Genitourinary Scintigraphy

Renal Imaging

The major renal functions include blood flow, glomerular filtration, tubular function and excretory system fuction.

Radionuclines

Diethylenetriamine pentaacetic acid (Tc-99m-DTPA) is only 5-10% protein bound, and so almost completely glomerular filtered, but has increased extravascular distribution hence lower target-to-background ratio than MAG3 or DMSA. There is also no significant resbsorption and does not reach the urine by any other means, hence is accurate to measure the GFR. GFR is reduced with reduced preglomerular pressure (renal artery stenosis, microvascular disorder, heart failure), increased postglomerular/Bowman space pressure (renal obstruction, acute tubular necrosis, or reduced glomerular membrane permeability (glomerulnephritis)

Glucoheptonate (Tc-99m-GH) is a glucose analog mostly glomerularly filtered, but 10% retained by proximule tubule allowing delayed cortical imaging.

Mercaptoacetyltriglycine (Tc-99m-MAG3) has 5% glomerular filtration, but 55% tubular extraction efficiency and high (90%) protein binding (thus high target-to-background ratio), useful for tubular functional imaging. Total extraction efficiency is 60% (compared to DTPA 20%), hence is agent of choise for imaging moderate to severe renal failure, immature kidneys and transplant kidneys. Since GFR and tubular fuction generally parallel each other, unless GFR required MAG3 is usually performed for GF/tubular function and collecting systems and ureter.

Dimercaptosuccinic acide (Tc-99m-DMSA) has <5% urunary excretion, and high cortical binding (50% at 4hrs) allowing excellent cortical imaging.

Gallium-67 (Ga-67) citrate is useful for infectious and neoplastic processes of the kidneys and perinephric spaces. Indium-111-labeled WBC specific for focal inflammatio and acute infection. Tc-99m-)4 used for scrotal imaging (thyroid should be blocked with oral potassium perchlorate).

Techniques

Flow images can be performed using DTPA, MAG3 or GH. Sequential 1-3sec images obtained (normal arrival to kidney at 1-2sec after reaching aorta) for the 1st min. The kidneys should be as hot or hotter than the spleen on image following aorta bolus. with DTPA and GH, peak activity reached after 6sec and declines before recirculation (only 20% 1st pass extraction) compared to MAG3 where decline in intensity less evident.

Uptake and excretion phases of DTPA and MAG3 15-60sec images over 20-30min.

Uptake/cortical phase continues for 3-4min where it would start to appear in the collecting systems. Differential function computed with ROI on this uptake phase or 4h delayed GH/DMSA with excellent intrapatient and inter-radiotracer reproducibility >95%; normal 45-55%.
Excretory phase starts with arrival to renal pelvis (should be noted), with prolonged/intense accumulations or structural displacement abnormality. In collecting system obstruction a catheter will ensure bladder decompression and monitor urine output; frusemide (20-40mg IV) given 15min before (useful if system known to be markedly dilated) or 20min after tracer; imaging continues for further 20-30min with max frusemide effect at 15min. ROIs over whole kidney, renal cortex, collecting system or renal pelvis. T1/2 = time from tracer or frusemide injection to half max activity of kidney or cortex; normal <10min, may not be able to be calculated in poor renal fuction or collcting system dilatation in a 20-30min exam. Residual cortical or kidney activity = ratio of 20min activity to maximum activity; normal <0.3. <br>

Cortical imaging (DMSA, GH) – static images at 4h (to allow collecting system washout) with post and post oblique of each kidney (or SPECT). Direct radionucline cystography for VUR obtained post upfight as 1min dymanic acquisitions during retrograde filling and voiding.

Renal tracer clearance GFR with DTPA or ERPF (effective renal plasma flow) with MAG3 extimated by assessing rate of disappearance of tracer from blood (cardiac blood pool and/or background), rate of appearance of renal cortical activity, or rate of appearance of urine (usually bladder) activity.

Supine position usually used, but physiologic upright/semiupright sitting can be used when ureteral draininge is evaluated or renal pelvic actity may interfere (but differential function may be inacurate due to mobility of kidneys). For dynamic studies, the injection site should be imaged as a small amount of infiltrated dose can affect quantitative analysis of excretion and uptake. Dehydration can cause false-positive renovascular HTN and collecting system obstruction, and cause variable washout parameters.

Applications

Compared with cysts that are cold, hydronephrosis and urinoma increase tracer with time. Renal masses never accumulate Tc.
Acute renal failure causes:

  • Acute vascular occlusion
  • Venous thrombosis – decreased perfusion, enlarged, prolonged cortical retention
  • Collecting system or bladder outlet obstruction – persistent activity in dilated collecting system
  • Acute tubular necrosis (ATN) – relatively maintained arterial flow. Glomerular filtration drops to near zero (DTPA no uptake), but tubular cell uptake of MAG3 contiues (reduced) as long as cells are viable. Differentiated from high grade obstruction by lack of dilated collecting system.

In transplant patients ARF causes as above plus ATN (1st week) cyclosporine toxicity (variable pattern) or transplant rejection (acute 2nd-4th weeks, chronic late and eventually occurs in all transplants). Rejection causes damage to small vessels with balanced loss of perfusion and function. Infarction and infection show as photopenic defects. Urinomas (early) differentiated from lymphocoeles (late) by presence of activity. Correlation with US required.

Renal artery stenosis (RAS) diagnosis enhanced with ACEI (captopril, enalapril). Haemodynamically significant RAS/renovascular HTN reduces BP in afferent glomerular arteriole, increasing renin by juxtaglomerular apparatus, stimulating conversion of angiotensin I to II and thus constriction of efferent arteriole to maintain glomerular perfusion pressure and thus GFR. ACEIs block conversion to angiotensin II, relaxing the efferent arteriole and dropping GFR increasing transit to renal pelvis. ACEIs have little effect on the unconstricted efferent arteriole of normal kidneys. Hence in RAS MAG3 before and after ACEI (changes less with DTPA and GH) demonstrate reduced and delayed flow with prolonged cortical retention peak and washout with ACEI. Sensitivity and specificity 90%.