Glomerulonephritis

Reported by:
Marivic J. Miagar
• Each kidney is composed of about 1 million nephrons which is
responsible for filtration and purification of the blood.
• Nephrons are responsible for formation of urine.
Nephrons are made up of 2 basic components:
1. Filtering element composed of an enclosed capillary network (the
glomerulus).
2.The attach tubule
Kidney convert blood plasma into urine in 4 stages:
1. Glomerular filtration
2. Tubular reabsorption
3. Tubular secretion
4. Water conservation

• Glomerulus – is a unique network of capillaries suspended between

the afferent and efferrent blood vessels.
• -The main filter of the nephron and is located within the Bowman’s
Capsule.
• The glomerulus is semipermeable allowing water and soluble
wastes to pass through and to be excreted out of the Bowman’s
capsule as urine.
Parts of Glomerular filtration
 Glomerular Filtration
• 1200mL/min- the normal blood flow through the
kidneys.
• As blood flows into the glomerulus from an afferent
arteriole, the filtration occurs.
• The filtered fluid also known as filtrate or ultrafiltrate,
then enters the renal tubules.
• Under normal conditions, about 20% of the blood
passing through the glomeruli is filtered into the
nephron, amounting to about 180L/day of filtrate.
• The filtrate normally consist of water, electrolytes and
other small molecules are allowed to pass, whereas
larger molecules stay in the blood stream.
 Glomerulonephritis
• Inflammation of the glomerular capillaries caused by
numerous factors including immunologic
abnormalities, ischemia, free radicals, drugs, toxins,
vascular disorders and systemic diseases.
Types of Glomerulonephritis:
1. Acute glomerulonephritis
2. Chronic glomerulonephritis

• In nearly all types of glomerulonephritis, the

epithelial or podocyte layer of the glomerular
membrane disturbed with loss of negative charges
and changes in membrane permeability.
 Types of Glomerular Lesions
Types Characteristics Other
Terms
Diffuse -Involves all glomeruli Primary Disease is mainly in
Focal -Involves some glomeruli glomeruli
Segmental –local -Involves portion of individual
glomeruli Secondary Glomerular diseases
Mesangial -Deposits of immunoglobulins that are the
in the mesanglial matrix, consequence of
mesanglial proliferation systemic diseases
Membranous -Thickening of the glomerular
capillary wall with immune Acute GN Benign and relatively
deposits quick to resolve
Proliferative -Increase in the number of
glomerular cells Rapidly Swiftly advancing
Sclerotic -Glomerular scarring from progressive disorder that can lead to
previous glomerular injury GN death in a matter of few
Crescentic -Accumulation of proliferating month
cells with Bowman space, Chronic GN A long term disease that
making the appearance of a may take years to run its
crescent. course.
 Acute glomerulonephritis
Primary glomerular diseases:
1.Postinfectious glomerulonephritis
2.Rapidly progressive glomerulonephritis
3.Mebrane proliferative glomerulonephritis
4.Membranous glomerulonephritis

• Also known as Acute Nephritic Syndrome, Acute glomerular

nephritis, Acute hemorrhagic glomerulonephritis, Acute
poststreptococcal glomerulonephritis.
• It is most common in boys ages 2 and above but it can
oocur at any age.
• The inflammatory process usually begins with and infection
or an injury (e.g. burn or trauma) then the protective
immune system fights off the infection, scar tissue forms
and the process complete.
• Postinfectious glomerulonephritis- are causes by
group A beta hemolytic streptoccocal infection of
the throat that precedes the onset of
glomerulonephritis by 2 to 3 weeks.
• It may also follow impetigo (infection of the skin)
and acute viral infections (URTI, mumps, varicella
zoster virus, hepatitis B and HIV infection)

• In some patients, antigens outside the body (e.g.

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.
 Acute glomerulonephritis
Signs and Symptoms:
• Hematuria
(microscopic/macroscopic). Urine may appear cola colored because of RBC’s
protein plugs or casts.
• Edema
• Hypertension
• Ascites
• Fever
• Albuminuria
• Muscle weakness
• Fatigue
• Poor appetite
• Decreased GFR
• Oliguria
• Proteinuria
due to increase permeability of the glomerular membrane
Child with papilledema
Diagnostic test:
• Electron microscopy
• Immunofluorescent analysis
• Kidney biopsy
• Urinalysis:
– Decreased output (oliguria)may approach anuria
– Microscopic or gross hematuria
– Specific gravity moderately elevated
– Proteinuria may be mild to severe
– Microscopicâ red blood cells, leukocytes, epithelial cells, and casts
– Low urinary sodium
• Blood urea nitrogen (BUN) and creatinine usually mildly to
moderately elevated; however, normal in 50% of the patients.
• Chest X-ray may show pulmonary congestion, cardiac enlargement
during the edematous phase.
• KUB- bilateral kidney enlargement
Normal kidney Acute Glomerulonephritis
 Complication
The following complications occur infrequently.
• Hypertensive encephalopathy
• Heart failure
• Uremia
• Anemia
 Rapidly Progressive Glomerulonephritis
• Also known as subacute, crescentic or extracapillary
glomerulonephritis.
• An autoimmune disease whereby antibodies are directed
against basal membrane antigens found in the kidney and
lungs.
• The disease develops over a period of days and weeks.
• By the time the RPGN diagnosed, renal insufficiency is
apparent.
• There is extensive proliferation of cells into Bowman space
with crescent formation
• Typically, the glomerular injury is a accompanied by a rapid
decline in glomerular function, progressing to renal failure in a
few weeks or months.
Risk Factors:
• 50’s and 60’s of age
• Idiopathic
• Associated with proliferative glomerular disease
Symptoms:
• Hematuria is common
• Proteinuria
• Edema
• Hypertension
Diagnostic test:
immunohistochemistry
Rapidly Progressive Glomerulonephritis
 Good Pasture Syndrome
• A type of RPGN
• Also known as Antiglomerular basement
membrane disease
• The disease is rare and associated with
antibody formation against both pulmonary
capillary and glomerular basement
membrane, with activation of complement
and neutrophils that damage the GBM.
Risk Factors
• Men, 20-30 of age /
• Often accompanied by pulmonary hemorrhage
• Renal failure
-RPGN has relatively poor prognosis if not
diagnosed and treated early
-Dialysis or Transplantation is required when failure
is irreversible.
-Plasma exchange (plasmepheresis) and treatment
with high-dose corticosteroids and cytotoxic
agents have been used to reduced the
inflammatory response.
 Chronic Glomerulonephritis
• May be due to repeated episodes of acute
nephritic syndrome, hypertensive nphrosclerosis,
hyperlipidemia, chronic tubulointerstitial injury.
• Secondary glomerular diseases that can have
systemic effects include Lupus erythomatosus,
good pastures syndrome , diabetic
glomerulosclerosis .
• There may be no history of renal disease before
the diagnosis.
Chronic Glomerulonephritis
 Signs and Symptoms
Two major changes in the urine are distinctive of more severe
glomerulonephritis:
1.Hematuria with rbc casts
2.Proteinuria exceeding 3 to 5 g/day, with albumin as the major protein.

• Hypertension
• Elevated BUN
• Elevated serum creatinine
• Loss of weight and strength
• Increasing irritability
• Increase need to urinate at night
• headaches
• Dizziness
• Poorly nourished
• With a yellow gray- pigmentation of the skin
• Periorbital and peripheral edema
 Diagnostic test
• Urinalysis- reveals a fixed specific gravity of about
1.010, variable proteinuria and urinary casts
• Chest X-rays may show cardiac enlargement and
pulmonary edema.
• ECG may be normal or may indicate left
ventricular hypertrophy associated with
hypertension
• CT scan and MRI shows a decrease in the size of
the renal cortex.
 Nursing diagnosis taxonomy pertinent to
problem or alteration in:
• Fluid volume excess related to decreased
glomerularfiltration rate
• Imbalanced body temperature related to unknown etiology
(possible infection)
• Imbalanced nutrition: less than body requirements related
to increased glomerular permeability
• Knowledge deficit related to medical management of the
disease
• Anxiety related to outcome of treatment
• Impaired parent-child interaction related to irritability of
the child
• Risk for impaired skin integrity related to edema/ altered
skin turgor
• Risk for infection related to ongoing disease process