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Hypertension is characterized by a systolic blood pressure of 130 mmHg or a diastolic blood pressure of 80 mmHg. One of the most prevalent chronic conditions, hypertension, is defined by a continuous rise in arterial pressure.
One of the most significant comorbidities influencing the emergence of stroke, myocardial infarction, heart failure, and renal failure, hypertension has been one of the most researched subjects of the past century.
There is consensus that persistent blood pressure readings of 140/90mmHg or above should be treated with the conventional therapeutic aim of 130/80mmHg or less. The definition and classifications of hypertension have been developing throughout time.
Around the world, more than a billion adults have hypertension, which impacts up to 45% of the adult population. All socioeconomic classes have significant rates of hypertension, which increase with age, reaching up to 60% over the age of 60.
Hypertension causes more cardiovascular disease-related deaths in the US than any other modifiable risk factor.
It is the second-leading preventable cause of death worldwide after cigarette smoking. Recent estimates suggest by 2025, there may be up to 1.5 billion people worldwide with hypertension, an increase of up to 15% or 20%.
An essential regulator of blood volume is sodium (Na+). High serum Na+ levels promote water retention, increasing blood volume and pressure. In normotensive adults, compensatory hemodynamic adjustments stabilize blood pressure as dietary Na+ increases. Nitric oxide generation from the endothelium increased, while renal and peripheral vascular resistance reduced.
However, blood pressure increases if nitric oxide’s impact is diminished or nonexistent. Endothelial dysfunction is a risk factor for the emergence of salt sensitivity and hypertension. Salt sensitivity is characterized by an increase in systolic blood pressure of at least 10 mmHg within a few hours of intake. It is defined as a considerable increase in blood pressure after a Na+ load of less than 5 g.
Renin- Angiotensin-Aldosterone System [RAAS]
RAAS is found in multiple organs at the cellular level. However, its most essential function is to assist in regulating pressure-volume balance in the kidney, where it maintains perfusion in states of volume depletion and is inhibited in circumstances of fluid excess. The juxtaglomerular cells of the kidney produce and store renin and its precursor, pro-renin, which are then released in response to various stimuli. Renin’s primary function is to break down angiotensinogen to create angiotensin I.
The pathogenetic significance of RAAS in hypertension is centered on how the angiotensin-converting enzyme (ACE) converts angiotensin I into angiotensin II. By enhancing the function of the sodium-hydrogen exchanger, sodium-bicarbonate exchanger, and sodium-potassium ATPase, as well as promoting aldosterone production and release from the adrenal glomerulosa, angiotensin II improves Na+ reabsorption in the proximal tubule.
Angiotensin II is also associated with endothelial dysfunction and causes renal, cardiac, and vascular damage. These effects are pro-fibrotic and pro-inflammatory and are mediated mainly by increased oxidative stress. Angiotensin II is strongly aligned to target organ damage in hypertension through these processes. Aldosterone plays a significant role in hypertension by binding to the mineralocorticoid receptor and inducing non-genomic effects.
These effects include activating the amiloride-sensitive sodium channel, also known as the epithelial sodium channel, which stimulates renal Na+ reabsorption in the cortical collecting duct. Additionally, aldosterone has a wide range of non-epithelial actions that support hypertension, vasoconstriction, and endothelial dysfunction. These include vascular fibrosis, extracellular matrix deposition, vascular remodeling, vascular smooth muscle cell proliferation, and elevated oxidative stress.
Idiopathic or essential hypertension is the most common type of hypertension. It has been hypothesized that consuming more salt increases the potential risk of hypertension.
The patient’s genetic ability for a salt response is identified as one of the elements contributing to the development of hypertension. Salt sensitivity affects 50 to 60 % of the patients, who are more likely to develop hypertension.
The prognosis depends on blood pressure control and is positive if blood pressure is well controlled; nevertheless, as hypertension is a progressive condition, complications may occur in a few patients.
Adequate lifestyle and management measures accomplish little more to delay the onset and progression of complications like chronic kidney disease and renal failure.
IR tablets
Initial dose:
100
mg
Orally
once a day
Maintenance dose: 100-450 mg orally once a day
ER tablets:
Initial dose: 25-100 mg orally once a day
Maintenance dose: 100-400 mg orally once a day
Initial:
1
mg
Orally
8 - 12
hrs
Maintenance: 6-15 mg once a day or divided 2 to 3 times a day alternatively
1
mg
Orally
once a day
; the dose can be titrated to double the dose up to 16 mg qDay based on blood pressure response
ER: not recommended for HTN
10 - 20
mg
Orally
every 12 hrs
Maintenance: 20-40 mg once a day
Do not exceed 60 mg per day
40 - 320
mg
Tablet
Orally
once a day
Initial:
1
mg
Orally
once a day
Maintenance: 1-5 mg per day for every 12hrsand can increase upto less than 20 mg per day
Dose Adjustments
Dosing considerations
To prevent syncope first dose and subsequent dose preferred at bedtime and can be taken with food
100
mg
Orally
every 12 hrs
initially; increased up to100 mg for 12hrs every 2-3 days Usual dosage range: 200-400 mg orally every 12hrs Do not exceed 2400 mg per day
Nonblack patients:
1
mg
orally
every day
black patients: 2 mg orally every day
Maintenance dose
2-4 mg orally every day or divided in every 12 hours
2.5
mg
Orally
twice a day
; increase to 2.5 mg for at least 2 days
Extended-release capsules:
Initial dose: 120-240mg orally once a day, increasing the dose as needed
Maintenance dose: 120 to 540mg orally once every day
Maximum dose:540mg/day
Extended-release coated capsules
Initial dose: 120-180mg orally once a day; increase the dose as needed
Maintenance dose: 240 to 360mg orally every day
Maximum dose: 480mg/day
Extended-release tablets
Initial dose: 180 to 240mg orally once a day; increase the dose as needed
Maintenance dose: 540mg orally every day
400 - 1200
mg/day
Capsule
Orally
every 12 hours
off-label:
1
mg
Intravenous (IV)
loading dose, followed by 0.5-2 mg/day oral divided every 12 hours.
Initial dose: Initiate with 40mg/5mg or 80mg/5mg orally every day. Do not exceed 80mg/10mg every day
Maximum dose: Telmisartan 80mg-amlodipine 10mg orally every day
Dose Adjustments
Hepatic impairment
Start with a lower dose of 2.5 mg amlodipine and increase the amount gradually
Renal impairment
Dosage adjustment is not required
Initial dose-12.5mg/150mg or 25mg/150mg orally every day; can increase the dose if needed after 2-4 weeks. Do not exceed 300mg/25mg
Maintenance dose-25mg/300mg orally every day
Dose Adjustments
Renal impairment
CrCl<30ml/min: caution is needed for the use. When CrCl is below 30 mL/min, hydrochlorothiazide is typically ineffective and contraindicated in anuric individuals; aliskiren has the potential to cause hyperkalemia and progressive renal failure
CrCl>30ml/min: No dosage adjustment is needed
Hepatic impairment
No dosage adjustment needed
Initial dose:5mg/20mg orally once a day, can increase the dose after 1-2 weeks
Maintenance dose-10mg/40mg orally once a day
lisinopril/hydrochlorothiazide
Initial dose-10 to 80mg/6.25 to 50mg orally once a day. May increase the dose after 2 to 3 weeks. Do not exceed 80mg/50mg per day
eprosartan/hydrochlorothiazide
600mg/12.5mg to 600mg/25mg orally everyday
Initial dose: 1 tablet (80-160mg valsartan/12.5-25mg hydrochlorothiazide) per day orally
Maintenance dose: May increase the dose after 1-2 weeks to a maximum dose of 320mg valsartan/25mg hydrochlorothiazide daily
Dose Adjustments
Renal impairment
CrCl less than 30 mL/min: Because hydrochlorothiazide is not anticipated to be filtered into the renal tubule, which is where it acts when the glomerular filtration rate is less than 30 mL/min, hydrochlorothiazide-valsartan is not advised
methyldopa/hydrochlorothiazide
methyldopa 500mg/hydrochlorothiazide 30 to 50mg orally every day
methyldopa 250mg/hydrochlorothiazide 25mg orally twice a day or
methyldopa 250mg/hydrochlorothiazide 15mg orally twice or thrice a day
Do not exceed 50mg of hydrochlorothiazide every day
Dose Adjustments
Renal impairment
In patients with creatinine clearance (CrCl) of less than 30 mL/min, valsartan/hydrochlorothiazide should be avoided due to the potential for azotemia (elevated blood urea nitrogen and creatinine levels)
moexipril 7.5mg to 15mg/hydrochlorothiazide 12.5 to 25mg orally before a meal once a day
If hydrochlorothiazide 25 mg once a day monotherapy is effective in controlling blood pressure, but considerable potassium loss still occurs, hydrochlorothiazide 6.25 mg-moexipril 3.75 mg may be used to manage blood pressure without causing electrolyte disturbances (one-half of a hydrochlorothiazide 12.5-moexipril 7.5 mg tablet)
25 - 15
mg-- captopril/hydrochlorothiazide
Orally
every day
Do not exceed 150 mg/50 mg captopril/hydrochlorothiazide
0.1 - 0.3
mg/15 mg
Orally
every day or divided into 2 times a day
Do not exceed 0.6 mg/30 mg per day
30 - 60
mg
Tablets (extended release)
Orally
once a day
7 - 14
days
when required<
should not exceed more than 120 mg/day (Procardia XL) or 90 mg/day (Adalat CC)
(10 mg/12.5 mg) or (20 mg/12.5 mg) orally each day Increase the dose from either of the drug components based on the clinical response Do not increase the hydrochlorothiazide part more than every 2-3 weeks
Dose Adjustments
Renal impairment- When CrCl ≥30 mL/min; no dose modification is required When CrCl <30 mL/min/1.73 m² or the serum creatinine ≥3 mg/dL, the drug is not recommended
metoprolol/hydrochlorothiazide
Renal impairment-
In case of renal impairment, use the medication with caution
Thiazides may develop a cumulative effect if given in the impaired renal function
:
Lopressor HCT: 50-100 mg metoprolol tartrate and 25-50 mg hydrochlorothiazide orally each day as single or divided doses
Dutoprol: 25-100mg metoprolol succinate and 12.5 mg hydrochlorothiazide orally each day as a single dose
The drug is not indicated for initial therapy
candesartan/hydrochlorothiazide
16-32 mg candesartan and 12.5-25 mg hydrochlorothiazide orally each day; the therapeutic effect is expected within 4 weeks
propranolol/hydrochlorothiazide
1 tablet (40/25 mg) orally every 12 hours. If the propranolol dose is more than 160 mg, do not use the combination of the two drugs
Dose Adjustments
Renal impairment-
In case of renal impairment, use the dose with caution
Hepatic impairment-
Adjust the dose in case of severe hepatic impairment
1 tablet (2.5/10 mg) orally each day. Titrate an appropriate dose to control the blood pressure.
Do not increase the dose to more than 10/80 mg per day
1 tablet (2.5/10 mg) orally each day. Titrate an appropriate dose to control the blood pressure.
Do not increase the dose to more than 10/80 mg per day
Dose Adjustments
Renal impairment-
In case of renal impairment, when CrCl<30 ml/min, decrease the dose
In case of severe renal impairment, co-administer the dose with a diuretic
Hepatic impairment-
2.5 mg based on the initial dose of amlodipine
1 tablet (2.5/10 mg) orally each day. Titrate an appropriate dose to control the blood pressure.
Do not increase the dose to more than 10/80 mg per day
Dose Adjustments
Renal impairment-
In case of renal impairment, when CrCl<30 ml/min, decrease the dose
In case of severe renal impairment, co-administer the dose with a diuretic
Hepatic impairment-
2.5 mg based on the initial dose of amlodipine
1 tablet (2.5/10 mg) orally each day. Titrate an appropriate dose to control the blood pressure.
Do not increase the dose to more than 10/80 mg per day
Dose Adjustments
Renal impairment-
In case of renal impairment, when CrCl<30 ml/min, decrease the dose
In case of severe renal impairment, co-administer the dose with a diuretic
Hepatic impairment-
2.5 mg based on the initial dose of amlodipine
benazepril/hydrochlorothiazide
1 tablet (2.5/10 mg) orally each day. Titrate an appropriate dose to control the blood pressure.
Do not increase the dose to more than 10/80 mg per day
Initially, 5 mg/160 mg orally each day
Titrate an appropriate dose to control the blood pressure.
Increase the dose after 2 weeks. Do not exceed the dose of more than 10 mg/day for amlodipine and 320 mg/day for valsartan
Dose Adjustments
Renal impairment-
In case of moderate renal impairment, dose adjustment is not required
In severe renal impairment (CrCl>30 ml/min), dose adjustment is not studied
Hepatic impairment-
Increase the dose in case of hepatic impairment
5
mg
Orally
twice a day; may increase up to 10 mg
3 - 4
week
amlodipine/valsartan/hydrochlorothiazide
12.5-25mg hydrochlorothiazide/
5-10mg amlodipine/160-320 mg valsartan/ every Day
if needed May increase dose after 2 weeks
But should not exceed more than 10 mg/320 mg/25 mg orally once daily
Dose Adjustments
Renal & Hepatic Impairment
Renal impairment
Dose adjustment is not necessary with mild to moderate
Safety and efficacy not established with severe
Hepatic impairment
amlodipine: half-life is increased to 56 hr with an impaired hepatic function and metabolised by liver
valsartan: dose adjustment not necessary with mild to severe hepatic impairment
hydrochlorothiazide: alterations of fluid and electrolyte balance in patients with impaired hepatic function may lead to hepatic coma
ER TABLETS
Age: > 6 years old
:
Initial dose: 1 mg/kg orally once a day
Maximum dose: 2 mg/kg orally once a day
0.5 - 1
mg/kg
Orally
once a day
; do not exceed 2 mg/kg per day
Off-label:
Initial: 0.05-0.1 mg/kg orally once a day
(Off-label)
IR:
1 - 4
mg
Orally
once a day
(Off-label) :
1
mg
Orally
once a day
increase up to 20 mg per day
13
mg/kg
Orally
once a day
or divided for every 12hr
do not exceed 1200 mg per day
1.5-2mg/kg/day orally divided every 8 hours. Do not exceed 6mg/kg/day
0.25 - 0.5
mg
Tablets(extended release)
Orally
once a day
should not exceed more than 3 mg/kg/day (120 mg/day)
Initial dose: 200-400mg/day divided orally. Do not exceed 800mg/day
30 - 60
mg
Tablets (extended release)
Orally
once a day
7 - 14
days
should not exceed more than 120 mg/day (Procardia XL)
metoprolol/hydrochlorothiazide
Lopressor HCT: 50-100 mg metoprolol tartrate and 25-50 mg hydrochlorothiazide orally each day as single or divided doses
Dutoprol: 25-100mg metoprolol succinate and 12.5 mg hydrochlorothiazide orally each day as a single dose
The drug is not indicated for initial therapy
amlodipine/valsartan/hydrochlorothiazide
Initiate with 2.5 mg orally every day, if needed May increase dose after 2 weeks
But should not exceed more than 10 mg/320 mg/25 mg orally once daily
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6477925/
www.ncbi.nlm.nih.gov/books/NBK539859/
ADVERTISEMENT
Hypertension is characterized by a systolic blood pressure of 130 mmHg or a diastolic blood pressure of 80 mmHg. One of the most prevalent chronic conditions, hypertension, is defined by a continuous rise in arterial pressure.
One of the most significant comorbidities influencing the emergence of stroke, myocardial infarction, heart failure, and renal failure, hypertension has been one of the most researched subjects of the past century.
There is consensus that persistent blood pressure readings of 140/90mmHg or above should be treated with the conventional therapeutic aim of 130/80mmHg or less. The definition and classifications of hypertension have been developing throughout time.
Around the world, more than a billion adults have hypertension, which impacts up to 45% of the adult population. All socioeconomic classes have significant rates of hypertension, which increase with age, reaching up to 60% over the age of 60.
Hypertension causes more cardiovascular disease-related deaths in the US than any other modifiable risk factor.
It is the second-leading preventable cause of death worldwide after cigarette smoking. Recent estimates suggest by 2025, there may be up to 1.5 billion people worldwide with hypertension, an increase of up to 15% or 20%.
An essential regulator of blood volume is sodium (Na+). High serum Na+ levels promote water retention, increasing blood volume and pressure. In normotensive adults, compensatory hemodynamic adjustments stabilize blood pressure as dietary Na+ increases. Nitric oxide generation from the endothelium increased, while renal and peripheral vascular resistance reduced.
However, blood pressure increases if nitric oxide’s impact is diminished or nonexistent. Endothelial dysfunction is a risk factor for the emergence of salt sensitivity and hypertension. Salt sensitivity is characterized by an increase in systolic blood pressure of at least 10 mmHg within a few hours of intake. It is defined as a considerable increase in blood pressure after a Na+ load of less than 5 g.
Renin- Angiotensin-Aldosterone System [RAAS]
RAAS is found in multiple organs at the cellular level. However, its most essential function is to assist in regulating pressure-volume balance in the kidney, where it maintains perfusion in states of volume depletion and is inhibited in circumstances of fluid excess. The juxtaglomerular cells of the kidney produce and store renin and its precursor, pro-renin, which are then released in response to various stimuli. Renin’s primary function is to break down angiotensinogen to create angiotensin I.
The pathogenetic significance of RAAS in hypertension is centered on how the angiotensin-converting enzyme (ACE) converts angiotensin I into angiotensin II. By enhancing the function of the sodium-hydrogen exchanger, sodium-bicarbonate exchanger, and sodium-potassium ATPase, as well as promoting aldosterone production and release from the adrenal glomerulosa, angiotensin II improves Na+ reabsorption in the proximal tubule.
Angiotensin II is also associated with endothelial dysfunction and causes renal, cardiac, and vascular damage. These effects are pro-fibrotic and pro-inflammatory and are mediated mainly by increased oxidative stress. Angiotensin II is strongly aligned to target organ damage in hypertension through these processes. Aldosterone plays a significant role in hypertension by binding to the mineralocorticoid receptor and inducing non-genomic effects.
These effects include activating the amiloride-sensitive sodium channel, also known as the epithelial sodium channel, which stimulates renal Na+ reabsorption in the cortical collecting duct. Additionally, aldosterone has a wide range of non-epithelial actions that support hypertension, vasoconstriction, and endothelial dysfunction. These include vascular fibrosis, extracellular matrix deposition, vascular remodeling, vascular smooth muscle cell proliferation, and elevated oxidative stress.
Idiopathic or essential hypertension is the most common type of hypertension. It has been hypothesized that consuming more salt increases the potential risk of hypertension.
The patient’s genetic ability for a salt response is identified as one of the elements contributing to the development of hypertension. Salt sensitivity affects 50 to 60 % of the patients, who are more likely to develop hypertension.
The prognosis depends on blood pressure control and is positive if blood pressure is well controlled; nevertheless, as hypertension is a progressive condition, complications may occur in a few patients.
Adequate lifestyle and management measures accomplish little more to delay the onset and progression of complications like chronic kidney disease and renal failure.
IR tablets
Initial dose:
100
mg
Orally
once a day
Maintenance dose: 100-450 mg orally once a day
ER tablets:
Initial dose: 25-100 mg orally once a day
Maintenance dose: 100-400 mg orally once a day
Initial:
1
mg
Orally
8 - 12
hrs
Maintenance: 6-15 mg once a day or divided 2 to 3 times a day alternatively
1
mg
Orally
once a day
; the dose can be titrated to double the dose up to 16 mg qDay based on blood pressure response
ER: not recommended for HTN
10 - 20
mg
Orally
every 12 hrs
Maintenance: 20-40 mg once a day
Do not exceed 60 mg per day
40 - 320
mg
Tablet
Orally
once a day
Initial:
1
mg
Orally
once a day
Maintenance: 1-5 mg per day for every 12hrsand can increase upto less than 20 mg per day
Dose Adjustments
Dosing considerations
To prevent syncope first dose and subsequent dose preferred at bedtime and can be taken with food
100
mg
Orally
every 12 hrs
initially; increased up to100 mg for 12hrs every 2-3 days Usual dosage range: 200-400 mg orally every 12hrs Do not exceed 2400 mg per day
Nonblack patients:
1
mg
orally
every day
black patients: 2 mg orally every day
Maintenance dose
2-4 mg orally every day or divided in every 12 hours
2.5
mg
Orally
twice a day
; increase to 2.5 mg for at least 2 days
Extended-release capsules:
Initial dose: 120-240mg orally once a day, increasing the dose as needed
Maintenance dose: 120 to 540mg orally once every day
Maximum dose:540mg/day
Extended-release coated capsules
Initial dose: 120-180mg orally once a day; increase the dose as needed
Maintenance dose: 240 to 360mg orally every day
Maximum dose: 480mg/day
Extended-release tablets
Initial dose: 180 to 240mg orally once a day; increase the dose as needed
Maintenance dose: 540mg orally every day
400 - 1200
mg/day
Capsule
Orally
every 12 hours
off-label:
1
mg
Intravenous (IV)
loading dose, followed by 0.5-2 mg/day oral divided every 12 hours.
Initial dose: Initiate with 40mg/5mg or 80mg/5mg orally every day. Do not exceed 80mg/10mg every day
Maximum dose: Telmisartan 80mg-amlodipine 10mg orally every day
Dose Adjustments
Hepatic impairment
Start with a lower dose of 2.5 mg amlodipine and increase the amount gradually
Renal impairment
Dosage adjustment is not required
Initial dose-12.5mg/150mg or 25mg/150mg orally every day; can increase the dose if needed after 2-4 weeks. Do not exceed 300mg/25mg
Maintenance dose-25mg/300mg orally every day
Dose Adjustments
Renal impairment
CrCl<30ml/min: caution is needed for the use. When CrCl is below 30 mL/min, hydrochlorothiazide is typically ineffective and contraindicated in anuric individuals; aliskiren has the potential to cause hyperkalemia and progressive renal failure
CrCl>30ml/min: No dosage adjustment is needed
Hepatic impairment
No dosage adjustment needed
Initial dose:5mg/20mg orally once a day, can increase the dose after 1-2 weeks
Maintenance dose-10mg/40mg orally once a day
lisinopril/hydrochlorothiazide
Initial dose-10 to 80mg/6.25 to 50mg orally once a day. May increase the dose after 2 to 3 weeks. Do not exceed 80mg/50mg per day
eprosartan/hydrochlorothiazide
600mg/12.5mg to 600mg/25mg orally everyday
Initial dose: 1 tablet (80-160mg valsartan/12.5-25mg hydrochlorothiazide) per day orally
Maintenance dose: May increase the dose after 1-2 weeks to a maximum dose of 320mg valsartan/25mg hydrochlorothiazide daily
Dose Adjustments
Renal impairment
CrCl less than 30 mL/min: Because hydrochlorothiazide is not anticipated to be filtered into the renal tubule, which is where it acts when the glomerular filtration rate is less than 30 mL/min, hydrochlorothiazide-valsartan is not advised
methyldopa/hydrochlorothiazide
methyldopa 500mg/hydrochlorothiazide 30 to 50mg orally every day
methyldopa 250mg/hydrochlorothiazide 25mg orally twice a day or
methyldopa 250mg/hydrochlorothiazide 15mg orally twice or thrice a day
Do not exceed 50mg of hydrochlorothiazide every day
Dose Adjustments
Renal impairment
In patients with creatinine clearance (CrCl) of less than 30 mL/min, valsartan/hydrochlorothiazide should be avoided due to the potential for azotemia (elevated blood urea nitrogen and creatinine levels)
moexipril 7.5mg to 15mg/hydrochlorothiazide 12.5 to 25mg orally before a meal once a day
If hydrochlorothiazide 25 mg once a day monotherapy is effective in controlling blood pressure, but considerable potassium loss still occurs, hydrochlorothiazide 6.25 mg-moexipril 3.75 mg may be used to manage blood pressure without causing electrolyte disturbances (one-half of a hydrochlorothiazide 12.5-moexipril 7.5 mg tablet)
25 - 15
mg-- captopril/hydrochlorothiazide
Orally
every day
Do not exceed 150 mg/50 mg captopril/hydrochlorothiazide
0.1 - 0.3
mg/15 mg
Orally
every day or divided into 2 times a day
Do not exceed 0.6 mg/30 mg per day
30 - 60
mg
Tablets (extended release)
Orally
once a day
7 - 14
days
when required<
should not exceed more than 120 mg/day (Procardia XL) or 90 mg/day (Adalat CC)
(10 mg/12.5 mg) or (20 mg/12.5 mg) orally each day Increase the dose from either of the drug components based on the clinical response Do not increase the hydrochlorothiazide part more than every 2-3 weeks
Dose Adjustments
Renal impairment- When CrCl ≥30 mL/min; no dose modification is required When CrCl <30 mL/min/1.73 m² or the serum creatinine ≥3 mg/dL, the drug is not recommended
metoprolol/hydrochlorothiazide
Renal impairment-
In case of renal impairment, use the medication with caution
Thiazides may develop a cumulative effect if given in the impaired renal function
:
Lopressor HCT: 50-100 mg metoprolol tartrate and 25-50 mg hydrochlorothiazide orally each day as single or divided doses
Dutoprol: 25-100mg metoprolol succinate and 12.5 mg hydrochlorothiazide orally each day as a single dose
The drug is not indicated for initial therapy
candesartan/hydrochlorothiazide
16-32 mg candesartan and 12.5-25 mg hydrochlorothiazide orally each day; the therapeutic effect is expected within 4 weeks
propranolol/hydrochlorothiazide
1 tablet (40/25 mg) orally every 12 hours. If the propranolol dose is more than 160 mg, do not use the combination of the two drugs
Dose Adjustments
Renal impairment-
In case of renal impairment, use the dose with caution
Hepatic impairment-
Adjust the dose in case of severe hepatic impairment
1 tablet (2.5/10 mg) orally each day. Titrate an appropriate dose to control the blood pressure.
Do not increase the dose to more than 10/80 mg per day
1 tablet (2.5/10 mg) orally each day. Titrate an appropriate dose to control the blood pressure.
Do not increase the dose to more than 10/80 mg per day
Dose Adjustments
Renal impairment-
In case of renal impairment, when CrCl<30 ml/min, decrease the dose
In case of severe renal impairment, co-administer the dose with a diuretic
Hepatic impairment-
2.5 mg based on the initial dose of amlodipine
1 tablet (2.5/10 mg) orally each day. Titrate an appropriate dose to control the blood pressure.
Do not increase the dose to more than 10/80 mg per day
Dose Adjustments
Renal impairment-
In case of renal impairment, when CrCl<30 ml/min, decrease the dose
In case of severe renal impairment, co-administer the dose with a diuretic
Hepatic impairment-
2.5 mg based on the initial dose of amlodipine
1 tablet (2.5/10 mg) orally each day. Titrate an appropriate dose to control the blood pressure.
Do not increase the dose to more than 10/80 mg per day
Dose Adjustments
Renal impairment-
In case of renal impairment, when CrCl<30 ml/min, decrease the dose
In case of severe renal impairment, co-administer the dose with a diuretic
Hepatic impairment-
2.5 mg based on the initial dose of amlodipine
benazepril/hydrochlorothiazide
1 tablet (2.5/10 mg) orally each day. Titrate an appropriate dose to control the blood pressure.
Do not increase the dose to more than 10/80 mg per day
Initially, 5 mg/160 mg orally each day
Titrate an appropriate dose to control the blood pressure.
Increase the dose after 2 weeks. Do not exceed the dose of more than 10 mg/day for amlodipine and 320 mg/day for valsartan
Dose Adjustments
Renal impairment-
In case of moderate renal impairment, dose adjustment is not required
In severe renal impairment (CrCl>30 ml/min), dose adjustment is not studied
Hepatic impairment-
Increase the dose in case of hepatic impairment
5
mg
Orally
twice a day; may increase up to 10 mg
3 - 4
week
amlodipine/valsartan/hydrochlorothiazide
12.5-25mg hydrochlorothiazide/
5-10mg amlodipine/160-320 mg valsartan/ every Day
if needed May increase dose after 2 weeks
But should not exceed more than 10 mg/320 mg/25 mg orally once daily
Dose Adjustments
Renal & Hepatic Impairment
Renal impairment
Dose adjustment is not necessary with mild to moderate
Safety and efficacy not established with severe
Hepatic impairment
amlodipine: half-life is increased to 56 hr with an impaired hepatic function and metabolised by liver
valsartan: dose adjustment not necessary with mild to severe hepatic impairment
hydrochlorothiazide: alterations of fluid and electrolyte balance in patients with impaired hepatic function may lead to hepatic coma
ER TABLETS
Age: > 6 years old
:
Initial dose: 1 mg/kg orally once a day
Maximum dose: 2 mg/kg orally once a day
0.5 - 1
mg/kg
Orally
once a day
; do not exceed 2 mg/kg per day
Off-label:
Initial: 0.05-0.1 mg/kg orally once a day
(Off-label)
IR:
1 - 4
mg
Orally
once a day
(Off-label) :
1
mg
Orally
once a day
increase up to 20 mg per day
13
mg/kg
Orally
once a day
or divided for every 12hr
do not exceed 1200 mg per day
1.5-2mg/kg/day orally divided every 8 hours. Do not exceed 6mg/kg/day
0.25 - 0.5
mg
Tablets(extended release)
Orally
once a day
should not exceed more than 3 mg/kg/day (120 mg/day)
Initial dose: 200-400mg/day divided orally. Do not exceed 800mg/day
30 - 60
mg
Tablets (extended release)
Orally
once a day
7 - 14
days
should not exceed more than 120 mg/day (Procardia XL)
metoprolol/hydrochlorothiazide
Lopressor HCT: 50-100 mg metoprolol tartrate and 25-50 mg hydrochlorothiazide orally each day as single or divided doses
Dutoprol: 25-100mg metoprolol succinate and 12.5 mg hydrochlorothiazide orally each day as a single dose
The drug is not indicated for initial therapy
amlodipine/valsartan/hydrochlorothiazide
Initiate with 2.5 mg orally every day, if needed May increase dose after 2 weeks
But should not exceed more than 10 mg/320 mg/25 mg orally once daily
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6477925/
www.ncbi.nlm.nih.gov/books/NBK539859/
Hypertension is characterized by a systolic blood pressure of 130 mmHg or a diastolic blood pressure of 80 mmHg. One of the most prevalent chronic conditions, hypertension, is defined by a continuous rise in arterial pressure.
One of the most significant comorbidities influencing the emergence of stroke, myocardial infarction, heart failure, and renal failure, hypertension has been one of the most researched subjects of the past century.
There is consensus that persistent blood pressure readings of 140/90mmHg or above should be treated with the conventional therapeutic aim of 130/80mmHg or less. The definition and classifications of hypertension have been developing throughout time.
Around the world, more than a billion adults have hypertension, which impacts up to 45% of the adult population. All socioeconomic classes have significant rates of hypertension, which increase with age, reaching up to 60% over the age of 60.
Hypertension causes more cardiovascular disease-related deaths in the US than any other modifiable risk factor.
It is the second-leading preventable cause of death worldwide after cigarette smoking. Recent estimates suggest by 2025, there may be up to 1.5 billion people worldwide with hypertension, an increase of up to 15% or 20%.
An essential regulator of blood volume is sodium (Na+). High serum Na+ levels promote water retention, increasing blood volume and pressure. In normotensive adults, compensatory hemodynamic adjustments stabilize blood pressure as dietary Na+ increases. Nitric oxide generation from the endothelium increased, while renal and peripheral vascular resistance reduced.
However, blood pressure increases if nitric oxide’s impact is diminished or nonexistent. Endothelial dysfunction is a risk factor for the emergence of salt sensitivity and hypertension. Salt sensitivity is characterized by an increase in systolic blood pressure of at least 10 mmHg within a few hours of intake. It is defined as a considerable increase in blood pressure after a Na+ load of less than 5 g.
Renin- Angiotensin-Aldosterone System [RAAS]
RAAS is found in multiple organs at the cellular level. However, its most essential function is to assist in regulating pressure-volume balance in the kidney, where it maintains perfusion in states of volume depletion and is inhibited in circumstances of fluid excess. The juxtaglomerular cells of the kidney produce and store renin and its precursor, pro-renin, which are then released in response to various stimuli. Renin’s primary function is to break down angiotensinogen to create angiotensin I.
The pathogenetic significance of RAAS in hypertension is centered on how the angiotensin-converting enzyme (ACE) converts angiotensin I into angiotensin II. By enhancing the function of the sodium-hydrogen exchanger, sodium-bicarbonate exchanger, and sodium-potassium ATPase, as well as promoting aldosterone production and release from the adrenal glomerulosa, angiotensin II improves Na+ reabsorption in the proximal tubule.
Angiotensin II is also associated with endothelial dysfunction and causes renal, cardiac, and vascular damage. These effects are pro-fibrotic and pro-inflammatory and are mediated mainly by increased oxidative stress. Angiotensin II is strongly aligned to target organ damage in hypertension through these processes. Aldosterone plays a significant role in hypertension by binding to the mineralocorticoid receptor and inducing non-genomic effects.
These effects include activating the amiloride-sensitive sodium channel, also known as the epithelial sodium channel, which stimulates renal Na+ reabsorption in the cortical collecting duct. Additionally, aldosterone has a wide range of non-epithelial actions that support hypertension, vasoconstriction, and endothelial dysfunction. These include vascular fibrosis, extracellular matrix deposition, vascular remodeling, vascular smooth muscle cell proliferation, and elevated oxidative stress.
Idiopathic or essential hypertension is the most common type of hypertension. It has been hypothesized that consuming more salt increases the potential risk of hypertension.
The patient’s genetic ability for a salt response is identified as one of the elements contributing to the development of hypertension. Salt sensitivity affects 50 to 60 % of the patients, who are more likely to develop hypertension.
The prognosis depends on blood pressure control and is positive if blood pressure is well controlled; nevertheless, as hypertension is a progressive condition, complications may occur in a few patients.
Adequate lifestyle and management measures accomplish little more to delay the onset and progression of complications like chronic kidney disease and renal failure.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6477925/
www.ncbi.nlm.nih.gov/books/NBK539859/
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