Thiazide Diuretics

Thiazide and thiazide-like diuretics make up a group of highly important antihypertensive agents, with some drugs being 1st-line agents. The class includes hydrochlorothiazide, chlorothiazide, chlorthalidone, indapamide, and metolazone. These drugs block sodium reabsorption in the distal convoluted tubule of the kidney by inhibiting the sodium-chloride cotransporter. As a result, the increased sodium excretion causes secondary water excretion because water follows the sodium. In addition to increasing sodium and water excretion, thiazide diuretics also cause the excretion of chloride, potassium, magnesium, and protons (H+).

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Editorial responsibility: Stanley Oiseth, Lindsay Jones, Evelin Maza

Table of Contents

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Overview

Overview of antihypertensive agents

Table: Drugs used to treat hypertension Hypertension Hypertension, or high blood pressure, is a common disease that manifests as elevated systemic arterial pressures. Hypertension is most often asymptomatic and is found incidentally as part of a routine physical examination or during triage for an unrelated medical encounter. Hypertension
Location of action Class Subclasses
Renal drugs Drugs affecting the RAAS
  • ACEis
  • ARBs
  • Direct renin inhibitors
Diuretics
  • Thiazide diuretics
  • Loop diuretics Loop diuretics Loop diuretics are a group of diuretic medications primarily used to treat fluid overload in edematous conditions such as heart failure and cirrhosis. Loop diuretics also treat hypertension, but not as a 1st-line agent. Loop Diuretics
  • Potassium-sparing diuretics Potassium-sparing diuretics Potassium-sparing diuretics are medications that act in the principal cells in the collecting ducts to induce diuresis that does not result in excretion of potassium. These diuretics include 2 subclasses: sodium channel blockers and aldosterone antagonists. Potassium-sparing Diuretics
Extrarenal drugs Direct vasodilators
  • Calcium channel blockers Calcium Channel Blockers Calcium channel blockers (CCBs) are a class of medications that inhibit voltage-dependent L-type calcium channels of cardiac and vascular smooth muscle cells. The inhibition of these channels produces vasodilation and myocardial depression. There are 2 major classes of CCBs: dihydropyridines and non-dihydropyridines. Class 4 Antiarrhythmic Drugs (Calcium Channel Blockers)
  • Potassium channel openers
  • Nitrodilators
  • Endothelin antagonists
Agents acting via the sympathetic nervous system Nervous system The nervous system is a small and complex system that consists of an intricate network of neural cells (or neurons) and even more glial cells (for support and insulation). It is divided according to its anatomical components as well as its functional characteristics. The brain and spinal cord are referred to as the central nervous system, and the branches of nerves from these structures are referred to as the peripheral nervous system. General Structure of the Nervous System
  • Drugs affecting CNS sympathetic outflow (e.g., clonidine)
  • Drugs affecting the ganglia (e.g., hexamethonium)
  • Drugs affecting the nerve terminals (e.g., guanethidine, reserpine)
  • Drugs affecting the α and β receptors

Drugs in the thiazide class

Drugs in this class include: 

  • Hydrochlorothiazide (HCTZ; prototypical drug in this class)
  • Chlorothiazide 
  • Chlorthalidone (1st-line agent in the treatment of hypertension Hypertension Hypertension, or high blood pressure, is a common disease that manifests as elevated systemic arterial pressures. Hypertension is most often asymptomatic and is found incidentally as part of a routine physical examination or during triage for an unrelated medical encounter. Hypertension)
  • Indapamide
  • Metolazone

Chemistry and Pharmacodynamics

Chemical structure

The chemical structure for HCTZ:

  • Molecular formula: C7H8ClN3O4S2
  • A benzothiadiazine that is 3,4-dihydro-2H-1,2,4-benzothiadiazine 1,1-dioxide with substitutions of:
    • A chloro group at position 6 
    • A sulfonamide Sulfonamide The sulfonamides are a class of antimicrobial drugs inhibiting folic acid synthesize in pathogens. The prototypical drug in the class is sulfamethoxazole. Although not technically sulfonamides, trimethoprim, dapsone, and pyrimethamine are also important antimicrobial agents inhibiting folic acid synthesis. The agents are often combined with sulfonamides, resulting in a synergistic effect. Sulfonamides and Trimethoprim at position 7
Hydrochlorothiazide

Skeletal formula of hydrochlorothiazide

Image: “Hydrochlorothiazide” by Yikrazuul. License: Public Domain

Mechanism of action (MOA)

  • Primary MOA: ↓ reabsorption of NaCl through the inhibition of the Na+/Cl cotransporter in the distal convoluted tubule (DCT)
    • With this channel blocked → ↓ Na+ reabsorption
    • Water always follows Na+:
      • Water stays with Na+ in the tubules (rather than being reabsorbed).
      • Diuresis results from the osmotic effect of Na+.
    • Diuresis → ↓ plasma volume → ↓ BP
      • Initially causes a transient ↑ in the RAAS and sympathetic tone to compensate for ↓ BP and cardiac output.
      • Transient ↑ in the RAAS explains why there is a synergistic effect between thiazides and ACEis/ARBs.
    • There is also a modest ↑ in vasodilation via an unclear mechanism.
  • Thiazide use results in:
    • ↑ Excretion of Na+, Cl, K+, and water 
    • ↑ Reabsorption of Ca2+
      • ↑ Na+ excretion → ↓ cellular Na+ levels → 
      • ↑ Compensatory exchange of Ca2+ for Na+ (via the basolateral Na+/Ca2+ exchanger)
  • Development of hypokalemia Hypokalemia Hypokalemia is defined as plasma potassium (K+) concentration < 3.5 mEq/L. Homeostatic mechanisms maintain plasma concentration between 3.5-5.2 mEq/L despite marked variation in dietary intake. Hypokalemia can be due to renal losses, GI losses, transcellular shifts, or poor dietary intake. Hypokalemia:
    • ↓ Na+ reabsorption in the DCT → 
    • ↑ Na+ delivered to the collecting ducts (CDs) → 
    • Stimulates ↑ aldosterone release
    • Aldosterone stimulates Na+/K+ exchanger to ↑ Na+ reabsorption and excrete K+ hypokalemia Hypokalemia Hypokalemia is defined as plasma potassium (K+) concentration < 3.5 mEq/L. Homeostatic mechanisms maintain plasma concentration between 3.5-5.2 mEq/L despite marked variation in dietary intake. Hypokalemia can be due to renal losses, GI losses, transcellular shifts, or poor dietary intake. Hypokalemia
  • Development of a metabolic alkalosis Metabolic alkalosis The renal system is responsible for eliminating the daily load of non-volatile acids, which is approximately 70 millimoles per day. Metabolic alkalosis also occurs when there is an increased loss of acid, either renally or through the upper GI tract (e.g., vomiting), increased intake of HCO3-, or a reduced ability to secrete HCO3- when needed. Metabolic Alkalosis:
    • ↑ K+ excretion in the CD → 
    • Aldosterone-stimulated ↑ in K+/H+ exchanger → 
    • Reabsorbs some of the extra K+ in the tubule in exchange for H+ (which is excreted) → metabolic alkalosis Metabolic alkalosis The renal system is responsible for eliminating the daily load of non-volatile acids, which is approximately 70 millimoles per day. Metabolic alkalosis also occurs when there is an increased loss of acid, either renally or through the upper GI tract (e.g., vomiting), increased intake of HCO3-, or a reduced ability to secrete HCO3- when needed. Metabolic Alkalosis via H+ loss
Thiazide diuretics acting

Thiazide diuretics acting on the Na/Cl cotransporter

Image by Lecturio. License: CC BY-NC-SA 4.0

Pharmacokinetics

Table: Pharmacokinetics of thiazide diuretics
Drug Absorption Distribution Metabolism Excretion
HCTZ
  • Well absorbed
  • Peak effect in 4 hours
  • Bioavailability 65%–75%
  • Vd: 3.6–7.8 L/kg
  • Protein binding 40%–68%
Not metabolized
  • Urine
  • Half-life: 6–15 hours
Chlorothiazide
  • Poor oral absorption
  • Peak effect: 30 minutes IV
Distributed throughout the extracellular space Not metabolized
  • Urine
  • Half-life: 45–120 minutes
Chlorthalidone Peak effect 2–6 hours
  • Vd: 3–13 L/kg
  • Protein binding: 75%
Hepatic
  • Urine
  • Half-life: 40 hours
Indapamide
  • Rapid and complete absorption
  • Peak effect: 2 hours
  • Vd: 25 L
  • Protein binding: approximately 75%
Extensive hepatic metabolism
  • Urine: 75%
  • Feces: 25%
Metolazone Onset of action: 1 hour
  • Vd: 113 L
  • Protein binding: 95%
Not metabolized Urine
HCTZ: hydrochlorothiazide
Vd: volume of distribution

Indications

Indications

Most thiazide diuretics share similar indications, including:

  • Hypertension
  • As an adjunctive therapy for edema Edema Edema is a condition in which excess serous fluid accumulates in the body cavity or interstitial space of connective tissues. Edema is a symptom observed in several medical conditions. It can be categorized into 2 types, namely, peripheral (in the extremities) and internal (in an organ or body cavity). Edema in the following conditions:
    • Heart failure
    • Hepatic cirrhosis Cirrhosis Cirrhosis is a late stage of hepatic parenchymal necrosis and scarring (fibrosis) most commonly due to hepatitis C infection and alcoholic liver disease. Patients may present with jaundice, ascites, and hepatosplenomegaly. Cirrhosis can also cause complications such as hepatic encephalopathy, portal hypertension, portal vein thrombosis, and hepatorenal syndrome. Cirrhosis resulting in ascites Ascites Ascites is the pathologic accumulation of fluid within the peritoneal cavity that occurs due to an osmotic and/or hydrostatic pressure imbalance secondary to portal hypertension (cirrhosis, heart failure) or non-portal hypertension (hypoalbuminemia, malignancy, infection). Ascites
    • Mild to moderate renal dysfunction ( CKD CKD Chronic kidney disease (CKD) is kidney impairment that lasts for ≥ 3 months, implying that it is irreversible. Hypertension and diabetes are the most common causes; however, there are a multitude of other etiologies. In the early to moderate stages, CKD is usually asymptomatic and is primarily diagnosed by laboratory abnormalities. Chronic Kidney Disease stages 1–3): 
      • Includes CKD CKD Chronic kidney disease (CKD) is kidney impairment that lasts for ≥ 3 months, implying that it is irreversible. Hypertension and diabetes are the most common causes; however, there are a multitude of other etiologies. In the early to moderate stages, CKD is usually asymptomatic and is primarily diagnosed by laboratory abnormalities. Chronic Kidney Disease due to nephrotic syndrome Nephrotic syndrome Nephrotic syndrome is characterized by severe proteinuria, hypoalbuminemia, and peripheral edema. In contrast, the nephritic syndromes present with hematuria, variable loss of renal function, and hypertension, although there is sometimes overlap of > 1 glomerular disease in the same individual. Nephrotic Syndrome, glomerulonephritis, chronic renal failure
      • Note: Thiazides are relatively contraindicated in patients with anuria/severe renal failure ( CKD CKD Chronic kidney disease (CKD) is kidney impairment that lasts for ≥ 3 months, implying that it is irreversible. Hypertension and diabetes are the most common causes; however, there are a multitude of other etiologies. In the early to moderate stages, CKD is usually asymptomatic and is primarily diagnosed by laboratory abnormalities. Chronic Kidney Disease stages 4 and 5).
    • Corticosteroid use
    • Estrogen therapy
  • Off-label uses: 
    • Hypercalciuria 
    • Diabetes insipidus Diabetes Insipidus Diabetes insipidus (DI) is a condition in which the kidneys are unable to concentrate urine. There are 2 subforms of DI: central DI (CDI) and nephrogenic DI (NDI). Both conditions result in the kidneys being unable to concentrate urine, leading to polyuria, nocturia, and polydipsia. Diabetes Insipidus 

Clinical pearls

  • All patients should be monitored for BP, creatinine, Na+, and K+.
  • Chlorthalidone and indapamide:
    • 1st-line agents for monotherapy when treating hypertension Hypertension Hypertension, or high blood pressure, is a common disease that manifests as elevated systemic arterial pressures. Hypertension is most often asymptomatic and is found incidentally as part of a routine physical examination or during triage for an unrelated medical encounter. Hypertension
    • 1.5–2× as potent and longer half-life than HCTZ 
    • ALLHAT (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial) showed reduction in cardiovascular events (has the most evidence of all the thiazides).
    • May have ↑ side effects and risk of hypokalemia Hypokalemia Hypokalemia is defined as plasma potassium (K+) concentration < 3.5 mEq/L. Homeostatic mechanisms maintain plasma concentration between 3.5-5.2 mEq/L despite marked variation in dietary intake. Hypokalemia can be due to renal losses, GI losses, transcellular shifts, or poor dietary intake. Hypokalemia
  • HCTZ:
    • Commonly used as 1st-line agent for hypertension Hypertension Hypertension, or high blood pressure, is a common disease that manifests as elevated systemic arterial pressures. Hypertension is most often asymptomatic and is found incidentally as part of a routine physical examination or during triage for an unrelated medical encounter. Hypertension, though less effective than chlorthalidone or indapamide
    • Comes in combination pills with ACEis, ARBs, and/or calcium-channel blockers
    • Not as effective with creatinine clearance < 30 ml/min
  • Metolazone:
    • May be more effective than other thiazides with CrCl < 30 ml/min
    • Often combined with other diuretics

Adverse Effects and Contraindications

Adverse effects

Table: Adverse effects of thiazide diuretics
Thiazide adverse effects Mechanism Management
Hypokalemia ↑ Urinary Na+ causes ↑ K+ exchange in the CD → ↑ K+ excretion ↑ Dietary intake of K+ or supplementation
Hyponatremia Hyponatremia Hyponatremia is defined as a decreased serum sodium (sNa+) concentration less than 135 mmol/L. Serum sodium is the greatest contributor to plasma osmolality, which is very tightly controlled via antidiuretic hormone (ADH) release from the hypothalamus and by the thirst mechanism. Hyponatremia and hypovolemia ↓ Na+ reabsorption results in ↓ serum Na+; water follows Na+, potentially leading to hypovolemia (most likely to occur in the 1st few weeks of therapy)
  • ↓ Starting dose
  • Without overt hypovolemia: ↓ Free water intake
  • With overt hypovolemia: Replete Na+ with IV saline.
Metabolic alkalosis ↑ Exchange of K+ for H+ ions in the CD Potassium supplementation and/or lower dose/switch agents
Hypomagnesemia Not fully elucidated Mg2+ supplementation
Hyperuricemia Thiazides ↑ urate reabsorption Avoid thiazides in patients with untreated gout Gout Gout is a heterogeneous metabolic disease associated with elevated serum uric acid levels (> 6.8 mg/dL) and abnormal deposits of monosodium urate in tissues. The condition is often familial and is initially characterized by painful, recurring, and usually monoarticular acute arthritis, or "gout flare," followed later by chronic deforming arthritis. Gout or at high risk for gout Gout Gout is a heterogeneous metabolic disease associated with elevated serum uric acid levels (> 6.8 mg/dL) and abnormal deposits of monosodium urate in tissues. The condition is often familial and is initially characterized by painful, recurring, and usually monoarticular acute arthritis, or "gout flare," followed later by chronic deforming arthritis. Gout.
Hypercalcemia Hypercalcemia Hypercalcemia (serum calcium > 10.5 mg/dL) can result from various conditions, the majority of which are due to hyperparathyroidism and malignancy. Other causes include disorders leading to vitamin D elevation, granulomatous diseases, and the use of certain pharmacological agents. Symptoms vary depending on calcium levels and the onset of hypercalcemia. Hypercalcemia Thiazide-induced ↑ of Ca2+ reabsorption Typically inconsequential in absence of CKD CKD Chronic kidney disease (CKD) is kidney impairment that lasts for ≥ 3 months, implying that it is irreversible. Hypertension and diabetes are the most common causes; however, there are a multitude of other etiologies. In the early to moderate stages, CKD is usually asymptomatic and is primarily diagnosed by laboratory abnormalities. Chronic Kidney Disease or hyperparathyroidism Hyperparathyroidism Hyperparathyroidism is a condition associated with elevated blood levels of parathyroid hormone (PTH). Depending on the pathogenesis of this condition, hyperparathyroidism can be defined as primary, secondary or tertiary. Hyperparathyroidism
Hyperglycemia
  • ↓ K+ → hyperpolarization in pancreatic β cells → ↓ insulin Insulin Insulin is a peptide hormone that is produced by the beta cells of the pancreas. Insulin plays a role in metabolic functions such as glucose uptake, glycolysis, glycogenesis, lipogenesis, and protein synthesis. Exogenous insulin may be needed for individuals with diabetes mellitus, in whom there is a deficiency in endogenous insulin or increased insulin resistance. Insulin secretion
  • Seen in higher doses in patients with underlying diabetes
  • Consider alternative agents in patients with diabetes.
  • ↓ Thiazide dose
  • Correct hypokalemia Hypokalemia Hypokalemia is defined as plasma potassium (K+) concentration < 3.5 mEq/L. Homeostatic mechanisms maintain plasma concentration between 3.5-5.2 mEq/L despite marked variation in dietary intake. Hypokalemia can be due to renal losses, GI losses, transcellular shifts, or poor dietary intake. Hypokalemia.
  • Treat diabetes.
Dyslipidemia
  • Not fully elucidated
  • Risk is ↓ with indapamide.
  • Lipid monitoring
  • Lipid-lowering diet and medications
Photosensitivity Not fully elucidated Wear sunscreen and protective clothing.
Hypersensitivity Underlying sulfonamide Sulfonamide The sulfonamides are a class of antimicrobial drugs inhibiting folic acid synthesize in pathogens. The prototypical drug in the class is sulfamethoxazole. Although not technically sulfonamides, trimethoprim, dapsone, and pyrimethamine are also important antimicrobial agents inhibiting folic acid synthesis. The agents are often combined with sulfonamides, resulting in a synergistic effect. Sulfonamides and Trimethoprim allergy Avoid thiazides.

Contraindications

  • Thiazide contraindications:
    • Hypersensitivity reactions
    • Anuria and/or renal failure
    • Hypotension Hypotension Hypotension is defined as low blood pressure, specifically < 90/60 mm Hg, and is most commonly a physiologic response. Hypotension may be mild, serious, or life threatening, depending on the cause. Hypotension
    • Hypokalemia
    • Allergy to sulfa drugs
    • Gout
  • Thiazide precautions:
    • Diabetes
    • Hypercalcemia Hypercalcemia Hypercalcemia (serum calcium > 10.5 mg/dL) can result from various conditions, the majority of which are due to hyperparathyroidism and malignancy. Other causes include disorders leading to vitamin D elevation, granulomatous diseases, and the use of certain pharmacological agents. Symptoms vary depending on calcium levels and the onset of hypercalcemia. Hypercalcemia
    • Hepatic impairment
    • Certain medications:
      • Lithium
      • Carbamazepine 
      • Corticosteroids 
      • NSAIDs
    • Pregnancy Pregnancy Pregnancy is the time period between fertilization of an oocyte and delivery of a fetus approximately 9 months later. The 1st sign of pregnancy is typically a missed menstrual period, after which, pregnancy should be confirmed clinically based on a positive β-hCG test (typically a qualitative urine test) and pelvic ultrasound. Pregnancy: Diagnosis, Maternal Physiology, and Routine Care and lactation

Comparison of Medications

Some of the other most common diuretics include loop diuretics (e.g., furosemide), potassium-sparing diuretics (e.g., spironolactone), carbonic anhydrase inhibitors Carbonic anhydrase inhibitors Carbonic anhydrase inhibitors (CAIs) block the carbonic anhydrase enzymes in the proximal convoluted tubule, inhibiting the reabsorption of sodium bicarbonate (NaHCO3), which results in diuresis and metabolic acidosis. Carbonic Anhydrase Inhibitors (e.g., acetazolamide), and osmotic diuretics Osmotic diuretics Osmotic diuretics increase tubular fluid osmolarity, pulling water into the collecting tubules and preventing water reabsorption, which results in osmotic diuresis. The primary osmotic diuretic used clinically is mannitol. The primary indication for mannitol is to treat cases of increased intracranial or intraocular pressure. Osmotic Diuretics (e.g., mannitol).

Table: Comparison of diuretics
Medication Mechanism Physiologic effect Indication
Thiazide diuretic: Hydrochlorothiazide ↓ Reabsorption of NaCl in the DCT through the inhibition of Na+/Cl cotransporter
  • ↓ Blood pressure
  • ↓ Edema
  • Hypertension
  • Edema
Loop diuretic: Furosemide Inhibits the luminal Na+/K+/Cl cotransporter in the thick ascending limb of the loop of Henle
  • ↓ Edema
  • ↓ Blood pressure
  • Edema/ ascites Ascites Ascites is the pathologic accumulation of fluid within the peritoneal cavity that occurs due to an osmotic and/or hydrostatic pressure imbalance secondary to portal hypertension (cirrhosis, heart failure) or non-portal hypertension (hypoalbuminemia, malignancy, infection). Ascites
  • CHF CHF Congestive heart failure refers to the inability of the heart to supply the body with normal cardiac output to meet metabolic needs. Echocardiography can confirm the diagnosis and give information about the ejection fraction. Congestive Heart Failure
  • Hypertension
Potassium-sparing diuretic: Spironolactone
  • ↓ Reabsorption of Na through the ENaC channels in the CD
  • Inhibition of aldosterone receptors in the CD
  • ↓ Blood pressure
  • ↓ Edema
  • Does not cause ↑ excretion of K+
  • Anti-androgenic effects
  • CHF CHF Congestive heart failure refers to the inability of the heart to supply the body with normal cardiac output to meet metabolic needs. Echocardiography can confirm the diagnosis and give information about the ejection fraction. Congestive Heart Failure
  • Edema/ ascites Ascites Ascites is the pathologic accumulation of fluid within the peritoneal cavity that occurs due to an osmotic and/or hydrostatic pressure imbalance secondary to portal hypertension (cirrhosis, heart failure) or non-portal hypertension (hypoalbuminemia, malignancy, infection). Ascites
  • Hypertension
  • Hirsutism in females
  • Primary hyperaldosteronism Hyperaldosteronism Hyperaldosteronism is defined as the increased secretion of aldosterone from the zona glomerulosa of the adrenal cortex. Hyperaldosteronism may be primary (resulting from autonomous secretion), or secondary (resulting from physiological secretion due to stimulation of the RAAS). Classically, hyperaldosteronism presents with hypertension, hypokalemia, and metabolic alkalosis. Hyperaldosteronism
Carbonic anhydrase inhibitor: Acetazolamide Inhibits both the hydration of CO2 in the PCT epithelial cells and the dehydration of H2CO3 in the PCT lumen; results in ↑ HCO3 and Na+ excretion
  • ↑ Urinary excretion of HCO3 metabolic acidosis Metabolic acidosis The renal system is responsible for eliminating the daily load of non-volatile acids, which is approximately 70 millimoles per day. Metabolic acidosis occurs when there is an increase in the levels of new non-volatile acids (e.g., lactic acid), renal loss of HCO3-, or ingestion of toxic alcohols. Metabolic Acidosis
  • ↓ Intraocular pressure
  • Edema in patients with metabolic alkalosis Metabolic alkalosis The renal system is responsible for eliminating the daily load of non-volatile acids, which is approximately 70 millimoles per day. Metabolic alkalosis also occurs when there is an increased loss of acid, either renally or through the upper GI tract (e.g., vomiting), increased intake of HCO3-, or a reduced ability to secrete HCO3- when needed. Metabolic Alkalosis
  • Altitude sickness Altitude Sickness Altitude sickness refers to a spectrum of symptoms caused by physiological changes in the human body at altitudes above 2,500 m. Altitude sickness includes acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). Altitude Sickness
  • ↑ Intraocular pressure
  • Off label: normal pressure hydrocephalus Normal Pressure Hydrocephalus Normal pressure hydrocephalus (NPH) is a neurodegenerative disorder characterized by the triad of gait abnormalities, dementia, and urinary urgency or incontinence. Normal pressure hydrocephalus can be either idiopathic or secondary to intraventricular or subarachnoid hemorrhage. Normal Pressure Hydrocephalus
Osmotic diuretics: Mannitol ↑ Osmotic pressure in the glomerular filtrate → ↑ tubular fluid and prevents water reabsorption
  • ↓ Free water
  • ↓ Cerebral blood volume
  • Increased intracranial pressure Increased Intracranial Pressure Normal intracranial pressure (ICP) is defined as < 15 mm Hg, whereas pathologically increased ICP is any pressure ≥ 20 mm Hg. Increased ICP may result from several etiologies, including trauma, intracranial hemorrhage, mass lesions, cerebral edema, increased CSF production, and decreased CSF absorption. Increased Intracranial Pressure (ICP)
  • Increased intraocular pressure
PCT: proximal convoluted tubule
DCT: distal convoluted tubule
CHF CHF Congestive heart failure refers to the inability of the heart to supply the body with normal cardiac output to meet metabolic needs. Echocardiography can confirm the diagnosis and give information about the ejection fraction. Congestive Heart Failure: congestive heart failure Congestive heart failure Congestive heart failure refers to the inability of the heart to supply the body with normal cardiac output to meet metabolic needs. Echocardiography can confirm the diagnosis and give information about the ejection fraction. Congestive Heart Failure
Diuretics

The sites of action within the nephron for the diuretic drug classes

Image by Lecturio. License: CC BY-NC-SA 4.0

References

  1. Akbari P, Khorasani-Zadeh A. (2020). StatPearls. https://www.ncbi.nlm.nih.gov/pubmed/30422513
  2. Heymann WR. (2019). The expanding saga of hydrochlorothiazide and skin cancer. J Am Acad Dermatol https://www.ncbi.nlm.nih.gov/pubmed/30529707
  3. Dhayat NA, et al. (2018). Efficacy of standard and low dose hydrochlorothiazide in the recurrence prevention of calcium nephrolithiasis (NOSTONE trial): protocol for a randomized double-blind placebo-controlled trial. BMC Nephrol. https://www.ncbi.nlm.nih.gov/pubmed/30526528
  4. Roush GC, Abdelfattah R, Song S, Ernst ME, Sica DA, Kostis JB. (2018). Hydrochlorothiazide vs chlorthalidone, indapamide, and potassium-sparing/hydrochlorothiazide diuretics for reducing left ventricular hypertrophy: a systematic review and meta-analysis. J Clin Hypertens (Greenwich). https://www.ncbi.nlm.nih.gov/pubmed/30251403
  5. Musini VM, Nazer M, Bassett K, Wright JM. (2014). Blood pressure-lowering efficacy of monotherapy with thiazide diuretics for primary hypertension. Cochrane Database Syst Rev. https://www.ncbi.nlm.nih.gov/pubmed/22526259
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  7. Sica DA, Carter B, Cushman W, Hamm L. (2011). Thiazide and loop diuretics. J Clin Hypertens (Greenwich). https://www.ncbi.nlm.nih.gov/pubmed/21896142
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  9. Mann, J.F., Hilgers, K.F. (2020). Use of thiazide diuretics in patients with primary (essential) hypertension. In Forman, J.P. (Ed.), UpToDate. Retrieved June 14, 2021, from https://www.uptodate.com/contents/use-of-thiazide-diuretics-in-patients-with-primary-essential-hypertension
  10.  Lexicomp Drug Topic Pages: Hydrochlorothiazide; Chlorothiazide; chlorthalidone; indapamide; metolazone. Retrieved June 14, 2021, from https://www.uptodate.com/contents/hydrochlorothiazide-drug-information
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