingham, Nottingham, United Kingdom. 5NIHR Nottingham Biomedical Research Centre, Nottingham, United Kingdom. 6Albert Einstein College of Medicine, Yeshiva University, New York, New York, USA. 7Clinical Pharmacology Unit, University of Cambridge, Cambridge, United Kingdom. 8Department of Diabetes and Endocrinology, Nottingham University Hospitals NHS Trust, Nottingham, United Kingdom. 9Duke-National University of Singapore, Singapore. 10National Heart Centre Singapore, Singapore. Authorship note: J.S. Ware, L.V. Wain, and S.K. Channavajjhala are cofirst authors. Address correspondence to: Mark Glover, Division of Therapeutics and Molecular Medicine, Queens Medical Centre, Nottingham, NG7 2UH, United Kingdom. Phone: 44.115.8231063; Email: [email protected] . Find articles by Ware, J. in: JCI | PubMed | Google Scholar 1NIHR Biomedical Research Unit in Cardiovascular Disease at Royal Brompton & Harefield, NHS Foundation Trust and Imperial College London, London, United Kingdom. 2National Heart and Lung Institute, Imperial College London, London, United Kingdom. 3Genetic Epidemiology Group, Department of Health Sciences, University of Leicester, Leicester, United Kingdom. 4Division of Therapeutics and Molecular Medicine, University of Nottingham, Nottingham, United Kingdom. 5NIHR Nottingham Biomedical Research Centre, Nottingham, United Kingdom Continue reading >>

Thiazides - An Overview | Sciencedirect Topics

Mark Kester PhD, ... Kent E. Vrana PhD, in Elsevier's Integrated Review Pharmacology (Second Edition) , 2012 Thiazides increase urine output by inhibiting the NaCl cotransporter on the luminal membrane of the earliest portion of the distal convoluted tubule, often called the cortical diluting segment (Fig. 9-5). Inhibition of the NaCl cotransporter increases luminal concentrations of Na+ and Cl ions in the late distal tubule; the large Na+ load downstream promotes K+ excretion in the late distal tubule and the collecting duct. Thiazides also lead to increased reabsorption of Ca++ into the blood and may lead to hypercalcemia. Thus thiazides increase urinary levels of Na+, K+, and Cl and decrease levels of Ca++ in the urine. Thiazides, as organic acids, are readily filtered and secreted but are less effective at mobilizing fluid than loop diuretics, especially at low (GFR). (Loop diuretics are preferred when creatine clearance is less than 40 to 50 mL/min.) In fact, hydrochlorothiazide decreases GFR without altering renal blood flow. Mark Kester PhD, ... Kent E. Vrana PhD, in Elsevier's Integrated Review Pharmacology (Second Edition) , 2012 Thiazides, Loop Diuretics, and Potassium-Sparing Drugs Thiazides include hydrochlorothiazide, chlorthalidone, metolazone, indapamide. Examples of loop diuretics are furosemide and bumetanide. K+-sparing drugs are spironolactone, triamterene, and amiloride. An initial strategy for managing hypertension is often to alter volumetric excess through dietary restriction of Na+. Diuretics (see Chapter 9) essentially capitalize on sodium restriction because these drugs facilitate sodium excretion. Diuretics are often included in antihypertensive treatment regimens. In hypertension management, diuretics initially decrease blood volume by facil Continue reading >>