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. [11]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:

  • Atypical hemolytic-uremic syndrome [12]
  • Refractory hypoxic respiratory failure from diffuse alveolar hemorrhage due to pulmonary renal syndrome [13]
  • Seizures and other central nervous system manifestations, from posterior reversible encephalopathy syndrome [1415]


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



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 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 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. [16]

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


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.

Laboratory Tests

Usually manifests clinically with varying grades of proteinuria and microscopic hematuria.

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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.



Kidney biopsy from a 7-yr old child with acute posKidney biopsy from a 7-yr 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.

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

Although many morphologic, clinical, and serologic features suggest that APSGN is an immune complex disorder, the precise nature of the antigen-antibody interaction is undefined. APSGN is believed to be an immune-mediated disease, 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 increased frequency of APSGN in children compared to that in adults.

The two antigens isolated from nephritogenic streptococci are under investigation in APSGN. These include the cationic cysteine protease streptococcal pyrogenic exotoxin B and nephritis-associated streptococcal plasmin receptor, which is a plasmin-binding protein with glyceraldehyde phosphate dehydrogenase (also known as presorbing antigen or PA-Ag). [4]These fractions have an affinity for glomeruli and have been shown to induce specific, long-lasting antibody responses in biopsy specimens from patients with APSGN.

The relevance of exotoxin B and glyceraldehyde phosphate dehydrogenase was evaluated in the same renal biopsy and serum samples of patients with well-defined APSGN. Glomerular deposits of and antibody response to exotoxin B were more consistently present in APSGN than were deposits of and antibody response to glyceraldehyde phosphate dehydrogenase. [5]

Antibodies to exotoxin B and PA-Ag are elevated in the majority of patients with APSGN. Intravenous injections of PA-Ag produce acute glomerulonephritis in animals. Antibodies to PA-Ag are found in 30 of 31 patients with APSGN but are low or absent in those with uncomplicated streptococcal infection or in patients with rheumatic fever.

PA-Ag is also known to activate the alternate pathway of the complement cascade, which happens to be preferentially activated in persons with APSGN. The observation that some patients may only have C3 deposition may relate to this mechanism.

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. [6]


This condition typically affects children aged 2-12 years. A large series reported that 5% are younger than 2 years and 10% are older than 40 years.


The treatment of HBV-GN revolves around antiviral therapy.


Complications of Injecting Drug Use

  • Local problems—Abscess (Figures 240-2 
    Image not available.

    A 32-year-old woman with type 1 diabetes developed large abscesses all over her body secondary to injection of cocaine and heroin. Her back shows the large scars remaining after the healing of these abscesses. (Courtesy of ­Richard P. Usatine, MD.)

    and 240-3; Abscess), cellulitis, septic thrombophlebitis, local induration, necrotizing fasciitis, gas gangrene, pyomyositis, mycotic aneurysm, compartmental syndromes, and foreign bodies (e.g., broken needle parts) in local areas.2
    • IDUs are at higher risk of getting methicillin-resistant Staphylococcus aureus(MRSA) skin infections that the patient may think are spider bites (Figure 240-4).
    • Some IDUs give up trying to inject into their veins and put the cocaine directly into the skin. This causes local skin necrosis that produces round atrophic scars (Figure 240-5).
  • IDUs are at risk for contracting systemic infections, including HIV and hepatitis B or hepatitis C.
    • Injecting drug users are at risk of endocarditis, osteomyelitis (Figures 240-6and 240-7), and an abscess of the epidural region. These infections can lead to long hospitalizations for intravenous antibiotics. The endocarditis that occurs in IDUs involves the right-sided heart valves (see Chapter 50, Bacterial Endocarditis).2 They are also at risk of septic emboli to the lungs, group A β-hemolytic streptococcal septicemia, septic arthritis, and candidal and other fungal infections.



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%. [8]

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%. [9] A study from Australia demonstrated that APSGN can add to the burden of chronic kidney disease. [10]


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Content 11


Question 1 of 1

A 42-year-old African-American man has been diagnosed with hypertension for the past 10 years and treated with medication. One morning, he is found unresponsive by his wife. He is taken to the emergency department and pronounced dead by the physician. An autopsy revealed cardiac hypertrophy and a narrowing of the aorta just distal to the ligamentum arteriosum, with dilation of the intercostal artery's ostia. How could the death have possibly been prevented?



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