TO THE EDITOR:
A recent interesting paper by Fine et al. (1) raises both conceptual and technical questions. Whether or not any test is necessary depends on one’s point of view. The authors conclude that mean transit time (MTT) analysis is not necessary for 99mTc-diethylenetriaminepentaacetic acid (DTPA) captopril renography. The authors acknowledge “the theoretic advantages” of parenchymal MTT compared with other renographically determined indices. As the authors state, the key issue is the attempt to move from what may be called “curveology” (i.e., taking 2 points on the time–activity curve with empirical evaluation) to measurements related to the underlying pathophysiology of renovascular disorder (RVD). In the study, the reduction in perfusion pressure was transduced into an MTT measurement that was prolonged in renovascular hypertension, because of the increased salt and water reabsorption in the proximal tubule and the increased water reabsorption in the collecting ducts in functionally significant RVD. To make this move, a robust technique of deconvolution was required. The authors appear to have deconvolved a 3-s frame rate for 8 min where counting rates per time interval are too low for good statistical analysis compared with 10-s intervals. Also, they used DTPA but only in a 185-MBq (5 mCi) dose instead of the 370-MBq (10 mCi) dose required for optional deconvolution and instead of the better-extracted mercaptoacetyltriglycine (MAG3). This may well explain the poor results in RVD obtained with both MTT and the empirical curveology methods they used. These results are all poor compared with the European multicenter trial of Fommei et al. (2) with 99mTc-DTPA.
The main criticism is the authors’ (1) lack of outcome data. The authors equate RVD with renal artery stenosis (RAS); yet, small vessel disease is the most common cause of RVD and, with such a high percentage of patients with poor overall renal function, small vessel disease is likely. Without evidence of correction of large vessel disease causing RVD with subsequent reduction of blood pressure, no certainty can be given that the RAS was functionally significant. Furthermore, the age range is not given for group II. If they are elderly, essential hypertension is common, as is atheroma, including that of the renal artery. This association does not imply causation.
Before MTT is considered to be unnecessary, the results should be obtained with the original validated method with 99mTc-MAG3 and a 10-s frame rate (3), which predicted a successful blood pressure lowering in 20 of 23 patients (87%) (4). It is this outcome that the pathophysiology measured by MTT predicts, not whether there is a narrowing of a renal artery. If a simpler index of MTT is required, then the corticopelvic transfer time—the time of the first appearance of activity at the kidney to the first appearance of activity in the pelvis—described by Makoba et al. (5), which has a respectable relation to MTT, is an objective alternative to empirical curveology.
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REPLY:
We have reviewed Dr. Britton’s comments regarding our investigation of diethylenetriaminepentaacetic acid (DTPA) mean transit time (MTT) in the evaluation of patients suspected of having renovascular hypertension (1). Several of Dr. Britton’s assertions require a response.
Dr. Britton suggests that we concluded that “MTT analysis is not necessary for 99mTc-DTPA captopril renography.” In fact, our conclusion was limited to patients with reduced renal function. In these individuals the value of MTT analysis using DTPA was not supported by our data. We drew no conclusion about the general utility of MTT, but it may be inferred from Figure 1 of our study (1) that the diagnostic value of MTT decreases with declining renal function and improves with improving renal function, similar to other methods of assessing renography.
He indicates that our deconvolution 3-s frame rate was too short for optimal statistics. In fact, we did acquire data at 3-s framing intervals but regrouped 7 frames at a time in our analysis. The 21-s intervals and other technical aspects referenced in the original study (1) are described by our colleagues, Rottman and Zhang (2).
Dr. Britton criticizes the fact that we used only 185-MBq (5 mCi) doses of DTPA. However, we actually used both 185-MBq (5 mCi; precaptopril) and 370-MBq (10 mCi; postcaptopril) activities of DTPA. We did not report our results for 370-MBq injections of DTPA because they were no different from the results for 185 MBq.
He also states that our results were poor compared with those of the European multicenter trial. We are uncertain what Dr. Britton means here because the European multicenter trial (3) did not report on MTT. In any event, using other measures of abnormality, their results for patients with renal dysfunction showed reduced accuracy (67% for postcaptopril examination) compared with their subjects with normal renal function. Our results for subjects with renal dysfunction were comparable (54%–61% accuracy).
His main criticism is our lack of outcome data. We heartily agree, and we acknowledge this limitation of our study. We disagree, however, that convincing outcome data exist in the literature supporting the value of MTT in patients with renal dysfunction. The study by Gruenewald et al. (4) includes eleven 2-kidney patients with renal artery stenosis without renovascular hypertension, only 4 of whom had a glomerular filtration rate of <50 mL/min. Three of these subjects had false-positive MTT values.
Mercaptoacetyltriglycine (MAG3) MTT may be superior to DTPA in subjects with renal dysfunction, though there are no data yet to support this assertion. The reference by Dr. Britton to a validated method using MAG3 is in error, because the article by Al-Nahhas et al. (5) uses DTPA and a method very similar to ours.
The coexistence of renal dysfunction in many of the subjects in our study certainly reflects small vessel disease, as suggested by Dr. Britton. Small vessel disease is a common endpoint for many kinds of renal insufficiency. In fact, we showed decreased usefulness of MTT as renal function declined. The observation that an abnormal MTT may have lower specificity for renovascular hypertension in patients with abnormal renal function is not refuted by the very limited data of Gruenewald et al. (4) (3 false-positives in the whole group [n = 11], and 3 false-positives in subjects with renal dysfunction [n = 4], as indicated above). Renal dysfunction is an unfortunate fact of life for many hypertensive individuals. MTT may provide complementary information, but, as we concluded, existing data do not support a unique role for MTT in these individuals.
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