GLOMERULONEPH

RITIS
MR. LUKUYU
 ACUTE GLOMERULONEPHRITIS

Glomerulonephritis is an inflammation of the

glomerular capillaries. Acute glomerulonephritis is
primarily a disease of children older than 2 years of age,
but it can occur at nearly any age.
 Pathophysiology

• In most cases of acute glomerulonephritis, a group A betahemolytic streptococcal

infection of the throat precedes the onset of glomerulonephritis by 2 to 3 weeks.
• It may also follow impetigo (infection of the skin) and acute viral infections (upper
respiratory tract infections, mumps, varicella zoster virus, Epstein-Barr virus,
hepatitis B, and human immunodeficiency virus infection).
• In some patients, antigens outside the body (eg, medications, foreign serum) initiate
the process, resulting in antigen-antibody complexes being deposited in the
glomeruli. In other patients, the kidney tissue itself serves as the inciting antigen.
Antigen (group A beta-hemolytic streptococcus)

Antigen-antibody product

Deposition of antigen–antibody complex in glomerulus

Increased production of epithelial cells lining the glomerulus

Leukocytes infiltrate the glomerulus

Thickening of the glomerular filtration membrane

Scarring and loss of glomerular filtration membrane

Decreased glomerular filtration rate (GFR)

 Clinical Manifestations

• The primary presenting feature of acute glomerulonephritis is hematuria (blood in the urine),
which may be microscopic or macroscopic or gross. The urine may appear cola-colored because of
RBCs and protein plugs or casts. (RBC casts indicate glomerular injury.)
• acute renal failure with oliguria.
• Azootemia
• Proteinuria (primarily albumin), which is present, is due to the increased permeability of the
glomerular membrane.
• BUN and serum creatinine levels may rise as urine output drops.
• The patient may be anemic.
• edema and hypertension
• headache, malaise, and flank pain.
• Elderly patients may experience circulatory overload with dyspnea,
engorged neck veins, cardiomegaly, and pulmonary edema.
• Atypical symptoms include confusion, somnolence, and seizures.
 Assessment and Diagnostic Findings

• Electron microscopy and immunofluorescent analysis help identify the

nature of the lesion;
• kidney biopsy may be needed for definitive diagnosis.
• Serial determinations of antistreptolysin O or anti-DNase B titers are
usually elevated in poststreptococcal glomerulonephritis.
• Urinalysis
 Medical Management

• Management consists primarily of treating symptoms, attempting to preserve kidney function, and
treating complications promptly.
• If residual streptococcal infection is suspected, penicillin is the agent of choice; however, other
antibiotic agents may be prescribed.
• Corticosteroids and immunosuppressant medications may be prescribed for patients with rapidly
progressive acute glomerulonephritis, but in most cases of poststreptococcal acute glomerulonephritis,
these medications are of no value and may actually worsen the fluid retention and hypertension.
• Dietary protein is restricted when renal insufficiency and nitrogen retention (elevated BUN) develop.
• Sodium is restricted when the patient has hypertension, edema, and heart failure.
• Loop diuretic medications and antihypertensive agents may be prescribed to control hypertension.
 Nursing Management

• Carbohydrates are given liberally to provide energy and reduce the catabolism of protein.
• Intake and output are carefully measured and recorded.
• Fluids are given according to the patient’s fluid losses and daily body weight. Insensible fluid loss
through the respiratory and GI tracts (500 to 1,000 mL) is considered when estimating fluid loss.
• patient education for safe and effective self-care at home.
 COMPLICATIONS
• Hyperkalemia due to decreased potassium excretion, acidosis, catabolism,
and excessive potassium intake from food and medications
• Metabolic acidosis from decreased acid secretion by the kidney and
inability to regenerate bicarbonate
• Anemia secondary to decreased erythropoiesis (production of RBCs)
• Hypoalbuminemia with edema secondary to protein loss through the
damaged glomerular membrane
 CHRONIC GLOMERULONEPHRITIS

Pathophysiology
• Chronic glomerulonephritis may be due to repeated episodes of acute glomerulonephritis, hypertensive
nephrosclerosis, hyperlipidemia, chronic tubulointerstitial injury, or hemodynamically mediated
glomerular sclerosis.
• The kidneys are reduced to as little as one-fifth their normal size (consisting largely of fibrous tissue).
• The cortex shrinks to a layer 1 to 2 mm thick or less.
• Bands of scar tissue distort the remaining cortex, making the surface of the kidney rough and irregular.
• Numerous glomeruli and their tubules become scarred, and the branches of the renal artery are
thickened. The result is severe glomerular damage that results in ESRD.
 CLINICAL FEATURES
• Usually asymptomatic: discovered when hypertension or elevated BUN and serum creatinine
levels are detected
• vascular changes or retinal hemorrhages
• severe nosebleed, a stroke, or a seizure.
• feet are slightly swollen at night.
• loss of weight and strength,
• increasing irritability,
• increased need to urinate at night (nocturia).
• Headaches, dizziness, and digestive disturbances are common.
 Late signs
• The patient appears poorly nourished, with a yellow-gray pigmentation of the skin and periorbital
and peripheral (dependent) edema.
• Blood pressure may be normal or severely elevated.
• Retinal findings include hemorrhage, exudate, narrowed tortuous arterioles, and papilledema.
• Mucous membranes are pale because of anemia.
• Cardiomegaly, a gallop rhythm, distended neck veins, and other signs and symptoms of heart
failure may be present.
• Crackles can be heard in the lungs.
• Peripheral neuropathy with diminished deep tendon reflexes and neurosensory changes
 Assessment and Diagnostic Findings

• A number of laboratory abnormalities occur. Urinalysis reveals a fixed specific gravity of about 1.010, variable proteinuria, and
urinary casts (protein plugs secreted by damaged kidney tubules). As renal failure progresses and the GFR falls below 50
mL/min, the following changes occur:
• Hyperkalemia due to decreased potassium excretion, acidosis, catabolism, and excessive potassium intake from food and
medications
• Metabolic acidosis from decreased acid secretion by the kidney and inability to regenerate bicarbonate
• Anemia secondary to decreased erythropoiesis (production of RBCs)
• Hypoalbuminemia with edema secondary to protein loss through the damaged glomerular membrane
• Increased serum phosphorus level due to decreased renal excretion of phosphorus
• Decreased serum calcium level (calcium binds to phosphorus to compensate for elevated serum phosphorus levels)
• Hypermagnesemia from decreased excretion and inadvertent ingestion of antacids containing magnesium
• Impaired nerve conduction due to electrolyte abnormalities and uremia
• Chest x-rays may show cardiac enlargement and pulmonary edema.
• The electrocardiogram may be normal or may indicate left ventricular
hypertrophy associated with hypertension and signs of electrolyte
disturbances, such as tall, tented (or peaked) T waves associated with
hyperkalemia.
• Serum markers, including vascular endothelial growth factor and
thrombospondin-1, are being evaluated for their reliability in assessing
renal disease
 management
• Treatment of hypertension
• diuretics
• dialysis
 assignment
• Nursing management and complications