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Figure 19. 99mTc-DPTA scan in a normal renal transplant. Both the flow (A) and 1 minute sequential images (B) are normal.

Pathophysiology

Renal artery stenosis causes a drop in pressure in the glomerulus. This would be expected to result in a loss of filtration were it not for compensatory mechanisms instigated by the juxtaglomerular apparatus (JGA). In response to inadequate pressure within the afferent arteriole of the glomerulus, the JGA produces renin which converts angiotensinogen to angiotensin I. Angiotensin I is subsequently converted to angiotensin II, a potent vasconstrictor. Angiotensin II causes constriction of the efferent arteriole and results in increased pressure in the glomerulus and restoration of glomerular filtration. Angiotensin II also stimulates aldosterone which potentiates sodium retention and potassium secretion in the distal nephron. Both angiotensin II and aldosterone contribute to an elevated blood pressure. ACE inhibitors are pharmacologic agents which block the formation of angiotensin II, interrupting the compensatory mechanism of efferent arteriolar vasoconstriction thus lowering GFR in the affected kidney. This serves as the basis for ACE inhibition renography (Fig.

Figure 20. 99mTc-DTPA scan in a renal transplant with moderate acute tubular necrosis (ATN). Perfusion (A) is normal, but on the sequential images (B) uptake in the kidney is impaired and there is poor contrast between kidney and background.

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