Guide — Renal
Glomerulonephritis Nursing Guide
Nephrotic vs nephritic syndrome differentiation, major glomerulonephritis types (IgA nephropathy, PSGN, minimal change disease, membranous nephropathy, lupus nephritis), diagnostic labs, and nursing priorities for renal nursing care.
11 min read · Renal
Educational use only. Glomerulonephritis diagnosis requires kidney biopsy and nephrology evaluation. Clinical presentations vary significantly — assessment and management are provider-directed. This material supports nursing education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional policy, or medical direction. Always follow facility protocols and current provider orders.
Nephrotic vs Nephritic Syndrome
The two fundamental glomerular syndromes differ in what the damaged glomerulus leaks — protein (nephrotic) or blood (nephritic). Distinguishing them drives diagnosis and management.
| Feature | Nephrotic Syndrome | Nephritic Syndrome |
|---|---|---|
| Proteinuria | > 3.5 g/day (massive) | < 3.5 g/day (mild-moderate) |
| Hematuria | Absent or mild | PRESENT — hallmark (RBC casts) |
| Edema | MASSIVE — periorbital, ascites, anasarca | Mild-moderate (periorbital, peripheral) |
| Blood pressure | Normal or mildly elevated | HYPERTENSION — hallmark |
| Albumin | Low (< 3 g/dL, often < 2) | Normal or mildly reduced |
| Cholesterol | HIGH — hyperlipidemia (compensatory hepatic lipoprotein synthesis) | Normal |
| Urine casts | Fatty casts, oval fat bodies, hyaline casts | RBC casts (pathognomonic for glomerular bleeding) |
| Complement (C3/C4) | Normal (usually) | LOW — consumed by immune complex activation |
| Classic examples | Minimal change disease, membranous nephropathy, FSGS, diabetic nephropathy | IgA nephropathy, PSGN, lupus nephritis (class III/IV), anti-GBM disease |
| Core mnemonic | NASTY PROTEIN: No hematuria, Albumin low, Swelling/edema massive, Triglycerides high, Yearlong (gradual onset) | PHARAOH: Proteinuria (mild), Hematuria (RBC casts), Azotemia, Rising BP, Acute onset, Oliguria, Hypertension |
Glomerulonephritis Types
IgA Nephropathy (Berger's Disease)
Syndrome: Nephritic (predominantly) · Most common primary glomerulonephritis worldwide; young males
| Pathophysiology | IgA immune complex deposition in mesangium → inflammation and mesangial proliferation |
| Presentation | Gross hematuria during or shortly after URI or GI infection ('synpharyngitic hematuria'). May have microscopic hematuria + mild proteinuria between episodes. |
| Key Labs | Elevated serum IgA (~50%); microscopic hematuria with RBC casts; mild-moderate proteinuria; normal complement |
| Treatment | ACE inhibitors/ARBs for proteinuria and BP. Immunosuppression for high-risk (fish oil, corticosteroids). Avoid NSAIDs. |
| Nursing Priority | Monitor for hematuria flares with illness. Teach BP management. Encourage low-sodium diet. Regular nephrology follow-up. |
Post-Infectious Glomerulonephritis (PSGN)
Syndrome: Nephritic · Children > adults; follows group A beta-hemolytic Streptococcus (throat or skin infection); peaks 1–3 weeks post-infection
| Pathophysiology | Streptococcal antigen-antibody immune complex deposition → complement activation → glomerular inflammation |
| Presentation | Acute nephritic syndrome: hematuria (cola/tea-colored urine), edema (periorbital in children), hypertension, oliguria, azotemia. Occurs 1–3 weeks after strep throat; 3–6 weeks after skin infection. |
| Key Labs | RBC casts (hallmark), low C3/C4 (complement consumed), elevated ASO titer, proteinuria (< 3.5 g/day), elevated BUN/Cr |
| Treatment | Supportive: antibiotics for active strep (does NOT prevent GN once established), fluid restriction, antihypertensives, diuretics for edema. No immunosuppression needed. |
| Nursing Priority | Strict I&O monitoring; daily weights; BP control; fluid restriction; salt restriction; check urine color improvements daily; observe for pulmonary edema. |
Minimal Change Disease (MCD)
Syndrome: Nephrotic · Most common nephrotic syndrome in children (ages 2–8); associated with allergies, NSAIDs, lithium, lymphoma (adults)
| Pathophysiology | Loss of glomerular polyanion (negative charge barrier) → selective loss of albumin without structural change visible on light microscopy (foot process effacement on electron microscopy) |
| Presentation | Acute nephrotic syndrome: massive proteinuria (> 3.5 g/day), hypoalbuminemia, generalized edema (periorbital, ascites, anasarca), hypercholesterolemia |
| Key Labs | Massive proteinuria, low albumin (often < 2 g/dL), hyperlipidemia, lipiduria (oval fat bodies, Maltese cross pattern); normal complement; NO hematuria or RBC casts |
| Treatment | Corticosteroids (prednisone) — first-line. Frequent relapsers: cyclophosphamide, mycophenolate, rituximab. Albumin infusion for severe edema. Salt restriction. |
| Nursing Priority | Daily weights (edema monitoring); strict I&O; skin care for edematous tissue; albumin infusion administration; steroid side effect teaching; infection prevention (immunosuppressed). |
Membranous Nephropathy
Syndrome: Nephrotic · Most common nephrotic syndrome in non-diabetic adults (40–60 years); associated with hepatitis B, autoantibodies (anti-PLA2R), drugs (gold, penicillamine, NSAIDs), malignancy
| Pathophysiology | Immune complex deposition on outer (subepithelial) surface of glomerular basement membrane → GBM thickening → protein loss |
| Presentation | Gradual onset nephrotic syndrome; often initially asymptomatic; edema and fatigue develop |
| Key Labs | Massive proteinuria (selective or non-selective), hypoalbuminemia, hyperlipidemia, elevated anti-PLA2R antibody (primary form); normal complement (unlike PSGN) |
| Treatment | ACE/ARBs, immunosuppression (cyclophosphamide + corticosteroids, rituximab for anti-PLA2R positive). Anticoagulation if hypercoagulable. |
| Nursing Priority | Monitor for thromboembolism (DVT/PE/renal vein thrombosis) — major complication. Anticoagulation monitoring. Lipid management. Protein-restricted diet education. |
Lupus Nephritis (Secondary GN)
Syndrome: Mixed nephrotic + nephritic (class III/IV) · Occurs in ~50% of SLE patients; young women of color disproportionately affected; class III/IV = most severe
| Pathophysiology | Anti-dsDNA and anti-Smith antibodies form immune complexes → deposit throughout glomerulus → complement activation → diffuse inflammation |
| Presentation | Variable by class. Ranges from asymptomatic hematuria/proteinuria (class I/II) to rapidly progressive GN with nephrotic + nephritic syndrome combined (class III/IV) |
| Key Labs | Anti-dsDNA antibodies, low C3/C4 (consumed), hematuria + RBC casts + proteinuria, elevated creatinine; biopsy required for classification |
| Treatment | Hydroxychloroquine (all SLE patients). Class III/IV: high-dose corticosteroids + mycophenolate or cyclophosphamide. Rituximab for refractory. Kidney transplant for ESRD. |
| Nursing Priority | BP management (target < 130/80); sun protection (photosensitivity worsens SLE); medication adherence (hydroxychloroquine, immunosuppression); monitor CBC, LFTs, creatinine on immunosuppression; infection vigilance. |
Nursing Priorities — Glomerular Disease
| Priority | Nursing Action |
|---|---|
| Fluid balance | Daily weights (same scale, same time, same clothing). Strict I&O. Edema assessment (1+ to 4+ grading). Fluid and sodium restrictions as ordered. |
| Blood pressure | Q4–8h BP monitoring. ACE inhibitors/ARBs reduce both BP and proteinuria (renoproductive effect). Sodium restriction supports BP control. Target BP < 130/80 mmHg. |
| Urine monitoring | Monitor urine output (oliguria indicates declining function). Urine dipstick for protein. Color assessment for hematuria resolution. 24h urine protein collection technique teaching. |
| Labs monitoring | Creatinine and BUN trends. Potassium (hyperkalemia risk with renal dysfunction + ACE/ARBs). Albumin levels. Complement levels (C3/C4). CBC on immunosuppression. |
| Infection prevention | Nephrotic patients: hypogammaglobulinemia (immunoglobulins lost in urine) → increased infection susceptibility. Immunosuppression adds risk. Pneumococcal vaccine, hand hygiene, avoid sick contacts. |
| Thromboembolism | Nephrotic syndrome: hypercoagulable state (loss of antithrombin III, protein C/S in urine). Watch for DVT, PE, renal vein thrombosis. Anticoagulation may be prescribed. Sequential compression devices. |
| Skin care | Severe edema → impaired skin integrity. Reposition frequently. Protect bony prominences. Scrotal or labial edema in nephrotic syndrome requires supportive care. |
| Nutrition | Adequate protein intake (replace urinary losses in nephrotic syndrome). Sodium restriction (< 2g/day for edema). Avoid high-potassium foods if hyperkalemic. |
NCLEX Pearls
RBC casts = glomerular bleeding = nephritic syndrome. No other cause produces RBC casts.
Massive proteinuria + edema + low albumin + high cholesterol = nephrotic syndrome. Hematuria absent or mild.
PSGN follows strep infection by 1–3 weeks (throat) or 3–6 weeks (skin). Not during the infection — AFTER. Low complement (C3) is hallmark.
Minimal change disease: most common nephrotic syndrome in children. Responds dramatically to prednisone. Normal light microscopy — electron microscopy shows foot process effacement.
Periorbital edema in children is characteristic of nephrotic syndrome — noticed first thing in morning (dependent edema redistributes overnight).
Nephrotic syndrome = hypercoagulable → watch for DVT, PE, and renal vein thrombosis.
ACE inhibitors/ARBs reduce proteinuria and slow CKD progression in glomerular disease regardless of BP.
Daily weight is the best method to monitor fluid balance in glomerular disease (1 kg = ~1 L).
Related Resources
Standards & sources
Fact-checked Jun 21, 2026This page is written to align with KDIGO Clinical Practice Guidelines · National Kidney Foundation (NKF). It is an educational summary, not a citation of any single document — always verify specific doses, values, and protocols against current guidelines and your facility policy. How we source content →