glomerular filtration

Glomerular filtration occurs at the filtration barrier composed of three layers: fenestrated capillary endothelium, glomerular basement membrane (GBM), and podocyte foot processes with slit diaphragms. This barrier permits free filtration of water and small solutes while restricting larger proteins (like albumin) based on both size and charge (the GBM is negatively charged, repelling anionic proteins). Net filtration pressure is determined by Starling forces: glomerular capillary hydrostatic pressure (P_GC, favors filtration) and Bowman's space hydrostatic pressure (P_BS, opposes filtration), along with glomerular capillary oncotic pressure (π_GC, opposes filtration) — Bowman's space oncotic pressure is normally negligible. GFR = Kf × [(P_GC - P_BS) - π_GC]. Afferent and efferent arteriolar tone regulate P_GC and thus GFR and renal blood flow (RBF); autoregulation via myogenic mechanism and tubuloglomerular feedback maintains stable GFR despite BP fluctuations. Clinically, GFR is estimated using creatinine clearance, Cockcroft-Gault, or MDRD/CKD-EPI equations, and is central to diagnosing and staging chronic kidney disease (CKD) and acute kidney injury (AKI). Pathologic changes affecting filtration include: increased GFR with afferent dilation/efferent constriction (early diabetic nephropathy, prostaglandins, ACE inhibitors' effect on efferent arteriole), decreased GFR with NSAIDs (block prostaglandin-mediated afferent dilation) or ACE inhibitors/ARBs (block angiotensin II-mediated efferent constriction) especially in bilateral renal artery stenosis. Loss of the negative charge barrier (e.g., minimal change disease) causes selective albuminuria, whereas structural damage to GBM/podocytes (e.g., diabetic nephropathy, FSGS, membranous nephropathy) causes non-selective proteinuria. Filtration fraction (FF = GFR/RPF) helps distinguish these hemodynamic effects on renal physiology, tested frequently via NSAID/ACEi comparative questions on boards.