Renal Pathophysiology

Na + -K +

Na +

Increased distal NaCl to

intracellular calcium

„ FIGURE 11.6. Vascular and tubular processes leading to reduced glomerular filtration rate (GFR) in ischemic acute tubular necrosis (ATN). eNOS, endothelial nitric oxide synthase; TJ, tight junction. (Modified with permission of American Society for Clinical Investigation from Schrier RW, Wang W, Poole B, et al. Acute renal failure: definitions, diagnosis, pathogenesis, and therapy. J Clin Invest . 2004;114[1]:5-14, permis sion conveyed through Copyright Clearance Center, Inc.) 321

Tubuloglomerular feedback

Increased

reabsorption

translocation

TJ disruption

macula densa

Decreased proximal

Backleak

Nitric oxide caspases

Increased necrosis Apoptosis

Increased tubular obstruction

Tubular effects

metalloproteinases

Cast

Aberrant

adhesion

formation

of viable and nonviable

tubular cells

Detachment

Renal ischemia

Decreased

prostaglandins

endothelial injury

GFR

Increased

Increased

endothelin

Vascular effects

Decreased

nitric oxide

from eNOS

adhesion

inflammatory cytokines

Increased

Increased

Increased

neutrophil

oxygen radicals

calcium

in afferent arteriole

cytosolic

Increased

Increased sensitivity to vasoconstrictor

and renal nerve stimulation; impaired autoregulation

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