## Analysis of GFR Determinants ### The Starling Equation for Filtration Net filtration pressure (NFP) determines GFR: $$NFP = (P_{GC} - P_{BS}) - (\pi_{GC} - \pi_{BS})$$ Where: - $P_{GC}$ = glomerular hydrostatic pressure - $P_{BS}$ = Bowman's space hydrostatic pressure - $\pi_{GC}$ = glomerular oncotic pressure - $\pi_{BS}$ = Bowman's space oncotic pressure ### Evaluation of Each Option | Statement | Correct? | Reason | |-----------|----------|--------| | Kf proportionality | ✓ Yes | GFR = Kf × NFP; Kf = hydraulic permeability × surface area | | Plasma oncotic pressure ↑ → GFR ↓ | ✓ Yes | ↑ $\pi_{GC}$ opposes filtration, reducing NFP | | Autoregulation (80–180 mmHg) | ✓ Yes | Myogenic + tubuloglomerular feedback maintain constant GFR | | Efferent constriction → ↑ GFR | ✗ **Wrong** | Efferent constriction increases $P_{GC}$ but **decreases** renal plasma flow and filtration fraction; net effect is **minimal or decreased GFR** | ### Why Option 3 Is Incorrect **Key Point:** Efferent arteriole constriction has **two opposing effects**: 1. ↑ Glomerular hydrostatic pressure (favors filtration) 2. ↓ Renal plasma flow (reduces filtration fraction and GFR) The **decrease in plasma flow dominates**, so GFR typically decreases or remains unchanged. This is unlike **afferent constriction**, which decreases both $P_{GC}$ and GFR. **Clinical Pearl:** Angiotensin II causes efferent > afferent constriction, maintaining GFR despite reduced renal blood flow — a mechanism of GFR preservation in volume depletion. **High-Yield:** In contrast, NSAIDs block prostaglandin-mediated afferent vasodilation, causing **afferent constriction** and **GFR decline** — especially dangerous in volume-depleted or CKD patients.
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