Poststreptococcal Glomerulonephritis 

Updated: Dec 16, 2020
Author: Duvuru Geetha, MD, MRCP; Chief Editor: Vecihi Batuman, MD, FASN 

Overview

Practice Essentials

Acute glomerulonephritis following streptococcal infection is characterized by the sudden appearance of hematuria, proteinuria, red blood cell casts in the urine, edema, and hypertension with or without oliguria.[1, 2] (See the image below.) Poststreptococcal glomerulonephritis was first recognized as a complication of the convalescence period of scarlet fever in the 18th century.[3] A link between hemolytic streptococci and acute glomerulonephritis was recognized in the 20th century.

Kidney biopsy from a 7-year-old child with acute p Kidney biopsy from a 7-year-old child with acute poststreptococcal glomerulonephritis. Periodic acid–Schiff stain (at 40x) shows the intracapillary and occasional mesangial neutrophil (arrows). Courtesy of Laura Kidd, MD, Pathology and Laboratory Medicine, Tulane University Medical School.

Although the incidence of poststreptococcal glomerulonephritis has declined in the United States, it continues to have high incidence in other parts of the world, especially in areas with tropical climates where skin infections are common.[4, 5]

The workup in patients with suspected acute poststreptococcal glomerulonephritis includes tests to provide evidence of preceding streptococcal infection, renal function studies, and serologic studies (see Workup). The major goal of treatment is to control edema and blood pressure (see Treatment and Medication).

See also Acute Poststreptococcal Glomerulonephritis, Acute Glomerulonephritis, and Emergent Management of Acute Glomerulonephritis.

Pathophysiology

Poststreptococcal glomerulonephritis follows infection with only certain strains of streptococci, designated as nephritogenic. The offending organisms have virtually always been group A streptococci. Acute poststreptococcal glomerulonephritis (APSGN) follows pyodermatitis with group A streptococci that have the surface antigen M protein types 47, 49, 55, 2, 60, and 57 and throat infection with streptococci that have M types 1, 2, 4, 3, 25, 49, and 12. Less often, group C streptococci (ie, Streptococcus zooepidemicus) may be involved.[6]

Many morphologic, clinical, and serologic features suggest that APSGN is an immune complex disorder in which an immune complex containing a streptococcal antigen is deposited in the affected glomeruli. The size of glomerular basement membrane (GBM) pores and the molecular size of the streptococcus-Ig complex are also important determinants. The molecular size of the streptococcus-Ig complex is about 15 nm (10 nm for streptococcus group A and 5 nm for immunoglobulin). The GBM pore sizes in children and adults are 2-3 nm and 4-4.5 nm, respectively. Therefore, the immune complex molecule can be more easily rodded into the glomerulus in children than in adults and, thus, may explain the higher frequency of APSGN in children than in adults.

Stamatiades et al determined that in PSGN and other type III hypersensitivity reactions, vascular endothelial cells in the kidney actively transport circulating immune complexes from the capillaries to the peritubular interstitial space, where they are detected and scavenged by resident macrophages. Uptake of the immune complexes by the resident macrophages triggers the release of pro-inflammatory cytokines, which in turn results in recruitment of monocytes and neutrophils into the kidney from the circulation.[7]

Two antigens isolated from nephritogenic streptococci are commonly implicated in APSGN: streptococcal pyrogenic exotoxin B (SPEB) and nephritis-associated plasmin receptor (NAPlr).[8, 9] Both SPEB and NAPlr bind plasmin, protecting it from physiological inhibitors, and thus could cause chemotaxis of inflammatory cells and degradation of glomerular basement membranes. Both can be found in the glomeruli of APSGN tissues[9] .

In addition to streptococcal antigens, rheumatoid factor, cryoglobulins, and antineutrophil cytoplasmic serum antibodies are present in some of these patients. The pathogenic significance of this autoimmune response is not defined.

There are also host susceptibility factors. In one study, HLA-DRB1*03011 was reported to be found at a significantly higher frequency in 32 unrelated patients with APSGN as compared to 380 healthy individuals.[10]

Etiology

Acute poststreptococcal glomerulonephritis (APSGN) follows infection with only certain strains of streptococci designated as nephritogenic. The offending organisms are virtually always group A streptococci. APSGN follows pyodermatitis with streptococci M types 47, 49, 55, 2, 60, and 57 and throat infection with streptococci M types 1, 2, 4, 3, 25, 49, and 12.

Less commonly, group C streptococcal infection may result in APSGN. Clusters of cases linked to infection with Streptococcus zooepidemicus have occurred in Brazil, England, and Romania. S zooepidemicus is an emerging opportunistic pathogen that is part of the normal respiratory and intestinal flora of horses.[6]

Epidemiology

The incidence of clinically detectable glomerulonephritis during an epidemic is up to 10% of children with pharyngitis and 25% of children with impetigo. One study reported a change in the epidemiology of APSGN and found that pharyngitis has replaced impetigo as the predominant cause of APSGN.[11]

APSGN can occur sporadically or epidemically. The incidence seems to be decreasing in the United States and Europe, but sporadic cases of the disease continue to be reported from all over the world. The prevalence of nephritis varies considerably among persons with sporadic infections with nephritogenic streptococci. The reason for this variability is not known.

A systematic review by Jackson et al demonstrated significant variation in the global incidence of APSGN, with the highest incidence of 239 per 10,000 in Australian Aborigines and lowest incidence of 0.04 in 100,000 in an Italian study of people younger than 60 years.[12]

Epidemic poststreptococcal glomerulonephritis occurs mainly in developing countries in areas such as Africa, the West Indies, and the Middle East. Reasons for this changing epidemiology relate to the nutritional status of the community, the more liberal use of antibiotic prophylaxis, and possibly the change in the nephritogenic potential of streptococci. Among epidemic infections with nephritogenic streptococci, the apparent clinical attack rate is 10-12%.[4, 5]

Studies suggest that indigenous populations—including Native Americans, Pacific Islanders, and Aboriginal Australians—have increased susceptibility to APSGN. Limm-Chan and colleagues reported that Hawaii has a higher incidence of APSGN (4 cases per 100,000 population) than most developed countries. Of the reported cases, 62% were in Pacific Islanders, although they represent only 10% of the population.[13]   In a study of 322 cases of APSGN in Australia, 94% were among Aboriginal Australians, who make up 30% of the population.[14]

Clinical cases of APSGN are twice as common in males than in females. If subclinical disease is considered, both sexes are affected equally. The familial incidence rate is nearly 40%, but no genetic marker has been identified. This condition typically affects children aged 2-12 years. A large series reported that 5% of patients are younger than 2 years and 10% are older than 40 years.  

Prognosis

In children, the immediate prognosis is excellent.[4]  Early death is extremely rare in children (< 1%) but is significantly more common in adults (25%). This is secondary to congestive heart failure and azotemia. Congestive heart failure is more common in adults (43%) than in children (< 5%). Nephrotic-range proteinuria is also more common in adults (20%) than in children (4-10%). Approximately 83% of adults have azotemia, compared with 25-40% of children.

Six cohort studies report case fatality rates from APSGN, with three revealing a case fatality rate of 0%, two studies from India reporting a case fatality rate of 1.4% and 2%, and one study from Turkey reporting a case fatality rate of 0.08%.[12]

The long-term prognosis is debatable. Fewer than 1% of children have elevated serum creatinine values after 10-15 years of follow-up. Adults who develop massive proteinuria often have the garlandlike pattern of immune deposits. Their prognosis is worse; approximately 25% progress to chronic kidney disease.

The long-term prognosis of children with APSGN has been the subject of several studies. Pooled data of studies published prior to 2000 with 5- to 18-year follow-up indicate abnormal urinalysis in 17.4%, proteinuria in 13.8%, hypertension in 13.8%, and azotemia in 1.3%.[15]  A study from Australia demonstrated that APSGN can add to the burden of chronic kidney disease.[16]  Araki and colleagues reported a case in a 15-year old boy with Alport syndrome that accelerated to end-stage kidney disease 15 months after the onset of APSGN.[17]

Complications in the acute phase include the following:

  • Congestive heart failure
  • Azotemia
  • Early death secondary to congestive heart failure and azotemia

Complications in the chronic phase include the following:

  • Nephrotic-range proteinuria
  • Chronic kidney disease and end-stage renal disease

Patient Education

Patients with skin infections should know the importance of personal hygiene. In epidemics, all close personal contacts and family members should be told to seek medical attention for prophylactic treatment of streptococcal infections.

For patient education resources, see Blood in the Urine (Hematuria) and Strep Throat.

 

Presentation

History

A history suggestive of preceding streptococcal infection may include a preceding infective episode such as pharyngitis, tonsillitis, or pyoderma. This is the sine qua non for the diagnosis of acute poststreptococcal glomerulonephritis (APSGN).

A latent period always occurs between the streptococcal infection and the onset of signs and symptoms of acute glomerulonephritis. In general, the latent period is 1-2 weeks after a throat infection and 3-6 weeks after a skin infection.[18] The onset of signs and symptoms at the same time as pharyngitis (also called synpharyngitic nephritis) is more likely to be immunoglobulin A (IgA) nephropathy rather than APSGN.

Dark urine (brown-, tea-, or cola-colored) is often the first clinical manifestation of APSGN. Dark urine is caused by hemolysis of red blood cells that have penetrated the glomerular basement membrane and have passed into the tubular system.

Periorbital edema is typical. The onset of puffiness of the face or eyelids is sudden. It is usually prominent upon awakening and, if the patient is active, tends to subside at the end of the day.

In some cases, generalized edema and other features of circulatory congestion, such as dyspnea, may be present. Edema is a result of a defect in renal excretion of salt and water. The severity of edema is often disproportionate to the degree of renal impairment.

Nonspecific symptoms of APSGN can include general malaise, weakness, and anorexia and are present in 50% of patients. Approximately 15% of patients complain of nausea and vomiting.

Unusual presentations of complicated APSGN include the following:

  • Refractory hypoxic respiratory failure from diffuse alveolar hemorrhage due to pulmonary renal syndrome [20]
  • Seizures and other central nervous system manifestations, from posterior reversible encephalopathy syndrome [21, 22]
  • Severe nephritis similar to that from systemic lupus erythematosus, including acute kidney injury, positive antinuclear antibody, and hematologic anomalies [23]

Physical Examination

Acute nephritic syndrome is the most frequent presentation of APSGN. Its manifestations are edema, hematuria, and hypertension, with or without oliguria. Hematuria is present in all cases, and is gross in 30% of cases. Approximately 95% of clinical cases have at least two manifestations, and 40% have the full-blown acute nephritic syndrome.

Edema

Edema is present in 80-90% of cases, and it is the presenting complaint in 60% of cases. Compromised intraglomerular blood flow due to glomerular hypercellularity results in progressive encroachment on the cross-sectional area of the glomerular capillaries. This leads to reduced blood flow that manifests as low fractional excretion of sodium and concentrated urine. This salt and water retention leads to edema.

Hypertension

Hypertension occurs in 60-80% of cases and is more common in elderly individuals. In 50% of cases, the hypertension can be severe; however, more often it is transient, with normalization of blood pressure upon restoration of the glomerular filtration rate, loss of edema, and normalization of plasma volume. If hypertension persists, it is more indicative of the progression to a more chronic stage or that the disease is not poststreptococcal glomerulonephritis.

Hypertension is thought to be the result of excessive salt and water retention. Despite excessive sodium retention, the plasma levels of atrial natriuretic peptide are increased. In this condition, this suggests that the kidneys are unresponsive to atrial natriuretic peptide.

Plasma renin activity is usually low, and studies by Parra et al have shown that an inhibition of angiotensin-converting enzyme could be an effective short-term treatment for this low-renin hypertension.[24]

Hypertensive encephalopathy occurs in no more than 5-10% of patients. Usually, clinical improvement occurs without any neurological sequelae.

Oliguria

Oliguria is present in 10-50% of cases. In 15% of cases, urine output is less than 200 mL. Oliguria is indicative of the severe crescentic form of the disease. It is often transient, with diuresis occurring within 1-2 weeks.

Left ventricular dysfunction

Left ventricular dysfunction with or without hypertension or pericardial effusion may be present during the acute congestive and convalescent phases.

In rare cases, persons with APSGN can show signs of pulmonary hemorrhage.

 

DDx

Diagnostic Considerations

Other conditions to consider in the differential diagnosis include the following:

  • Bacterial endocarditis
  • Essential cryoglobulinemia
  • IgA nephropathy
  • Microscopic polyarteritis
  • Shunt nephritis
  • Visceral abscess
  • Other infection-related glomerulonephritis

With the increase in antibiotic-resistant staphylococcus strains such as methicillin-resistant Staphylococcus aureus (MRSA), the incidence of glomerulonephritis associated with S aureus infection has been rising. Differentiating staphylococcal glomerulonephritis from poststreptococcal glomerulonephritis is important because staphylococcal glomerulonephritis involves active infection and requires different management.[25, 26]

Differential Diagnoses

 

Workup

Laboratory Studies

Laboratory studies in acute poststreptococcal glomerulonephritis (APSGN) include tests to provide evidence of preceding streptococcal infection, renal function studies, and serologic studies.

Evidence of preceding streptococcal infection can be determined as follows:

  • Antibody titers to extracellular products of streptococci are positive in more than 95% of patients with pharyngitis and 80% of patients with skin infections.

  • The antistreptolysin (ASO), antinicotinamide adenine dinucleotidase (anti-NAD), antihyaluronidase (AHase), and anti–DNAse B are commonly positive after pharyngitis, and anti–DNAse B and AHase titers are more often positive following skin infections

  • ASO titers are frequently used to document streptococcal infection, but a more sensitive test is the streptozyme test, which tests antibodies to ASO, anti–DNAse B, AHase, and anti-NAD

  • Studies suggest that the relatively unavailable antizymogen titer test is superior to both anti–DNAse B and ASO titers

  • Antizymogen titers that are two dilutions higher than the mean in healthy controls are reported to have a sensitivity of 88% and a specificity of 85% in the diagnosis of streptococcal infection in patients with glomerulonephritis

  • High antibody titers to glyceraldehyde phosphate dehydrogenase are also found in persons with APSGN

  • In general, the antibody titers are elevated at 1 week, peak at 1 month, and fall toward preinfection levels after several months

Kidney function studies

Elevated blood urea nitrogen (BUN) and serum creatinine values reflect the decrease in the glomerular filtration rate that occurs in the acute phase. The elevations are usually transient.Their failure to normalize within several weeks or months indicates that the patient may not have a true APSGN and suggests seeking an alternative diagnosis. Patients who have the crescentic form of glomerulonephritis have rapid deterioration and, often, incomplete recovery of kidney function.

Serology

Serologic findings are as follows:

  • Low serum complement levels indicative of an antigen-antibody interaction are a universal finding in the acute phase of APSGN

  • Most patients have marked depression of serum hemolytic component CH50 and serum concentrations of C3

  • The decrease in C3 concentration typically occurs before the increase in ASO titers[18]

  • The activation of the alternative pathway of the complement system is thought to be responsible for the hypocomplementemia

  • In some patients, the levels of C2 and C4 may also be decreased, but to a lesser extent, suggesting that both classic and alternate pathways of the complement system are activated

  • In most uncomplicated cases, the complement levels return to normal in 6-8 weeks. Prolonged hypocomplementemia suggests an alternative diagnosis

  • Occasionally, low complement levels persist for 3 months

  • The level of reduction of serum complement levels does not have any prognostic significance

  • Circulating immune complexes and cryoglobulins are found in 60% of cases, and rheumatoid factor is found in 43% of cases

Urinalysis

Findings are as follows:

  • Results are always abnormal

  • Hematuria and proteinuria are present in all cases

  • Urine sediment has red blood cells, red blood cell casts, white blood cells, granular casts, and, rarely, white blood cell casts

  • Dysmorphic red blood cells indicative of glomerular hematuria can usually be detected by performing phase-contrast microscopy

  • Red blood cell casts are best detected in first, early-morning urine specimens examined by the physician immediately after the patient voids

  • Hematuria usually resolves within 3-6 months but may persist as long as 18 months

  • Microscopic hematuria may be present in patients in whom the disease has otherwise clinically resolved

  • Proteinuria may be mild or so severe that it causes nephrotic syndrome

  • Approximately 5-10% of patients with APSGN have nephrotic-range proteinuria

  • Proteinuria usually disappears in 6 months. A mild increase in urinary protein excretion is present in 15% at 3 years and 2% at 10 years

  • Patients with nephrotic-range proteinuria in the acute phase or persistent heavy proteinuria have a worse prognosis. This is often associated with an evolution to a garlandlike pattern of immune deposits as the disease progresses

Other studies

In a study of 28 pediatric patients with APSGN, Taskesen et al found that on clinic admission, the plasma levels of NT-proBNP (an N-terminal peptide left over when the prohormone for brain natriuretic peptide [proBNP] is cleaved to produce active BNP) were higher in these patients than in the 26 healthy children making up the control group.[27] Moreover, the NT-proBNP levels were significantly higher in six patients with APSGN who were found to have left ventricular dysfunction than they were in the patients with APSGN in whom no ventricular dysfunction was diagnosed. The authors suggested that in some patients with APSGN, determination of NT-proBNP levels may prove helpful in the assessment of left ventricular volume overload and cardiac function.

Imaging Studies

Imaging study results may include the following:

  • Chest radiographs may show findings of congestive heart failure.
  • Renal ultrasound images usually reveal normal-sized kidneys bilaterally.

Histologic Findings

Pathologic findings of changes in gross appearance findings are as follows:

  • The kidneys are symmetrically enlarged to approximately 25-50% of normal.
  • They are pale in appearance, and the cut surfaces bulge because of interstitial edema.
  • The glomeruli may stand out as reddish or gray translucent dots.
  • The cut surfaces may have tiny red speckles caused by red blood cells in the lumen of the Bowman space and tubules.

Light microscopy findings are as follows:

  • The most striking finding is hypercellularity of the glomeruli. All glomeruli are affected (diffuse) and usually to an approximately equal degree. The glomerular tufts are larger than normal, and the cells are more numerous.
  • The cell types typically present include endothelial and mesangial cells and migrant inflammatory cells, which include polymorphonuclear leukocytes and monocytes. [28]
  • Polymorphonuclear leukocytes are present in large numbers, hence the term exudative glomerulonephritis.
  • Necrosis in the glomerular tuft is not typically found.
  • The individual lobules are wider than usual and may have a clubbed appearance.
  • Generally, the glomerular capillary walls are not thick.
  • In some patients, crescent formation may be found, but usually, only a small percentage of glomeruli are affected by crescents.
  • The tubules are normal in the majority of cases.
  • When proteinuria is present, hyaline droplets (protein reabsorption droplets) may be present in the proximal convoluted tubules.
  • In patients with severe exudative glomerulonephritis, polymorphonuclear leukocytes may be present in the lumen.
  • The degree of interstitial involvement is variable. The interstitial areas show edema and infiltration with polymorphonuclear leukocytes and mononuclear cells. The arteries and arterioles are normal.

Immunofluorescence findings (see the image below) are as follows:

  • In biopsy samples taken in the first 2-3 weeks of illness, deposits of immunoglobulin G and C3 in a diffuse granular pattern are present along the glomerular capillary wall and mesangium.
  • Immunoglobulin M may be present in small amounts. Significant amounts of IgA suggest an alternative diagnosis.
  • Sorger et al have described 3 different patterns of immunofluorescence called the garland pattern, the starry sky pattern, and the mesangial pattern. [29]
  • The starry sky pattern is an irregular, finely granular pattern with small deposits often situated on the glomerular basement membrane overlying the mesangium. This pattern is often seen in the early phase of the disease.
  • The starry sky pattern may turn into the mesangial pattern, which is characterized by granular deposition of C3 with or without immunoglobulin G. It seems to be most closely related to a resolving pattern.
  • In approximately 25% of patients, the deposits are large and densely packed and aggregate into a ropelike or garlandlike pattern. These correspond to the humps on the subepithelial side of the glomerular capillary wall seen with electron microscopy. These types of deposits may persist for months and may be associated with the persistence of proteinuria and the development of glomerulosclerosis.
Kidney biopsy from a 7-year-old child with acute p Kidney biopsy from a 7-year-old child with acute poststreptococcal glomerulonephritis. Immunofluorescence (C3) shows a granular capillary and mesangial staining pattern with segmental areas of “lumpy-bumpy” staining (white arrows). Courtesy of Laura Kidd, MD, Pathology and Laboratory Medicine, Tulane University Medical School.

Electron microscopy findings are as follows:

  • Many of the ultrastructural changes confirm the findings from light microscopy evaluations.
  • The number of endothelial, mesangial, and infiltrating inflammatory cells is increased.
  • The glomerular basement membrane is usually normal in thickness and contour, although occasionally patchy thickening may be noted.
  • The most consistent and classic diagnostic finding is the presence of glomerular subepithelial electron-dense immune-type deposits, often referred to as humps (see the image below). The deposits are discrete and are commonly found on the part of the glomerular basement membrane overlying the mesangium.
Kidney biopsy from a 7-year-old child with acute p Kidney biopsy from a 7-year-old child with acute poststreptococcal glomerulonephritis. Electron microscopy image shows rare large subepithelial deposits, or “humps” (arrows). Courtesy of Laura Kidd, MD, Pathology and Laboratory Medicine, Tulane University Medical School.

Kidney Biopsy

Atypical features in the early phase of APSGN that suggest the need for kidney biopsy include the following:

  • Absence of the latent period between streptococcal infection and acute glomerulonephritis
  • Anuria
  • Rapidly deteriorating renal function
  • Normal serum complement levels
  • No rise in antistreptococcal antibodies
  • Extrarenal manifestations of systemic disease
  • No improvement or continued decrease in the glomerular filtration rate at 2 weeks
  • Persistence of hypertension beyond 2 weeks

Atypical features in the recovery phase that mandate a kidney biopsy include the following:

  • Failure of glomerular filtration rate to normalize by 4 weeks
  • Persistent hypocomplementemia beyond 6 weeks
  • Persistent microscopic hematuria beyond 18 months
  • Persistent proteinuria beyond 6 months
 

Treatment

Medical Care

Symptomatic therapy is recommended for patients with acute poststreptococcal glomerulonephritis (APSGN), and it should be based on the clinical severity of the illness. The major goal is to control edema and blood pressure. Those sequelae are most likely to arise in the first 7 to 10 days of APSGN.[18]

During the acute phase of the disease, restrict salt and water. If significant edema or hypertension develops, administer diuretics. Loop diuretics increase urinary output and consequently improve cardiovascular congestion and hypertension.

Most patients do not require any medications after the acute phase, but antihypertensives may be needed in the chronic phase if the blood pressure remains high. For hypertension not controlled by diuretics, the usual second-line choices are calcium channel blockers, angiotensin-converting enzyme inhibitors (ACEIs), or angiotensin receptor blockers (ARBs), although ACEIs and ARBs carry the risk of hyperkalemia and temporarily impairing recovery of renal function.[18] For malignant hypertension, intravenous nitroprusside or other parenteral agents are used.

In the acute phase, admit for observation and treatment of hypertension and congestive heart failure.  

Other features of therapy are as follows:

  • Indications for dialysis include life-threatening hyperkalemia and clinical manifestations of uremia.
  • Restricting physical activity is appropriate in the first few days of the illness but is unnecessary once the patient feels well.
  • Steroids, immunosuppressive agents, and plasmapheresis are not generally indicated.

A kidney biopsy is indicated for patients with rapidly progressive renal failure. If the biopsy findings show evidence of crescentic glomerulonephritis with more than 30% of the glomeruli involved, a short course of intravenous pulse steroid therapy is recommended (500 mg to 1 g/1.73 m2 of methylprednisone qd for 3-5 d). However, no controlled clinical trials have evaluated such therapy. Long-term treatment with steroids or immunosuppressives is not recommended.

Admit for monitoring and to initiate dialysis (when indicated) if kidney function progressively worsens. Transfer may be necessary if kidney biopsy facilities are not available and the diagnosis is in doubt or if rapidly progressive renal failure develops. Transfer may also be necessary if azotemia worsens and dialysis facilities are not available on site.

Specific therapy for streptococcal infection is an important part of the therapeutic regimen. Throat cultures should be performed on patients, family members, and close personal contacts, and treatment should be provided for all patients found to be infected or colonized. Treat with oral penicillin G (250 mg qid for 7-10 d) or with erythromycin (250 mg qid for 7-10 d) for patients allergic to penicillin. This helps prevent nephritis in carriers and helps prevent the spread of nephritogenic strains to others.

Patients with skin infections must practice good personal hygiene. This is essential.

During epidemics, recommend that high-risk individuals, including close contacts and family members, receive empirical prophylactic treatment.

 

Consultations

The following consultations may be beneficial:

  • Nutritionist or dietitian
  • Nephrologist

Diet and Activity

Dietary measures are as follows:

  • Low-salt diet - Two grams of sodium per day
  • Fluid restriction - One liter per day

Restricting physical activity is appropriate in the first few days of the illness but is not necessary once the patient feels well.

Prevention

Preventive measures are as follows:

  • The patient and any family member or close personal contact should have a throat culture.
  • Treatment with penicillin G or erythromycin (if allergic to penicillin) helps prevent nephritis in carriers and helps prevent the spread of nephritogenic strains to others.
  • Patients with skin infections must pay close attention to personal hygiene.
  • Epidemics should prompt empirical prophylactic treatment for high-risk individuals (family and close personal contacts).

Long-Term Monitoring

Patients who have had acute poststreptococcal glomerulonephritis should be monitored according to the following schedule:

  • Monitor blood pressure every month for 6 months and then every 6 months thereafter.
  • Monitor BUN and serum creatinine levels every 3 months after the acute phase for 1 year and then yearly after that.
  • Check serum complement levels at 6-8 weeks to make sure they have returned to normal.
  • Check urine for hematuria and proteinuria every 3-6 months.
 

Medication

Medication Summary

Therapy for patients with acute poststreptococcal glomerulonephritis is symptomatic in nature and depends on the clinical severity of the illness. The major aims are to control the edema and blood pressure. 

During the acute phase of the disease, salt and water should be restricted. If significant edema or hypertension develops, diuretics should be administered. Loop diuretics increase urinary output and consequently improve cardiovascular congestion and hypertension.

For hypertension not controlled by diuretics, calcium channel blockers or angiotensin-converting enzyme inhibitors are generally useful. For malignant hypertension, intravenous nitroprusside or other parenteral agents are used.

The indications for dialysis include life-threatening hyperkalemia and clinical manifestations of uremia. Steroids, immunosuppressive agents, and plasmapheresis are not generally indicated. In patients with rapidly progressive renal failure, a renal biopsy is indicated. If the biopsy findings show evidence of crescentic glomerulonephritis with more than 30% of the glomeruli involved, a short course of intravenous pulse steroid therapy is recommended (500 mg to 1 g/1.73 m2 of methylprednisone qd for 3-5 d). However, no controlled clinical trials have evaluated such therapy. Long-term treatment with steroids or immunosuppressives is not recommended.

Diuretics

Class Summary

Used to control edema and circulatory congestion.

Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. Dose must be individualized to patient. Depending on response, administer at increments of 20-40 mg, no sooner than 6-8 h after the previous dose, until desired diuresis occurs. When treating infants, titrate with increments of 1 mg/kg/dose until a satisfactory effect is achieved.

Calcium channel blockers

Class Summary

In specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. Calcium channel blockers inhibit movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and conduction velocity.

Amlodipine (Norvasc)

Relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery. Benefits nonpregnant patients with systolic dysfunction, hypertension, or arrhythmias. Can be used during pregnancy if clinically indicated.

Angiotensin-converting enzyme inhibitors

Class Summary

Decrease aldosterone secretion.

Captopril (Capoten)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

Enalapril (Vasotec)

Competitive inhibitor of angiotensin-converting enzyme. Reduces angiotensin II levels, decreasing aldosterone secretion. Clinical response usually observed within 15 min of administration.

Vasodilators

Class Summary

Used to treat hypertensive emergencies. Vasodilators reduce SVR, which, in turn, may allow forward flow, improving cardiac output.

Nitroprusside (Nitropress)

Produces vasodilation and increases inotropic activity of heart. At higher dosages, may exacerbate myocardial ischemia by increasing heart rate. Should not be used to treat compensatory hypertension (arteriovenous shunt or coarctation of aorta).

Hydralazine (Apresoline)

Decreases systemic resistance through direct vasodilation of arterioles.

 

Questions & Answers

Overview

What is poststreptococcal glomerulonephritis?

What is the pathophysiology of poststreptococcal glomerulonephritis?

What causes poststreptococcal glomerulonephritis?

What is the prevalence of poststreptococcal glomerulonephritis in the US?

What is the global prevalence of poststreptococcal glomerulonephritis?

What are the racial predilections of poststreptococcal glomerulonephritis?

Which patient groups have the highest prevalence of poststreptococcal glomerulonephritis?

What is the prognosis of poststreptococcal glomerulonephritis?

What are the possible complications of acute poststreptococcal glomerulonephritis?

What are the possible complications of chronic poststreptococcal glomerulonephritis?

What is included in patient education about poststreptococcal glomerulonephritis?

Presentation

Which clinical history findings are characteristic of poststreptococcal glomerulonephritis?

What are the signs and symptoms of complicated acute poststreptococcal glomerulonephritis (APSGN)?

Which physical findings are characteristic of poststreptococcal glomerulonephritis?

What are the signs and symptoms of edema in poststreptococcal glomerulonephritis?

Which physical findings are characteristic of hypertension in poststreptococcal glomerulonephritis?

What causes hypertension in poststreptococcal glomerulonephritis?

How prevalent is hypertensive encephalopathy in poststreptococcal glomerulonephritis?

What are the signs and symptoms of oliguria in poststreptococcal glomerulonephritis?

What are the possible cardiovascular findings in poststreptococcal glomerulonephritis?

What is the prevalence of pulmonary hemorrhage in poststreptococcal glomerulonephritis?

DDX

Which conditions are included in the differential diagnoses of poststreptococcal glomerulonephritis?

What are the differential diagnoses for Poststreptococcal Glomerulonephritis?

Workup

What is the role of lab tests in the workup of poststreptococcal glomerulonephritis?

What is the role of kidney function studies in the workup of poststreptococcal glomerulonephritis?

Which serologic findings are characteristic of poststreptococcal glomerulonephritis?

Which urinalysis findings are characteristic of poststreptococcal glomerulonephritis?

What is the role of NT-proBNP measurement in the workup of poststreptococcal glomerulonephritis?

Which imaging studies are characteristic of poststreptococcal glomerulonephritis?

Which pathologic findings are characteristic of poststreptococcal glomerulonephritis?

Which light microscopy findings are characteristic of poststreptococcal glomerulonephritis?

Which immunofluorescence findings are characteristic of poststreptococcal glomerulonephritis?

Which electron microscopy findings are characteristic of poststreptococcal glomerulonephritis?

When is renal biopsy indicated in the workup of acute poststreptococcal glomerulonephritis (APSGN)?

Treatment

How is poststreptococcal glomerulonephritis treatment?

What is the role of kidney biopsy in the treatment of poststreptococcal glomerulonephritis?

When are inpatient care and/or transfer indicated for the treatment of poststreptococcal glomerulonephritis?

What is the role of throat cultures in the treatment of poststreptococcal glomerulonephritis?

How are skin infections treated in poststreptococcal glomerulonephritis?

When is empirical prophylactic treatment for poststreptococcal glomerulonephritis indicated?

Which specialist consultations are beneficial to patients with poststreptococcal glomerulonephritis?

Which dietary and activity modifications are used in the treatment of poststreptococcal glomerulonephritis?

How is poststreptococcal glomerulonephritis prevented?

What is included in the long-term monitoring of poststreptococcal glomerulonephritis?

Medications

What is the role of medications in the treatment of poststreptococcal glomerulonephritis?

Which medications in the drug class Vasodilators are used in the treatment of Poststreptococcal Glomerulonephritis?

Which medications in the drug class Angiotensin-converting enzyme inhibitors are used in the treatment of Poststreptococcal Glomerulonephritis?

Which medications in the drug class Calcium channel blockers are used in the treatment of Poststreptococcal Glomerulonephritis?

Which medications in the drug class Diuretics are used in the treatment of Poststreptococcal Glomerulonephritis?