ANGIOGRAPHY BARRY
ARON,
ARTHUR PABLO
IN HYDRONEPHROSIS
M.D.
TESSLER, MORALES,
M.D. M.D.
From the Department of Urology, New York University Medical Center, New York, New York
ABSTRACT-In hydronephrosis, the angiogram enables assessment of the vascular architecture of the kidney, the amount of parenchyma present, or the possibility of a vascular cause for the obstruction. The loss or amputation of arcuate or interlobular arteries on the angiogram is an early sign of hydronephrotic atrophy. Pathophysiologically, these changes antedate the narrowing of the renal artery reported to be indicative of irreversible renal damage. The presence of normal peripheral renal vasculature is a favorable prognostic indicator for recovery of renal function following relief of hydronephrosis. The loss of arcuate and interlobular vessels on the angiogram of a hydronephrotic kidney, regardless of renal artery diameter, augurs poorly for functional improvement following corrective surgery.
In treating hydronephrosis, the urologist must weigh the risks of corrective surgery with the prospect of success against the alternative of nephrectomy. Utilizing newer diagnostic methods, attempts at preserving salvageable kidneys can be planned with greater prospects of success.r Gibson2 illustrated a case in which intravenous and retrograde pyelograms portrayed a large, hydronephrotic, nonfunctioning kidney, which was found to have substantial parenchyma at nephrectomy. Conventional urologic studies may not adequately delineate the status of the renal vascular supply, the amount of functional renal substance, or the presence of a vascular cause for the obstruction. Angiography, because it provides additional information about the status of the renal vasculature and parenchyma, has been advocated as part of the routine preoperative evaluation of patients with hydronephrosis.3 Doss4z5 reported the use of translumbar aortography to evaluate the vasculature of hydronephrotic kidneys in 1946 and 1947. Idbohrn’j subsequently reported on 17 cases of hydronephrosis which were studied by angiography. He found a significant decrease in the caliber of the main renal artery of patients who required nephrectomy because of moderate to severe destruction
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of the renal parenchyma. Experimentally, when rabbit ureters were ligated to produce complete obstruction, the decrease in function and in the caliber of the main renal artery was proportional to the duration of the obstruction. If the renal artery diameter decreased to less than 55 per cent of the original caliber, functional improvement failed to occur after relief of the obstruction by ureterostomy.7 As demonstrated by Widen8jg relief of obstruction up to twenty days after occlusion resulted in a complete return of the width of the renal artery to preocclusion levels, although renal function, as measured by para-aminohippuric acid clearance, did not return completely. After forty to fifty days of complete ureteral occlusion, no recovery, either in arterial diameter or in function, occurred. Based on these studies, OlsenlO concluded that a loss of greater than 50 per cent in the diameter of the renal artery corresponded to a permanent loss of renal function, whereas a renal artery of normal width indicated that the kidney is capable of recovery. Hinmanll described the pathologic vascular derangements during progressive hydronephrosis which affects the nephron through the particular relationship of the blood vessels to the renal parenchyma. The arcuate arteries and veins swing around the calyces at the corticomedullary
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FIGURE 1. Case 1. (A) Retrograde pyelogram demonstrating right hydronephrosis with ureteral obstruction (lucent calculus). (B) Selective right renal arteriogram reveals renal artery narrowing with narrowing and amputation of distal vessels. (C) Nephrogram phase illustrating loss of cortex. (D) Nephrectomy gross specimen shows hydronephrotic atrophy.
junction in a plane parallel to the surface of the kidney as well. as parallel to the surface of the renal pelvis and of the dilating calyces. This arrangement places the vital portion of the kidney (glomeruli, proximal and distal convoluted tubules) peripheral to this network of major vessels. These vessels become elongated and compressed by pelvic dilatation, so that the blood supply to- the cortex gradually decreases. The renal capsule is not distensible and may aggravate the process. Necrosis and atrophy then occur, progressing more rapidly as the blood supply to the already ischemic cortex dwindles. Since compression of the arcuate and intralobular vessels is responsible for the earliest ischemic lesions in hydronephrotic atrophy, the angiogram, which visualizes these vessels, may demonstrate early irreversible changes occurring before the renal artery diameter has decreased to accommodate the diminished renal blood flow.
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In contrast to Hinman’s explanation for renal ischemia in hydronephrosis, Gillenwater12 and associates have postulated active vasoconstriction of the blood vessels of the renal cortex from either a neurogenic or humoral mechanism during obstructive uropathy. In most patients, obstruction is rarely complete and usually of indeterminate duration so that information regarding the status of the blood supply to the renal cortex becomes highly significant in assessing the reversibility of damage from hydronephrosis. Method Radiograms of 17 patients with hydronephrosis who had undergone angiography were reviewed. Particular attention was directed to the pyelographic appearance, the renal artery diameter, the appearance of the interlobular and arcuate arteries, and the amount of cortex seen on the
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FIGURE 2. Case 2. (A) Intravenous pyelogram reveals calcijic density at pelvic brim on left with nonfunction of left kidney. (B) Selective left renal arteriogram shows renal artery diameter is 80 to 90 per cent of normal, but peripheral amputation of interlobular and arcuate arteries is demonstrated. (C) Nephrogram phase of arteriogram shows presence of cortex. (D) Nephrectomy specimen showing substantial atrophy.
nephrographic phase. Of the 17 patients, 7 had pathologic or operative confirmation of the appearance of the renal parenchyma; this latter group forms the basis of this discussion. Results Case
1
A sixty-four-year-old woman was admitted with right flank pain, chills, and fever. The excretory urogram failed to visualize the right kidney. A retrograde pyelogram demonstrated right hydronephrosis with ureteral obstruction (Fig. 1A). The angiogram revealed a small right renal artery with no distal renal vessels (Fig. 1B). The cortex was almost completely absent (Fig. 1C). At surgery an infected, atrophic, hydronephrotic kidney was removed (Fig. 1D). Case
2
A seventy-year-old woman, with a history of recurrent urinary tract calculi, was admitted because of left flank pain, chills, and fever. The intravenous pyelogram demonstrated a stone obstructing the left ureter (Fig. 2A). The angiogram
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revealed a slightly decreased renal artery on the left which, however, was not less than 50 per cent of the diameter on the right. However, a loss of arcuate and interlobular vasculature was seen (Fig. 2B). The renal cortex was present on the nephrogram phase (Fig. 2C). At surgery a large retroperitoneal pus collection was encountered. A nephrectomy was performed; the specimen consisted of an infected, atrophied kidney with little remaining parenchyma (Fig. 2D). The preoperative angiogram illustrated the degree of atrophy to be expected with a loss of peripheral renal vasculature without a significant decrease in renal artery diameter. Case
3
A sixty-year-old man was admitted with a ninemonth history of right flank pain. The intravenous pyelogram showed delayed visualization of the
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FIGURE 3. Intravenous
Case 6. (A) p yelogram
showing grade III to IV pyelocaliectasia resulting from ureteropelvic junction obstruction. (B) Flush aortogram demonstrating two right renal arteries with
preservation of
peripheral vessels. (C) Nephrogram phase of arteriogram showing thin cortex. (D) Postoperative intravenous p yelogram following right pyeloplasty showing improved visualization and increased cortical thickness.
right kidney with grade III hydronephrosis. The angiogram showed two right renal arteries, normal intrarenal vessels, and a renal cortex measuring 0.5 to 1.2 cm. A nephrectomy was performed. At pathologic examination, a thin but adequate renal cortex (0.5 to 1.2 cm.) was found which corresponded to the estimated measurement obtained during angiography.
right renal artery had a normal diameter, and the left renal artery had a slightly decreased diameter. Peripheral arteries were present on the right side, with substantial cortex seen. A right pyelolithotomy was performed with improvement in urographic appearance and a fall in the patient’s blood urea nitrogen to 40 mg. per 100 ml.
Case 4
Case 5
A sixty-nine-year-old man was admitted with bilateral renal calculi. The intravenous pyelogram showed nonvisualization of the left kidney and faint visualization of the right. Blood urea nitrogen was 59 mg. per 100 ml., serum creatinine was 3.6 mg. per 100 ml. On the angiogram, the
A forty-four-year-old man with severe hypertension was found to have bilateral ureteropelvic junction obstruction. Angiograms showed normal size renal arteries, with arcuate and interlobular arteries demonstrated bilaterally. The patient responded to bilateral pyeloplasties with stabili-
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zation of his blood pressure and improvement in the urographic appearance of his kidneys. Two years following surgery, the patient was readmitted in coma with renal failure due to acute tubular necrosis as a consequence of a drug overdose. Retrograde pyelograms showed no obstruction. Case 6 A twenty-seven-year-old man with chronic right flank pain was found to have a right ureteropelvic junction obstruction (Fig. 3A). The angiogram demonstrated a separate artery to the lower pole. The renal arteries, interlobular, arcuate, and interlobar arteries were normal (Fig. 3B). Despite cortical thinning, good peripheral vasculature was demonstrated (Fig. 3C). A right pyeloplasty produced an excellent functional result (Fig. 3D). Case 7 A twenty-three-year-old Vietnam veteran was admitted with nausea and vomiting. His blood urea nitrogen was 76 mg. per 100 ml. with a serum creatinine level of 7 mg. per 100 ml. The creatinine clearance was 23 cc. per minute. An intravenous pyelogram revealed no evidence of a right kidney. There was a faint nephrogram phase on the left, with massive ureteropyelo-
caliectasia to the left ureterovesical junction (Fig. 4A). The angiogram revealed absence of a right renal artery and a large left renal artery, amputation of parenchymal vessels, and diminution of cortical thickness (Fig. 4B). The patient underwent two surgical procedures entailing Y-V plasty of the bladder neck, reimplantation of the ureter with tailoring of the entire ureter from kidney to bladder, and a nephrostomy. At surgery, the parenchyma was thinned and contained multiple small cysts. Creatinine clearance following surgery stabilized at 30 cc. per minute. Despite the presence of a large renal artery on the angiogram, a limited functional result was obtained following elimination of the obstruction, suggesting that the abnormal intrarenal vasculature was more indicative of the functional status of the kidney than the large renal artery. Comment In Cases 2 and 7 angiography demonstrated nearly normal arterial diameter, but amputation and loss of peripheral vasculature was noted. Despite the presence of a dense nephrogram phase (Case 2) at surgery, the kidney was damaged beyond repair. The patient in Case 7 responded poorly to attempts at reconstruction despite adequate drainage. Patients in Cases 4, 5, and 6, with normal main renal, interlobar,
FIGURE 4. Case 7. (A) Eight-hour delayed intravenous pyelogram illustrated delayed visualization of solitary left kidney with hydronephrosis and columning to ureterovesical junction. (B) Flush aortogram shows large single renal artery on left, amputation of peripheral arcuate and interlobular vessels, and substantial cortical thinning. Despite extensive reconstruction with nephrostomy drainage, creatinine clearance did not improve after surgery.
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arcuate, and interlobular arteries responded well to the relief of hydronephrosis. In particular, the patient in Case 6, with a thin renal cortex on the nephrogram, had good peripheral vasculature, and an excellent functional result was obtained. Case 1 was beyond salvage; the angiogram showed atrophy and attenuation of all vessels with no demonstrable cortex. In Case 3, with good vasculature and adequate cortex, the kidney was removed because of the patient’s advanced age and poor general condition. The loss of arcuate and interlobular vessels in the angiograms of “poor” kidneys is a manifestation of the early changes leading to hydronephrotic atrophy. This so-called “pruning” of vessels, although reported in the radiologic literature, has not been emphasized by urologists.13,14 In our cases these changes were associated with failure to regain function after relief of the obstruction. With the progression of atrophy, blood flow through the peripheral renal bed would decrease further, eventually resulting in a diminished renal arterial flow; as flow diminishes, the renal artery would be expected to be narrow. The cross sectional area decreases with the square of the diameter; a 50 per cent decrease in diameter wouId reduce blood flow to only 25 per cent of normal, which may supply only the metabolic needs of the nonexcretory portion of the kidney. The earliest irreversible changes in hydronephrosis appear to occur at the periphery, possibly explaining the failure of hydronephrotic kidneys with normal renal arteries to regain function after relief of the obstruction, Renal artery
narrowing represents a later vascular change in hydronephrosis, reflecting ischemic changes occurring in the peripheral renal vascular bed.
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University Hospital 560 First Avenue New York, New York 10016 (DR. MORALES) References 1. 2. 3.
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ANDERSEN, J. C.: Hydronephrosis: a fourteen years’ survey of results, Proc. Roy. Sot. Med. 55: 93 (1962). Hydronephrosis: diagnosis and treatment GIBSON, J. E.: of ureteropelvic obstructions, J. Urol. 75: 1 (1956). LEARY, D. J., JR., TEMPLETON, A. W., THOMPSON, I. M., Preoperative angiography in hydroand SIBALA, J. L.: nephrosis, ibid. 107: 542 (1972). DOSS, A. K.: Translumbar aortography: its diagnostic value in urology, ibid. 55: 594 (1946). IDEM: The management of ureteropelvic juncture obstruction: translumbar aortography an adjunct, ibid. 57: 521 (1947). IDBOHRN, H.: Renal angiography in cases of delayed excretion in intravenous urography, Acta Radiol. 42: 333 (1954). IDEM: Renal angiography in experimental hydroneohrosis. ibid. SUDDI. 136: 1 (1956). WIDEN, T.: Restoration of lkdney function after induced urinary stasis of varying duration, Acta Chir. Stand. 131: 507 (1957). IDEM: Renal angiography during and after unilateral ureteric occlusion, Acta Radiol. suppl. 162: 1 (1958). OLSEN, 0.: Hydronephrosis, in Abrams, H. L.: Angiography, Boston, Little, Brown and Co., 1971, p. 786. HINMAN, F., JR.: The pathophysiology of urinary obstruction, in Campbell, M. F.: Urology, Philadelphia, W. B. Saunders Co., 1970, p. 322. GILLENWATER, J.: Personal communication. HALPERN, M.: Angiography in chronic renal disease and renal failure, Radiol. Clin. North Am. 10: 467 (1972). GILL, W. M., JR., and PUDVAN, W. R.: The arteriographic diagnosis of renal parenchymal diseases, Radiology 96: 81 (1970).
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