Medication Summary
The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Medications used to treat chronic glomerulonephritis include angiotensin-converting enzyme inhibitors (ACEIs), angiotensin II receptor blockers (ARBs), diuretics, calcium channel blockers, beta-adrenergic blockers, and alpha-adrenergic agonists. Medications used in chronic glomerulonephriits caused by diabetes mellitus includeusing agents such as sodium-glucose cotransporter–2 inhibitors (SGLT2i) and nonsteroidal minercalocorticoid receptor antagonists.
ACE Inhibitors
Class Summary
ACEIs are renoprotective agents. They decrease intraglomerular pressure and, consequently, glomerular protein filtration by decreasing efferent arteriolar constriction.
Enalapril (Vasotec)
Enalapril is a competitive inhibitor of ACE. It reduces angiotensin II levels, thus decreasing aldosterone secretion. It decreases intraglomerular pressure and glomerular protein filtration by decreasing efferent arteriolar constriction.
Captopril
Captopril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. It is rapidly absorbed, but bioavailability is significantly reduced with food intake. Captopril achieves a peak concentration in 1 hour and has a short half-life. It is cleared by the kidney; impaired renal function requires reduction of the dosage. The drug is absorbed well orally.
It decreases intraglomerular pressure and glomerular protein filtration by decreasing efferent arteriolar constriction. Give captopril at least 1 hour before meals. If it is added to water, use it within 15 minutes. The dose can be low initially, then titrated upward as needed and as tolerated by the patient.
Lisinopril (Prinivil, Zestril)
Lisinopril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. It decreases intraglomerular pressure and glomerular protein filtration by decreasing efferent arteriolar constriction.
Benazepril (Lotensin)
Benazepril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.
It decreases intraglomerular pressure and glomerular protein filtration by decreasing efferent arteriolar constriction.
Fosinopril
Fosinopril is a competitive ACE inhibitor. It prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. It decreases intraglomerular pressure and glomerular protein filtration by decreasing efferent arteriolar constriction.
Quinapril (Accupril)
Quinapril is a competitive ACE inhibitor. It reduces angiotensin II levels, decreasing aldosterone secretion. It decreases intraglomerular pressure and glomerular protein filtration by decreasing efferent arteriolar constriction.
Diuretics, Loop
Class Summary
Diuretics are used to treat edema and hypertension. They increase urine excretion by inhibiting sodium and chloride transporters.
Furosemide (Lasix)
Furosemide is the diuretic of choice. It increases excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and the distal renal tubule.
Bumetanide (Bumex)
Bumetanide increases the excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium, potassium, and chloride reabsorption in the ascending loop of Henle. These effects increase the urinary excretion of sodium, chloride, and water, resulting in profound diuresis. Renal vasodilation occurs after administration, renal vascular resistance decreases, and renal blood flow is enhanced. In terms of effect, 1 mg of bumetanide is equivalent to approximately 40 mg of furosemide.
Ethacrynic acid (Edecrin)
Ethacrynic acid increases the excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. This agent is used only in refractory cases. Continuous IV infusion is preferable in many cases. It is indicated for temporary treatment of edema associated with heart failure when greater diuretic potential is needed.
Diuretics, Thiazide
Class Summary
Diuretics are used to treat edema and hypertension. They increase urine excretion by inhibiting sodium and chloride transporters.
Metolazone (Zaroxolyn)
Metolazone treats edema in congestive heart failure. It increases excretion of sodium, water, potassium, and hydrogen ions by inhibiting reabsorption of sodium in distal tubules. It may be more effective in cases of impaired renal function.
Hydrochlorothiazide (Microzide)
Hydrochlorothiazide inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water as well as potassium and hydrogen ions.
Calcium Channel Blockers
Class Summary
Calcium channel blockers are used to treat hypertension, angina, and atrial fibrillation.
Amlodipine (Norvasc)
Amlodipine blocks slow calcium channels, causing relaxation of vascular smooth muscles.
Nifedipine (Procardia)
Nifedipine relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery. Sublingual administration is generally safe, theoretical concerns notwithstanding.
Felodipine
Felodipine relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery. It benefits nonpregnant patients with systolic dysfunction, hypertension, or arrhythmias. It can be used during pregnancy if clinically indicated.
Calcium-channel blockers potentiate ACE inhibitor effects. Renal protection is not proven, but these agents reduce morbidity and mortality rates in congestive heart failure. Calcium channel blockers are indicated in patients with diastolic dysfunction. They are effective as monotherapy in black patients and elderly patients.
Isradipine (DynaCirc)
Isradipine is a dihydropyridine calcium channel blocker. It inhibits calcium from entering select voltage-sensitive areas of vascular smooth muscle and myocardium during depolarization. This causes relaxation of coronary vascular smooth muscle, which results in coronary vasodilation. Vasodilation reduces systemic resistance and blood pressure, with a small increase in resting heart rate. Isradipine also has negative inotropic effects.
Verapamil (Calan, Isoptin, Verelan)
During depolarization, verapamil inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium. It can diminish premature ventricular contractions (PVCs) associated with perfusion therapy and decrease risk of ventricular fibrillation and ventricular tachycardia. By interrupting re-entry at the AV node, it can restore normal sinus rhythm (NSR) in patients with paroxysmal supraventricular tachycardias.
Diltiazem (Cardizem, Dilacor XR, Diltzac, Matzim LA)
During depolarization, diltiazem inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.
Beta-Blockers, Beta-1 Selective
Class Summary
Beta-adrenergic blockers compete with beta-adrenergic agonists for available beta-receptor sites. These agents inhibit mainly beta1 receptors (located mainly in cardiac muscle).
Metoprolol (Lopressor, Toprol XL)
Metoprolol is a selective beta1-adrenergic blocker that decreases the automaticity of contractions. During intravenous (IV) administration, carefully monitor blood pressure, heart rate, and electrocardiographic readings.
Bisoprolol (Zebeta)
Bisoprolol is a selective beta1-adrenergic receptor blocker that decreases automaticity of contractions.
Esmolol (Brevibloc)
Esmolol is an ultra–short-acting beta2-blocker. It is particularly useful in patients with labile arterial pressure, especially if surgery is planned, because it can be discontinued abruptly if necessary. It may be useful as a means to test beta-blocker safety and tolerance in patients with a history of obstructive pulmonary disease who are at possible risk of bronchospasm from beta-blockade. The elimination half-life of esmolol is 9 minutes.
Atenolol (Tenormin)
Atenolol selectively blocks beta-1 receptors with little or no effect on beta-2 receptors.
Beta-Blockers, Nonselective
Class Summary
Nonselective beta-blockers inhibit both beta1 receptors (located mainly in cardiac muscle) and beta2 receptors located in the bronchial and vascular musculature. These agents slow the sinus rate and decrease AV nodal conduction. Carefully monitor blood pressure.
Propranolol (Inderal LA, InnoPran XL)
Propranolol is a class II antiarrhythmic nonselective beta-adrenergic receptor blocker. It has membrane-stabilizing activity and decreases the automaticity of contractions.
Sotalol (Betapace, Sorine)
This class III antiarrhythmic agent blocks K+ channels, prolongs action potential duration (APD), and lengthens the QT interval. It is a non–cardiac selective beta-adrenergic blocker. Sotalol is shown to be effective in the maintenance of sinus rhythm, even in patients with underlying structural heart disease.
Labetalol (Trandate)
Labetalol blocks alpha-, beta1-, and beta2-adrenergic receptor sites, decreasing blood pressure.
Penbutolol
Pindolol has mild intrinsic sympathomimetic activity and negative chronotropic and inotropic effects.
Penbutolol (Levatol)
Penbutolol has mild intrinsic sympathomimetic activity and negative chronotropic and inotropic effects.
Alpha-Blockers, Antihypertensives
Class Summary
Alpha1 antagonists may be used to achieve the target pressure. Peripheral 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 marked hypotension after the first dose. High doses are likely to cause postural hypotension. Of the peripheral alpha-antagonists, doxazosin and terazosin are selective for alpha1 -receptors. Prazosin is nonselective and inhibits both alpha1- and alpha2-receptors.
Doxazosin (Cardura, Cardura XL)
Doxazosin, a quinazoline compound, is a selective alpha1-adrenergic antagonist. It inhibits postsynaptic alpha-adrenergic receptors, causing vasodilation of veins and arterioles and decreases total peripheral resistance and blood pressure.
Prazosin (Minipress)
Prazosin treats prostatic hypertrophy. It improves urine flow rates through relaxation of smooth muscle, accomplished by blocking alpha1-adrenoceptors in the bladder neck and prostate. When increasing the dose, administer the first dose of each increment at bedtime to reduce syncopal episodes. Although doses higher than 20 mg/day usually do not increase efficacy, some patients may benefit from doses as high as 40 mg/day.
Terazosin
Terazosin decreases arterial tone by allowing peripheral postsynaptic blockade. It has minimal alpha2 effect.
Vasodilators
Class Summary
These drugs act directly on the smooth muscle in the peripheral vasculature to cause vasodilation. Tachycardia and fluid retention are common adverse effects. Prolonged use of minoxidil can cause hypertrichosis. Hydralazine can cause a lupuslike syndrome in certain populations of slow acetylators. Examples of direct vasodilators are minoxidil and hydralazine. Vasodilators may be used to achieve the target pressure.
Minoxidil
Minoxidil relaxes arteriolar smooth muscle, causing vasodilation, which, in turn, may reduce blood pressure.
Hydralazine
Hydralazine decreases systemic resistance through direct vasodilation of arterioles. It is used to treat hypertensive emergencies. The use of a vasodilator reduces systemic vascular resistance, which, in turn, may allow forward flow, improving cardiac output.
Nitroprusside sodium (Nitropress)
Nitroprusside sodium produces vasodilation and increases inotropic activity of the heart. At higher dosages, it may exacerbate myocardial ischemia by increasing the heart rate.
Nitroglycerin (Nitro-Bid, Nitrostat, Nitro-Dur, Nitrolingual, NitroMist)
Nitroglycerin is primarily a venodilator that decreases both preload and afterload.
Alpha2 Agonists, Central-Acting
Class Summary
Alpha-adrenergic agonists are used in combination with other agents for management of hypertension.
Clonidine (Catapres, Duraclon, Nexiclon XR)
Clonidine stimulates presynaptic (central) alpha2-adrenergic receptors, thereby reducing norepinephrine release and peripheral vasoconstriction.
Sodium Glucose Transport Inhibitors (SGLTi)
Class Summary
SGLTi inhibit glucose absorption in proximal tubules and indirectly inhibit sodium transport by inhibiting sodium Hydrogen exhanger.. Several classes of these agents are now available. Caution is advised in indiividuals prone to hypotension, UTI's, DKA and PVD. .
Non steroidal mineralocorticoid receptor antagonists
Finerenone
Thes drugs inhibit the action of mineralocorticoids such as aldosterone on their receptors without causing significant hyperkalemia, thus reducing volume and inihbiting fibrosis mediated via aldosterone pathways.
ARBs
Class Summary
Angiotensin II receptor blockers (ARBs) are renoprotective agents that have been found to retard the progression of CKD.
Irbesartan (Avapro)
Angiotensin II receptor blocker; inhibits vasoconstrictor and aldosterone-secreting effects of angiotensin II
Valsartan (Diovan)
Blocks binding of angiotensin II to type 1 angiotensin II receptors, causing a lowering in blood pressure; blocks vasoconstrictor and aldosterone-secreting effects of angiotensin II
Candesartan (Atacand)
Prevents angiotensin II from binding to its receptor, which in turn blocks the vasoconstriction and aldosterone secreting effects of angiotensin II.
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Renal corpuscle.
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Photomicrograph of a kidney biopsy from a patient with crescentic glomerulonephritis showing prominent fibrocellular crescent formation and moderate mesangial proliferation in a glomerulus. Hematoxylin and eosin stain. Image courtesy of Wikipedia.
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Membranoproliferative glomerulonephritis (MPGN) type I. Glomerulus with lobular accentuation from increased mesangial cellularity. A segmental increase occurs in the mesangial matrix, and the peripheral capillary walls are thickened (hematoxylin and eosin stained section; original magnification × 250). Courtesy of John A. Minielly, MD.
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- Overview
- Presentation
- DDx
- Workup
- Treatment
- Medication
- Medication Summary
- ACE Inhibitors
- Diuretics, Loop
- Diuretics, Thiazide
- Calcium Channel Blockers
- Beta-Blockers, Beta-1 Selective
- Beta-Blockers, Nonselective
- Alpha-Blockers, Antihypertensives
- Vasodilators
- Alpha2 Agonists, Central-Acting
- Sodium Glucose Transport Inhibitors (SGLTi)
- Non steroidal mineralocorticoid receptor antagonists
- ARBs
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