Glomerulonephritis

Marivic J. Miagar
Reported by:

 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 Bowmans Capsule. The glomerulus is semipermeable allowing water and soluble wastes to pass through and to be excreted out of the Bowmans 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 Diffuse Focal Segmental local Mesangial Characteristics -Involves all glomeruli -Involves some glomeruli -Involves portion of individual glomeruli -Deposits of immunoglobulins in the mesanglial matrix, mesanglial proliferation -Thickening of the glomerular capillary wall with immune deposits -Increase in the number of glomerular cells -Glomerular scarring from previous glomerular injury -Accumulation of proliferating cells with Bowman space, making the appearance of a crescent. Other Terms Primary Disease is mainly in glomeruli Glomerular diseases that are the consequence of systemic diseases

Secondary

Membranous

Acute GN

Proliferative Sclerotic Crescentic

Benign and relatively quick to resolve

Swiftly advancing disorder that can lead to death in a matter of few month A long term disease that may take years to run its course.

Rapidly progressive GN Chronic GN

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 RBCs 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 Microscopic 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: 50s and 60s 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