Chart — Renal
Nephrotic vs Nephritic Syndrome Chart
Side-by-side comparison of nephrotic and nephritic syndrome — proteinuria levels, hematuria, edema type and severity, blood pressure, albumin, cholesterol, complement levels, urine casts, classic examples by age group, treatment approach, and NCLEX memory aids.
Chart · Renal
Educational use only. Many glomerular diseases (e.g., lupus nephritis Class III/IV) present with MIXED features of both syndromes. Kidney biopsy is required for definitive diagnosis. 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 Syndrome
Protein leaks out
Massive proteinuria → hypoalbuminemia → edema → hyperlipidemia
NEPHRITIC Syndrome
Blood leaks out
Inflammation → hematuria → hypertension → oliguria → azotemia
| Feature | Nephrotic Syndrome | Nephritic Syndrome |
|---|---|---|
| Core mechanism | Glomerular filtration barrier PERMEABILITY to PROTEIN lost → massive protein leak into urine | Glomerular INFLAMMATION → hematuria + mild protein leak + edema + hypertension |
| Proteinuria | MASSIVE — > 3.5 g/day (adult). May reach 15–30 g/day. Often described as 'heavy' or 'nephrotic-range' proteinuria. | Mild-moderate — < 3.5 g/day. Protein present but NOT the dominant feature. |
| Hematuria | ABSENT or minimal. No RBCs in urine (protein leaks, not blood). No RBC casts. | PRESENT — hallmark finding. Gross (cola/tea-colored urine) or microscopic. RBC casts pathognomonic. |
| Edema | MASSIVE — periorbital edema (classic in children — worse on waking), peripheral pitting edema, ascites, pleural effusions, scrotal/labial edema, anasarca (4+ edema). Caused by hypoalbuminemia → reduced oncotic pressure. | Mild-moderate — periorbital or facial edema, peripheral edema. Caused by sodium and water retention (RAAS activation). |
| Blood pressure | Often NORMAL or mildly elevated (though can be hypertensive depending on underlying disease). | HYPERTENSION — hallmark. Sodium and water retention → volume-mediated hypertension. Can be severe. |
| Serum albumin | LOW — typically < 3 g/dL, often < 2 g/dL in severe cases. Albumin lost in urine faster than liver can synthesize. | Normal or mildly reduced (protein leakage is less, liver can compensate). |
| Cholesterol / Lipids | HIGH — hyperlipidemia (elevated LDL, VLDL, total cholesterol). Compensatory hepatic lipoprotein synthesis triggered by hypoalbuminemia and decreased oncotic pressure. | Normal — liver synthesis not triggered (albumin levels maintained). |
| Lipiduria | PRESENT — lipids in urine. Oval fat bodies (lipid-laden tubular cells). Fatty casts with Maltese cross pattern under polarized light. | Absent. |
| Urine casts | Fatty casts, oval fat bodies (Maltese cross), hyaline casts. No RBC casts. | RBC casts — PATHOGNOMONIC for glomerular bleeding (hallmark). Also granular casts. |
| Complement (C3/C4) | Usually NORMAL — immune complex deposition not a feature of most nephrotic diseases. | Usually LOW (consumed) — C3/C4 decreased in immune complex deposition diseases (PSGN, lupus nephritis, MPGN). Exception: IgA nephropathy has normal complement. |
| Azotemia / Creatinine | Usually normal early. Rises with advanced disease or when thrombosis occludes renal vessels. | Elevated — AKI common in acute nephritic syndrome. Reduced GFR from inflammation and reduced filtration surface. |
| Thrombosis risk | HIGH — hypercoagulable state from loss of antithrombin III, protein C/S in urine. DVT, PE, renal vein thrombosis. Renal vein thrombosis most associated with membranous nephropathy. | Low-normal thrombosis risk. |
| Onset | Often gradual — edema noticed over days to weeks. | Often ACUTE — sudden onset of hematuria, hypertension, oliguria. |
| Classic examples — PEDIATRIC | Minimal Change Disease (MCD) — most common nephrotic syndrome in children. Responds to steroids in 90% within 8 weeks. Normal light microscopy (electron microscopy: foot process effacement). | Post-Infectious GN (PSGN) — follows strep throat (1–3 weeks) or skin infection (3–6 weeks). Most common nephritic syndrome in children. Hematuria + cola-colored urine. |
| Classic examples — ADULT | Membranous Nephropathy — most common in non-diabetic adults (40–60y). Anti-PLA2R antibody. High DVT/renal vein thrombosis risk. Secondary: hepatitis B, lupus, drugs. Focal Segmental Glomerulosclerosis (FSGS) — most common in African Americans; associated with HIV, heroin. Diabetic Nephropathy — most common cause of nephrotic syndrome in diabetics and most common cause of ESRD worldwide. | IgA Nephropathy (Berger's disease) — most common primary GN worldwide. Hematuria during URI ('synpharyngitic'). Normal complement. Lupus Nephritis (Class III/IV) — mixed nephrotic + nephritic features. Low complement, anti-dsDNA antibodies. Anti-GBM disease (Goodpasture's) — hemoptysis + hematuria. Linear IgG deposits on GBM. |
| Treatment approach | Corticosteroids (especially MCD — dramatic response). Immunosuppressants for steroid-resistant. ACE/ARB to reduce proteinuria. Sodium restriction for edema. Salt-poor albumin infusion for severe edema. Statins for hyperlipidemia. Anticoagulation if high thrombosis risk. | Treat underlying cause. Antibiotics (PSGN — if active strep infection; does NOT reverse established GN). Fluid/salt restriction for hypertension and edema. Antihypertensives. Pulse steroids for acute necrotizing GN. Immunosuppression for lupus nephritis. |
| Nursing priority | Daily weights + strict I&O for fluid monitoring. Edema assessment and skin protection. Infection prevention (hypogammaglobulinemia from protein loss). DVT prevention + anticoagulation monitoring. Steroid side effect education (hyperglycemia, HTN, adrenal suppression). | BP monitoring (frequent). Fluid restriction. I&O monitoring (oliguria). Urine color assessment. Electrolyte monitoring (hyperkalemia with AKI). Educate on strep exposure prevention (PSGN recurrence). |
| NCLEX memory aid | THINK OIL: protein goes OUT (proteinuria), cholesterol goes IN (hyperlipidemia), albumin goes DOWN (hypoalbuminemia), edema goes UP (anasarca). Fatty casts = oil droplets. NO blood in urine. | THINK BLOOD: hematuria (cola-colored), hypertension, oliguria, RBC casts, low complement. Like a kidney that is BLEEDING and INFLAMED. BPH (Blood + Pressure + Hyaline cast → wrong, it's RBC casts). |
Nephrotic — Quick Review
- > 3.5 g/day proteinuria
- Hypoalbuminemia (< 3 g/dL)
- Hyperlipidemia (elevated LDL, cholesterol)
- Massive edema (anasarca, ascites)
- Fatty casts / oval fat bodies
- NO RBC casts; NO significant hematuria
- Thromboembolism risk (antithrombin III loss)
- Normal complement (most types)
Nephritic — Quick Review
- Hematuria (gross: cola/tea-colored)
- RBC casts — pathognomonic
- < 3.5 g/day proteinuria (mild)
- Hypertension (hallmark)
- Oliguria + azotemia (elevated Cr)
- Low complement (C3/C4) in most types
- Mild edema (less than nephrotic)
- Acute onset (often follows infection)
NCLEX Key Distinctions
Massive proteinuria + edema = NEPHROTIC. Even without knowing the disease, massive foam/protein + anasarca = nephrotic.
RBC casts + cola urine = NEPHRITIC. RBC casts are pathognomonic — only produced by glomerular bleeding.
Periorbital edema in a child + proteinuria = Minimal Change Disease (most common nephrotic in children). Dramatic steroid response.
Cola-colored urine in a child 1–3 weeks after strep throat = PSGN (most common nephritic in children). Low C3. Expect full recovery.
Membranous nephropathy = highest DVT/renal vein thrombosis risk in nephrotic diseases. Watch for flank pain, asymmetric leg swelling.
Fatty casts / Maltese cross under polarized light = nephrotic syndrome.
Daily weight is the best way to monitor edema and fluid status in glomerular disease. 1 kg = ~1 L fluid.
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 →