glomerulonefritis kronik emed

8/18/2019 Glomerulonefritis Kronik Emed

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ackground

Nearly all forms of acute glomerulonephritis have a tendency to progress to chronic

glomerulonephritis. The condition is characterized by irreversible and progressive

glomerular and tubulointerstitial fibrosis, ultimately leading to a reduction in the

glomerular filtration rate (GFR) and retention of uremic toins. !f disease progression isnot halted "ith therapy, the net results are chronic #idney disease ($%&), end'stage renal

disease (R&), and cardiovascular disease. $hronic glomerulonephritis is the third

leading cause and accounts for about *+ of all causes of $%&.

The eact cause of $%& in patients "ith chronic glomerulonephritis may never be #no"nin some patients. Therefore, it has generally been accepted that the diagnosis of $%& can

be made "ithout #no"ledge of the specific cause.-*

The National %idney Foundation (N%F) defines $%& on the basis of either of the

follo"ing/

vidence of #idney damage based on abnormal urinalysis results (eg, proteinuria or

hematuria) or structural abnormalities observed on ultrasound images 0 GFR of less than 1+ m23min for 4 or more months

!n accordance "ith this definition, the N%F developed guidelines that classify the progression of renal disease into five stages, from #idney disease "ith a preserved GFR

to end'stage #idney failure. This classification includes treatment strategies for each

progressive level, as follo"s/

tage * – This stage is characterized by #idney damage "ith a normal GFR (≥ 5+

m23min)6 the action plan consists of diagnosis and treatment, treatment of comorbidconditions, slo"ing of the progressing of #idney disease, and reduction of

cardiovascular disease ris#s

tage 7 – This stage is characterized by #idney damage "ith a mild decrease in the

GFR (1+'5+ m23min)6 the action plan is estimation of the progression of #idney

disease

tage 4 – This stage is characterized by a moderately decreased GFR (to 4+'85

m23min)6 the action plan consists of evaluation and treatment of complications

tage 9 – This stage is characterized by a severe decrease in the GFR (to *8'75

m23min)6 the action plan is preparation for renal replacement therapy tage 8 – This stage is characterized by #idney failure6 the action plan is #idney

replacement if the patient is uremic

0t the later stages of glomerular in:ury, the #idney are small and contracted and biopsy

results cannot help distinguish the primary disease. ;istology and clues to the etiology

are often derived from other systemic diseases (if present). $onsiderable cause'specific

variability is observed in the rate at "hich acute glomerulonephritis progresses to chronicglomerulonephritis.

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The prognosis depends on the type of chronic glomerulonephritis (see tiology). R&

and death are common outcomes unless renal replacement therapy is instituted.

Pathophysiology

Reduction in nephron mass from the initial in:ury reduces the GFR. This reduction leads

to hypertrophy and hyperfiltration of the remaining nephrons and to the initiation of intraglomerular hypertension. These changes occur in order to increase the GFR of theremaining nephrons, thus minimizing the functional conse


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Dembranoproliferative glomerulonephritis/ ' 0bout 9+ of patients "ith

membranoproliferative glomerulonephritis progress to $RF and R& in *+ years !g0 nephropathy – 0bout *+ of patients "ith !g0 nephropathy progress to $RF

and R& in *+ years -4

@oststreptococcal glomerulonephritis ' 0bout *'7 of patients "ith poststreptococcal

glomerulonephritis progress to $RF and R&6 older children "ho present "ithcrescentic glomerulonephritis are at greatest ris#

2upus nephritis – Everall, about 7+ of patients "ith lupus nephritis progress to

$RF and R& in *+ years6 ho"ever, patients "ith certain histologic variants (eg,class !C) may have a more rapid decline

Epidemiology

!n the >nited tates, chronic glomerulonephritis is the third leading cause of R& andaccounts for *+ of patients on dialysis.

!n apan and some 0sian countries, chronic glomerulonephritis has accounted for asmany as 9+ of patients on dialysis6 ho"ever, subse


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@ericardial friction rub in pericarditis

Tenderness in the epigastric region or blood in the stool (possible indicators of

uremic gastritis or enteropathy)

&ecreased sensation and asteriis (indicators of advanced uremia)

Complications

The presence of the follo"ing complications generally indicates a need for urgent

dialysis/

Detabolic acidosis

@ulmonary edema

@ericarditis

>remic encephalopathy

>remic gastrointestinal bleeding

>remic neuropathy

evere anemia and hypocalcemia

;yper#alemia

DD

The presence of the follo"ing complications generally indicates a need for urgentdialysis/

Detabolic acidosis

@ulmonary edema

@ericarditis

>remic encephalopathy

>remic gastrointestinal bleeding

>remic neuropathy

evere anemia and hypocalcemia

;yper#alemia


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Laboratory Studies

Urinalysis

The presence of dysmorphic red blood cells (R=$s), albumin, or R=$ casts suggests

glomerulonephritis as the cause of renal failure. Aay or broad casts are observed in all

forms of chronic #idney disease ($%&), including chronic glomerulonephritis. 2o"urine'specific gravity indicates loss of tubular concentrating ability, an early finding in

persons "ith $%&. ee >rinalysis.

Urinary protein excretion

>rinary protein ecretion can be estimated by calculating the protein'to'creatinine ratioon a spot morning urine sample. The ratio of urinary protein concentration (in mg3d2) to

urinary creatinine (in mg3d2) reflects 79'hour protein ecretion in grams. For instance, if

the spot urine protein value is 4++ mg3d2 and the creatinine value is *8+ mg3d2, the

protein'to'creatinine ratio is 7. Thus, in this eample, the 79'hour urine protein ecretionis 7 g.-?

The estimated creatinine clearance rate is used to assess and monitor the glomerular

filtration rate (GFR). The 7 formulas available for calculation of the GFR are the

$oc#croft'Gault formula, "hich estimates creatinine clearance, and the Dodification of &iet in Renal &isease (D&R&) tudy formula, "hich is used to calculate the GFR

directly.

The $oc#croft'Gault formula is simple to use but overestimates the GFR by *+'*8

because creatinine is both filtered and secreted. The D&R& formula is much morecomple but can be determined "ith a smartphone and tablet application available from

the National %idney Foundation or can be calculated online through the ;ypertension,&ialysis, and $linical Nephrology Aeb site.

The estimated creatinine clearance rate is also used to monitor response to therapy and toinitiate an early transition to renal replacement therapy (eg, dialysis access placement and

transplantation evaluation). The degree of proteinuria, especially albuminuria, helps

predict the renal prognosis in patients "ith chronic glomerulonephritis. @atients "ith

proteinuria eceeding * g3day have an increased ris# of progression to end'stage renalfailure.

Complete blood count

0nemia is a significant finding in patients "ith some decline in the GFR. @hysicians must be a"are that anemia can occur even in patients "ith serum creatinine levels lo"er than 7

mg3d2. ven severe anemia can occur at lo" serum creatinine levels. 0nemia is the result

of mar#ed impairment of erythropoietin production.

Serum chemistry

erum creatinine and urea nitrogen levels are elevated. !mpaired ecretion of potassium,

free "ater, and acid results in hyper#alemia, hyponatremia, and lo" serum bicarbonate

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levels, respectively. !mpaired vitamin &'4 production results in hypocalcemia,

hyperphosphatemia, and high levels of parathyroid hormone. 2o" serum albumin levels

may be present if uremia interferes "ith nutrition or if the patient is nephrotic. Recently, ahigh fibroblast gro"th factor 7* (FGF7*) "as found to be significantly elevated in

patients "ith $%& and the high levels of FGF7* may eplain the ecess overall and

cardiovascular mortality in patients "ith $%&. These adverse effects of elevated FGF7*are not clearly understood but research is under"ay to elucidate its biologic effects.

ther Studies!enal ultrasonography

Ebtain a renal ultrasonogram to determine renal size, to assess for the presence of both

#idneys, and to eclude structural lesions that may be responsible for azotemia. mall#idneys often indicate an irreversible process.

"idney biopsy

!f the #idney is small, #idney biopsy is usually unnecessary6 no specific pattern of disease

can be discerned at this point. 0 #idney biopsy may be considered in the minority of patients "ho ehibit an acute eacerbation of their chronic disease. This may be

particularly pertinent to patients "ith preserved #idney size and in those "ith lupus

nephritis.

!n early stages, the glomeruli may still sho" some histologic evidence of the primarydisease. !n advanced stages, the glomeruli are hyalinized and obsolescent. The tubules are

disrupted and atrophic, and mar#ed interstitial fibrosis and arterial and arteriolar sclerosis

occur.

#pproach Considerations@atients "ith chronic #idney disease ($%&) "ho are admitted to the hospital should

receive careful monitoring of "eight, inta#e, output, and renal function so that acute renalfailure (0RF) can be diagnosed and treated early if it occurs,. 0ll potentially nephrotoic

agents must be ad:usted for the degree of $%&. Furthermore, agents such as nonsteroidal

anti'inflammatory drugs (N0!&s), aminoglycosides, and intravenous (!C) contrast

media must be avoided unless the benefits clearly out"eigh the ris#s6 they are stronglyassociated "ith 0RF.

@rogression from $%& to end'stage renal disease (R&) can be slo"ed by a variety of

measures, including aggressive control of diabetes, hypertension, and proteinuria. &ietary

protein restriction, phosphate restriction, and hyperlipidemia control may have significantimpact on retarding disease progression.

pecific therapies for some glomerular diseases (eg, lupus) should be implemented in

appropriate settings. 0ggressively manage anemia and renal osteodystrophy (eg,

hyperphosphatemia, hypocalcemia, or hyperparathyroidism) before initiating renalreplacement therapy. 0lso, aggressively manage comorbid conditions, such as heart

disease and diabetes.

http://emedicine.medscape.com/article/2054430-overviewhttp://emedicine.medscape.com/article/2054430-overview


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Nephrotic patients (urinary protein ecretion 4.8 g3day) may have hyperlipidemia. 0s a

part of cardiovascular health care, the lipid profile should be chec#ed, and lipid'lo"ering

therapy should be started for patients "ith hyperlipidemia.

teroid therapy may induce or eacerbate diabetes, hypertension, "eight gain, fatredistribution in the trun# (buffalo hump) and face (moon facies), cosmetic problems (eg,

hirsutism and acne), and osteoporosis.

Donitor fasting blood glucose levels and blood pressure. Ebtain baseline bone

densitometry values. Repeat bone densitometry for bone pain. Eral calcium supplements(* g3day) and vitamin & (9++'B++ !>3day) are recommended for prophylais against

osteoporosis.

Pharmacologic $herapy lood pressure management

The target blood pressure for patients "ith proteinuria in ecess of * g3day is less than*783?8 mm ;g6 for patients "ith proteinuria of less than * g3day, the target pressure is

less than *4+3B+ mm ;g.

0ngiotensin'converting enzyme inhibitors (0$!s) are commonly used and are usually

the first choice for treatment of hypertension in patients "ith chronic #idney disease($%&). 0$!s are renoprotective agents that have additional benefits beyond lo"ering

pressure. They effectively reduce proteinuria, in part by reducing the efferent arteriolar

vascular tone, thereby decreasing intraglomerular hypertension.

!n particular, 0$!s have been sho"n to be superior to conventional therapy in slo"ing

the decline of the glomerular filtration rate (GFR) in patients "ith diabetic and

nondiabetic proteinuric nephropathies. Therefore, 0$!s should be considered for treatment of even normotensive patients "ith significant proteinuria.-B

The role of angiotensin !! receptor bloc#ers (0R=s) in renal protection is increasingly

being established, and these medications have been found to retard the progression of $%& in patients "ith diabetic or nondiabetic nephropathy, much as 0$!s do.-5

0 combination of 0$! therapy and 0R= therapy has been sho"n to achieve better

pressure control and preservation of renal function than either therapy alone could.

Therefore, in patients "ithout hyper#alemia or an acute rise in serum creatinine levelsafter the use of either therapy, combination therapy should be attempted.-*+

;o"ever, in patients "ith vascular disease or diabetes, combination 0$! and 0R=therapy has been associated "ith increased adverse effects, including hyper#alemia,

"orsening renal function, and mortality. 0s such, combination 0$! and 0R= therapy

should not be used to treat hypertension in these groups of patients "ith $%&.-**

&iuretics are often re


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and 0R=s. ;o"ever, they should be used "ith caution "hen given together "ith 0$!s

or 0R=s because the decline in intraglomerular pressure induced by 0$!s or 0R=s may

be eacerbated by the volume depletion induced by diuretics, potentially precipitating0RF.

=eta bloc#ers, calcium channel bloc#ers,-*7 central alpha7 agonists (eg, clonidine),

alpha* antagonists, and direct vasodilators (eg, minoidil and nitrates) may be used to

achieve the target pressure.

%ibrosis inhibition

=ecause progressive fibrosis is the hallmar# of chronic glomerulonephritis, some

investigators have focused on finding inhibitors of fibrosis in an attempt to slo"

progression. Ef the many compounds that have been considered, pirfenidone, an inhibitor of transforming gro"th factor beta and hence of collagen synthesis, has emerged as the

best candidate.

$ho et al, in an open'label study involving 7* patients "ith idiopathic and postadaptive

focal segmental glomerulosclerosis, found that pirfenidone yielded a median 78improvement in the rate of decline of the estimated GFR6 the drug did not affect

proteinuria or blood pressure.-*4 0mong the adverse events attributed to therapy "ere

dyspepsia, sedation, and photosensitive dermatitis. !t is hoped that pirfenidone therapy

"ill prove an effective means of slo"ing progressive fibrosis6 ho"ever, more studies areneeded.

!ole o& antioxidants 'bardoxolone(

$ells have the ability to produce antioidants, anti'inflammatory and detoifyingenzymes that are useful for cell viability, but this path"ay is constantly being inhibited by

an enzyme called %0@. !nhibition of %0@ may therefore improve the antioidant

activity of cells and promote cell viability. =ardoolone, an oleanolic acid derivative, bloc#s %eap and has been postulated as a potential mechanism to retard progression of $%&. !n one study, patients receiving bardoolone had significant increases in the mean

(H standard deviation) estimated GFR, as compared "ith placebo, at 79 "ee#s. The

improvement persisted at 87 "ee#s, suggesting that bardoolone may have promise for the treatment of $%&, ho"ever a phase 4 randomized clinical trial failed to achieve the

primary end point and "as associated "ith side effects and so the study "as stopped. -*9 !t

is not li#ely that =ardoolone "ill be used for renoprotection any time soon.

!ole o& sodium bicarbonate

odium bicarbonate has been sho"n to reduce tubulointerstitial in:ury and endothelin

production "ith substantial benefits in slo"ing progressive #idney damage. !n one studyon patients "ith advanced #idney failure, the administration of sodium bicarbonate preserved GFR decline.-*9 ven in patients "ith relatively preserved GFR in stage 7

$%&, the administration of sodium bicarbonate "as sho"n to preserve #idney function

over 8 years.-*8 0 study in patients "ith stage 9 $%& found that * year of consuming adiet that included fruits and vegetables dosed to reduce dietary acid by half had effects

comparable to those of daily oral sodium bicarbonate at *.+ m


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!ole o& direct renin inhibitors

@reliminary studies using alis#iren,-*? a direct renin inhibitor, sho" reductions in proteinuria over 1 months, but larger studies did not sho" benefit.

)anagement o& other problems

Renal osteodystrophy can be managed early by replacing vitamin & and by administering

phosphate binders. ee# and treat nonuremic causes of anemia, such as iron deficiency, before instituting therapy "ith erythropoietin.

Treat hyperlipidemia (if present) to reduce overall cardiovascular comorbidity, even

though evidence for lipid lo"ering in renal protection is lac#ing.

!enal !eplacement $herapy&iscuss options for renal replacement therapy (eg, hemodialysis, peritoneal dialysis, and

renal transplantation).

0rrange permanent vascular access "hen the GFR falls belo" 7+'78 m23min, "hen theserum creatinine level eceeds 9 mg3d2, or "hen the rate of increase in the serum

creatinine level indicates the need for dialysis "ithin * year. 0rteriovenous fistulas are preferred to arteriovenous grafts because of their long'term high'patency rates and should

be placed "henever possible. @lace peritoneal dialysis catheters 7'4 "ee#s before

anticipated dialysis therapy.

@reemptive transplantation before the initiation of dialysis results in better survival thantransplantation after the initiation of dialysis. Therefore, preemptive transplantation

should be eplored from live donors. @atients "ithout live donors can be placed on the

deceased donor "ait list "hen the GFR falls belo" 7+ m23min to accrue time. @atients"ho opt for no treatment "hen it is indicated should be informed of imminent renal

failure in a shorter time.

pose patients to educational programs for early rehabilitation from dialysis or

transplantation.

Consultations

@atients "ith any evidence of #idney disease should be referred to a #idney specialist (ie,

a nephrologist). arly referral of patients "ith $RF (serum creatinine, *.8'7 mg3d2) to a

nephrologist is important for managing complications and organizing the transition torenal replacement therapy. ome evidence indicates that early referral of $RF patients to

a nephrologist improves the short'term outcome. The nephrologist "ill usually determine

the fre


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@rotein'restricted diets (+.9'+.1 g3#g3day) are controversial but may be beneficial in

slo"ing the decline in the GFR and reducing hyperphosphatemia (serum phosphate 8.8

mg3d2) in patients "ith serum creatinine levels higher than 9 mg3d2. Donitor these patients for signs of malnutrition, "hich may contraindicate protein restriction. ducate

patients about ho" potassium'rich diets help control hyper#alemia. Dany dietary

restrictions are no longer necessary "ith the initiation of renal replacement therapy.

ncourage patients to increase their activity level as tolerated. !ncreased activity may aidin blood pressure control.

!n obese patients "ith mild to moderate $%&, "eight loss may help reverse renal

dysfunction, manifesting as reduction in proteinuria and albuminuria.-*B, *5

)edication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Dedications used to treat chronic glomerulonephritis include angiotensin'converting

enzyme (0$) inhibitors (0$!s), diuretics, calcium channel bloc#ers, beta'adrenergic

bloc#ers, and alpha'adrenergic agonists.

#CE ,nhibitors

Class Summary

0$!s are renoprotective agents. They decrease intraglomerular pressure and,

conse


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decreases intraglomerular pressure and glomerular protein filtration by decreasing

efferent arteriolar constriction.Cie" full drug information

ena0epril 'Lotensin(

=enazepril prevents conversion of angiotensin ! to angiotensin !!, a potent

vasoconstrictor, resulting in increased levels of plasma renin and a reduction inaldosterone secretion.

!t decreases intraglomerular pressure and glomerular protein filtration by decreasing

efferent arteriolar constriction.Cie" full drug information

%osinopril

Fosinopril is a competitive 0$ inhibitor. !t prevents conversion of angiotensin ! to

angiotensin !!, a potent vasoconstrictor, resulting in increased levels of plasma renin and

a reduction in aldosterone secretion. !t decreases intraglomerular pressure and glomerular protein filtration by decreasing efferent arteriolar constriction.Cie" full drug information

1uinapril '#ccupril(

Iuinapril is a competitive 0$ inhibitor. !t reduces angiotensin !! levels, decreasingaldosterone secretion. !t decreases intraglomerular pressure and glomerular protein

filtration by decreasing efferent arteriolar constriction.

*iuretics. Loop

Class Summary

&iuretics are used to treat edema and hypertension. They increase urine ecretion by

inhibiting sodium and chloride transporters.Cie" full drug information

%urosemide 'Lasix(

Furosemide is the diuretic of choice. !t increases ecretion of "ater by interfering "ith

the chloride'binding cotransport system, "hich, in turn, inhibits sodium and chloride

reabsorption in the ascending loop of ;enle and the distal renal tubule. Cie" full druginformation

umetanide ' umex(

=umetanide increases the ecretion of "ater by interfering "ith the chloride'binding

cotransport system, "hich, in turn, inhibits sodium, potassium, and chloride reabsorptionin the ascending loop of ;enle. These effects increase the urinary ecretion of sodium,

chloride, and "ater, resulting in profound diuresis. Renal vasodilation occurs after administration, renal vascular resistance decreases, and renal blood flo" is enhanced. !nterms of effect, * mg of bumetanide is e


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ascending loop of ;enle and distal renal tubule. This agent is used only in refractory

cases. $ontinuous !C infusion is preferable in many cases. !t is indicated for temporary

treatment of edema associated "ith heart failure "hen greater diuretic potential is needed.

*iuretics. $hia0ide

Class Summary

&iuretics are used to treat edema and hypertension. They increase urine ecretion by

inhibiting sodium and chloride transporters.

Cie" full drug information

)etola0one '/aroxolyn(

Detolazone treats edema in congestive heart failure. !t increases ecretion of sodium,

"ater, potassium, and hydrogen ions by inhibiting reabsorption of sodium in distal

tubules. !t may be more effective in cases of impaired renal function.Cie" full druginformation

Hydrochlorothia0ide ')icro0ide(

;ydrochlorothiazide inhibits reabsorption of sodium in distal tubules, causing increased

ecretion of sodium and "ater as "ell as potassium and hydrogen ions.

Calcium Channel lockers

Class Summary

$alcium channel bloc#ers are used to treat hypertension, angina, and atrialfibrillation.Cie" full drug information

#mlodipine '2or+asc(

0mlodipine bloc#s slo" calcium channels, causing relaation of vascular smooth

muscles.Cie" full drug information

2i&edipine 'Procardia(

Nifedipine relaes coronary smooth muscle and produces coronary vasodilation, "hich,

in turn, improves myocardial oygen delivery. ublingual administration is generallysafe, theoretical concerns not"ithstanding.Cie" full drug information

%elodipine

Felodipine relaes coronary smooth muscle and produces coronary vasodilation, "hich,

in turn, improves myocardial oygen delivery. !t benefits nonpregnant patients "ithsystolic dysfunction, hypertension, or arrhythmias. !t can be used during pregnancy if

clinically indicated.

$alcium'channel bloc#ers potentiate 0$ inhibitor effects. Renal protection is not

proven, but these agents reduce morbidity and mortality rates in congestive heart failure.

$alcium channel bloc#ers are indicated in patients "ith diastolic dysfunction. They areeffective as monotherapy in blac# patients and elderly patients.Cie" full drug information

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,sradipine '*ynaCirc(

!sradipine is a dihydropyridine calcium channel bloc#er. !t inhibits calcium from enteringselect voltage'sensitive areas of vascular smooth muscle and myocardium during

depolarization. This causes relaation of coronary vascular smooth muscle, "hich results

in coronary vasodilation. Casodilation reduces systemic resistance and blood pressure,

"ith a small increase in resting heart rate. !sradipine also has negative inotropiceffects.Cie" full drug information

Verapamil (Calan, Isoptin, Verelan)

&uring depolarization, verapamil inhibits calcium ions from entering slo" channels and

voltage'sensitive areas of vascular smooth muscle and myocardium. !t can diminish

premature ventricular contractions (@C$s) associated "ith perfusion therapy anddecrease ris# of ventricular fibrillation and ventricular tachycardia. =y interrupting re'

entry at the 0C node, it can restore normal sinus rhythm (NR) in patients "ith

paroysmal supraventricular tachycardias.Cie" full drug information

*iltia0em 'Cardi0em. *ilacor 3!. *ilt0ac. )at0im L#(

&uring depolarization, diltiazem inhibits calcium ions from entering slo" channels and

voltage'sensitive areas of vascular smooth muscle and myocardium.

eta4 lockers. eta45 Selecti+e

Class Summary

=eta'adrenergic bloc#ers compete "ith beta'adrenergic agonists for available beta'

receptor sites. These agents inhibit mainly beta* receptors (located mainly in cardiacmuscle).Cie" full drug information

)etoprolol 'Lopressor. $oprol 3L(

Detoprolol is a selective beta*'adrenergic bloc#er that decreases the automaticity of contractions. &uring intravenous (!C) administration, carefully monitor blood pressure,

heart rate, and electrocardiographic readings.Cie" full drug information

isoprolol '/ebeta(

=isoprolol is a selective beta*'adrenergic receptor bloc#er that decreases automaticity of contractions.Cie" full drug information

Esmolol ' re+ibloc(

smolol is an ultra–short'acting beta7'bloc#er. !t is particularly useful in patients "ithlabile arterial pressure, especially if surgery is planned, because it can be discontinuedabruptly if necessary. !t may be useful as a means to test beta'bloc#er safety and tolerance

in patients "ith a history of obstructive pulmonary disease "ho are at possible ris# of

bronchospasm from beta'bloc#ade. The elimination half'life of esmolol is 5minutes.Cie" full drug information

#tenolol '$enormin(

http://reference.medscape.com/drug/isradipine-342376http://reference.medscape.com/drug/calan-sr-isoptin-sr-verapamil-342380http://reference.medscape.com/drug/calan-sr-isoptin-sr-verapamil-342380http://reference.medscape.com/drug/cardizem-cd-diltiazem-342374http://reference.medscape.com/drug/cardizem-cd-diltiazem-342374http://reference.medscape.com/drug/lopressor-toprol-xl-metoprolol-342360http://reference.medscape.com/drug/lopressor-toprol-xl-metoprolol-342360http://reference.medscape.com/drug/monocor-zebeta-bisoprolol-342367http://reference.medscape.com/drug/monocor-zebeta-bisoprolol-342367http://reference.medscape.com/drug/brevibloc-esmolol-342358http://reference.medscape.com/drug/brevibloc-esmolol-342358http://reference.medscape.com/drug/tenormin-atenolol-342356http://reference.medscape.com/drug/tenormin-atenolol-342356http://reference.medscape.com/drug/isradipine-342376http://reference.medscape.com/drug/calan-sr-isoptin-sr-verapamil-342380http://reference.medscape.com/drug/calan-sr-isoptin-sr-verapamil-342380http://reference.medscape.com/drug/cardizem-cd-diltiazem-342374http://reference.medscape.com/drug/cardizem-cd-diltiazem-342374http://reference.medscape.com/drug/lopressor-toprol-xl-metoprolol-342360http://reference.medscape.com/drug/lopressor-toprol-xl-metoprolol-342360http://reference.medscape.com/drug/monocor-zebeta-bisoprolol-342367http://reference.medscape.com/drug/monocor-zebeta-bisoprolol-342367http://reference.medscape.com/drug/brevibloc-esmolol-342358http://reference.medscape.com/drug/brevibloc-esmolol-342358http://reference.medscape.com/drug/tenormin-atenolol-342356http://reference.medscape.com/drug/tenormin-atenolol-342356


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0tenolol selectively bloc#s beta'* receptors "ith little or no effect on beta'7 receptors.

Beta4Blockers. 2onselecti+eClass Summary

Nonselective beta'bloc#ers inhibit both beta* receptors (located mainly in cardiac

muscle) and beta7 receptors located in the bronchial and vascular musculature. Theseagents slo" the sinus rate and decrease 0C nodal conduction. $arefully monitor blood

pressure.

Cie" full drug information

Propranolol ',nderal L#. ,nnoPran 3L(

@ropranolol is a class !! antiarrhythmic nonselective beta'adrenergic receptor bloc#er. !t

has membrane'stabilizing activity and decreases the automaticity of contractions.Cie"

full drug information

Sotalol ' etapace. Sorine(

This class !!! antiarrhythmic agent bloc#s %J channels, prolongs action potential duration

(0@&), and lengthens the IT interval. !t is a non–cardiac selective beta'adrenergic bloc#er. otalol is sho"n to be effective in the maintenance of sinus rhythm, even in patients "ith underlying structural heart disease.Cie" full drug information

Labetalol '$randate(

2abetalol bloc#s alpha', beta*', and beta7'adrenergic receptor sites, decreasing blood

pressure.Cie" full drug information

Penbutolol

@indolol has mild intrinsic sympathomimetic activity and negative chronotropic andinotropic effects.Cie" full drug information

Penbutolol 'Le+atol(

@enbutolol has mild intrinsic sympathomimetic activity and negative chronotropic andinotropic effects.

#lpha4 lockers. #ntihypertensi+es

Class Summary

0lpha* antagonists may be used to achieve the target pressure. @eripheral alpha'

antagonists inhibit postsynaptic alpha'adrenergic receptors, resulting in vasodilation of veins and arterioles and decreasing total peripheral resistance and blood pressure. These

drugs often cause mar#ed hypotension after the first dose. ;igh doses are li#ely to cause

postural hypotension. Ef the peripheral alpha'antagonists, doazosin and terazosin are

selective for alpha* 6'receptors. @razosin is nonselective and inhibits both alpha*' andalpha7'receptors.Cie" full drug information

*oxa0osin 'Cardura. Cardura 3L(

http://reference.medscape.com/drug/inderal-inderal-la-propranolol-342364http://reference.medscape.com/drug/inderal-inderal-la-propranolol-342364http://reference.medscape.com/drug/betapace-af-sotalol-342365http://reference.medscape.com/drug/betapace-af-sotalol-342365http://reference.medscape.com/drug/betapace-af-sotalol-342365http://reference.medscape.com/drug/trandate-labetalol-342359http://reference.medscape.com/drug/trandate-labetalol-342359http://reference.medscape.com/drug/levatol-penbutolol-342370http://reference.medscape.com/drug/levatol-penbutolol-342370http://reference.medscape.com/drug/levatol-penbutolol-342370http://reference.medscape.com/drug/levatol-penbutolol-342370http://reference.medscape.com/drug/cardura-xl-doxazosin-342343http://reference.medscape.com/drug/cardura-xl-doxazosin-342343http://reference.medscape.com/drug/inderal-inderal-la-propranolol-342364http://reference.medscape.com/drug/inderal-inderal-la-propranolol-342364http://reference.medscape.com/drug/betapace-af-sotalol-342365http://reference.medscape.com/drug/betapace-af-sotalol-342365http://reference.medscape.com/drug/betapace-af-sotalol-342365http://reference.medscape.com/drug/trandate-labetalol-342359http://reference.medscape.com/drug/trandate-labetalol-342359http://reference.medscape.com/drug/levatol-penbutolol-342370http://reference.medscape.com/drug/levatol-penbutolol-342370http://reference.medscape.com/drug/levatol-penbutolol-342370http://reference.medscape.com/drug/levatol-penbutolol-342370http://reference.medscape.com/drug/cardura-xl-doxazosin-342343http://reference.medscape.com/drug/cardura-xl-doxazosin-342343


16/17

&oazosin, a


17/17

#lpha7 #gonists. Central4#cting

Class Summary

0lpha'adrenergic agonists are used in combination "ith other agents for management of

hypertension.Cie" full drug information

Clonidine 'Catapres. *uraclon. 2exiclon 3!(

$lonidine stimulates presynaptic (central) alpha7'adrenergic receptors, thereby reducing

norepinephrine release and peripheral vasoconstriction.
http://reference.medscape.com/drug/catapres-tts-clonidine-342382http://reference.medscape.com/drug/catapres-tts-clonidine-342382http://reference.medscape.com/drug/catapres-tts-clonidine-342382http://reference.medscape.com/drug/catapres-tts-clonidine-342382

glomerulonefritis kronik emed

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