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Acute Glomerulonephritis

8 min read

References:

  1. Wong’s Nursing Care of Infants and Children, 10th Edition, ISBN 978-0-323-54939-4, by Marilyn J. Hockenberry, David Wilson, and Cheryl C. Rodgers (pp. 1012-1016)

Acute glomerulonephritis (AGN) as a classification includes a number of distinct entities. It may be a primary event or a manifestation of a systemic disorder (e.g., systemic lupus erythematosus, sickle cell disease, bacterial endocarditis), and the disease can range from minimum to severe. The common features include oliguria, edema, hypertension and circulatory congestion, hematuria, and proteinuria.

  1. Most casts are postinfectious and have been associated with pneumococcal, streptococcal (most common), and viral infections, all being associated with immune complex formation and glomerular deposition. Postinfectious glomerulonephritis exhibits a better clinical course than other acute proliferative glomerulonephritis.
  2. Acute poststreptococcal glomerulonephritis (APSGN) is the most common of the noninfectious renal diseases in childhood, established in the majority of cases. It primarily affects early school-age children, with a median age of onset between 6 and 8 years. It is uncommon in children younger than 2 years of age.
  3. APSGN is also considered to cause immune-complex disease—that is, a reaction that occurs as a by-product of an antecedent streptococcal infection with certain strains of the group A β-hemolytic streptococci, although other bacteria and viruses have also been implicated. However, most streptococcal infections do not cause APSGN.

Pathophysiology

  1. Immune complexes become trapped in the glomerular capillary loop.
  2. The kidney undergoes a proliferative and exudative process.
  3. Glomerular capillary loops are almost obliterated by swelling, making them appear dense and lobulated. Deposits of immune complexes can be visualized via electron microscope as discrete nodules or “humps” in the basement membrane.
  4. Occlusion of the capillary lumen of affected glomeruli and probable constriction of the afferent arteriole reduces glomerular filtration rate. This does not affect renal blood flow, but results in reduced capacity to form filtrate from glomerular plasma flow.
  5. Decreased filtration of plasma results in an excessive accumulation of water and retention of sodium. Volume increases in both plasma and interstitial fluid, leading to circulatory congestion and edema.
  6. Hypertension also occurs, but its specific cause is unexplained. Hypervolemia may be a factor. Plasma renin activity is also low during the acute phase.

Clinical Manifestations

Typically, affected children are in good health until they experience the antecedent infection. Some infections may be described as a “mild cold”. However, while most cases are postinfectious, other cases may not have a history of infection.

  1. The onset of nephritis occurs after a latent period. It varies according to the infectious agent but is 1–2 weeks for streptococcal throat infections and 3–4 weeks for streptococcal skin infections.
  2. Initial signs of nephritic reaction include puffiness, especially around the eyes; periorbital edema, anorexia, and the passage of cola-colored urine.
    • Edema is more prominent in the face in the morning but spreads during the day to involve the extremities, genitalia, and abdomen.
    • Edema is only moderate— those unfamiliar with the child’s face may perceive it as a normal appearance.
    • The urine may appear cloudy, smoky brown, or what parents describe as resembling tea or cola, and it is severely reduced in volume.
  3. The child is pale, irritable, and lethargic and appears unwell but seldom expresses specific complaints. Older children may complain of headaches, abdominal discomfort, or dysuria.
  4. On examination, there is usually a mild to moderate elevation in blood pressure compared with normal values for age, although severe hypertension may be present.
  5. Occasionally, a child will present with severe symptoms such as seizures from hypertensive encephalopathy, pulmonary and circulatory congestion, or hematuria in the absence of hypertension and edema.

Clinical Course

During the Edematous Acute Phase (4 to 10 days), the child remains listless, anorexic, and apathetic. Weight fluctuates, and urine appears smoky brown. Blood pressure may suddenly reach dangerously high levels at any time during this phase.

The first sign of improvement is an increase in urinary output with a corresponding decrease in body weight. With diuresis the child begins to feel better, the appetite improves, and the blood pressure decreases to normal with the reduction of edema. Gross hematuria diminishes, in part because of dilution of the red blood cells in the more dilute urine. Renal function and hypocomplementemia usually normalize by 8 weeks.

Complications

  1. Hypertensive Encephalopathy— acute and severe hypertension overtakes the autoregulatory vasoconstriction experienced by the brain to protect from hypertension. With the failure of this protective mechanism, hyperperfusion and cerebral edema occur. Headache, dizziness, abdominal discomfort, and vomiting appear as premonitory signs of encephalopathy. Transient loss of vision, hemiparesis, disorientation, and generalized tonic-clonic seizures may occur.
  2. Acute Cardiac Decompensation due to hypervolemia (not congestion, which may also be present). The heart becomes enlarged, and increased pulmonary vascular markings are evident on x-ray examination.
  3. Acute Renal Failure with persistent oliguria or anuria is uncommon, but requires an appropriate treatment regimen.

Diagnostic Evaluation

  1. Urinalysis shows (characteristically) hematuria, proteinuria, and increased specific gravity are noted. Proteinuria often parallels hematuria, and is not found in massive amounts like in nephrotic syndrome.

    • Urine cultures are negative; bacteria are not seen. Microscopic examination shows red blood cells, leukocytes, epithelial cells, and granular and red blood cell casts.
    • If proteinuria does become severe, changes seen in nephrotic syndrome may also begin to appear: transient hypoproteinemia and hyperlipidemia.

  2. Blood examination shows normal electrolytes in the acute phase and carbon dioxide levels unless renal failure has occurred. Azotemia (↑ BUN, ↑ Crea) can be seen in at least 50% of cases.

  3. Streptococcal cultures from the pharynx or family members can be helpful, but is only seen in a few cases. Numbers are also rarely significantly higher than in normal carrier incidence in many communities.

  4. Serologic tests are required for diagnosis.

    1. Testing for response of antibodies to streptococci provide indirect evidence of previous streptococcal infection— antistreptolysin O (ASO) titer being the most familiar and readily available test for streptococcal antibodies. ASO appears in the serum approximately 10 days after the initial infection. Reminder that it is only a useful diagnostic tool when nephritis follows a pharyngeal infection but is of less value after pyoderma.
      • An ASO titer of 250 Todd units or higher is of diagnostic significance along with a rising titer in two samples taken 1 week apart.
      • More consistent and reliable antibody tests following streptococcal skin infections are elevated antihyaluronidase (AHase) and antidioxyribonuclease-B (ADNase-B) titers.
    2. Of more importance for clinical serologic diagnosis is measurement of the serum complement level (C3). Serum C3 level is decreased initially but returns to normal 8 to 10 weeks after onset of the glomerulonephritis.

  5. Others: chest x-ray examination: appearance of generalized cardiac enlargement, pulmonary congestion, and pleural effusion during the edematous acute phase. Renal biopsy is seldom required.

Therapeutic Management

No specific treatment is available for AGN, but recovery is spontaneous and uneventful in most cases. Management consists of general supportive measures and early recognition and treatment of complications. Children with normal blood pressure and satisfactory urine output may be treated at home.

  1. General Measures: most children voluntarily restrict their activities (listlessness, fatigue, malaise) during the most active phase of the disease, but ambulation does not seem to have an adverse effect on the course of the disease. Bed rest is not required.
  2. Fluid Balance: regular monitoring of vital signs, body weight (best assessment for fluid balance; done daily), and I&O is essential to monitor the disease’s progress and detect complications.
    • Sodium and water restriction is used when urine output is significantly reduced (<200 to 300 mL/day). Water restriction is based on calculations of insensible loss plus the volume of urine excreted.
    • Diuretics are rarely of value when severe renal failure is present, since little sodium reaches the distal tubules as a result of the reduced filtration rate. Otherwise, diuretic therapy is helpful if significant edema and fluid overload are present.
    • If acute renal failure with oliguria does occur, careful management may include peritoneal dialysis or hemodialysis.
    • Electrolyte imbalances can appear in severe forms of APSGN. These often include hyperkalemia, acidosis, hypocalcemia, and hyperphosphatemia. Review acute renal failure for this discussion.
    • Acute Hypertension must be anticipated and identified early. Blood pressure is measured every 4 to 6 hours. Loop diuretics can control significant but not severe hypertension. Antihypertensive drugs may be needed in severe cases. Seizure activity from hypertensive encephalopathy will necessitate anticonvulsant therapy and hypertensive agents.
  3. Nutrition: a regular diet is permitted in uncomplicated cases, but sodium intake is usually limited.
    • Moderate sodium restriction is usually instituted for children with hypertension or edema.
    • Oliguria will warrant limitation of high-protein foods.
    • Protein restriction is limited to children with severe azotemia from prolonged oliguria. However, anorexia as a symptom often already limits protein intake.
  4. Antibiotics are used for those with evidence of persistent streptococcal infections. Antibiotics do not alter the course of the disease but are often recommended to prevent transmission of nephritogenic streptococci to other family members.
  5. Nursing Care Management: careful assessment, regular monitoring (vital signs, fluid balance, behavior, urine characteristics and output, weight)
    • The nurse educates parents and friends against bringing items such as potato chips or pretzels. However, the total amount of salt ingested is usually less than prescribed because of poor appetite. Fluid restriction is more difficult to control.
    • Follow-up care should be advised. Parents are instructed about the care of the child (activity, diet, infection prevention) and health supervision is continued with weekly, then monthly visits

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