Clinical Radiology (1987) 38, 45%462

Annotation: Renal Failure Radiology- 1987 COLIN EVANS

Cardiff Royal Infirmary, Newport Road, Cardiff CF2 1SZ

A patient presenting with newly diagnosed renal failure usually undergoes radiological evaluation to assess the number of kidneys, their size, shape and position, and whether they are obstructed and perfused. An underly- ing cause such as calculi, retroperitoneal fibrosis or poly- cystic disease should also be sought.

The development of new imaging techniques, par- ticularly real time ultrasound together with advances in interventional uroradiology in the past 10 years have revolutionised the management of the renal failure patient. These advances have led to the rapid identifica- tion and treatment of the most important group, those with surgically remediable causes.

Prior to the mid sixties, retrograde pyelography reigned supreme as the primary investigation. Whilst it had the potential disadvantage of invasiveness leading to sepsis, and the need for general anaesthesia and urological expertise, it did have the advantage of rapid and reliable diagnosis of obstructive uropathy. It also gave an indication of renal size, and thus the chronicity of the process, and demonstrated pelvicalyceal abnor- malities, e.g., papillary necrosis, and the distorted architecture of polycystic disease. The use of this tech- nique in renal failure was stongly advocated by Kingston and colleagues as recently as 1977, suprisingly, the last article on renal failure in Clinical Radiology.

Prior to the landmark paper by Schwartz and col- leagues (1963) highlighting the 'benignity' of intra- venous urography in renal insufficiency, the procedure had always been considered both dangerous and unrewarding in this group of patients. Subsequent authors (Mahaffy et al., 1969, Brown et al., 1970) con- firmed that even in advanced renal failure both calyceal systems and renal outlines could be visualised in over 90% of all patients, and high dose urography rapidly became the cornerstone of renal failure radiology. Good renal failure urography however demands a high dose of contrast medium (600 mg Iodine/kg), no dehydration, linear tomography pre- and post-injection of contrast medium, delayed films up to 24 h, low and constant kilovoltage setting for maximum contrast, and above all a meticulous radiographic technique. Obtaining the lat- ter was not helped in our hospital by most new renal failure patients arriving on Friday, and thus urograms were sometimes performed over the weekend by chang- ing shifts of radiographers. Never were so many films taken by so many different people for such a long time for the benefit of so few with so little supervision.

Initial enthusiasm was somewhat dampened by reports, mostly from the United States of America, that contrast medium might precipitate further renal impair- ment. Although mainly a problem in America, Webb et al. (1981) showed transient deterioration of function in three out of 40 patients (7.5%) with renal failure after intravenous urography. Rahimi et al. (1981) however, showed no deterioration of function in a group of 15

patients who had varying degrees of renal failure and were monitored for 3 days after the procedure. Risk factors which have been identified include myeloma, diabetes mellitus, hyperuricaemia, dehydration or fluid restriction before the urogram, large doses of contrast medium, repeated contrast examination over a short period, and elderly patients. Dawson (1985) in a review concluded that contrast medium nephrotoxicity was a real entity and stated that caution should be exercised in the high risk group. The radiologist who is concerned about the risks of intravenous contrast medium should always convince himself that the study is absolutely necessary before proceeding. There must also be adequ- ate hydration before, during and after the procedure.

There is a recommendation that the limited number of high dose urograms now being performed should be carried out with low osmolar contrast media (Grainger, 1984). Despite the cost, this is no doubt prudent because of the less significant haemodynamic effects of these agents and their lower toxicity. We have studied a group of 30 patients with uraemia who were randomly allo- cated to undergo high dose urography using ioxaglate or iohexol by carrying out pre-examination serum creatinine, urea, urinary N acetyl-B glucosaminidase and B 2 microglobulin estimations and repeating these 48 h after the procedure. There was no evidence of increased renal damage in either group (unpublished data).

As well as demonstrating renal size and excluding obstruction, claims were made that specific radiographic patterns on urography could point to certain parenchy- mal disease (Fry and Cattell, 1972). In clinical practice however, these were of limited value, the only specific nephrographic patterns being the increasingly dense nephrogram of acute obstruction, the Gruyere cheese nephrogram of polycystic disease, and the nephrogram or 'negative pyelogram' of chronic obstruction. In no other situation in my experience did the nephrographic pattern alone obviate the need for a renal biospy.

It took the development of Gray scale, the replace- ment of static B-scanning by real time ultrasound, many clinical meetings and a prospective study (Denton et al., 1984) to convince our nephrologists that ultrasound should replace high dose urography as the first line investigation in renal failure This was despite earlier reports (Ellenbogen et al., 1978; Talner et al., 1981) which showed ultrasound to be highly sensitive in the detection of hydronephrosis. This high sensitivity is important as a false negative examination would be disastrous for the particular patient. By now however, despite an increased overall workload, the number of high dose urograms carried out in our department has decreased from 130 per annum in the late seventies, to single figures in 1986. High dose urography in renal failure is now confined to mild or moderate dysfunction (say a serum creatinine of 300/~mol/litre or less) when

458 CLINICAL RADIOLOGY

adequate views of the renal outline and calyces would be expected which might point to the underlying disease process. Acceptability of ultrasound has been aided by its mobility- use at the bedside became possible, and the rapidity with which post renal obstruction can be con- firmed or excluded. The 'Friday renal failure' is now investigated, diagnosed and treated on Friday.

Sonographic renal size caused initial confusion to our clinicians. Sonographic length is always less than urographic length due to lack of radiographic magnifica- tion: ultrasonic size is thus true renal size (Lewis and Ritchie, 1980). Intravenous contrast medium also increases renal size transiently. Thus it has to be made clear to colleagues that a sonographic length of 10 cm, for example, is normal in an adult male although 10 cm kidneys would be somewhat small on tomography, sug- gesting chronic disease. In every new case of renal failure however, we carry out plain tomography which, as well as excluding calculi, gives an indication of renal size in most cases. It is also my impression that errors of underestimation are possible on ultrasound in inex- perienced hands when true pole tO pole renal lengths are not obtained. Conversely, on B-scanning, renal size may be overestimated if there is respiratory movement dur- ing the scan sweep.

Ultrasound has many limitations. There may be difficulty in outlining the kidneys in obese patients, especially the left side. The field of view on sector scan- ners may be too small to visualise a whole kidney. Small end stage kidneys may be difficult to localise. This difficulty is accentuated because the organs become more echogenic in chronic disease, lose their normal ultrasonic characteristic appearance, and are often only visualised because of their respiratory excursion. Know- ing whether a kidney is absent or ectopic may be difficult or impossible on ultrasound examination alone.

The cause of obstruction may not be detectable on ultrasound in many cases despite scanning the pelvis and retroperitoneum (which is mandatory when there is hydronephrosis), such patients then usually progressing to a more invasive technique or computed tomography.

The presence of a dilated system does not always mean obstruction; ultrasound, though highly sensitive for dilatation, is not specific for obstruction. False posi- tive rates of 8 to 26% have been reported, when 'baggy' systems, parapelvic cysts, and reflux nephropathy can simulate obstruction. Calyceal cysts, congenital megacalyces, and polycystic disease may also lead to confusion. Excluding obstruction in patients with adult polycystic disease may be impossible with this tech- nique. There is a variable increase in cortical echogenicity in renal parenchymal disease on ultra- sound examination, but this is too non-specific to point to a particular histological diagnosis (Hricak et al. , 1982). Although comparison of cortical echoes with the echogenicity of adjacent liver and spleen should be car- ried out, many technical errors are still possible. Rosen- field and Siegel (1981) showed no correlation between sonographic findings and glomerular disease, but echogenicity increased with the severity of interstitial nephritis.

Moccia and colleagues (1980) demonstrated no rela- tionship between echogenicity of kidneys, kidney size, pathological diagnosis, or degree of renal function. Echogenic kidneys imply a 'medical' cause of renal failure warranting biopsy if the kidneys are of a suitable

size. In small end stage kidneys, ultrasound may demonstrate the development of acquired cystic disease.

Failure to detect acute renal obstruction because of the absence of dilatation is a well known pitfall of ultra- sound. It has been shown that in one-third of kidneys acutely obstructed by calculi, ultrasound detects no dilatation at 48 h (Brooke et al. , 1984). We encountered one such case in our series (Denton et al. , 1984). Other authors have also emphasised the importance of further evaluation in the presence of even minor calyceal dilata- tion when dealing with a uraemic patient (Curry et al., 1982).

Unfortunately, dilatation of the collecting system does not occur in every patient with obstructive uropa- thy. This phenomenon, albeit rare, has been described in a few cases by several authors (Rascoff et al. , 1983; Maillet et al. , 1986). Lalli (1977) encountered this in relation to idiopathic retroperitoneal fibrosis and post- ulated that the disease may interfere with ureteric peri- stalsis and cause non-mechanical obstruction with minimal dilatation. Others have noted it in association with malignancy and suggest an acute precipitating event, e.g. oedema obstructing a single functioning kidney, the other having been previously obstructed by the underlying disease process (Naidich et al . , 1986). Further theories include encasement of the kidney by neoplasia or fibrosis preventing dilatation, and an intra- renal pelvis again with no dilatation. Whatever the cause, this entity must be considered in patients with renal failure who are at high risk of urinary obstruction, e.g., known pre-existing retroperitoneal malignancy. To place things in perspective however, the total num- ber of reported cases is less than 20 and this should not depose ultrasound from its position as the first line investigation in acute renal failure.

Isotope examinations of the urinary tract provide functional information, in contrast to the anatomical information provided by radiological studies. This reliance on renal function relegates isotope studies to a secondary role in acute or advanced renal failure. It has one useful role in this situation, that of providing a 'poor man's angiogram' in the detection of renal artery occlu- sion. In acute tubular necrosis there is usually an almost normal perfusion phase on a 99m Tc diethylene triamine penta-acetic acid (DTPA) study which gives optimism to the clinician and hope of a return of renal function in due course. But when there is severe parenchymal dis- ease with renal shutdown, isotope renal perfusion may be so poor as even to be inconclusive regarding the presence of patent renal arteries. In mild chronic renal failure on the other hand, serial radio-isotope studies which are non-invasive, reproducible and inexpensive are helpful in quantitating total and split renal function during long term follow-up.

In the presence of obstructive uropathy it would be useful to predict the degree of recoverable function. Staab et al. (1973) showed that an 131I-hippuran study predicted outcome in 12 of 15 patients. Perry and col- leagues (1977) using both Dimercaptosuccinic acid (DMSA) and 13q-hippuran concluded that when the kidneys were visualised with both agents, there was some recovery of function. Many others disagree; Chisholm (1974) considered predictions for recovery in obstructive uropathy unreliable, and another study showed that even in the absence of any isotope uptake

ANNOTATION 459

some patients had significant recovery of function (Chibber et al. , 1981). They considered that the scan was an indicator of function at the time of the study and not an absolute indicator of the amount of viable renal tissue in the presence of urinary obstruction. In our centre, potential for recovery of renal function in obstructive uropathy is often based on the quantity and quality of the urine draining through the nephrostomy tubes, and the consequent improvement in the patient's biochemi- cal parameters.

Computed tomography (CT) provides good anatomi- cal delineation of the kidneys with or without contrast medium regardless of their size, configuration or posi- tion, and is a useful adjunct to ultrasound in the investigation of the patient with renal failure. It is of value in locating small or ectopic kidneys and can locate small calculi, even those non-opaque on conventional radiographs. Uric acid calculi are no longer radiolucent. Obstruction can be confirmed or excluded in many cases without intravenous contrast medium (Webb et al . , 1984). Minor degrees of dilatation can be missed. Occa- sionally renal cysts, especially in a parapelvic position may cause confusion and excluding obstruction in poly- cystic kidneys may also be difficult, but use of contrast medium resolves both issues.

CT gives a subjective impression of renal size, but does not permit accurate renal length measurement. Renal volume, which CT can estimate, is not a widely used parameter. Parenchymal thickness may give an impression of recovery potential. Good views of the retroperitoneum are obtained in all but the thinnest of patients, thus elucidating the cause of obstruction (Bosniak et al. , 1982). The dilated ureter is visualised without contrast medium and the level of obstruction can be determined, which is often impossible with ultra- sound. Unfortunately, many district general hospitals have no on-site access to CT, which obviously influences uroradiological practice. Ultrasound and plain tomo- grams provide acceptable substitutes in most cases, and CT even when available, should be reserved for difficult cases.

Nuclear magnetic resonance imaging has shown great promise in the investigation of the central nervous sys- tem, but data regarding renal investigations is limited, and indications for its use have not yet been defined (Leung et al. , 1984; Lipuma, 1984). Whilst anatomical demonstration of the kidneys may be as good as CT, it has the disadvantages of poor demonstration of calculi, motion degradation of the images, prolonged examina- tion time and not yet being widely available. A combina- tion of calyceal dilatation and loss of cortico-medullary differentiation with certain pulse sequences has been reported to be characteristic of hydronephrosis on mag- netic resonance imaging. Changes in the cortico-medull- ary junction occur in physiological and pathological states (Hricak et al., 1983) and this should prove a fruitful area for future research. The use of gadolinium DTPA, a paramagnetic contrast agent in magnetic reso- nance imaging of the kidney is also currently under investigation (Leung et al . , 1984).

Invasive procedures, particularly renal biopsy, ante- grade pyelography percutaneous nephrostomy and retrograde pyelography, go hand in hand with imaging techiques in the investigation of patients with renal failure. Close collaboration between nephrologists and radiologists in carrying out renal biopsies seems wise as

the technique may be hazardous. Fine needle antegrade pyelography is a routine procedure to ascertain the level of obstruction and often the cause. This, like renal biopsy, is usually carried out in a fluoroscopy room also using mobile ultrasound equipment for guidance. The renal outlines may be faintly visible on fluoroscopy even without contrast medium giving an idea of the position of the calyces. Multiple attempts at calyceal puncture may sometimes be necessary and though this causes no problems, it would be of great help if someone were to devise a method whereby the needle tip was consistently well visualised on ultrasound. There is no reason why the pelvis should not be punctured directly in mildly dilated systems, when calyceal puncture is difficult. Urine should be aspirated before injection of contrast medium to avoid overdistension. Antibiotic cover is recommended if there is a suspicion of infection. The patient may need to be tilted head upwards so that the contrast medium displaces non-opacified urine to give the true level of obstruction. If antegrade pyelography fails, or no expertise is available, one must resort to retrograde pyelography to delineate the cause of hydronephrosis.

Establishment of a percutaneous nephrostomy has been described in detail by several authors since the original description in 1955, and should be part of every radiologists' armamentarium (Saxton et al. , 1972; Pfis- ter and Newhouse, 1979; Barbaric, 1984). The Setdinger technique is obviously preferred by most radiologists though the brave may prefer trocar and cannula methods in dilated systems. Methods facilitat- ing catheter placement after a single fine needle punc- ture offer no particular advantage, are more difficult to use and should be avoided.

Complications are very unusual, haematuria being expected. The most likely problem is dislodgement of the tube. This occurs whatever method of attachment is used, but nursing staff should be instructed not to change the dressings. If the tube falls out from a fairly mature track, a 5 gauge dilator will usually find the way into the calyceal system, and the tube can then be replaced. Blockage of the tube may occur when draining a pyonephrosis but this can be avoided by regular flush- ing with saline.

Controversy still exists regarding the wisdom of relief of uraemia in patients with obstructive uropathy due to pelvic malignancy. If the patient is pain free at the time of presentation, drainage is often carried out and the nephrostomy track may then be used for antegrade stent insertion for long term drainage. Polyethylene stents are easier to insert but if too long may cause irritation of the trigone and urinary frequency. Softer silicone stents tend to concertina when pushed into the calyces often leading to technical failure. Alternatively, the track may be dilated to accommodate a Foley or Malecot catheter for long term external drainage, and major surgery in a patient with a predicted short life span can be avoided. Nephrostomy tracks may also be used to dilate benign ureteric strictures (Banner and Pollack, 1984) and for percutaneous stone extraction (Alken et al. , 1981).

Angiographic procedures in renal failure are fairly uncommon but attention has been drawn to uraemia due to bilateral arterial stenosis or occlusion (Sheil et al . , 1973). This entity is now more eagerly sought because of the possibility of renal artery angioplasty. Whilst the primary effect of this technique is on blood pressure,

460 CLINICAL R A D I O L O G Y

many authors have shown improvement and preserva- tion of renal function after angioplasty (Tegtmeyer et al., 1981; Madias et al., 1982).

Some authors found improvement of function delayed for several months (Kremer-Hovinga et al. , 1986). Overall, Tegtmeyer et al. (1981) found functional improvement in 56% of patients, and a gradual increase in renal length after angioplasty has also been observed (Sos et al., 1983). Knowing that patients with atheromatous stenoses in their renal arteries often pro- gress to occlusion (Meaney et al . , 1968) and that angio- plasty can preserve function in unilateral and bilateral disease will inevitably lead to more active investigation of uraemic patients with hypertension, presumably by intravenous digital angiography which is now becoming more widely available. Some cases will be highlighted by uraemia resulting from therapy with angiotension con- verting enzyme inhibitors such as captopril which strongly suggests bilateral renal artery stenoses or stenosis in a single functioning kidney (Hricak et al., 1983, Greminger et al., 1986).

Renal transplant dysfunction may be due to ureteric obstruction, arterial occlusion, rejection, acute tubular necrosis (or preservation injury) and cyclosporin tox- icity. The first two can conclusively be detected by ultra- sound and radionuclide studies respectively. Although the calyceal system in a newly transplanted kidney is often distended, due to oedema at the ureteric anasto- mosis, an intense diuresis, or denervation, ultrasound has been shown to be accurate in the diagnosis of obstruction. Doubtful cases are evaluated either by serial scans or ultrasound guided antegrade pyelography which is both safe and easy in the transplanted kidney. In transplantation the difficulty lies in distinguishing acute tubular necrosis, rejection and cyclosporin tox- icity. One can confidently say at the outset, that despite much literature (often contradictory) from many authors advocating all the imaging modalities in turn, no single satisfactory imaging technique exists in this clini- cal situation.

Many descriptions of the sonographic changes in acute rejection and acute tubular necrosis have been published (Maklad et al. , 1979; Hricak et al., 1982; Fried et al. , 1983; Griffin et al . , 1986). Features suggesting rejection include decrease in cortico-medullary differentiation, increased volume of the kidney, enlarged renal pyramids and a decreased echodensity of the renal sinuses. Although accuracy rates of up to 85% for the ultrasonic detection of acute rejection have been quoted (Frick et al. , 1981), experience in our centre has been less favourable. The conclusion of Griffin et al. (1986) that ultrasound alone should not be used to diag- nose rejection is in our experience sound. A recent study in our department emphasises the need for baseline scans of the kidney in all patients soon after transplanta- tion so that changes in calyceal dilatation, renal volume and of the renal parenchyma may be more accurately assessed. Since the advent of cyclosporin, the sonographic changes of rejection appear to be sup- pressed and are seldom as florid as seen previously.

Recently attention has been focused on duplex Dop- pler ultrasound of renal transplants (Berland et al. , 1982; Rigsby et al. , 1986). Animal studies have shown good differentiation between rejection and acute tubu- lar necrosis (Taylor et al . , 1985). Renal transplant artery stenosis may also be diagnosed in this way. It is perhaps

too early to determine whether duplex Doppler studies will be of value in patient management.

Radionuclide studies using either 13~I-hippuran or 99mTC DTPA can provide valuable information regarding transplant function. Acute tubular necrosis may be differentiated from acute rejection by calcula- tion of a perfusion index (Hilson et al., 1978). Serial studies are required, diminishing perfusion and excre- tion suggesting rejection. All this takes time which transplant surgeons find unacceptable, thus clinical decisions are taken often before conclusive radiological evidence has been obtained. However, a normal ultra- sound scan and normal perfusion index on renography suggests acute tubular necrosis whereas an oedematous kidney on ultrasound and a high perfusion index sug- gests acute rejection. There have been promising reports of the use of rain-labelled platelets in acute rejection though the complex preparation has prevented adoption of the technique in clinical practice (Fawwaz, 1984). In-labelled leucocyte scans have been shown to be non-specific for rejection (McAfee et al . , 1985). Dis- tinction of rejection from cyclosporin toxicity by 99mTC DTPA scintigraphy has been shown to be of limited value presumably because of diminished graft perfusion in both conditions. Biopsy remains the only reliable means of differentiation at present (Gedroyc et al., 1986).

Urography has no place in renal transplant evaluation because when there is deranged function there is little likelihood of obtaining useful diagnostic information. CT of renal transplants duplicates information obtained from ultrasound scanning. Although it has been advo- cated for the differentiation of rejecting and normal kidneys, this has not been widely accepted, and the role of CT is therefore limited.

Angiography is limited to the diagnosis and treatment of renal artery stenosis (Clements et al., 1987). Initial reports of the use of magnetic resonance imaging (MRI) are, as often with a new technique, very encouraging (Geisinger et al., 1984; Hricak et al., 1986) but will doubtlessly be somewhat tempered by time and further experience. Indeed a recent paper on MRI in renal transplants quotes an 8% false negative rate for rejec- tion with 24% of studies indeterminate (Baumgarten et al., 1986).

The use of fine needle intrarenal pressure measure- ments is an interesting and repeatable alternative to radiology (Salaman and Griffin, 1985) but unfortunately in this field, despite advances in medical imaging, the gold standard for diagnosis of rejection remains needle biopsy.

And what of the results of these refinements of old technology and introduction of the new? Although developments in dialysis techniques and transplantation have improved the prospects for patients with chronic renal failure, the overall mortality in patients with acute renal failure remains as it was 30 years ago (Wheeler et al., 1986).

Acknowledgement. I wish to thank my secretary, Miss Rosslyn Jones, for typing the manuscript.

REFERENCES

Alken, P, Hutschenreiter, G, Gunther, R & Marberger, M (1981). Percutaneous stone manipulation. Journal of Urology, 125, 463- 466.

ANNOTATION 461

Banner, MP & Pollack, HM (1984). Dilatation of ureteral stenoses: techniques and-experience in 44 patients. American Journal of Roentgenology, 143, 789-793.

Barbaric, ZL (1984). Percutaneous nephrostomy for urinary tract obstruction. American Journal of Roentgenology, 143, 803-809.

Baumgarten, BR, Nelson, RC, Ball, TI, Wyly, JB, Bourke, E, Delaney, V et al. (1986). MR imaging of renal transplants. Amer- cian Journal of Roentgenology, 147, 949-953.

Berland, LL, Lawson, TL, Adams, MB, Melrose, BL & Foley, WD (1982). Evaluation of renal transplants with pulsed Doppler duplex sonography. Journal of Ultrasound in Medicine, 1,215-222.

Bosniak, MA, Megibow, AJ, Ambos, MA, Mitnick, JS, Lefleur, RS & Gordon, R (1982). CT of ureteral obstruction. Amercian Journal of Roentgenology, 138, 1107-1113.

Brooke, JR, Laing, FC & Wing, VW (1984). Sonography vs excretory urography in acute ureteral obstruction. Radiology, 153, 202 (Abstract).

Brown, CB, Glancy, JJ, Fry, IK & Cattell, WR (1970). High dose excretion urography in oliguric renal failure. Lancet, ii, 952-955.

Chibber, PJ, Chisholm, GD, Hargreave, TB & Merrick, MV (1981). 99m Technetium DMSA and the prediction of recovery in obstruc- tive uropathy. British Journal of Urology, 53, 492-495.

Chisholm, GD (1974). Obstructive uropathy. In Postgraduate Surgery Lectures, No. 2, pp. 51-66. Butterworths, London.

Clements, R, Evans, C & Salaman, JR (1987). Percutaneous trans- luminal angioplasty in renal transplant artery stenosis. Clinical Radiology, 38, 235-237.

Curry, NS, Gobien, RP & Schabel, SI (1982). Minimal dilatation obstructive nephropathy. Radiology, 143, 531-534.

Dawson, P (1985). Contrast agent nephrotoxicity. An appraisal. Bri- tish Journal of Radiology, 58, 121-124.

Denton, T, Cochlin, DL & Evans, C (1984). The value of ultrasound in previously undiagnosed renal failure. British Journal of Radiology, 57, 673-675.

Ellenbogen, PH, Scheible, FW, Talner, LB & Leopold, GR (1978). Sensitivity of gray scale ultrasound in detecting urinary tract obstruction. American Journal of Roentgenology, 130, 731-733.

Fawwaz, RA (1984), Clinical utility of labelled cells for detection of allograft rejection and myocardial infarction. Seminars in Nuclear Medicine, 14, 198-207.

Frick, MP, Feinberg, SB, Sibley, RK & Idstrom, ME (1981). Ultra- sound in acute transplant rejection. Radiology, 138, 657-660.

Fried, AM, Woodring, JH, Loh, FK, Lucas, BA & Kryscio, RJ (1983). Medullary pyramid index. An objective assessment of prominence in renal transplant rejection. Radiology, 149,787-791.

Fry, IK & Cattell, WR (1972). Nephrographic patterns during excre- tion urography. British Medical Bulletin, 23, 227-232.

Gedroyc, W, Taube, D, Fogelman, I, Neild, G, Cameron, S. and Maisey, M (1986). Tc99m - DTPA scans in renal allograft rejection and cyclosporin nephrotoxicity. Transplantation, 425, 494-497.

Geisinger, MA, Risius, B, Jordan, ML, Zelch, MG, Novick, AC & George, CR (1984). Magnetic resonance imaging of renal trans- plants. American Journal of Roentgenology, 143, 1229-1234.

Grainger, R (1984). The clinical and financial implications of the low- osmolar radiological contrast media. Clinical Radiology, 35, 251- 252.

Greminger, P, Vetter, H, Steurer, J, Siegenthaler, W & Vetter, W (1986). Captopril and kidney function in renovascular and essential hypertension. Nephron, 44, Suppl. 1, 91-95.

Griffin, JF, Short, CD, Lawler, W, Malick, NP & Johnson, RWG (1986). Diagnosis of disease in renal allografts: correlation between ultrasound and histology. Clinical Radiology, 37, 59-62.

Hilson, AJW, Maisey, MN, Brown, CB, Ogg, CS & Bewick, MS (1978). Dynamic renal transplant imaging with TC-99m DTPA supplemented by a transplant perfusion index in the management of renal transplants. Journal of Nuclear Medicine, 19, 994-1000.

Hricak, H, Crooks, LE, Sheldon, P & Kaufman, L (1983). Nuclear magnetic resonance imaging of the kidney. Radiology, 146, 425- 432.

Hricak, H, Cruz, C, Romanski, R, Uniewski, MH, Levin, NW, Madrazo, MD et al. (1982). Renal parenchymal disease: sonographic - histologic correlation. Radiology, 144, 141-147.

Hricak, H, Romanski, RN & Eyler, WR (1982). The renal sinus during allograft rejection: sonographic and histopathologic find- ings. Radiology, 142, 693-699.

Hricak, H, Terrier, F & Demas, BE (1986). Renal allografts: evalua- tion by MR imaging. Radiology, 159, 435-441.

Hricik, DE, Browning, PJ, Kopelman, R, Goorno, WE, Madias, NE & Dzau, VJ (1983). Captopril induced functional renal insuffi- ciency in patients with bilateral renal artery stenoses or renal artery

stenosis in a solitary kidney. New England Journal of Medicine, 308, 373-376.

Kingston, RD, Shah, KJ & Dawson-Edwards, P (1977). Ascending ureteropyelography in renal failure. Clinical Radiology, 28, 483- 489.

Kremer-Hovinga, TK, de Jong, PE, de Zeeuw, D, Donker, AJM, Schuur, KH & van der Hem, GK (1986). Restenosis prevalance and long term effects on renal function after percutaneous trans- luminal renal angioplasty. Nephron, 44, Suppl. 1, 64-67.

Lalli, AF (1977). Retroperitoneal fibrosis and inapparent obstructive uropathy. Radiology, 122, 339-342.

Leung, AWL, Bydder, GM, Steiner, RE, Bryant, DJ & Young, IR (1984). Magnetic resonance imaging of the kidneys. American Journal of Roentgenology, 143, 1215-1227.

Lewis, E & Ritchie, WGM (1980). A simple ultrasonic method for assessing renal size. Journal of Clinical Ultrasound, 8, 417-420.

Lipuma, JP (1984). Magnetic resonance imaging of the kidney. Radio- logic Clinics of North America, 22, 925-941.

Madias, NE, Kwon, OJ & Millan, VG (1982). Percutaneous trans- luminal renal angioplasty: a potentially effective treatment for preservation of renal function. Archives of Internal Medicine, 142, 693-697.

Mahaffy, RG, Matheson, NA & Caridis, DT (1969). Infusion urogra- phy in acute renal failure. Clinical Radiology, 20, 320-323.

Maillet, PJ, Pelle-Francoz, D, Laville, M, Gay, F. & Pinet, A. (1986). Non-dilated obstructive acute renal failure: diagnostic procedures and therapeutic management. Radiology, 160, 659-662.

Maklad, NF, Wright, CH & Rosenthal, SJ (1979). Gray scale ultra- sonic apperances of renal transplant rejection. Radiology, 131, 711-717.

McAfee, JG & Samin, A (1985). Into-labelled leucocytes: a review of problems in image interpretation. Radiology, 155, 221-229.

Meaney, TF, Dunstan, HP & McCormack, LJ (1986). Natural History of renal arterial disease. Radiology, 91, 881-887.

Moccia, WA, Kaude, JV, Wright, PG & Gaffney, E.F. (1980). Evaluation of chronic renal failure by digital Gray-scale ultra- sound. Urologic Radiology, 2, 1-7.

Naidich, JB, Rackson, ME, Mossey, RT & Stein, HL (1986). Non- dilated obstructive nephropathy: percutaneous nephrostomy per- formed to reverse renal failure. Radiology, 160, 653-657.

Perry, JR, McCartney, WH, Bateman, WB, Mattern, WD & Staab, EV (1977). Assessment of recoverable renal function. A compari- son of two radiopharmaceuticals. Journal of Nuclear Medicine, 18, 595 (Abstract).

Pfister, RC & Newhouse, JH (1979). Interventional percutaneous pyeloureteral techniques. II: Percutaneous nephrostomy and other procedures. Radiologic Clinics of North America, 351-363.

Rahimi, A, Edmondson, RPS & Jones, NF (1981). Effect of radio- contrast media on kidneys of patients with renal disease. British Medical Journal, 282, 1194-1195.

Rascoff, JH, Gold, RA Spinowitz, BS & Charytan, C. (1983). Non- dilated obstructive nephropathy. Archives of Internal medicine, 143, 696--698.

Rigsby, CM, Taylor, KJW, Weltin, G, Burns, PN, Bia, M, Princenthal, RA et al. (1986). Renal allografts in acute rejec- tion: evaluation using duplex sonography. Radiology, 158, 375- 378.

Rosenfield, AT & Siegel, NJ (1981). Renal parenehymal disease: histopathologic - sonographic correlation. American Journal of Roentgenology, 137, 793-798.

Salaman, JR & Griffin, PJA (1985). The use of fine needle intrarenal manometry in the management of renal transplant patients receiv- ing cyclosporin. Transplantation, 39, 523-526.

Saxton, HM, Ogg, CS & Cameron, JS (1972). Needle nephrostomy. British Medical Bulletin, 28, 210-213.

Schwartz, WB, Hurwit, A & Ettinger, A (1963). Intravenous urogra- phy in the patient with renal insufficiency. New England Journal of Medicine, 269, 277-283.

Sheil, AGR, Stokes, GS, Tiller, DJ, May, J, Johnson, JR & Stewart, JH (1973). Reversal of renal failure by revascularization of kidneys with thrombosed renal arteries. Lancet, ii, 865-866.

Sos, TA, Pickering, TG, Sniderman, K, Saddekni, S, Case, DB, Silane, MF et al. (1983). Percutaneous transluminal renal angio- plasty in renovascular hypertension due to atheroma or fibro- muscular hyperplasia. New England Journal of Medicine, 309,274- 279.

Staab, EV, Hopkins, J, Patton, DD, Hanchet, J & Stone, WJ (1973). The use of radionuelide studies in the prediction of function in renal failure. Radiology, 106, 141-146.

Talner, LB, Seheible, W, Ellenbogen, PH, Beck, CH & Gosink, BB

462 CLINICAL RADIOLOGY

(1981). How accurate is ultrasonography in detecting hydro- nephrosis in azotaemic patients? Urologic Radiology, 3, 1-6.

Taylor, KJW, Piccirillo, M, Weltin, GG & Flye, MW (1985). Differen- tiation between ATN and acute vascular rejection by Doppler waveforms in porcine renal allografts. Radiology, 157, 119 (Abstract).

Tegtmeyer, CJ, Teates, CD, Crigler, N, Gander, RW, Ayers, CR, Stoddard, M, et al. (1981). Percutaneous transluminal angioplasty in patients with renal artery stenosis. Radiology, 140, 323-330.

Wcbb, JAW, Rezneck, RH, Cattell, WR & Fry, IK (1981). ~ Renal function after high dose urography in patients with renal failure. British JouPnal of Radiology, 54, 47%483.

Webb, JAW, Reznek, RH, White, FE, Cattell, WR, Fry, IK & Baker, LRI (1984). Can ultrasound and computed tomography replace high-dose urography in patients with impaired renal function? Quarterly Journal of Medicine, 211, 411-425.

Wheeler, DC, Fcehally, J & Walls, J (1986). High risk acute renal failure. Quarterly Journal of Medicine, 61,977-984.