157. Nephritic and nephrotic syndrome - etiology, pathogenesis, clinical manifestations.

Nephritic syndrome

Definition

A clinical syndrome characterized by glomerular inflammation leading to hematuria, reduced GFR, mild proteinuria, and hypertension.

Etiology

• Post-infectious glomerulonephritis (e.g., after streptococcal pharyngitis or skin infection).
• IgA nephropathy (Berger disease).
• Lupus nephritis.
• Membranoproliferative GN.
• Goodpasture syndrome (anti- GBM disease).
• Crescentic (rapidly progressive) GN.

Pathogenesis

1. Immune complex deposition or autoantibody binding in glomeruli.
2. Complement activation → attraction of neutrophils and monocytes.
3. Release of proteases and reactive oxygen species → glomerular basement membrane (GBM) damage.
4. Proliferation of mesangial and endothelial cells → hypercellularity and decreased filtration surface.
5. Reduced GFR → oliguria, azotemia, sodium and water retention → hypertension.

Clinical manifestations

• Hematuria (cola or tea- colored urine), RBC casts.
• Oliguria (reduced urine output).
• Mild to moderate proteinuria (<3.5 g/day).
• Hypertension.
• Edema (mild, usually periorbital or dependent areas).
• Possible azotemia (elevated BUN, creatinine).

Nephrotic syndrome

Definition

A clinical syndrome marked by heavy proteinuria (>3.5 g/day), hypoalbuminemia, severe generalized edema, hyperlipidemia, and lipiduria.

Etiology

• Primary glomerular diseases:
• Minimal change disease (most common in children).
• Focal segmental glomerulosclerosis (FSGS).
• Membranous nephropathy.
• Membranoproliferative GN.
• Secondary causes:
• Diabetes mellitus (diabetic nephropathy).
• Lupus nephritis.
• Amyloidosis.
• Infections (e.g., hepatitis B, C).

Pathogenesis

1. Podocyte injury or GBM damage → increased permeability to proteins.
2. Massive protein loss in urine → hypoalbuminemia.
3. Decreased plasma oncotic pressure → fluid moves into interstitial space → generalized edema (anasarca).
4. Compensatory hepatic synthesis of lipoproteins → hyperlipidemia, lipiduria.
5. Loss of antithrombin III and other anticoagulant factors → hypercoagulable state.

Clinical manifestations

• Severe generalized edema (anasarca), often first seen as periorbital swelling.
• Heavy proteinuria (>3.5 g/day).
• Hypoalbuminemia.
• Hyperlipidemia and lipiduria (fat bodies in urine — "Maltese cross" appearance).
• Increased risk of thromboembolism.
• Possible infections (loss of immunoglobulins).

Summary table

Conclusion

Nephritic and nephrotic syndromes represent distinct patterns of glomerular diseases, with nephritic syndrome dominated by inflammation and hematuria, while nephrotic syndrome is characterized by severe protein loss and massive edema.

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Here’s a complete, clear, and detailed note on interstitial nephritis and polycystic kidney disease, including classification, etiology, pathogenesis, and clinical manifestations —fully academic but easy to understand and memorize.