Acute Glomerulonephritis

Description

 Hippocrates originally described the natural history of acute glomerulonephritis (GN), writing of
back pain and hematuria followed by oliguria or anuria. Richard Bright (1789-1858) described acute GN
clinically in 1827, which led to the eponymic designation Bright disease. With the development of the
microscope, Theodor Langhans (1839-1915) was later able to describe the pathophysiologic glomerular
changes.

 Acute glomerulonephritis (GN) comprises a specific set of renal diseases in which an immunologic

mechanism triggers inflammation and proliferation of glomerular tissue that can result in damage to the
basement membrane, mesangium, or capillary endothelium.
 Acute GN is defined as the sudden onset of hematuria, proteinuria, and red blood cell (RBC) casts in the
urine.
 Acute GN is a condition that appears to be an allergic reaction to a specific infection, most often group A
beta-hemolytic streptococcal infection.

Pathophysiology

 Acute Glomerulonephritis involves both structural changes and functional changes.

 Structurally, cellular proliferation leads to an increase in the number of cells in the glomerular tuft
because of the proliferation of endothelial, mesangial, and epithelial cells.
 The proliferation may be endocapillary (i.e., within the confines of the glomerular capillary tufts) or
extracapillary (ie, in the Bowman space involving the epithelial cells).
 In extracapillary proliferation, proliferation of parietal epithelial cells leads to the formation of crescents,
a feature characteristic of certain forms of rapidly progressive GN.
 Leukocyte proliferation is indicated by the presence of neutrophils and monocytes within the glomerular
capillary lumen and often accompanies cellular proliferation.
 Glomerular basement membrane thickening appears as thickening of capillary walls on light microscopy.
 Electron-dense deposits can be subendothelial, subepithelial, intramembranous, or mesangial, and they
correspond to an area of immune complex deposition.
 Hyalinization or sclerosis indicates irreversible injury.
 These structural changes can be focal, diffuse or segmental, or global.
 Functional changes include proteinuria, hematuria, reduction in GFR (ie, oliguria or anuria), and active
urine sediment with RBCs and RBC casts.
 The decreased GFR and avid distal nephron salt and water retention result in expansion of intravascular
volume, edema, and, frequently, systemic hypertension.

Statistics and Incidences

 Acute Glomerulonephritis represents 10-15% of glomerular diseases.

 Acute GN has a peak incidence in children 6 to 7 years of age and occurs twice as often in boys.
 In the United States, GN comprises 25-30% of all cases of end-stage renal disease (ESRD).
 About one fourth of patients present with acute nephritic syndrome.
 Worldwide, IgA Nephropathy (Berger disease) is the most common cause of GN.
 In Port Harcourt, Nigeria, the incidence of acute GN in children aged 3-16 years was 15.5 cases per year,
with a male-to-female ratio of 1.1:1; the current incidence is not much different.
 A study from a regional dialysis center in Ethiopia found that acute GN was second only
to hypovolemia as a cause of acute kidney injury that required dialysis, accoujting for approximately 22%
of cases.
 Postinfectious GN can occur at any age but usually develops in children.
 Most cases occur in patients aged 5-15 years; only 10% occur in patients older than 40 years.
 Acute GN predominantly affects males (2:1 male-to-female ratio).
Causes

The causal factors that underlie acute GN can be broadly divided into infectious and noninfectious groups.

 Infectious. The most common infectious cause of acute GN is infection by Streptococcus species (ie,

group A, beta-hemolytic).
 Noninfectious. Noninfectious causes of acute GN may be divided into primary renal diseases, systemic
diseases, and miscellaneous conditions or agents.

Clinical Manifestations

 Presenting symptoms appear 1 to 3 weeks after the onset of a streptococcal infection.

 Hematuria. Usually the presenting symptom is grossly bloody urine; the caregiver may describe the urine
as smoky or bloody.
 Periorbital edema. Periorbital edema and/or pedal edema may accompany or precede hematuria.
 Fever. Fever may be 103°F to 104°F at the onset but decreases in a few days to about 100°F.
 Hypertension. Hypertension occurs in 60% to 70% of patients during the first 4 or 5 days.
 Oliguria. Oliguria (production of a subnormal volume of urine) is usually present, and the urine has a high
specific gravity and contains albumin, red and white blood cells, and casts.
 Fluid overload. Observe for periorbital and/or pedal edema; edema and hypertension due to fluid
overload (in 75% of patients); crackles (ie, if pulmonary edema); elevated jugular venous pressure; ascites
and pleural effusion (possible).
 Cerebral symptoms. Cerebral symptoms consisting mainly of headache, drowsiness, convulsions, and
vomiting occur in connection with hypertension in a few cases.

Assessment and Diagnostic Findings

 There are a lot of renal syndromes that may mimic the symptoms of acute GN, so accurate assessment and
diagnosis is essential.

 Initial blood tests. A CBC is performed; a decrease in the hematocrit may demonstrate a dilutional anemia;
in the setting of an infectious etiology, pleocytosis may be evident; electrolyte levels are measured
(particularly the serum potassium), along with BUN and creatinine (to allow estimation of the glomerular
filtration rate [GFR]); the BUN and creatinine levels will exhibit a degree of renal compromise and GFR
may be decreased.
 Complement levels. Differentiation of low and normal serum complement levels may allow the physician
to narrow the differential diagnosis.
 Urinalysis. The urine is dark; its specific gravity is greater than 1.020; RBCs and RBC casts are present; and
proteinuria is observed.
 Streptozyme tests. The streptozyme tests test includes many streptococcal antigens that are sensitive for
screening but are not quantitative, such as DNAase, streptokinase, streptolysin O, and hyaluronidase; the
antistreptolysin O (ASO) titer is increased in 60-80% of patients; increasing ASO titers or streptozyme
titers confirm recent infection.
 Blood and tissue cultures. Blood culture is indicated in patients with fever, immunosuppression,
intravenous (IV) drug use history, indwelling shunts, or catheters; cultures of throat and skin lesions to
rule out Streptococcus species may be obtained.

Medical Management

 Treatment of acute glomerulonephritis (AGN) is mainly supportive, because there is no specific therapy for
renal disease.

 Diet. Sodium and fluid restriction should be advised for treatment of signs and symptoms of fluid
retention (eg, edema, pulmonary edema); protein restriction for patients with azotemia should be
advised if there is no evidence of malnutrition.
  Activity. Bed rest is recommended until signs of glomerular inflammation and circulatory congestion
subside as prolonged inactivity is of no benefit in the patient recovery process.
 Long term monitoring. Long-term studies on children with AGN have revealed few chronic sequelae.

Pharmacologic Management

 The goals of pharmacotherapy are to reduce morbidity, to prevent complications, and to eradicate the
infection.

 Antibiotics. In streptococcal infections, early antibiotic therapy may prevent antibody response to
exoenzymes and render throat cultures negative but may not prevent the development of AGN.
 Loop diuretics. Loop diuretics decrease plasma volume and edema by causing diuresis. The reductions in
plasma volume and stroke volume associated with diuresis decrease cardiac output and,
consequently, blood pressure.
 Vasodilators. These agents reduce systemic vascular resistance, which, in turn, may allow forward flow,
improving cardiac output.
 Calcium channel blockers. Calcium channel blockers inhibit the movement of calcium ions across the cell
membrane, depressing both impulse formation (automaticity) and conduction velocity.

Nursing Management

 Physical examination. Obtain complete physical assessment

 Assess weight. Monitor daily weight to have a measurable account on the fluid elimination.
 Monitor intake and output. Monitor fluid intake and output every 4 hours to know progressing condition
via glomerular filtration.
 Assess vital signs. Monitor BP and PR every hour to know progression of hypertension and basis for
further nursing intervention or referral.
 Assess breath sounds. Assess for adventitious breath sounds to know for possible progression in the
lungs.

Nursing Diagnoses

 Ineffective breathing pattern related to the inflammatory process.

 Altered urinary elimination related to decreased bladder capacity or irritation secondary to infection.
 Excess fluid volume related to a decrease in regulatory mechanisms (renal failure) with the potential of
water.
 Risk for infection related to a decrease in the immunological defense.
 Imbalanced nutrition less than body requirements related to anorexia, nausea, vomiting.
 Risk for impaired skin integrity related to edema and pruritus.
 Hyperthermia related to the ineffectiveness of thermoregulation secondary to infection.

Nursing Care Planning and Goals

 Excretion of excessive fluid through urination.

 Demonstration of behaviors that would help in excreting excessive fluids in the body.
 Improvement of distended abdominal girth.
 Improvement of respiratory rate.
 Participation and demonstration of various ways to achieve effective tissue perfusion.

Nursing Interventions

 Activity. Bed rest should be maintained until acute symptoms and gross hematuria disappear.
 Prevent infection. The child must be protected from chilling and contact with people with infections.
 Monitor intake and output. Fluid intake and urinary output should be carefully monitored and recorded;
special attention is needed to keep the intake within prescribed limits.
 Monitor BP. Blood pressure should be monitored regularly using the same arm and a properly fitting cuff.
 Monitor urine characteristics. The urine must be tested regularly for protein and hematuria using dipstick
tests.