Glomerulonephritis, Poststreptococcal Clinical Presentation

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 APSGN.

• Latent period

  • 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.
  • 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)

  • This is often the first clinical symptom.
  • 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

  • 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

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

• Acute nephritic syndrome

  • Acute nephritic syndrome presenting as edema, hematuria, and hypertension with or without oliguria is the most frequent presentation of APSGN.
  • Approximately 95% of clinical cases have at least 2 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 among 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.^[8]
  • Hypertensive encephalopathy occurs in no more than 5-10% of patients. Usually, clinical improvement occurs without any neurological sequelae.
• Oliguria

  • This is present in 10-50% of cases, and, in 15%, 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.
• Hematuria

  • This is present universally.
  • In 30% of cases, gross hematuria is present.
• 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.
  • 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.^[9] Moreover, the NT-proBNP levels were significantly higher in 6 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.

• Poststreptococcal glomerulonephritis 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.