Glomerulonephritis

Key Points

• Glomerulonephritis is inflammation of renal glomeruli that impairs filtration of fluid and metabolic waste.
• Acute cases are often immune-triggered after infection; chronic cases can be driven by autoimmune disease and ongoing inflammatory injury.
• Typical findings include hematuria, proteinuria, oliguria, edema, hypertension, and rising BUN/creatinine with falling GFR.
• Severe disease can progress to uremic complications, acute kidney failure, or chronic kidney damage.
• Nursing priorities are infection management, fluid-balance surveillance, blood-pressure control, and structured self-management teaching.

Pathophysiology

Glomerular inflammation damages the filtration membrane and reduces selective permeability control. As inflammation increases, protein and blood can leak into urine while overall filtration capacity declines.

Acute glomerulonephritis commonly follows immune activation after infection (for example streptococcal triggers). Chronic glomerulonephritis reflects sustained inflammatory injury, frequently associated with autoimmune conditions such as systemic-lupus-erythematosus and vasculitic disease patterns.

Classification

• Acute glomerulonephritis: Abrupt inflammatory onset after immune trigger with rapid clinical change.
• Chronic glomerulonephritis: Progressive, long-duration inflammatory damage with ongoing nephron loss.
• Immune-mediated forms: Autoantibody or immune-complex activity driving persistent glomerular injury.
• Secondary inflammatory forms: Infection-, toxin-, or medication-associated inflammatory damage.

Nursing Assessment

NCLEX Focus

Prioritize signs of filtration failure plus fluid-overload and blood-pressure deterioration trends.

• Assess urinary cues: hematuria, proteinuria, oliguria, and changing urine output pattern.
• Assess cardiovascular cues: hypertension, edema, jugular venous distention, and overload-related murmur changes.
• Assess neurologic and GI uremic cues: confusion, nausea, vomiting, poor appetite, and metallic taste.
• Assess integumentary and hematologic cues: pallor, pruritus, petechiae/easy bruising, and anemia-related fatigue.
• Trend kidney and inflammatory diagnostics: BUN, creatinine, GFR, electrolytes, CBC, and urinalysis.
• Review diagnostics for etiology and severity: renal ultrasound or CT, and kidney biopsy when ordered.

Nursing Interventions

• Support treatment of the underlying cause (infectious and immune-mediated pathways) and monitor for response failure.
• Administer and monitor ordered medications (antibiotics, immunosuppressive agents, diuretics, and antihypertensives).
• Monitor daily weights, intake/output, and 24-hour trends to detect early fluid-overload progression.
• Implement ordered sodium/fluid restrictions and edema-reduction supports (for example extremity elevation).
• Coordinate renal-replacement escalation when acute failure develops, including dialysis preparation and monitoring.
• Support plasmapheresis pathways when excessive immune-complex burden is targeted by the treatment plan.
• Teach medication adherence, symptom escalation reporting (worsening edema, reduced urine output), and follow-up attendance.
• Reinforce nutrition planning, including individualized protein guidance based on renal stage and current status.

Renal Deterioration Risk

Delayed control of active glomerular inflammation can progress to acute kidney failure, persistent uremia, and chronic renal damage.

Pharmacology

Drug Class	Examples	Key Nursing Considerations
antibiotics	class-based agents	Use when bacterial trigger is identified; monitor culture/lab response trends.
immunosuppressants	corticosteroids, other agents	Reduce immune-mediated inflammation; monitor infection risk and therapy toxicity.
diuretics	class-based agents	Reduce edema/fluid burden; monitor urine output and electrolytes.
ace-inhibitors	class-based agents	Control blood pressure and reduce proteinuria progression risk.
angiotensin-ii-receptor-blockers	class-based agents	Alternative blood-pressure/proteinuria pathway when clinically indicated.

Clinical Judgment Application

Clinical Scenario

A client with recent streptococcal illness presents with edema, hypertension, oliguria, hematuria, and rising creatinine.

• Recognize Cues: Filtration injury pattern with fluid overload and renal decline.
• Analyze Cues: Active glomerular inflammation is impairing kidney function and increasing complication risk.
• Prioritize Hypotheses: Highest priority is preventing acute decompensation from fluid overload and worsening renal failure.
• Generate Solutions: Intensify monitoring, implement medication/fluid plans, and coordinate diagnostic clarification.
• Take Action: Administer ordered therapy, trend labs and output closely, and escalate deterioration promptly.
• Evaluate Outcomes: Edema and blood pressure improve, urine output stabilizes, and renal trend worsening slows.

Related Concepts

• acute-kidney-injury - Severe glomerular inflammation can precipitate acute renal failure.
• kidney-disease - Chronic progression pathway after persistent glomerular injury.
• peritoneal-and-hemodialysis-nursing-management - Renal replacement support when kidney failure progresses.
• urinalysis-reference-ranges-ua - Hematuria/proteinuria interpretation in glomerular disease.
• serum-creatinine - Primary trend marker for declining renal filtration.
• systemic-lupus-erythematosus - Common autoimmune contributor to chronic glomerular inflammation.

Self-Check

1. Which cue cluster most strongly suggests active glomerular filtration injury rather than isolated lower UTI?
2. Why are daily weight and urine-output trends central to early deterioration detection in glomerulonephritis?
3. When should dialysis or plasmapheresis escalation be considered in severe glomerular disease?