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688 PART V Urinary Tract Disorders
Tubular Leak
Normal Afferent Arteriolar Constriction Normal glomerular
VetBooks.ir Normal glomerular plasma flow plasma flow
Decreased
plasma flow
Afferent Efferent
Normal Normal Normal Normal
glomerular glomerular Decreased pressure GFR
hydrostatic filtration hydrostatic Diminished
pressure rate pressure GFR
Normal Leakage
intratubular
pressure
A B C
Obstruction Diminished Permeability
Normal glomerular Normal glomerular Normal glomerular
plasma flow plasma flow plasma flow
Diminished
permeability
Normal Diminished
pressure GFR Diminished Normal Diminished
Normal GFR pressure GFR
pressure
Loss of Loss of
microvilli Increased microvilli
tubular
pressure
D E
FIG 41.2
Mechanisms contributing to decreased GFR and oliguria in AKI. (A) Normal nephron.
Glomerular filtration pressure normally is not impeded to any appreciable extent by the
normally low intratubular pressure. The healthy renal tubular epithelium prevents tubular
fluid from leaking between or across tubular cells. No obstructing material is present
within the tubular lumen and the lumen is completely patent. (B) Afferent arteriolar
vasoconstriction (i.e., vasomotor nephropathy). Glomerular filtration is severely decreased
by constriction of the afferent arteriole. Decreased intraglomerular pressure can result in
azotemia and decreased urine production. (C) Tubular backleak. Filtration pressure may
be normal, but filtered fluid leaks back across the damaged tubular epithelium into the
interstitium. Some fluid also may accumulate within the damaged tubule. Tubular backleak
occurs in patients with more severe tubular injury. Backleak is increased by any concurrent
increase in tubular pressure (see D). (D) Obstruction-increased intratubular pressure.
Increased intratubular pressure occurs proximal to the obstructed segment of the nephron.
The obstruction can be intraluminal or extraluminal, and the resultant increase in pressure
opposes glomerular filtration. The obstructing material can be cellular debris, precipitated
proteins, or occasionally crystalline precipitates. Interstitial edema or cellular infiltrates can
cause extraluminal obstruction and decrease renal blood flow by compressing interstitial
blood vessels. Tubular swelling also can contribute to increased intraluminal pressure.
(E) Decreased glomerular permeability. In this example, the disease process has
decreased the surface area available for glomerular filtration. Decreased glomerular
permeability can arise as a consequence of mesangial cell contraction and decreases in
the number and diameter of the glomerular fenestrae (pores).