Emergent Management of Acute Glomerulonephritis 

Acute glomerulonephritis refers to a specific set of renal diseases in which an immunologic mechanism triggers inflammation and proliferation of glomerular tissue that can result in damage to the basement membrane, mesangium, or capillary endothelium.^{[1, 2]}

The condition is defined as the sudden onset of hematuria, proteinuria, and red blood cell casts. This clinical picture is often accompanied by hypertension, edema, and impaired renal function.

The most common causes of acute glomerulonephritis are postinfectious Streptococcus species, but other bacteria, as well as viruses, fungi, and parasites, can be the cause. The disease can also result from systemic and renal disorders.^[3]

Go to Acute Poststreptococcal Glomerulonephritis and Acute Glomerulonephritis for complete information on these topics.

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 central nervous system (CNS) symptoms.

Emergency department (ED) treatment is etiology dependent and includes correction of electrolyte abnormalities (ie, hypocalcemia, hyperkalemia) and acidosis, if present.

Poststreptococcal glomerulonephritis

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 the use of diazoxide and hydralazine often is described, neither commonly is used.

Base treatment of hypertensive emergencies on 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, the 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 on 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
• Systemic lupus erythematosus
• Wegener granulomatosis
• Idiopathic rapidly progressive glomerulonephritis
• Goodpasture syndrome

With regard to 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.

In systemic lupus erythematosus, pulse therapy with methylprednisolone has been reported to be more rapidly effective than conventional oral therapy for treating lupus nephritis.

In 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.

In patients with idiopathic rapidly progressive glomerulonephritis, pulse intravenous methylprednisolone is used to reduce the 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.

In 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 blood pressure (BP), hemoptysis, or any other concerning symptoms can be sent home with thorough follow-up instructions and close follow-up with a nephrologist.

A nephrologist may need to be consulted immediately for dialysis of the rare oliguric patient.

Urgency for referral depends on the glomerular filtration rate (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.

Inpatient care may be necessary, based on the type and/or etiology of acute glomerulonephritis (eg, shunt nephritis), the extent of renal involvement, or the existence of signs and symptoms indicative of potentially serious complications (eg, pulmonary edema, severe hypertension, encephalopathy). A follow-up evaluation by a nephrologist is essential for all patients who do not meet admission criteria. Goals include the following:

• Ensure appropriate evaluation of the etiology
• Reassess and address the course the illness takes in its progression
• Provide any intervention or treatment indicated based on the specific etiology and the course it follows in that specific patient

Outpatient care should include the following:

• Urinalysis at 2, 4, and 6 weeks and at 4, 6, and 12 months
• Cessation of follow-up care when urinalysis is normal
• Blood pressure monitoring during each visit
• Serum creatinine level monitoring at 2, 6, and 12 months
• Serum complement usually normal by 6 weeks

Early penicillin therapy does not prevent development of acute poststreptococcal glomerulonephritis. Although antibiotic therapy should be administered to abolish the streptococcal infection, no evidence indicates that such therapy influences the course of glomerulonephritis. Some clinicians have justified penicillin prophylaxis in populations at risk during epidemics and in siblings of index cases; however, epidemiologic evidence does not favor such use.

Upon discharge from the ED, patient education should emphasize the importance of close follow-up care.

Indicate that strenuous exercise should be avoided, because exercise can induce proteinuria, hematuria, and cylindruria (renal cylinders or casts in the urine) in healthy individuals.

Limit the patient to a diet with no added salt until edema, hypertension, and azotemia clear.

Restrict fluids in patients with significant edema.

Restrict protein in the presence of azotemia and metabolic acidosis (ie, approximately 0.5 g/kg/d).

The patient should avoid high-potassium foods.

For patient education information, see Blood in the Urine.