Poststreptococcal Glomerulonephritis Clinical Presentation

Updated: Nov 08, 2021
  • Author: Duvuru Geetha, MD, MRCP; Chief Editor: Vecihi Batuman, MD, FASN  more...
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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. [19] 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 [21]
  • Seizures and other central nervous system manifestations, from posterior reversible encephalopathy syndrome [22, 23]
  • Severe nephritis similar to that from systemic lupus erythematosus, including acute kidney injury, positive antinuclear antibody, and hematologic anomalies [24]

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 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. [25]

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.