Glomerulonephritis, Acute


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. Hippocrates originally described the manifestation of back pain and hematuria, which lead to oliguria or anuria. With the development of the microscope, Langhans was later able to describe these pathophysiologic glomerular changes.

Most original research focuses on the poststreptococcal patient. Acute glomerulonephritis 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. As will be discussed, acute glomerulonephritis can be due to a primary renal or systemic disease. 

This article addresses the aspects of glomerulonephritis relevant to emergency physicians during its acute management.


Glomerular lesions in acute glomerulonephritis are the result of glomerular deposition or in situ formation of immune complexes. On gross appearance, the kidneys may be enlarged up to 50%. Histopathologic changes include swelling of the glomerular tufts and infiltration with polymorphonucleocyte. Immunofluorescence reveals deposition of immunoglobulins and complement.

With the exception of poststreptococcal glomerulonephritis, the exact triggers for the formation of the immune complexes are unclear. In streptococcal infection, involvement of derivatives of streptococcal proteins has been reported. A streptococcal neuramidase may alter host immunoglobulin G (IgG). IgG combines with host antibodies. IgG/anti-IgG immune complexes are formed and then collect in the glomeruli. In addition, elevations of antibody titers to other antigens, such as antistreptolysin O or antihyaluronidase, DNAase-B, and streptokinase, provide evidence of a recent streptococcal infection.


United States

Glomerulonephritis represents 10-15% of glomerular diseases. Variable incidence has been reported due in part to the subclinical nature of the disease in more than one half the affected population. Despite sporadic outbreaks, incidence of poststreptococcal glomerulonephritis has fallen over the last few decades. Factors responsible for this decline may include better health care delivery and improved socioeconomic conditions.


With some exceptions, a reduction in the incidence of poststreptococcal glomerulonephritis has occurred in most western countries. It remains much more common in regions such as Africa, the Caribbean, India, Pakistan, Malaysia, Papua New Guinea, and South America. Immunoglobulin A (IgA) nephropathy glomerulonephritis (ie, Berger disease) is the most common cause of glomerulonephritis worldwide.


  • Most epidemic cases follow a course ending in complete patient recovery (as many as 100%).
  • Sporadic cases of acute nephritis often progress to a chronic form. This progression occurs in as many as 30% of adult patients and 10% of pediatric patients.
  • Glomerulonephritis is the most common cause of chronic renal failure (25%).
  • The mortality rate of acute glomerulonephritis in the most commonly affected age group, pediatric patients, has been reported at 0-7%.


  • A male-to-female ratio of 2:1 has been reported.


  • Most cases occur in patients aged 5-15 years.
  • Only 10% occur in patients older than 40 years.
  • Acute nephritis may occur at any age, including infancy.



  • A thorough history should focus on the identification of an underlying systemic disease (if any) or recent infection.
  • Most often, the patient is a boy, aged 2-14 years, who suddenly develops puffiness of the eyelids and facial edema in the setting of a poststreptococcal infection. The urine is dark and scanty, and the blood pressure may be elevated.
  • Onset of symptoms is usually abrupt.
  • Nonspecific symptoms include weakness, fever, abdominal pain, and malaise.
  • In the setting of a postinfectious acute nephritis, a latent period of up to 3 weeks occurs before onset of symptoms. However, the latent period may vary; typically 1-2 weeks for postpharyngitis cases and 2-4 weeks for cases of postdermal infection (ie, pyoderma).
  • Onset of nephritis within 1-4 days of streptococcal infection suggests preexisting renal disease.
  • Symptoms of acute glomerulonephritis include the following:
    • Hematuria is a universal finding, even if it is microscopic. Gross hematuria is reported in 30% of pediatric patients.
    • Oliguria
    • Edema (peripheral or periorbital) is reported in approximately 85% of pediatric patients; edema may be mild (involving only the face) to severe, bordering on a nephrotic appearance.
    • Headache may occur secondary to hypertension; confusion secondary to malignant hypertension may be seen in as many as 5% of patients.
    • Shortness of breath or dyspnea on exertion secondary to heart failure or pulmonary edema; usually uncommon, particularly in children.
    • Possible flank pain secondary to stretching of the renal capsule.
  • Patients may also present with symptoms specific to an underlying systemic disease that can precipitate an acute glomerulonephritis. These disease entities are briefly described in Causes. Classic presentations include the following:
    • Triad of sinusitis, pulmonary infiltrates, and nephritis suggesting Wegener granulomatosis
    • Nausea/vomiting, abdominal pain, and purpura observed with Henoch-Schönlein purpura
    • Arthralgias associated with systemic lupus erythematosus (SLE)
    • Hemoptysis occurring with Goodpasture syndrome or idiopathic progressive glomerulonephritis
    • Skin rashes observed with a hypersensitivity vasculitis or systemic lupus erythematosus; also possibly due to the purpura that can occur in hypersensitivity vasculitis, cryoglobulinemia, and Henoch-Schönlein purpura


This description does not include all the physical findings that can be associated with the nonnephritic features of an infectious process (eg, fever), renal etiology, or systemic etiology, as such a description is beyond the scope of this article. Patients often have a normal physical examination and blood pressure; most frequently, however, patients present with a combination of edema, hypertension, and oliguria.

  • Edema frequently involves the face, specifically the periorbital area.
  • Hypertension is seen in as many as 80% of affected patients.
  • Hematuria, either macroscopic (gross) or microscopic, may be noted.
  • Skin rashes (ie, malar rash frequently seen with lupus nephritis) may be observed.
  • Abnormal neurologic examination or altered level of consciousness occurring because of malignant hypertension or hypertensive encephalopathy.
  • Arthritis may be noted.
  • Other signs 
    • Pharyngitis
    • Impetigo
    • Respiratory infection
    • Pulmonary hemorrhage
    • Heart murmur may indicate endocarditis
    • Scarlet fever
    • Weight gain
    • Abdominal pain
    • Anorexia
    • Back pain
    • Skin pallor
    • Palpable purpura in patients with Henoch-Schönlein purpura
    • Oral ulcers


Causes of acute glomerulonephritis include postinfectious, renal, and systemic etiologies. Each is described briefly.
  • Postinfectious etiologies
    • The most common cause is postinfectious Streptococcus species (ie, group A, beta-hemolytic). Two types have been described as (1) attributed to serotype 12, poststreptococcal nephritis due to an upper respiratory infection occurring primarily in the winter months, and (2) attributed to serotype 49, poststreptococcal nephritis due to a skin infection usually observed in the summer and fall and more prevalent in southern regions of the United States.
    • Other specific agents include viruses and parasites, systemic and renal disease, visceral abscesses, endocarditis, infected grafts or shunts, and pneumonia.
    • Bacterial causes other than group A streptococci may be diplococcal, streptococcal, staphylococcal, or mycobacterial. Salmonella typhosa, Brucella suis, Treponema pallidum, Corynebacterium bovis, and actinobacilli have also been identified.
    • Cytomegalovirus, coxsackievirus, Epstein-Barr virus, hepatitis B, rubella, rickettsial scrub typhus, and mumps are accepted as viral causes only if it can be documented that a recent group A beta-hemolytic streptococcal infection did not occur.
    • Fungal and parasitic: Attributing glomerulonephritis to a parasitic or fungal etiology requires the exclusion of a streptococcal infection. Identified organisms include Coccidioides immitis and the following parasites: Plasmodium malariae, Plasmodium falciparum, Schistosoma mansoni, Toxoplasma gondii, filariasis, trichinosis, and trypanosomes.
  • Systemic causes
    • Vasculitis (ie, Wegener granulomatosis causes glomerulonephritis that combines upper and lower granulomatous nephritides).
    • Collagen vascular diseases (ie, systemic lupus erythematosus causes glomerulonephritis through renal deposition of immune complexes).
    • Hypersensitivity vasculitis encompasses a heterogeneous group of disorders featuring small vessel and skin disease.
    • Cryoglobulinemia causes abnormal quantities of cryoglobulin in plasma that result in repeated episodes of widespread purpura and cutaneous ulcerations upon crystallization.
    • Polyarteritis nodosa causes nephritis from a vasculitis involving the renal arteries.
    • Henoch-Schönlein purpura causes a generalized vasculitis resulting in glomerulonephritis.
    • Goodpasture syndrome causes circulating antibodies to type IV collagen and often results in a rapidly progressive oliguric renal failure (weeks to months).
    • Drug-induced (ie, gold, penicillamine)
  • Renal diseases
    • Membranoproliferative glomerulonephritis is due to the expansion and proliferation of mesangial cells as a consequence of the deposition of complements.
    • Type I refers to the granular deposition of C3; type II refers to an irregular process.
    • Berger disease (IgG-immunoglobulin A [IgA] nephropathy) glomerulonephritis results from a diffuse mesangial deposition of IgA and IgG.
    • Idiopathic rapidly progressive glomerulonephritis is a form of glomerulonephritis characterized by the presence of glomerular crescents. Three types have been distinguished. Type I is an antiglomerular basement membrane disease, type II is mediated by immune complexes, and type III is identified by antineutrophil cytoplasmic antibody.

Differential Diagnoses

Amyloidosis, Familial Renal
Pediatrics, Fever
Pediatrics, Pharyngitis
Renal Failure, Acute
Diabetes Mellitus, Type 2
Rheumatic Fever
Guillain-Barré Syndrome
Scarlet Fever
Heart Failure
Serum Sickness
Hypertensive Emergencies
Systemic Lupus Erythematosus
Thrombocytopenic Purpura
Necrotizing Fasciitis
Transplants, Renal

Other Problems to Be Considered

Bacterial, viral, and fungal etiologies
Chronic glomerulonephritis
Acute interstitial nephritis
Membranoproliferative glomerulonephritis
Rapidly progressive glomerulonephritis
Idiopathic hematuria
Irradiation of Wilms tumor
Hemolytic-uremic syndrome 
IgA nephropathy

The following 4 renal syndromes commonly mimic the early stage of acute glomerulonephritis:

Anaphylactoid purpura with nephritis
Chronic glomerulonephritis with an acute exacerbation
Idiopathic hematuria
Familial nephritis


Laboratory Studies

  • Complete blood cell count
    • A decrease in hematocrit may demonstrate a dilutional anemia.
    • In the setting of an infectious etiology, pleocytosis may be evident.
  • Electrolytes, including BUN and creatinine (to estimate the glomerular filtration rate [GFR]): The BUN and creatinine levels will exhibit a degree of renal compromise.
  • Urinalysis
    • Urine is dark.
    • Specific gravity is greater than 1020 osm.
    • Proteinuria is observed.
    • RBCs and red cell casts are present.
    • Although not indicated in the ED setting, a 24-hour urine protein excretion and creatinine clearance may be helpful to document the degree of renal dysfunction and proteinuria.
  • Streptozyme test: This test includes many streptococcal antigens that are sensitive for screening but are not quantitative.
  • Antistreptolysin O (ASO)
    • This quantitative titer is increased in 60-80% of patients.
    • Increase begins in 1-3 weeks, peaks in 3-5 weeks, and returns to normal in 6 months.
    • Antistreptolysin O titer is unrelated to severity, duration, or prognosis of renal disease.
  • Erythrocyte sedimentation ratio (ESR) usually is increased.
  • Urine or plasma creatinine level greater than 40; decreased renin level is noted.
  • Cultures of throat and skin lesions to rule out Streptococcus species may be obtained.
  • Blood cultures
    • Indicated in patients with fever, immunosuppression, intravenous drug use history, indwelling shunts, or catheters.
    • Blood culture may indicate hypertriglyceridemia, decreased glomerular filtration rate, or anemia.

Imaging Studies

  • Radiography
    • Chest radiography is needed in patients with a cough, with or without hemoptysis (ie, Wegener granulomatosis, Goodpasture syndrome, pulmonary congestion).
    • Abdominal radiographic imaging (ie, computed tomography) is needed if visceral abscesses are suspected; also look for chest abscesses.
  • Echocardiography in patients with a new cardiac murmur or a positive blood culture to rule out endocarditis or a pericardial effusion.
  • Bedside renal ultrasonography may be appropriate to evaluate kidney size as well as to determine the extent of fibrosis. A kidney size of less than 9 cm is suggestive of extensive scarring and a low likelihood of reversibility.

Other Tests

  • Serology and complement levels
    • Various etiologies largely are differentiated by serum complement levels.
    • Results are not readily available to the emergency physician but may be useful to the consultant.
  • Antinuclear antibody: This test is useful for patients with acute glomerular nephritis and symptoms of underlying systemic illness, such as systemic lupus erythematosus and polyarteritis nodosa.
  • Serum complement (C3, C4)
    • Differentiation of low and normal serum complement levels may allow the ED physician to narrow the differential diagnosis.
    • Low serum complement levels suggest the following systemic diseases: cryoglobulinemia, systemic lupus erythematosus, bacterial endocarditis, and shunt nephritis.
    • Under the same conditions, renal diseases characteristic of membranoproliferative or poststreptococcal glomerulonephritis also may be considered.
    • Normal serum complement levels suggest a visceral abscess, polyarteritis nodosa, Goodpasture syndrome, or Henoch-Schönlein purpura. In addition, normal complement levels suggest renal diseases such as immune complex disease, idiopathic rapidly progressive glomerulonephritis, and IgG or IgA nephropathy.
  • Others include anti-DNA antibodies, triglyceride levels, hepatitis B and C serologies, antineutrophil cytoplasmic antibodies (ANCA), c-ANCA (ie, if Wegener granulomatosis is suspected).


  • Renal biopsy
    • Acute glomerulonephritis usually has a self-limited course with a good prognosis.
    • Renal biopsy is required for definitive diagnosis, particularly in primary renal diseases.
    • Candidates for biopsy are patients with an individual or family history of renal disease and patients with an atypical presentation, including massive proteinuria, nephrotic syndrome, or a rapid rise in creatinine level without resolution.
    • Renal biopsy is not indicated as an ED procedure.


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.


  • 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.


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


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.



500 mg PO q6h


<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



C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus


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.



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


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



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


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.



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


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



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


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


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.



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


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



C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus


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.



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


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



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


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


Further Inpatient Care

  • 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.
  • 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).

Further Outpatient Care

  • 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.
  • Treat streptococcal infections aggressively.


  • Progression to sclerosis is rare in the typical patient; however, in 0.5-2% of patients with acute glomerulonephritis, the course progresses toward renal failure, resulting in kidney death in a short period.
  • Abnormal urinalysis (ie, microhematuria) may persist for years.
  • Marked decline in glomerular filtration rate is rare.
  • Other complications, resulting in relevant end-organ damage in the central nervous and cardiopulmonary systems, can develop in patients who present with severe hypertension, encephalopathy, and pulmonary edema. Those complications include the following:
    • Hypertensive retinopathy
    • Hypertensive encephalopathy
    • Rapidly progressive glomerulonephritis
    • Chronic renal failure
    • Nephrotic syndrome


  • In poststreptococcal nephritis, the long-term prognosis generally is good. More than 98% of individuals are asymptomatic after 5 years, with chronic renal failure reported 1-3% of the time.
  • The prognosis for nonstreptococcal postinfectious glomerulonephritis depends on the underlying agent, which must be identified and addressed.
  • Generally, the prognosis is worse in patients with heavy proteinuria, severe hypertension, and significant elevations of creatinine level.
  • Other causes of acute glomerulonephritis have outcomes varying from complete recovery to complete renal failure. Prognosis depends on the underlying disease and the overall health of the patient.
  • Occurrence of cardiopulmonary or neurologic complications worsens the prognosis.

Patient Education

  • 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.
  • Fluid restriction 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 excellent patient education resources, visit eMedicine's Kidneys and Urinary System Center. Also, see eMedicine's patient education article Blood in the Urine.


Medicolegal Pitfalls

  • Failure to detect an underlying complicated course or infectious etiology
  • Failure to address in a timely manner any of the severe complicated presentations, such as severe hypertension, encephalopathy, or pulmonary edema
  • Failure to consider acute glomerulonephritis in the differential diagnosis of patients with early signs, symptoms, or findings, such as mild headaches, flank pain, hematuria, proteinuria, facial edema, or renal insufficiency
  • Failure to document patient education given regarding the importance of close follow-up care before discharge from the ED

Special Concerns

  • Pediatric patients
    • Long-term studies on children with poststreptococcal acute glomerulonephritis have revealed few chronic sequelae.
    • Results of such studies are controversial because homogenous populations suitable for proper epidemiologic analysis have not been assembled.
  • Elderly patients
    • Long-term studies show higher mortality rates in elderly patients, particularly those on dialysis.
    • Patients may be predisposed to crescent formation.