eMedicine Specialties > Pediatrics: General Medicine > Nephrology

Acute Poststreptococcal Glomerulonephritis

Robert G Schacht, MD, Professor, Department of Pediatrics, New York University Medical Center
Yang Sun Kim, MD, Assistant Professor, Department of Pediatrics, Division of Neonatology, New York University Medical Center; Clinical Director, Neonatology Intensive Care Unit, Bellevue Hospital; Luther Travis, MD, William W Glauser Professor of Pediatrics and Pediatric Nephrology, Department of Pediatrics, Divisions of Nephrology and Diabetes, University of Texas Medical Branch and Children's Hospital

Updated: Jun 18, 2009

Introduction

Background

Glomerulonephritis (GN) is the term generally reserved for the various renal diseases in which inflammation of the glomerulus, manifested by proliferation of cellular elements, is secondary to an immunologic mechanism. The modification of this term by the adjective acute (eg, acute glomerulonephritis [AGN], poststreptococcal acute glomerulonephritis [PSAGN]) has imposed temporal restrictions and, as most commonly used by the clinician, defines an almost characteristic clinicopathologic correlation. The term also implies certain distinctive features concerning etiology, pathogenesis, course, and prognosis.

Prior to the development of precise serologic methodologies, coupled with clinicopathologic studies, acute glomerulonephritis was often known inappropriately as Bright disease, and almost any clinical presentation of gross hematuria was labeled erroneously as such. Most incidents of acute glomerulonephritis appear to be associated with a postinfectious state, whether bacterial or viral infections are incriminated in causation. Proven acute glomerulonephritis has been observed after staphylococcal and pneumonococcal infections, coxsackievirus B, echovirus type 9, influenza virus, and mumps. The most commonly recognized clinical picture (ie, poststreptococcal acute glomerulonephritis) follows infection with group A beta hemolytic streptococci. The physician must distinguish between poststreptococcal acute glomerulonephritis and acute glomerulonephritis secondary to other causes because the ultimate outcomes may differ.¹

Pathophysiology

Most forms of acute glomerulonephritis are mediated by an immunologic process. For poststreptococcal acute glomerulonephritis, the evidence suggests that immune complexes, preformed by the combination of specific antibodies against streptococcal antigens, localize on the glomerular capillary wall and activate the complement system. The immunologic system may also be activated by streptococcal antigens that adhere to the glomerular structures and act as "planted antigens" or by alterations in endogenous antigens. The activation of the complement cascade then generates chemotactic plasma-activated complement 5 (C5a) and platelet-derived inflammatory mediators. Various cytokines and other cellular immunity factors initiate an inflammatory response manifested by cellular proliferation and edema of the glomerular tuft.

Only a few strains of streptococci produce acute glomerulonephritis. Studies performed approximately 50 years ago led to the identification of certain strains of group A streptococci that are nephritogenic. More recently, non-group A streptococci, particularly group C, have also been demonstrated to produce glomerulonephritis.

At least 2 antigens isolated from nephritogenic streptococci, zymogen (a precursor of exotoxin B [SPEB]) and glyceraldehyde phosphate dehydrogenase (GAPDH), have been identified and are believed to be capable of initiating the immunologic response.² These fractions have a particular affinity for the glomerulus and have been demonstrated to induce an antibody response. This leads to the activation of a number of proinflammatory mediator pathways in both infiltrating and resident glomerular cells.

Although streptococcal infections are associated intimately with poststreptococcal acute glomerulonephritis, the mechanism of renal injury is still defined incompletely. Current evidence suggests that the inflammatory lesion in the glomerulus is associated with the fixation of soluble streptococcal antigen-antibody complexes. Studies have also demonstrated the ability of both SPEB and NAPlr, a streptococcal plasmin receptor, to bind and activate plasmin, thereby initiating an inflammatory cascade.

Several investigators have detected streptococcal antigen in renal biopsy material obtained early in the course of infection; however, the major evidence supporting an immune complex type of nephritis has been the finding of nodular deposits of immunoglobulin G (IgG) and the third component of complement (C3) on the capillary basement membrane. The finding of C3 in the renal glomerulus is usually associated with decreased serum concentrations of C3 and total hemolytic complement.

Decreased concentration of properdin and C3 proactivator and inconsistent decreases in the early components of complement indicate that complement activation occurs primarily by the alternate pathway. Reduced serum concentrations of C3 have been demonstrated in 80-92% of children with poststreptococcal acute glomerulonephritis. Values return to normal in most children within 6-8 weeks. The fourth component of complement (C4) value may also be depressed; however, this is an inconsistent finding.

Poststreptococcal acute glomerulonephritis can occur in epidemics or, more commonly, it can be sporadic. The sporadic form is seasonal; the winter-spring peak is associated with respiratory infection, and the summer-fall peak is most often associated with pyoderma. The most common serotype of group A beta hemolytic streptococci associated with nephritis from nasopharyngeal infections is type 12, whereas type 49 is most often recovered during outbreaks of pyoderma-related poststreptococcal acute glomerulonephritis. In individuals with pharyngitis-related acute glomerulonephritis, the latent period is approximately 10 days, and more than 80% of patients exhibit a significant rise in serum titer of antistreptolysin-O (ASO).

Conversely, a latent period is difficult to define in persons with impetigo-related acute glomerulonephritis, and a rise in the titer of ASO is observed in only 50% of patients. Serum concentrations of other streptococcal indicators (eg, antihyaluronidase [AH] titer, antideoxyribonuclease B titer [anti-DNase B]) are usually elevated in individuals with poststreptococcal acute glomerulonephritis secondary to either pharyngeal or skin infections. When various antibody titers are used, almost 95% of patients with poststreptococcal acute glomerulonephritis demonstrate evidence of a prior streptococcal infection.

Although renal biopsies are now indicated rarely in children with typical poststreptococcal acute glomerulonephritis, they have contributed substantially to the understanding of this disease. Irrespective of the degree of severity of the initial inflammatory response, the histologic picture is consistent and specific. As observed by light microscopy, glomerular changes are generalized and diffuse. The glomerular tufts usually appear enlarged and swollen, and a moderate-to-marked increase in proliferation of mesangial and epithelial cells is present.

Polymorphonuclear leukocytes are also often observed as part of the inflammatory process. In persons with the most severe disease, the glomeruli appear bloodless because of the associated edema of the capillary walls, which impedes glomerular perfusion. A direct correlation exists between the severity of the histologic process and the clinical manifestations of the disease during the acute phase and possibly the prognosis.

Granular deposits of IgG and C3 are typically found when the specimen is studied by immunofluorescent microscopy; other immunoglobulins (Igs) and fibrinogen often are observed. Electron microscopy of renal tissue from patients with poststreptococcal acute glomerulonephritis usually reveals subepithelial electron-dense deposits (humps).

In most patients with moderate-to-severe acute glomerulonephritis, a measurable reduction in volume of glomerular filtrate (GF) is present, and the capacity to excrete salt and water is usually diminished, leading to expansion of the extracellular fluid (ECF) volume. The expanded ECF volume is responsible for edema and, in part, for hypertension, anemia, circulatory congestion, and encephalopathy.

Frequency

United States

Acute postinfectious glomerulonephritis was the most common nonsuppurative disease of the kidneys; its incidence declined only to increase again in recent years, albeit slightly. Because a high percentage of persons affected with acute postinfectious glomerulonephritis have mild disease and are asymptomatic (estimates of the ratio of asymptomatic to symptomatic patients vary from 2:1-3:1), the actual incidence of the disease is not known. Less crowded living conditions may have contributed to the apparent decline in incidence of poststreptococcal acute glomerulonephritis over the past few decades; however, other factors, including decreased prevalence or infectivity of the nephritogenic streptococci, may also have contributed to the decline. The recently observed increase in incidence is more difficult to explain.

Mortality/Morbidity

The ultimate prognosis in persons with acute glomerulonephritis depends largely on the severity of the initial insult. In an extremely small proportion of hospitalized patients, the initial injury is so severe that either persistent renal failure or progression to renal failure generally occurs. However, in most patients, histologic regression of the disease is the rule, and the ultimate prognosis is good. Clinical manifestations of the disease rarely recur after the first 3 months, and second episodes of acute glomerulonephritis are uncommon.

Epidemic poststreptococcal acute glomerulonephritis appears to end in virtually complete resolution and healing in all patients. The prognosis is also favorable for approximately 95% of children with sporadic poststreptococcal acute glomerulonephritis. The prognosis for persons with acute glomerulonephritis secondary to other causes is less certain. The disease appears to have a poorer prognosis in adults, particularly in elderly individuals. The cause of this difference is unknown.

The clinical course is largely predictable. Edema usually resolves within 5-10 days, and blood pressure (BP) usually returns to normal within 2-3 weeks, although persistence of elevated pressures for as many as 6 weeks is compatible with complete resolution. Gross hematuria usually disappears within 1-3 weeks; however, it subsequently may recur following physical activity. The C3 concentration returns to normal by 6-8 weeks after onset in more than 95% of patients.

Urinary abnormalities resolve at a slower pace. Proteinuria may disappear within the first 2-3 months or may decrease slowly over 6 months. Intermittent or postural proteinuria has been noted in a few patients for as long as 1-2 years after onset. Microscopic hematuria usually disappears after 6 months; however, its presence for as long as 1 year is not uncommon. Even more prolonged hematuria (1-3 y) has been observed in some patients who ultimately have demonstrated complete resolution of their renal disease. Strongly consider the possibility that the disease has entered a chronic phase if both hematuria and proteinuria persist for more than 12 months.

While clinical resolution occurs in most patients, several authors report time-related reduction in precise measurements of renal function, as well as diminished renal functional reserve. These studies further support the thesis that any significant loss of nephrons leads to hyperfiltration of the remaining units.

Race

No racial predilection is noted; the condition is reported in all ethnic and cultural groups. In urban populations, a predilection toward minority populations is noted; however, this may be related more to the socioeconomic factor of overcrowding than to any racial predilection.

Sex

The disease is more prevalent in males in all regions of the world; the male-to-female ratio range is 1.7-2:1. The reasons for this male predominance are not known.

Age

Acute glomerulonephritis has been reported in infants as young as 1 year and in adults as old as 90 years; however, the disease occurs with the greatest frequency in children aged 4-12 years, with a peak prevalence in individuals aged approximately 5-6 years.³

Clinical

History

• Most patients with acute glomerulonephritis (AGN) exhibit milder symptoms and/or signs somewhere between the extremes described below.
  • At one extreme is the asymptomatic child whose disease is discovered only by examination of the urine. Based on surveillance studies of the siblings and/or household contacts of children affected with poststreptococcal acute glomerulonephritis (PSAGN), at least 50% of persons with laboratory evidence of nephritis (ie, abnormal urinalysis) appear to have no symptoms or signs of clinical illness.
  • At the other extreme is the child who presents with severe disease manifested by oliguria, edema, hypertension, and azotemia and with proteinuria, hematuria, and urinary casts (cylindruria).
• In those patients whose acute glomerulonephritis is the result of a postinfectious cause (ie, poststreptococcal acute glomerulonephritis being the most common), a latent period of 7-21 days between onset of the streptococcal infection and development of clinical glomerulonephritis is characteristic.⁴
• This latent period, more clearly defined after pharyngeal infections than after pyoderma, averages approximately 10 days.
• The development of clinical nephritis (ie, hematuria and/or edema) either during or within 2-5 days after the onset of a respiratory tract infection is atypical and suggests the possibility of some other form of glomerulonephritis.
• Gross hematuria and/or edema represent the most common clinical presentation.
• One or both findings usually appear abruptly and may be associated with various degrees of malaise, lethargy, anorexia, fever, abdominal pain, and headache. Observant parents may also note oliguria.
• An insidious onset of edema is more indicative of other forms of renal disease.
• An occasional child may have a scarlatiniform rash or evidence of a viral exanthema, but petechial or purpuric rashes suggest other conditions.
• Almost characteristic by their absence are arthralgia, arthritis, carditis, hepatic involvement, and GI bleeding.
• Edema is the most frequent manifesting symptom.
  • According to some investigators, edema is found in approximately 85% of patients.
  • Edema usually appears abruptly and first involves the periorbital area, but it may be generalized.
  • The degree of edema widely varies and depends on a number of factors, including the severity of glomerular involvement, the fluid intake, and the degree of hypoalbuminemia.
• Gross hematuria occurs at onset in 30-50% of children with poststreptococcal acute glomerulonephritis who require hospitalization.
  • The urine is usually described as being smoky, cola colored, tea colored, or rusty. The color is usually dependent on the amount of blood present and the pH of the urine.
  • Observant parents may note oliguria.
  • Clots are exceedingly rare in persons with acute glomerulonephritis.
• Hypertension is the third cardinal feature of poststreptococcal acute glomerulonephritis and is reported in 50-90% of children who are hospitalized with acute glomerulonephritis.
• The pathogenesis of the hypertension is unknown; however, pathogenesis is probably multifactorial and related only in part to extracellular fluid (ECF) volume expansion.
• The magnitude of the increase in blood pressure (BP) widely varies; however, systolic pressures greater than 200 mm Hg and diastolic pressures greater than 120 mm Hg are not unusual.
• Hypertensive encephalopathy has been reported in approximately 5% of hospitalized children and is the most serious early complication of this disease.
  • In these patients, hypertension is usually severe and is accompanied by signs of CNS dysfunction such as headache, vomiting, depressed sensorium, confusion, visual disturbances, aphasia, memory loss, coma, and convulsions.
  • Hypertensive encephalopathy has been reported in the occasional individual with minimal or no edema and with minimal urinary abnormalities.
• Circulatory congestion is apparent in most children admitted to the hospital but is responsible only rarely for significant early symptoms.
• Dyspnea, orthopnea, and cough may be present.
• Pulmonary rales are often audible.
• At times, the only evidence of congestion is detected on chest radiograph. A prominent cardiac shadow may be present until onset of diuresis.
• In the patient with an otherwise normal cardiovascular system, cardiac failure is unusual.
• Pallor is common at onset and is not explained entirely by the anemia.

Physical

• Edema is the most frequent and sometimes the only clinical finding. Edema may be either local (eg, periorbital) or generalized.
• Both systolic and diastolic hypertension may be present to a varying degree.
• Pallor is common.
• In some patients, pulmonary rales are audible.
• Either bradycardia or tachycardia may be observed.
• The sensorium may be depressed, and the degree of depression depends on the severity of encephalopathy.
• Other postinfectious causes of acute glomerulonephritis must be considered in the differential diagnosis (see Differentials) of poststreptococcal acute glomerulonephritis since the syndrome of acute glomerulonephritis has been reported following many other bacterial illnesses (eg, Streptococcus pneumoniae, Staphylococcus aureus, Staphylococcus epidermidis, Rickettsia rickettsiae, Mycoplasma species, Meningococcus species, Leptospira species).
  • In addition, certain viral illnesses have preceded the onset of fairly typical acute glomerulonephritis; among the most common are varicella-zoster virus, cytomegalovirus, and the Epstein-Barr virus.
  • In the evaluation of a patient with acute glomerulonephritis, if evidence of a prior streptococcal infection is missing or inconclusive, then a search for another infectious cause appears appropriate.
• Immunoglobulin A (IgA)-associated glomerulonephritis may be confused with poststreptococcal acute glomerulonephritis.⁵
  • In the form of IgA nephropathy associated with a typical anaphylactoid purpura (ie, Henoch-Schönlein purpura [HSP] nephritis), the characteristic rash and the associated symptoms of either abdominal pain or arthritis and/or arthralgia help in the differentiation; however, in atypical cases, marked similarity may be present.
  • All of the clinical manifestations of poststreptococcal acute glomerulonephritis have been reported in persons with HSP nephritis, although significant hypertension and edema are found less commonly in individuals with HSP than in those with poststreptococcal acute glomerulonephritis.
  • Urticarial or purpuric rashes, abdominal complaints, and arthritis and/or arthralgia are found almost exclusively in persons with HSP.
  • Evidence of a prior streptococcal illness is usually lacking in individuals with HSP nephritis, and complement values (C3 and/or C4) are usually normal.
• Berger disease or IgA nephropathy usually presents as an episode of gross hematuria occurring during the early stages of a respiratory illness; no latent period exists, and hypertension or edema is uncommon.
  • Recurrent episodes of gross hematuria, associated with respiratory illnesses, followed by persistent microscopic hematuria, are highly suggestive of IgA nephropathy.
  • In contrast, poststreptococcal acute glomerulonephritis usually does not recur, and second episodes are rare.
• Mesangiocapillary or membranoproliferative glomerulonephritis (MPGN) may have a presentation that is virtually identical to that of poststreptococcal acute glomerulonephritis. Distinguishing features include the following:
  • The initial manifestations are often more serious in persons with MPGN than in those with IgA nephropathy; the renal function is reduced markedly (ie, large elevation of serum creatinine).
  • Evidence of preexisting streptococcal infection is absent, although cases of MPGN have been reported in which clear evidence of such an infection is present.
  • In most cases, C3 levels are depressed persistently, past 6 weeks.
  • Urinary abnormalities persist past the time of expected resolution for poststreptococcal acute glomerulonephritis.
• Crescentic glomerulonephritis is the term used to describe a histologic picture of severe proliferative glomerulonephritis.
  • In persons with crescentic glomerulonephritis, in addition to inflammatory changes within the glomerular tuft, extensive proliferation exists within the Bowman space, leading to the formation of synechiae between the glomerular tuft and Bowman capsule.
  • The clinical picture is generally referred to as rapidly progressive glomerulonephritis and may be secondary to numerous causes, including an immune-complex mediated poststreptococcal nephritis. The initial clinical picture is generally severe, and resolution appears delayed.
• Other forms of glomerulonephritis (eg, systemic lupus erythematosus [SLE] nephritis, familial nephritis, chronic glomerulonephritis) may occasionally be confused with poststreptococcal acute glomerulonephritis when an acute exacerbation of the previously present nephropathy is present. In addition to the lack of expected complete resolution, other features suggest a condition other than poststreptococcal acute glomerulonephritis.

Causes

• Clinical manifestations are either the direct or indirect result of the glomerular inflammatory response, and the degree of involvement determines the severity of symptoms and signs.
  • Glomerular inflammation (ie, cellular proliferation, edema) reduces glomerular filtration without a coexistent decrease in total renal blood flow.
  • The reduced volume of glomerular filtration and the normal tubular function lead to an increase in the reabsorption of salt and water, with resulting oliguria and edema.
    • The edema first collects in those sites where tissue resistance is low, such as the periorbital area.
    • Later, it becomes more generalized, and, in those few patients in whom loss of albumin and/or vascular congestion is exaggerated with resultant hypoalbuminemia, the edema even may simulate that of the nephrotic syndrome.
• The precise etiology of the hypertension is less well explained and probably multifactorial.
  • ECF volume is increased, but the elevated systemic pressure does not always return to normal levels with diuresis.
  • Plasma renin levels are expected to be low due to the expanded ECF volume; however, plasma renin levels have been reported variously as low, normal, or slightly increased.
  • The lack of response to drug-induced blockade of the renin-angiotensin system does not support this system as a primary cause for hypertension.
  • Various cytokines known to have pressor effects are increased and may have an important role in the etiology of hypertension.

Differential Diagnoses

Hematuria
Nephritis

Other Problems to Be Considered

A number of disorders can produce an acute proliferative glomerulonephritis (GN). Any of these disorders may be confused with poststreptococcal acute glomerulonephritis (PSAGN). The following are the most common diseases that may present as acute nephritic syndrome (see Physical):

• Mesangiocapillary and/or membranoproliferative glomerulonephritis (MPGN)
• Postinfectious glomerulonephritis
  • Poststreptococcal
  • After other bacterial infections
  • Postviral infections
  • Postparasitic infections
• Immunoglobulin A (IgA)-associated glomerulonephritis
  • Henoch-Schönlein purpura (HSP) nephritis
  • Other IgA nephritis (Berger disease)
• Others (less common)
  • Chronic glomerulonephritis (recurrence and/or relapse)
  • Shunt nephritis
  • Familial nephritis
  • Rapidly progressive (crescentic) glomerulonephritis
  • Systemic lupus erythematosus (SLE) nephritis

Workup

Laboratory Studies

• Urine
  • Urine output most is often reduced in acute glomerulonephritis (AGN), and urine is concentrated and acidic.
  • Glucosuria occurs occasionally, and proteinuria is commonly present.
  • The urine reaction for protein rarely exceeds 3+ by dipstick, corresponding to fewer than 2 g/m²/d when assessed quantitatively.
  • Approximately 2-5% of children with poststreptococcal acute glomerulonephritis  (PSAGN) have massive proteinuria and a nephrotic picture.
  • Hematuria is the most consistent urinary abnormality, although histologic findings consistent with poststreptococcal acute glomerulonephritis have been reported in children who had no or minimal urinary abnormalities.
  • Polymorphonuclear leukocytes and renal epithelial cells are common in the urine of patients with poststreptococcal acute glomerulonephritis, particularly during the early phase of the disease.
  • Hyaline and/or cellular casts are almost always present.
  • RBC casts have been found in 60-85% of hospitalized children with poststreptococcal acute glomerulonephritis. RBC casts, although characteristic of a glomerular lesion, are often not detected because the urine is not fresh or is examined by an inexperienced person.
• Streptococcal infection
  • Look for evidence of streptococcal infection in all patients.
  • Cultures from either the pharynx or skin may be positive; however, high streptococcal antibody titers are more compelling.
  • Numerous laboratory tests can be used to measure antibodies to various streptococcal antigens (eg, ASO, AH, anti-DNase B) or to combinations of antigens (eg, streptozyme test).
  • Whatever test is used, a rise in the titer of the antibody, measured at an interval of 2-3 weeks, is more meaningful than a single measurement. An ASO titer of 250 U or higher is highly suggestive of recent streptococcal infection.
• Hemolytic complement
  • Total hemolytic complement and some of its components are low during poststreptococcal acute glomerulonephritis.
  • The concentration of C3 has been found to be decreased in more than 90% of patients with poststreptococcal acute glomerulonephritis when measured serially during the first 2 weeks of the illness.
  • Total hemolytic complement values are also depressed.
  • These tests help to differentiate poststreptococcal from other postinfectious forms of acute glomerulonephritis.
  • C4 levels are most often normal.
  • Serum levels of fifth component of complement (C5) and properdin are usually decreased.
  • The complement levels generally return to normal by 6-8 weeks after onset.
• Renal
  • The extent of renal functional impairment is correlated directly to the severity of the glomerular injury.
  • The elevation in the serum concentrations of creatinine and blood urea nitrogen (BUN) is usually modest, although some patients may have severe azotemia at onset.
  • The electrolyte profile is usually normal; hyperkalemia and metabolic acidosis are only present in patients with significant renal functional impairment. The same applies to hyperphosphatemia.
  • Total serum calcium, but not ionized calcium levels, may be low in patients who have a nephrotic picture.
• Blood
  • A mild anemia (normocytic, normochromic) is common in persons in the early phase of acute glomerulonephritis; its degree tends to parallel the degree of extracellular (ECF) volume expansion.
  • Erythropoiesis may decline in the aftermath of acute glomerulonephritis, particularly in individuals with severe cases.
  • WBC and platelet counts are usually normal, although an occasional patient exhibits a leukocytosis; rarely, a mild thrombocytopenia may be present.
  • A few patients have hypoproteinemia and hyperlipidemia. A nephrotic picture has been reported in approximately 5% of hospitalized patients with poststreptococcal acute glomerulonephritis.

Imaging Studies

• No specific radiologic studies are particularly helpful in either the evaluation or the treatment of patients with acute glomerulonephritis.
  • Renal ultrasonography generally demonstrates normal to slightly enlarged kidneys bilaterally with some evidence of increased echogenicity.
  • Chest radiographs commonly demonstrate central venous congestion in a hilar pattern, the degree of which parallels the increase in ECF volume. Occasionally, an enlarged cardiac shadow is evident.

Other Tests

• Currently, no other tests provide any meaningful data regarding acute glomerulonephritis.

Procedures

• No procedures are recommended routinely in the evaluation of patients with acute glomerulonephritis.
• The performance of a renal biopsy is indicated in patients whose clinical presentation, laboratory findings, or course is atypical. In such persons, study of the histology by light, immunofluorescent, and electron microscopy may be diagnostic.

Histologic Findings

• Histologic findings depend on the etiology of the acute glomerulonephritis, the severity of the inflammatory process, and the stage of the disease at the time of the biopsy. The section below concentrates on the findings observed in individuals with poststreptococcal acute glomerulonephritis. The severity of the histologic process correlates with the clinical severity of the initial phase of the disease, and it may correlate with the ultimate prognosis (ie, severe lesions have worse prognoses).
• By light microscopy, the glomerular tufts appear enlarged and swollen, often filling Bowman space. A moderate-to-marked increase in proliferation of both mesangial and epithelial cells is present. Polymorphonuclear leukocytes often are observed, and monocytes also may be present. The increased cell mass expands the central lobular area in a centrifugal pattern, leading to narrowing of the capillary lumens. When the inflammatory process is extensive, the epithelial cells of Bowman capsule proliferate, forming crescents. Few, if any, tubular changes are noted.
• Granular deposits of immunoglobulin G (IgG) and C3 along the capillary walls generally are observed when the specimen is studied by immunofluorescent microscopy early in the course of the disease. Other immunoglobulins (eg, immunoglobulin M [IgM]), complement components (eg, C4), properdin, and fibrinogen often are observed. Later in the course of the disease, the immunoreactants are observed primarily in the mesangium. In the nonstreptococcal forms of postinfectious glomerulonephritis, no significant deposition of complement components is present, although either IgG or IgM may be observed (as may immunoglobulin A [IgA] in persons with Henoch-Schönlein purpura (HSP) or IgA nephropathy).
• Electron microscopy of renal tissue from patients with poststreptococcal acute glomerulonephritis usually reveals electron-dense deposits (humps) in the subepithelial space. During the recovery process, these deposits rapidly disappear, although fragments still may be found in the mesangium.
• Renal biopsy is not needed in most patients with poststreptococcal acute glomerulonephritis (see Procedures).

Treatment

Medical Care

• General management begins with a decision to admit the child with acute glomerulonephritis (AGN) to the hospital or merely have him or her undergo frequent outpatient examinations. Hospitalization is indicated if the child has significant hypertension or a combination of oliguria, generalized edema, and elevation of serum creatinine or potassium.
• Severe hypertension, or that associated with signs of cerebral dysfunction, demands immediate attention.
  • Debate exists regarding the agent that is most effective in patients with severe hypertension. Three drugs are commonly cited as having a high benefit-to-risk ratio: labetalol (0.5-2 mg/kg/h intravenously [IV]), diazoxide, and nitroprusside (0.5-2 mcg/kg/min IV, in patients with severe hypertension that is refractory to the previous agents); with any of these agents, the simultaneous IV administration of furosemide at doses of 2 mg/kg may be merited. Diazoxide use for blood pressure (BP) control is limited because, once administered, no further control of pressure is possible, unlike labetalol or nitroprusside.
  • Severe hypertension without encephalopathy can be treated in the manner just described or, more commonly, by administration of vasodilator drugs such as hydralazine or nifedipine.
    • The doses of these drugs can be administered either by injection or by mouth and can be repeated every 10-20 minutes until a suitable response is obtained.
    • For most children, the need for more than 2-3 doses is unusual.
• Mild-to-moderate hypertension does not warrant emergency management.
  • Mild-to-moderate hypertension is treated most effectively with bedrest, fluid restriction, and less-frequent doses of the preceding medications.
  • The use of loop diuretics, such as furosemide (1-3 mg/kg/d oral [PO], administered 1-2 times daily), may hasten resolution of the hypertension.
  • For patients resistant to treatment, either hydralazine or nifedipine is indicated.
  • ACE inhibitors are effective, although they have the potential to produce hyperkalemia and usually are not first-line drugs in acute glomerulonephritis.
• Edema and circulatory congestion are usually not sufficiently marked to produce more than minimal discomfort.
  • Restriction of fluids to those amounts needed to replace insensible losses is the best treatment for edema and circulatory congestion.
  • Loop diuretics (furosemide) administered PO have been reported to reduce the length of hospitalization in children who are edematous.
  • If congestion is marked, administer furosemide parenterally (2 mg/kg).
  • Phlebotomy, rotating tourniquets, dialysis, or digitalization is rarely necessary.
• Anuria or severe and persistent oliguria may occur in 3-6% of children with acute glomerulonephritis and may necessitate hospitalization.
  • Fortunately, anuria or severe and persistent oliguria is usually transient.
  • Because they may be ototoxic, avoid large doses of furosemide in children with these symptoms.
  • Osmotic diuretics, such as mannitol, are contraindicated as they might increase vascular volume.
• A course of penicillin can be administered to avoid contamination of contacts with a nephritogenic strain of streptococci; however, in most instances, these contacts do not develop overt acute glomerulonephritis. Such therapy does not influence the course of the disease in the index patient, but it may alter the response that confers type-specific immunity. Throat cultures of immediate family members might detect patients who are asymptomatic but infected.
• Steroid therapy is indicated only in patients with severe crescentic glomerulonephritis or in those with rapidly progressive glomerulonephritis.
  • Selected patients with Henoch-Schönlein purpura (HSP) nephritis and membranoproliferative glomerulonephritis (MPGN) also may benefit from such agents.
  • An experienced nephrologist should make decisions regarding the indication for such treatment.

Surgical Care

• If indicated at any time during the course of the disease, an experienced nephrologist should perform renal biopsy percutaneously.

Consultations

• Severe hypertension
• Severe oliguria
• Severe edema
• Nephrotic-range proteinuria
• Azotemia (moderate to marked)
• Recurrent episodes of gross hematuria
• Persistently depressed C3 (past 8-10 wk)
• Atypical onset
  • Absence of latent period
  • No evidence of streptococcal illness
• Failure of expected resolution of clinical signs
  • Gross hematuria within the preceding 10-14 days
  • Microscopic hematuria within 1 year
  • Edema within 2 weeks
  • Proteinuria (>50 mg/dL) within 6 months
  • Azotemia within 1 week
  • Hypertension within 6 weeks

Diet

• A low-sodium, low-protein diet should be prescribed during the acute phase, when edema and hypertension are in evidence; however, prolonged dietary restrictions are not warranted.
• Limitation of fluid and salt intake is recommended in the child who has either oliguria or edema. Curtailment of fluid to amounts consistent with insensible losses helps to minimize vascular overload and hypertension.

Activity

• Limited activity is probably indicated during the early phase of the disease, particularly if hypertension is present.
• Bedrest may lessen the degree and duration of gross hematuria if present; however, longer periods of bedrest do not appear to influence the course or long-term prognosis; therefore, they are generally not recommended.

Medication

Need for medicines are 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 poststreptococcal acute glomerulonephritis (PSAGN) and if risk of contamination is present. Some clinicians use this treatment only when evidence suggests an active infection.

Antihypertensives (see Medical Care) usually are 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, long-acting nifedipine), or ACE inhibitor (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 necessary after the first 2 days; hypertension persisting beyond the first week may suggest a diagnosis other that acute glomerulonephritis.

Antihypertensives

These agents are commonly used during initial phase. Indications for use are covered in appropriate sections. Specific agents are mentioned below.

Diazoxide (Hyperstat)

Diuretic benzothiazine antihypertensive agent that may be indicated for emergency reduction of severe hypertension. Only administer IV. Produces direct smooth muscle relaxation of peripheral arterioles, which decreases BP.

Dosing

Adult

1-3 mg/kg IV as single injection, not to exceed 150 mg/dose; repeat dose in 5-15 min prn until BP is reduced adequately

Pediatric

2-3 mg/kg IV administered over 30 min; may repeat in 30-60 min

Interactions

May decrease serum hydantoins, possibly resulting in decreased anticonvulsant effects; thiazide diuretics may potentiate hyperuricemic and antihypertensive effects

Contraindications

Documented hypersensitivity; aortic coarctation; pheochromocytoma; arteriovenous shunts; aortic aneurysm; significant hypoproteinemia (serum albumin <2.5 g/dL)

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Carefully monitor BP while administering medication and for succeeding few hours; hypotension is relatively common adverse effect; may produce hyperglycemia with administration of multiple doses; patients with diabetes mellitus may require insulin; when administered prior to delivery, may produce fetal or neonatal hyperbilirubinemia, thrombocytopenia, altered carbohydrate metabolism, and other adverse reactions

Furosemide (Lasix)

Loop diuretic useful in patients with AGN who are edematous. Also has some BP-lowering effect. In acute hypertensive states, administer IV furosemide. Increases excretion of salt and water by interfering with chloride-binding cotransport system in ascending loop of Henle.

Dosing

Adult

20-80 mg/d PO/IV/IM; titrate not to exceed 600 mg/d for severe edematous states

Pediatric

1-2 mg/kg/dose PO, not to exceed 6 mg/kg/dose; do not administer more frequently than q6h; 1 mg/kg IV/IM slowly under close supervision, not to exceed 6 mg/kg

Interactions

Metformin decreases concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides; 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

Contraindications

Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Perform serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN measurements

Labetalol (Normodyne, Trandate)

Blocks beta1-adrenergic, alpha-adrenergic, and beta2-adrenergic receptor sites, decreasing BP.

Dosing

Adult

0.5-3 mg/kg/h IV; gradually titrate dose according to BP response

Pediatric

Not established; limited data suggest 0.4-1 mg/kg/h IV; not to exceed 3 mg/kg/h

Interactions

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

Contraindications

Documented hypersensitivity; cardiogenic shock; pulmonary edema; bradycardia; atrioventricular block; uncompensated congestive heart failure; reactive airway disease; severe bradycardia; asthma and/or obstructive airway disease

Precautions

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

Hydralazine (Apresoline)

Decreases systemic resistance through direct vasodilation of arterioles.

Dosing

Adult

Acute hypertension: 0.15-0.3 mg/kg/dose PO/IM q10-20 min
Chronic hypertension: 0.75-5 mg/kg/d PO divided q6-12h; gradually titrate over 3-4 weeks; not to exceed 200 mg/d

Pediatric

Administer as in adults

Interactions

MAOIs and beta-blockers may increase toxicity; pharmacologic effects may be decreased by indomethacin

Contraindications

Documented hypersensitivity; mitral valve rheumatic heart disease

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Has been implicated in myocardial infarction; caution required in suspected coronary artery disease

Nifedipine (Adalat, Procardia)

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

Dosing

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

Acute hypertension: 0.05-0.1 mg/kg/dose PO/SL q10-20min
Chronic hypertension: 0.25-0.5 mg/kg/dose PO tid/qid prn

Interactions

Caution with coadministration of any agent that can lower BP, including beta-blockers and opioids; H2 blockers (cimetidine) may increase toxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

May cause lower extremity edema; allergic hepatitis has occurred but is rare

Nitroprusside (Nitropress)

Produces vasodilation and increases inotropic activity of heart. Higher dosages may exacerbate myocardial ischemia by increasing heart rate.

Dosing

Adult

Begin infusion at 0.3-0.5 mcg/kg/min IV and titrate upward by increments of 0.5 mcg/kg/min; titrate to desired effect; average dose is 1-6 mcg/kg/min
Infusion rates >10 mcg/kg/min may lead to cyanide toxicity

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; subaortic stenosis; idiopathic hypertrophic and atrial fibrillation or flutter

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

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; sodium nitroprusside has the ability to lower BP, thus use only in those patients with mean arterial pressures >70 mm Hg

Antibiotics

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

Penicillin (Beepen-VK, Betapen-VK, Pen-Vee K, V-Cillin K)

Inhibits biosynthesis of cell wall mucopeptide. Bactericidal against sensitive organisms when adequate concentrations are reached; most effective during stage of active multiplication.

Dosing

Adult

250-500 mg PO q6-8h for 10 d

Pediatric

<12 years: 25-50 mg/kg/d PO divided tid/qid, not to exceed 3 g/d for 10 d
>12 years: Administer as in adults

Interactions

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

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in renal impairment

Erythromycin (E.E.S., E-Mycin, Eryc, Ery-Tab, Erythrocin)

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

Dosing

Adult

250 mg erythromycin stearate and/or base (or 400 mg ethylsuccinate) PO q6h 1 h ac, or 500 mg q12h
Alternatively, 333 mg q8h for 10 d

Pediatric

30-50 mg/kg/d (15-25 mg/lb/d) PO divided q6-8h for 10 d

Interactions

Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis

Contraindications

Documented hypersensitivity; hepatic impairment

Precautions

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI adverse effects are common (administer doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occurs

Follow-up

Further Inpatient Care

• Only a small percentage of patients with acute glomerulonephritis (AGN) require initial hospitalization, and most of those are ready for discharge in 2-4 days.
• As soon as the blood pressure (BP) is under relatively good control and diuresis has begun, most children can be discharged and monitored as outpatients.

Further Outpatient Care

• Follow up at 0-6 weeks as frequently as necessary to determine the following:
  • Hypertension has been controlled.
  • Edema has started to resolve.
  • Gross hematuria has resolved.
  • Azotemia has resolved.
• Follow up 8-10 weeks after onset to determine the following:
  • Azotemia has subsided.
  • Anemia has been corrected.
  • Hypertension has resolved.
  • C3 and C4 concentrations have returned to normal.
• Follow up at 3, 6, and 9 months after onset to check the following:
  • Hematuria and proteinuria are subsiding gradually.
  • BP is normal.
• Follow up at 12 months after onset to determine the following:
  • Proteinuria has disappeared.
  • Microscopic hematuria has disappeared.
• Follow up at 2, 5, and 10 years after onset to check the following:
  • Urine is normal.
  • BP is normal.
  • Serum creatinine level is normal.

Inpatient & Outpatient Medications

• See Medical Care.

Transfer

• Transfer of responsibility for the patient with acute glomerulonephritis rarely indicated except in those instances in which a consultation with a nephrologist is not easily obtainable in the local area or by telephone, facsimile, or e-mail.
• See Consultations for instances that necessitate consultation with a pediatric nephrologist.

Complications

• Acute complications as part of the initial syndrome are discussed in History.
• The most common acute complication is hypertension with or without CNS manifestations.
• Anemia is common early and is due primarily to dilution. Anemia tends to resolve with diuresis. A few patients may have diminished erythropoiesis in the recovery phase and have some persisting anemia.
• An occasional patient develops pulmonary edema because of the marked increase in vascular volume that is present in the early phase of the disease.
• Congestive heart failure is rare but has been reported. Definite myocarditis has also been documented.
• Azotemia is discussed in History, but its persistence or worsening is always troubling and may suggest acute renal failure (ARF). ARF may suggest an alternate diagnosis (eg, membranoproliferative glomerulonephritis [MPGN], Henoch-Schönlein purpura [HSP], systemic lupus erythematosus [SLE]) or a severe or worsening poststreptococcal acute glomerulonephritis, such as observed in those with crescentic glomerulonephritis or rapidly progressive glomerulonephritis.

Prognosis

• Epidemic poststreptococcal acute glomerulonephritis appears to end in virtually complete resolution and healing in all patients, and the prognosis is favorable for most children with sporadic poststreptococcal acute glomerulonephritis.
  • Edema usually resolves within 5-10 days, and BP usually returns to normal after 2-3 weeks, even though persistence of elevated pressures for as many as 6 weeks is compatible with complete resolution.
  • Gross hematuria usually disappears within 1-3 weeks but may be exacerbated by physical activity.
  • C3 concentration returns to normal in more than 95% of patients by the end of 8-10 weeks.
• Urinary abnormalities resolve at various times after onset.
  • Proteinuria may disappear within the first 2-3 months or may slowly decrease over 6 months. Intermittent or postural proteinuria has been noted for 1-2 years after onset.
  • Microscopic hematuria usually disappears after 6 months, but its presence for as long as 1 year should not cause undue concern, and even more prolonged hematuria (1-3 y) has been observed.
  • Consider the possibility of chronic renal disease when both hematuria and proteinuria persist longer than 12 months.
• The ultimate prognosis in individuals with poststreptococcal acute glomerulonephritis depends largely on the severity of the initial insult.
  • In a few hospitalized patients, the initial injury is so severe that either persistent renal failure or progressive renal failure ensues.
  • However, histologic regression of the disease in most patients is predictable, and the ultimate prognosis is good.
  • Clinical manifestations of the disease rarely recur after the first 3 months, and second episodes of acute glomerulonephritis are rare.

Patient Education

• Clearly and specifically explain the nature of the disease, its course, and the eventual prognosis of the condition to the child (if old enough to understand) and the parents and/or caregivers. They need to understand that, while complete resolution is expected, a small possibility exists for persistent disease, and that an even smaller possibility exists for progression. This information is necessary for some patients to ensure that compliance with the follow-up program occurs.
• Clearly outline a follow-up plan and discuss the plan with the family. BP measurements and urine examinations for protein and blood constitute the basis of the follow-up plan. Perform examinations at 4-week to 6-week intervals for the first 6 months and at 3-month to 6-month intervals thereafter until both hematuria and proteinuria have been absent and BP has been normal for 1 year. Documenting that the low C3 has returned to normal after 8-10 weeks may be useful.
• For excellent patient education resources, visit eMedicine's Kidneys and Urinary System Center. Also, see eMedicine's patient education article Blood in the Urine.

Miscellaneous

Medicolegal Pitfalls

• Failure to perform a thorough and complete history
• Failure to perform a complete physical examination
• Failure to inform the parents and/or child of the working diagnosis
• Failure to pay attention to the troublesome problems of hypertension, edema, and azotemia
• Failure to reassure the parents and/or child at intervals
• Failure to perform only the necessary examinations and discuss the results with the family
• Failure to obtain consultations as needed with an appropriate explanation of the purpose of the consultation
• Failure to develop a follow-up plan
• Failure to keep the family informed of the child's progress and how this progress relates to the diagnosis, management, and prognosis

Special Concerns

No special concerns are pertinent other than those noted in the History and Medical Care sections. Emphasizing other situations is also worthwhile.

• Diagnosis: The course and prognosis for poststreptococcal acute glomerulonephritis (PSAGN) well known and almost always favorable. This is not so with nonstreptococcal forms of postinfectious glomerulonephritis. For that reason, attempting to identify the etiology of the condition is prudent.
• Complement profiles in poststreptococcal acute glomerulonephritis: Theoretically, the complement (or C3) levels should be decreased in all such patients; however, the duration of low values may be quite brief and, therefore, missed, even when examined serially. When the serum level is low in individuals with poststreptococcal acute glomerulonephritis, a depressed level for longer than 6-8 weeks is unusual. Thus, if the value remains low after this period of time, thinking of some other nephritic process, such as membranoproliferative glomerulonephritis (MPGN), is wise.
• Renal biopsy is usually not indicated in the person who presents with relatively typical poststreptococcal acute glomerulonephritis. However, in individuals whose initial presentation or early course is atypical, an examination of renal tissue may be indicated.
• Hypertensive encephalopathy can be the presenting feature of postinfectious glomerulonephritis and is the most serious of the acute complications of this disease. Since the urinalysis in such patients may exhibit minimal abnormalities, the underlying cause may not be readily apparent. A high index of suspicion is required to make an appropriate diagnosis.
• The prognosis for individuals with poststreptococcal acute glomerulonephritis is not as good for adults as it appears to be for children. Prolonged follow-up observation appears to be indicated.

References

1. Ahn SY, Ingulli E. Acute poststreptococcal glomerulonephritis: an update. Curr Opin Pediatr. Apr 2008;20(2):157-62. [Medline].

2. Yoshizawa N, Yamakami K, Oda T. Nephritogenic antigen for acute poststreptococcal glomerulonephritis. Kidney Int. Mar 2006;69(5):942-3; author reply 942. [Medline].

3. Wu SH, Liao PY, Yin PL, Zhang YM, Dong L. Elevated expressions of 15-lipoxygenase and lipoxin A4 in children with acute poststreptococcal glomerulonephritis. Am J Pathol. Jan 2009;174(1):115-22. [Medline].

4. Tokura T, Morita Y, Yorimitsu D, Horike H, Sasaki T, Kashihara N. Co-occurrence of poststreptococcal reactive arthritis and acute glomerulonephritis. Mod Rheumatol. 2008;18(5):526-8. [Medline].

5. Haas M, Racusen LC, Bagnasco SM. IgA-dominant postinfectious glomerulonephritis: a report of 13 cases with common ultrastructural features. Hum Pathol. Sep 2008;39(9):1309-16. [Medline].

6. [Guideline] Choyke PL, Bluth EI, Bush WH Jr. Hematuria. [online publication]. American College of Radiology (ACR). 2005;[Full Text].

7. [Guideline] Finnish Medical Society Duodecim. Nephropathia epidemica (NE). EBM Guidelines. Evidence-Based Medicine [Internet]. Apr 4 2007;[Full Text].

8. Baldwin DS, Gluck MC, Schacht RG, Gallo G. The long-term course of poststreptococcal glomerulonephritis. Ann Intern Med. Mar 1974;80(3):342-58. [Medline].

9. Brouhard BH, Travis LB. Acute postinfectionus glomerulonephritis. In: Edelman CM, ed. Pediatric Kidney Disease. 1992:1169-221.

10. Clark G, White RH, Glasgow EF, et al. Poststreptococcal glomerulonephritis in children: clinicopathological correlations and long-term prognosis. Pediatr Nephrol. Oct 1988;2(4):381-8. [Medline].

11. Cleper R, Davidovitz M, Halevi R, Eisenstein B. Renal functional reserve after acute poststreptococcal glomerulonephritis. Pediatr Nephrol. Aug 1997;11(4):473-6. [Medline].

12. Cole BR, Salinas-Madrigal L. Acute Proliferative Glomerulonephritis and Crescentic Glomerulonephritis. In: Barratt TM, Avner ED, Harmon WE, eds. Pediatric Nephrology. 4^th ed. Lippincott; 1999:669-89.

13. Dodge WF, Spargo BH, Travis LB, et al. Poststreptococcal glomerulonephritis. A prospective study in children. N Engl J Med. Feb 10 1972;286(6):273-8. [Medline].

14. Haycock GB. The treatment of glomerulonephritis in children. Pediatr Nephrol. Apr 1988;2(2):247-55. [Medline].

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16. Hoyer JR, Michael AF, Fish AJ, Good RA. Acute poststreptococcal glomerulonephritis presenting as hypertensive encephalopathy with minimal urinary abnormalities. Pediatrics. Mar 1967;39(3):412-7. [Medline].

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20. Popovic-Rolovic M, Kostic M, Antic-Peco A, et al. Medium- and long-term prognosis of patients with acute poststreptococcal glomerulonephritis. Nephron. 1991;58(4):393-9. [Medline].

21. Rodriguez-Iturbe B, Herrera J, Garcia R. Response to acute protein load in kidney donors and in apparently normal postacute glomerulonephritis patients: evidence for glomerular hyperfiltration. Lancet. Aug 31 1985;2(8453):461-4. [Medline].

22. Roy S 3rd, Stapleton FB. Changing perspectives in children hospitalized with poststreptococcal acute glomerulonephritis. Pediatr Nephrol. Nov 1990;4(6):585-8. [Medline].

23. Schacht RG, Gallo GR, Gluck MC, et al. Irreversible disease following acute poststreptococcal glomerulonephritis in children. J Chronic Dis. 1979;32(7):515-24. [Medline].

24. Sesso R, Pinto SW. Five-year follow-up of patients with epidemic glomerulonephritis due to Streptococcus zooepidemicus. Nephrol Dial Transplant. Sep 2005;20(9):1808-12. [Medline].

25. Simckes AM, Spitzer A. Poststreptococcal acute glomerulonephritis. Pediatr Rev. Jul 1995;16(7):278-9. [Medline].

26. Soto HM, Parra G, Rodriguez-Itrube B. Circulating levels of cytokines in poststreptococcal glomerulonephritis. Clin Nephrol. Jan 1997;47(1):6-12. [Medline].

27. Tejani A, Ingulli E. Poststreptococcal glomerulonephritis. Current clinical and pathologic concepts. Nephron. 1990;55(1):1-5. [Medline].

28. Travis LB. Acute postinfectious glomerulonephritis. In Rudolph AM, Hoffman JI, Rudolph CD, eds. Rudolph's Pediatrics. Appleton & Lange;1996:1356-1358.

29. Travis LB, Dodge WF, Beathard GA, et al. Acute glomerulonephritis in children. A review of the natural history with emphasis on prognosis. Clin Nephrol. May-Jun 1973;1(3):169-81. [Medline].

30. White AV, Hoy WE, McCredie DA. Childhood post-streptococcal glomerulonephritis as a risk factor for chronic renal disease in later life. Med J Aust. May 21 2001;174(10):492-6. [Medline].

31. Yoshizawa N, Yamakami K, Oda T. Nephritogenic antigen for acute poststreptococcal glomerulonephritis. Kidney Int. Mar 2006;69(5):942-3; author reply 942. [Medline].

Keywords

acute poststreptococcal glomerulonephritis, acute glomerulonephritis, AGN, acute nephritis, acute postinfectious glomerulonephritis, poststreptococcal acute glomerulonephritis, PSAGN, acute proliferative glomerulonephritis, Bright disease, Bright's disease, acute diffuse proliferative glomerulonephritis, coxsackievirus B, echovirus type 9, influenza virus, mumps, treatment, diagnosis, hypertensive encephalopathy, CNS dysfunction, pulmonary rales, Streptococcus pneumoniae, Staphylococcus aureus, Staphylococcus epidermidis, Rickettsia rickettsiae, Mycoplasma species, Meningococcus species, Leptospira species, IgA nephropathy, Berger disease

Contributor Information and Disclosures

Author

Robert G Schacht, MD, Professor, Department of Pediatrics, New York University Medical Center
Robert G Schacht, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Federation for Clinical Research, American Society of Pediatric Nephrology, International Society of Nephrology, New York Academy of Medicine, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Coauthor(s)

Yang Sun Kim, MD, Assistant Professor, Department of Pediatrics, Division of Neonatology, New York University Medical Center; Clinical Director, Neonatology Intensive Care Unit, Bellevue Hospital
Yang Sun Kim, MD is a member of the following medical societies: American Academy of Pediatrics and Eastern Society for Pediatric Research
Disclosure: Nothing to disclose.

Luther Travis, MD, William W Glauser Professor of Pediatrics and Pediatric Nephrology, Department of Pediatrics, Divisions of Nephrology and Diabetes, University of Texas Medical Branch and Children's Hospital
Luther Travis, MD is a member of the following medical societies: Alpha Omega Alpha, American Federation for Medical Research, International Society of Nephrology, and Texas Pediatric Society
Disclosure: Nothing to disclose.

Medical Editor

Richard Neiberger, MD, PhD, Director of Pediatric Renal Stone Disease Clinic, Associate Professor, Department of Pediatrics, Division of Nephrology, University of Florida College of Medicine and Shands Hospital
Richard Neiberger, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Medical Association, American Society of Nephrology, American Society of Pediatric Nephrology, Christian Medical & Dental Society, Florida Medical Association, International Society for Peritoneal Dialysis, International Society of Nephrology, National Kidney Foundation, New York Academy of Sciences, Shock Society, Sigma Xi, Southern Medical Association, Southern Society for Pediatric Research, and Southwest Pediatric Nephrology Study Group
Disclosure: The Osler Institute Honoraria Speaking and teaching

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Adrian Spitzer, MD, Professor, Department of Pediatrics, Albert Einstein College of Medicine; Director of NIH Training Program, Children's Hospital at Montefiore Medical Center
Adrian Spitzer, MD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Pediatric Society, American Society of Nephrology, American Society of Pediatric Nephrology, International Society of Nephrology, and Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Howard Trachtman, MD, Program Director, Pediatrics Research, Schneider Children's Hospital, Department of Pediatrics, Division of Nephrology, Professor, Albert Einstein College of Medicine
Howard Trachtman, MD is a member of the following medical societies: American Society of Hypertension, American Society of Nephrology, American Society of Pediatric Nephrology, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Chief Editor

Craig B Langman, MD, The Isaac A Abt, MD, Professor of Kidney Diseases, Feinberg School of Medicine, Northwestern University; Division Head of Kidney Diseases, Children's Memorial Hospital, Chicago
Craig B Langman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, and International Society of Nephrology
Disclosure: Amgen Grant/research funds None; Altus Pharmaceuticals Grant/research funds None; Genzyme Grant/research funds None; Merck Grant/research funds None; NIH Grant/research funds None

• Relevant clinical guidelines include the following:
  • American College of Radiology Appropriateness Criteria for hematuria ⁶
  • Nephropathia epidemica (NE) ⁷
• Relevant clinical trials include the following:
  • Efficacy of Combined Pentoxifylline and Conventional Immunosuppressive Regimens on Rapidly Progressive Glomerulonephritis
  • Immune System Related Kidney Disease
  • Research Network for Neonatal Diseases Induced by Tissular Fetomaternal Alloimmunization
• Related eMedicine topics include the following:
  • Glomerulonephritis, Acute (Emergency Medicine)
  • Glomerulonephritis, Acute (Nephrology)
  • Glomerulonephritis, Poststreptococcal (Nephrology)
  • Renal Failure, Acute
  • Streptococcal Infection, Group A

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