eMedicine Specialties > Emergency Medicine > Genitourinary

Glomerulonephritis, Acute: Treatment & Medication

Author: Dimitrios Papanagnou, MD, MPH, Staff Physician, Department of Emergency Medicine, Bellevue Hospital Center
Coauthor(s): Nancy S Kwon, MD, MPA, Assistant Professor of Clinical Surgery, Consulting Staff, Department of Emergency Medicine, New York University School of Medicine and Bellevue Hospital Center
Contributor Information and Disclosures

Updated: Oct 2, 2009

Treatment

Prehospital Care

  • In most patients, acute glomerulonephritis is not an acute life-threatening emergency if the patient has normal vital signs and lacks underlying illness.
  • Give highest priority to patients who present with hypertension or pulmonary or CNS symptoms.

Emergency Department Care

ED treatment is etiology dependent.

  • Correction of electrolyte abnormalities (ie, hypocalcemia, hyperkalemia) and acidosis, if present.
  • Poststreptococcal
    • Eradicate streptococcal causes by oral antibiotic therapy.
    • Penicillin is indicated in nonallergic patients. Note that early antibiotic therapy does not affect the development of poststreptococcal glomerulonephritis.
    • Admit patients who present with oliguria and renal failure.
    • Consider renal biopsy.
  • Acute nephritic syndrome
    • Restrict fluids in patients with significant edema.
    • Loop diuretics are indicated for patients with nephrotic syndrome (4% of patients) or massive proteinuria.
    • Consider admission for patients with underlying compromised renal function or immunosuppression.
    • Admission is recommended for patients with anuria, nephrotic syndrome, massive proteinuria, significant hypertension, or pulmonary symptoms.
  • Hypertensive encephalopathy
    • Severe hypertension associated with signs of cerebral dysfunction is a hypertensive emergency requiring immediate aggressive treatment.
    • Manifestations include headache, nausea/vomiting, blurry vision, seizures, and coma.
    • Address the airway first. Intubation may be required for patients who present with severe CNS depression, signs of active or impending herniation, or status epilepticus.
    • Although use of diazoxide and hydralazine often is described, neither commonly is used.
    • Base treatment of hypertensive emergencies upon the specific organ involved. Tailor therapy to the depressed renin states and the degree of renal insufficiency.
  • Severe hypertension with or without end-organ insufficiency
    • Agents useful in treating hypertension include calcium channel blockers and nitroprusside. Note that beta-blocking agents or angiotensin-converting enzyme (ACE) inhibitors administered alone may not be useful unless administered with vasodilators and diuretics, because plasma renin activity levels are reduced.
    • In most patients with less severe hypertension, captopril should decrease blood pressure in less than 1 hour. Note that since renin activity is depressed, use of captopril carries the risk of hyperkalemia. Monitor serum potassium level closely.
  • Circulatory congestion and pulmonary edema
    • The patient often presents with only mild edema. In this setting, the most effective treatment is sodium and fluid restriction.
    • Diuretics such as furosemide are effective in more advanced disease; however, potassium-sparing diuretics are contraindicated because of an increased risk of hyperkalemia.
    • Manage the airway based upon the degree of pulmonary congestion and respiratory distress.
    • Dialysis or bloodless phlebotomy (rotating tourniquets) can be used to treat patients with pulmonary edema who are unresponsive, particularly when those patients are oliguric.
    • Digitalis is ineffective.
    • Preload and afterload reductions are indicated for hypertensive pulmonary edema (eg, nitrates, morphine, diuretics).
  • Therapies in nonstreptococcal glomerulonephritis: Steroids and cytotoxic agents may be indicated in the following conditions:
    • Glomerulonephritis secondary to hypersensitivity
    • Vasculitis
    • Cryoglobulinemia
    • Henoch-Schönlein purpura
    • Serum sickness: First-line therapy includes nonsedating antihistamines such as cetirizine, astemizole, loratadine, desloratadine, terfenadine, and acrivastine. In nonresponsive patients, a short course of oral steroids may be indicated as a second-line treatment.
    • Systemic lupus erythematosus: Pulse therapy with methylprednisolone has been reported to be more rapidly effective than conventional oral therapy for treating lupus nephritis.
    • Wegener granulomatosis: Oral cyclophosphamide, an antineoplastic immunosuppressant, is combined with oral steroid therapy. Such therapy is beyond the scope of ED care. Cyclophosphamide is continued until clinical remission, while steroids are tapered over 6 months to 1 year. Adjunctive use of azathioprine has also been described.
    • Idiopathic rapidly progressive glomerulonephritis: Pulse intravenous methylprednisolone is used to reduce risk of progression to end-stage renal disease. Cyclophosphamide is also used in conjunction with steroids. Dialysis should be considered to remove antigen-antibody complexes in patients with biopsy-proven, extensive, and irreversible glomerular and interstitial damage.
    • Goodpasture syndrome: Plasmapheresis is combined with immunosuppression (ie, prednisone and cyclophosphamide). High-dose pulse steroids are effective for pulmonary hemorrhage.
  • Disposition: ED physicians should have a low threshold for admitting patients with suspected acute glomerulonephritis. Patients who present with hematuria only without renal impairment, elevations in BP, hemoptysis, or any other concerning symptoms can be sent home with thorough follow-up instructions and close follow-up with a nephrologist.

Consultations

  • A nephrologist may need to be consulted immediately for dialysis of the rare oliguric patient.
  • Urgency for referral depends on the GFR; if the GFR is abnormal or rapidly deteriorating, or if systemic symptoms are present, immediate consultation is indicated.
  • Consultations are often indicated in the evaluation and follow-up care of patients with glomerulonephritis.
  • Surgical referral for biopsy is indicated in selected cases.

Medication

Treatment involves specific pharmacologic and supportive therapy to prevent and/or treat the sequelae, such as edema, hypertension, and progression of renal disease.

Antibiotics

Therapy must cover all likely pathogens in the context of the clinical setting. Penicillin is the DOC in treating acute glomerulonephritis of a poststreptococcal group A beta-hemolytic etiology.


Penicillin V (Veetids)

Derivative of 6-aminopenicillanic acid with a beta-lactam ring structure essential for bactericidal activity. Inhibits enzymes and cell wall receptors, resulting in cell wall synthesis inhibition. Other autolytics enzymes are also activated, degrading the bacterial cell wall. Bacterial resistance via beta-lactamase can be prevented with addition of clavulanic acid, sulbactam, or tazobactam. Other forms of bacterial resistance include alteration of bacterial PBPs and decreased permeability of cell wall to penicillin.

Adult

500 mg PO q6h

Pediatric

<12 years: 40 mg/kg/d PO divided q4-6h; not to exceed adult dose
>12 years: Administer as in adults

Probenecid may increase effectiveness by decreasing clearance; tetracyclines are bacteriostatic, causing decrease in effectiveness of penicillins when administered concurrently

Documented hypersensitivity; renal function impairment; bleeding disorder; congestive heart failure; cystic fibrosis; GI disease or antibiotic-associated colitis; mononucleosis

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 renal impairment

Nonselective beta-blocker with cardioselective alpha1 blocker

Labetalol is used for hypertensive encephalopathy and malignant hypertension.


Labetalol (Normodyne)

Has nonselective beta-antagonist and cardioselective alpha1-antagonist effects. Beta-blocking effects predominate, particularly when used IV. Low lipid solubility means bioavailability is reduced by first pass metabolism and enhanced by coadministration of food. Drug is not removed by hemodialysis.

Adult

20 mg (0.25 mg/kg for 80-kg patient) IV microdrip labetalol hydrochloride injection slowly over 2 min; desired BP may be achieved with continued injections of 40-80 mg at 10-min intervals or until 300 mg has been administered prn; to reduce possibility of postural hypotension, patients should remain supine for 3 h after administration

Pediatric

Not established
Suggested dose: 0.4-1 mg/kg/h IV; not to exceed 3 mg/kg/h

Decreases effect of diuretics and increases toxicity of methotrexate, lithium, and salicylates; may diminish reflex tachycardia, resulting from nitroglycerin use, without interfering with hypotensive effects; cimetidine may increase labetalol blood levels; glutethimide may decrease labetalol effects by inducing microsomal enzymes

Documented hypersensitivity; cardiogenic shock; atrioventricular block; uncompensated congestive heart failure; pulmonary edema; bradycardia; reactive airway disease; severe bradycardia

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in impaired hepatic function; discontinue therapy if signs of liver dysfunction; in elderly patients, lower response rate and higher incidence of toxicity may be observed

Loop diuretics

Loop diuretics are used for hypertensive encephalopathy with CNS signs and circulatory congestion or pulmonary edema. Furosemide is DOC for this indication.


Furosemide (Lasix)

Inhibits resorption of sodium and water in ascending limb of loop of Henle by interfering with Na+/K+/Cl- channel. An antihypercalcemic effect is mediated by an increased excretion of calcium.
Plasma volume, blood pressure, and cardiac output are reduced. Calcium excretion is increased.
Absorption of oral furosemide is reduced with renal disease or nephrotic syndrome as a result of edematous bowel. Parenteral administration may be indicated in patients with compromised kidneys; metabolized by hepatic biotransformation and renal excretion; onset of action is 20-60 min PO and 5 min IV. Children with nephrotic syndrome may require higher dosing beyond the scope of ED care.

Adult

20-80 mg PO/IV once initially, followed by once qd, or once qod after titrating for optimum efficacy, or by dividing daily dose bid/tid

Pediatric

Initially: 2 mg/kg PO/IV once; titrate with additional 1-2 mg/kg q6h

Metformin decreases furosemide 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; increased plasma lithium levels and toxicity are possible when taken concurrently

Documented hypersensitivity; hepatic coma; anuria; renal function impairment; diabetes mellitus; gout; MI; pancreatitis; state of severe electrolyte depletion

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter

Corticosteroids

Methylprednisolone is used for nonstreptococcal etiologies of acute glomerulonephritis, particularly in lupus nephritis and in idiopathic progressive glomerulonephritis.


Methylprednisolone (Medrol)

Has anti-inflammatory effect and is immunosuppressive. Metabolized by hepatic transformation and renal excretion.

Adult

Pulse therapy of 30 mg/kg IV over minimum of 30 min

Pediatric

Administer as in adults

Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels of methylprednisolone; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics

Documented hypersensitivity; viral, fungal, or tubercular skin infections

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

Adverse effects include allergy, cataracts, Cushing syndrome, severe acne, GI irritation, and pancreatitis
Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use

Antineoplastics and immunosuppressants

Cyclophosphamide is used for etiology-dependent treatment of acute glomerulonephritis due to Wegener granulomatosis.


Cyclophosphamide (Cytoxan, Neosar, Procytox)

Acts as alkylating agent that cross-links strands of DNA and RNA. Other actions include inhibition of protein synthesis, immunosuppression, and cholinesterase inhibition. Not within the scope of ED care.

Adult

For long-term therapy, the following doses are used:
400-1800 mg/m2 (30-40 mg/kg) IV in divided doses over 2-5 d; may repeat at 2- to 4-wk intervals; alternatively, 10-15 mg/kg IV q7-10d or 3-5 mg/kg twice weekly

Pediatric

Long-term therapy: Administer as in adults

Allopurinol may increase risk of bleeding or infection and enhance myelosuppressive effects; may potentiate doxorubicin-induced cardiotoxicity; may reduce digoxin serum levels and antimicrobial effects of quinolones
Chloramphenicol may increase half-life while decreasing metabolite concentrations; may increase effect of anticoagulants; coadministration with high doses of phenobarbital may increase rate of metabolism and leukopenic activity; thiazide diuretics may prolong cyclophosphamide-induced leukopenia and neuromuscular blockade by inhibiting cholinesterase activity

Documented hypersensitivity; severely depressed bone marrow function

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Regularly examine hematologic profile (particularly neutrophils and platelets) to monitor for hematopoietic suppression; regularly examine urine for RBCs, which may precede hemorrhagic cystitis

More on Glomerulonephritis, Acute

Overview: Glomerulonephritis, Acute
Differential Diagnoses & Workup: Glomerulonephritis, Acute
Treatment & Medication: Glomerulonephritis, Acute
Follow-up: Glomerulonephritis, Acute
References

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Further Reading

Contributor Information and Disclosures

Author

Dimitrios Papanagnou, MD, MPH, Staff Physician, Department of Emergency Medicine, Bellevue Hospital Center
Dimitrios Papanagnou, MD, MPH is a member of the following medical societies: American College of Emergency Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Student Association/Foundation, and Emergency Medicine Residents Association
Disclosure: Nothing to disclose.

Coauthor(s)

Nancy S Kwon, MD, MPA, Assistant Professor of Clinical Surgery, Consulting Staff, Department of Emergency Medicine, New York University School of Medicine and Bellevue Hospital Center
Nancy S Kwon, MD, MPA is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Edward A Michelson, MD, Program Director, Associate Professor, Department of Emergency Medicine, University Hospital Health Systems in Cleveland
Edward A Michelson, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Richard H Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Steven C Dronen, MD, FAAEM, Director of Emergency Services, Director of Chest Pain Center, Department of Emergency Medicine, Ft Sanders Sevier Medical Center
Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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