eMedicine Specialties > Nephrology > Glomerular Diseases
Glomerulonephritis, Acute: Treatment & Medication
Updated: Jul 2, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
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Treatment
Medical Care
Treatment of acute PSGN is mainly supportive because there is no specific therapy for renal disease. Treat the underlying infections when acute GN is associated with chronic infections.
- Antimicrobial therapy
- Antibiotics (eg, penicillin) are used to control local symptoms and to prevent spread of infection to close contacts.
- Antimicrobial therapy does not appear to prevent the development of GN, except if given within the first 36 hours.
- Loop diuretic therapy
- Loop diuretics may be required in patients who are edematous and hypertensive in order to remove excess fluid and to correct hypertension.
- Relieves edema and controls volume, thereby helping to control volume-related elevation in BP.
- Vasodilator drugs (eg, nitroprusside, nifedipine, hydralazine, diazoxide) may be used if severe hypertension or encephalopathy is present.
- Glucocorticoids and cytotoxic agents are of no value, except in severe cases of PSGN.
Consultations
Nephrologist
Diet
- Sodium and fluid restriction - For treatment of signs and symptoms of fluid retention (eg, edema, pulmonary edema)
- Protein restriction for patients with azotemia - If no evidence of malnutrition
Activity
Recommend bed rest until signs of glomerular inflammation and circulatory congestion subside. Prolonged inactivity does not benefit in the patient recovery process.
Medication
The goals of pharmacotherapy are to reduce morbidity, to prevent complications, and to eradicate the infection.
Antimicrobials (antibiotics)
In streptococcal infections, early antibiotic therapy may prevent antibody response to exoenzymes and render throat cultures negative, but may not prevent the development of PSGN.
Penicillin V (Pen VEE K, V-Cillin K)
More resistant than penicillin G to hydrolysis by acidic gastric secretions and is absorbed rapidly after oral administration. 250 mg of penicillin V = 400,000 U of penicillin.
Adult
500,000 U PO q6-8h
Pediatric
25,000-90,000 U/kg/d PO in 3-6 divided doses
Probenecid can increase effects; coadministration of tetracyclines can decrease effects; aminoglycosides show synergistic bactericidal effect in vitro against some strains of enterococci and viridans streptococci
Documented hypersensitivity
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Patient with impaired renal function (ie, CrCl <0.17 mL/sec) requires modification of dose and interval
Loop diuretics
Decrease plasma volume and edema by causing diuresis. The reduction in plasma volume and stroke volume associated with diuresis decreases cardiac output and, consequently, BP.
Furosemide (Lasix)
Increases excretion of water by interfering with chloride-binding cotransport system, inhibiting sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.
Rapidly absorbed from the GI tract. The diuretic effect is apparent within 1 h of PO administration, peaks by second h and effect lasts for 4-6 h. Following IV administration diuresis occurs within 30 min; duration of action is about 2 h; 66% of dose is excreted in the urine.
Adult
Edema:
Initial: 40-80 mg PO, titrate to satisfactory diuresis in 20- to 40-mg increments q6h; not to exceed 200 mg per dose; once effective single dose determined, may repeat qd/tid
Hypertension:
20-40 mg PO bid; titrated to desired response; if 40 mg PO bid does not lead to clinically significant response, add another antihypertensive agent rather than increasing the dose
Pediatric
0.5-1 mg/kg PO/IV; not to exceed 2 mg/kg PO qd or 1 mg/kg IV qd; in newborn and premature babies, daily dose should not exceed 1 mg/kg
Metformin decreases concentrations; furosemide interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides and furosemide; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently with this medication; increased plasma lithium levels and toxicity are possible when taken concurrently with this medication; potentiate hypotensive effect of various antihypertensive agents; may enhance the nephrotoxicity of cephaloridine; sucralfate may reduce absorption; increases risk of salicylate toxicity; NSAIDs, probenecid, anticonvulsants may attenuate effect of furosemide
Documented hypersensitivity; hepatic coma, anuria, and state of severe electrolyte depletion
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Perform frequent serum electrolyte, CO2, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter; increase in blood glucose in diabetics or alteration of GTT may occur; asymptomatic hyperuricemia is common and gout may occur; renal function may worsen because of volume depletion; in jaundiced newborn babies furosemide displaces bilirubin from albumin and may worsen hyperbilirubinemia and may cause kernicterus
Vasodilators
Reduce SVR, which, in turn, may allow forward flow, improving cardiac output.
Sodium nitroprusside (Nitropress)
Potent, rapidly acting IV antihypertensive agent. Effect is immediate and usually ends as soon as infusion is stopped because of its rapid biotransformation. Produces vasodilation and increases inotropic activity of the heart. At higher dosages may exacerbate myocardial ischemia by increasing heart rate. Use only for treatment of acute severe hypertension or malignant hypertension refractory to standard therapy.
Adult
0.5-8 mcg/kg/min IV infusion
Pediatric
Not established
Not established
Documented hypersensitivity; subaortic stenosis, idiopathic hypertrophic and atrial fibrillation or flutter
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in increased intracranial pressure, hepatic failure, severe renal impairment, and hypothyroidism; in renal or hepatic insufficiency, nitroprusside levels may increase and can cause cyanide toxicity (fatalities have occurred); sodium nitroprusside can lower BP and should therefore be used only in patients with mean arterial pressures >70 mm Hg; frequent and vigilant monitoring of BP; once dissolved, nitroprusside deteriorates in light, so protect by wrapping container with aluminum foil; solution should not be kept or used longer than 12 h
Calcium channel blockers
In specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. The calcium channel blockers inhibit movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and conduction velocity.
Nifedipine (Adalat, Adalat CC, Procardia, Procardia XL)
A dihydropyridine calcium channel blocker. The specific mechanisms by which nifedipine reduces BP have not been fully determined but are believed to be brought about largely by its vasodilatory action on peripheral blood vessels. Relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery.
Adult
10-30 mg IR cap PO tid; not to exceed 120-180 mg/d
30-60 mg SR tab PO qd; not to exceed 90-120 mg/d
Pediatric
Not established
Caution with coadministration of any agent that can lower BP, including beta-blockers and opioids; H2 receptor blockers (eg, cimetidine) may increase toxicity; increased efficacy when administered with grapefruit juice
Documented hypersensitivity; sick sinus syndrome; hypotension; acute myocardial infarction, severe aortic stenosis, A-V block
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause lower extremity edema; allergic hepatitis has occurred but is rare
Hydralazine (Apresoline)
Lowers BP by exerting a peripheral vasodilating effect through direct relaxation of vascular smooth muscle. Sodium retention and excessive sympathetic stimulation of the heart may be precluded by coadministration of a thiazide diuretic and a beta-blocker.
Adult
10 mg PO qid, gradually titrate to 25-50 mg qid; alternatively, 5-10 mg slow IV initially; repeat dose after 20-30 min if necessary
Maintenance dose: 50-200 mg PO qd in divided doses
Pediatric
Not established
MAOIs and beta-blockers may increase toxicity; pharmacologic effects may be decreased by indomethacin; alcohol may enhance hypotensive effect
Documented hypersensitivity; mitral valve rheumatic heart disease; dissecting aortic aneurysm
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Implicated in myocardial infarction; use caution in suspected coronary artery disease; SLE may occur, half of the patients taking this agent may have positive ANA test findings
More on Glomerulonephritis, Acute |
| Overview: Glomerulonephritis, Acute |
| Differential Diagnoses & Workup: Glomerulonephritis, Acute |
 Treatment & Medication: Glomerulonephritis, Acute |
| Follow-up: Glomerulonephritis, Acute |
| Multimedia: Glomerulonephritis, Acute |
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References
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Bazzi C, Petrini C, Rizza V, et al. A modern approach to selectivity of proteinuria and tubulointerstitial damage in nephrotic syndrome. Kidney Int. Oct 2000;58(4):1732-41. [Medline].
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Oda T, Yamakami K, Omasu F, et al. Glomerular plasmin-like activity in relation to nephritis-associated plasmin receptor in acute poststreptococcal glomerulonephritis. J Am Soc Nephrol. Jan 2005;16(1):247-54. [Medline].
Rodriguez-Iturbe B. Nephritis-associated streptococcal antigens: where are we now?. J Am Soc Nephrol. Jul 2004;15(7):1961-2. [Medline].
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Yoshizawa N, Yamakami K, Fujino M, et al. Nephritis-associated plasmin receptor and acute poststreptococcal glomerulonephritis: characterization of the antigen and associated immune response. J Am Soc Nephrol. Jul 2004;15(7):1785-93. [Medline].
Further Reading
Keywords
acute glomerulonephritis, acute nephritis, Bright disease, acute poststreptococcal glomerulonephritis, PSGN, acute postinfectious glomerulonephritis
