Acute Poststreptococcal Glomerulonephritis Medication

Updated: Nov 02, 2016
  • Author: Rajendra Bhimma, MB, MD, ChB, PhD, DCH (SA), FCP(Paeds)(SA), MMed(Natal); Chief Editor: Craig B Langman, MD  more...
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Medication

Medication Summary

The need for medicines in acute poststreptococcal glomerulonephritis (ASPGN) is usually limited in scope and in length. Administer antibiotics (penicillin or erythromycin) for 10 days to ensure eradication of the streptococcus if the disease is believed to be acute poststreptococcal glomerulonephritis and if risk of contamination is present. Some clinicians use this treatment only when evidence suggests an active infection.

Antihypertensives are usually not necessary after the child leaves the hospital, although mild hypertension may persist for as many as 6 weeks. The medications that can be used span the entire range of antihypertensives, such as vasodilators (eg, hydralazine), calcium channel-blocking agents (eg, amlodipine), or angiotensin-converting enzyme (ACE) inhibitors (eg, enalapril).

Carefully monitor blood pressure (BP) for at least 1 week after the drug is discontinued to ensure that rebound hypertension does not occur.

Diuretic agents (eg, furosemide) are rarely needed in the long term; hypertension persisting beyond the first week may suggest a diagnosis other than acute glomerulonephritis.

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Antihypertensives

Class Summary

Antihypertensive agents are commonly used during initial phase of acute glomerulonephritis.

Amlodipine (Norvasc)

Amlodipine is generally regarded as a dihydropyridine, although experimental evidence suggests that it may also bind to the nondihydropyridine binding sites.

Amlodipine blocks postexcitation release of calcium ions into cardiac and vascular smooth muscle, thereby inhibiting the activation of ATPase on myofibril contraction. The overall effect is reduced intracellular calcium levels in cardiac and smooth muscle cells of the coronary and peripheral vasculature, resulting in dilatation of the coronary and peripheral arteries. This drug may also potentiate angiotensin-converting enzyme (ACE) inhibitor effects.

During depolarization, amlodipine inhibits calcium ions from entering the slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium, which benefits nonpregnant patients with systolic dysfunction, hypertension, or arrhythmias. This agent a substantially longer half-life than nifedipine and diltiazem and is administered once daily.

Furosemide (Lasix)

Furosemide is a loop diuretic that is useful in patients with acute glomerulonephritis who are edematous. This agent also has some BP-lowering effect by increasing excretion of salt and water via interfering with the chloride-binding cotransport system in the ascending loop of Henle. In acute hypertensive states, administer furosemide intravenously (IV).

Labetalol (Trandate)

Labetalol blocks beta1-adrenergic, alpha-adrenergic, and beta2-adrenergic receptor sites, thereby decreasing BP.

Hydralazine

Hydralazine decreases systemic resistance through direct vasodilation of arterioles.

Nifedipine (Adalat, Procardia, Nifediac)

Nifedipine relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery.

Nitroprusside (Nitropress)

Nitroprusside produces vasodilation and increases the inotropic activity of the heart. However, higher dosages may exacerbate myocardial ischemia by increasing the heart rate.

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Antibiotics

Class Summary

Administer antibiotics for 10 days to ensure eradication of streptococci, if the disease is believed to be poststreptococcal acute glomerulonephritis and risk of contamination is present.

Penicillin VK

Penicillin VK inhibits biosynthesis of cell wall mucopeptide and is bactericidal against sensitive organisms when adequate concentrations are reached. This agent is most effective during the stage of active multiplication.

Erythromycin base (E.E.S., EryPed, Ery-Tab, Erythrocin)

Erythromycin inhibits bacterial growth, possibly by blocking the dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

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