Glomerulonephritis: Definition, Pathophysiology, and Management, Lecture notes of Nursing

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GLOMERULONEPHRITIS

Objectives

• (^) By the end of this presentation the students should be able

to:-

1. Define glomerulonephritis

2. Describe the pathophysiology in glomerulonephritis

3. List at least 5 s/s of glomerulonephritis

4. Outline at least 3 assessments and diagnostic finding in

glomerulonephritis

5. Describe the medical and nursing management of

glomerulonephritis

6. Differentiate acute and chronic glomerulonephritis

Glomerular Structure

Composition: A glomerulus consists

of a network of tiny blood vessels

called capillaries, surrounded by as

Bowman's capsule.

Blood Supply: Blood enters the

glomerulus through the afferent

arterioles and exits through the

efferent arterioles.

Intro Glomerulus function

Filtration : The primary function of

the glomeruli is to filter blood. As

blood flows through the capillaries,

water, electrolytes, and small

molecules pass into Bowman's

capsule, forming a filtrate that will

eventually become urine.

Selective Permeability: The

glomerular filtration barrier

selectively allows certain substances

Primary Glomerular Diseases

• (^) A variety of diseases can affect the glomerular capillaries, including acute and chronic glomerulonephritis, rapidly progressive glomerulonephritis, and nephrotic syndrome.
• (^) Antigen–antibody complexes form in the blood and become trapped in the glomerular capillaries (the filtering portion of the kidney), inducing an inflammatory response.
• (^) IgG, the major immunoglobulin (antibody) found in the blood, can be detected in the glomerular capillary walls.

Primary Glomerular Disease

• (^) Major clinical manifestations of glomerular injury include

proteinuria,

• (^) hematuria,
• (^) decreased glomerular filtration rate , and alterations in

excretion of sodium (leading to edema and hypertension).

Proliferative

Glomerulonephritis

• (^) Defin: This type involves an increase in the number of cells within the glomeruli, often in response to injury or inflammation.
• (^) Characteristics:
• (^) Cell Proliferation: Increased numbers of glomerular cells, including mesangial cells and endothelial cells.
• (^) Common Causes: Often associated with autoimmune diseases (e.g., Lupus nephritis), infections (e.g., post-streptococcal glomerulonephritis), and conditions like IgA nephropathy.
• (^) Symptoms: May result in hematuria, proteinuria,

Non-Proliferative

Glomerulonephritis

• (^) Definition: This type is characterized by minimal or no increase in the number of glomerular cells. It mainly affects the structure of the glomeruli rather than causing significant proliferation.
• (^) Characteristics:
• (^) Minimal Change Disease: A common cause in children, characterized by effacement of podocytes and significant proteinuria.
• (^) Focal Segmental Glomerulosclerosis (FSGS): Involves scarring in some glomeruli, leading to proteinuria and potential nephrotic syndrome.
• (^) Symptoms: Typically presents with heavy proteinuria, edema, and hypoalbuminemia, but

Pathophysiology

• (^) In most cases of acute glomerulonephritis, a group A beta

hemolytic 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).

Pathophysiology cont’d…

• (^) 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.

Clinical Manifestations

• (^) Primary presenting feature of acute glomerulonephritis is

hematuria (blood in the urine), which may be microscopic

(identifiable through microscopic examination) or macroscopic

or gross (visible to the eye).

• (^) Urine may appear cola-colored because of RBCs and

protein plugs or casts. (RBC casts indicate glomerular injury.)

Clinical manifestations cont’d…

• (^) Glomerulonephritis may be so mild, that hematuria is

discovered incidentally through a routine microscopic

urinalysis or the disease may be so severe that the patient

has acute renal failure with oliguria.

• (^) Acute glomerulonephritis typically has an abrupt onset

preceded by a latent period between the streptococcal

infection and indications of renal involvement

averaging 10 days

• (^) Proteinuria (primarily albumin), which is present, is due to

the increased permeability of the glomerular membrane.

What areAtypical symptoms

Delirium ( and somnolence

• (^) Uremia: Accumulation of waste products in the blood due to impaired kidney function. High levels of urea and creatinine can lead to neurological symptoms, including drowsiness and confusion.
• (^2). Electrolyte Imbalance
• (^) Common Imbalances: Conditions such as hyperkalemia (high potassium) or hyponatremia (low sodium) can affect brain function.
• (^) Impact on CNS: Electrolyte disturbances can lead to altered mental status, including somnolence and delirium.
• (^) 3. Fluid Overload
• (^) Consequences: Excess fluid retention can lead to hypertension and cerebral edema (swelling of the brain).
• (^) Symptoms: Increased intracranial pressure can result in confusion and lethargy.

Atypical symptoms Delirium ( and somnolence ct

• (^) Infection
• (^) Underlying Conditions: In some cases, glomerulonephritis may follow infections (e.g., post-streptococcal glomerulonephritis).
• (^) Systemic Effects: Infections can lead to fever, malaise, and altered mental status.
• (^) 5. Medications
• (^) Treatment Side Effects: Some medications used to manage glomerulonephritis or its complications may have side effects that cause sedation or confusion