Ultrasound
Evaluation of Acute Post-Transplant Renal Failure by Ultrasound 1 Hedvig Hricak, M.D., Luis H. Toledo-Pereyra, M.D., Ph.D., William R. Eyler, M.D., Beatrice L. Madrazo, M.D., and Guat 5. 5y, M.D.
Autotransplantation of the kidney was performed in seven adult mongrel dogs. A model of acute tubular necrosis (ATN) was developed by subjecting the kidney to warm ischemia (37°C) for 40 to 60 minutes. Serial ultrasound examinations were performed every 12 hours until the animal died or was killed. Sonographic findings were correlated with laboratory and histological data. Throughout the course of ATN, the characteristic normal echo pattern of the kidney remained unchanged in six of seven dogs. In one animal there were changes in the renal cortex, while the medullary pyramids showed no alteration from the base-line study. This contrasts with extensive abnormalities found during rejection. INDEX TERMS:
Kidneys, failure. Kidneys, necrosis • Kidneys, transplantation, 8 [1] .455 • Kidneys, ultrasound stud-
ies,8[1].1298 Radiology 133:443-447, November 1979
is a valuable noninvasive procedure in the monitoring of the renal transplant patient. It is used to demonstrate hydronephrosis, to detect perirenal fluid collections (1, 10), and recently to assess transplant rejection (2, 7). Immediately after transplantation, acute tubular necrosis (ATN) is a frequent complication which can be confused with rejection both clinically and by laboratory parameters (9, 12). To our knowledge, there are no studies describing sonographic parenchymal changes during ATN. Using a canine kidney as the model, this study was undertaken to evaluate parenchymal changes following post-transplant tubular necrosis.
An ultrasound examination was performed four to six hours after surgery, then every 12 hours until the animal died or was killed. Picker 80-L analog and digital units and a 5-MHz focused transducer were used. The sonograms were evaluated by two authors, first independently and then together. Observations were made regarding kidney size, cortical thickness, the distribution of the echoes throughout the cortex, distinction of the corticomedullary boundary, appearance of the medullary pyramids, and amplitude of the echoes within the renal sinus.
MATERIALS AND METHODS
Acute tubular necrosis was diagnosed by laboratory and pathological examination in all seven dogs. In two cases the immediate postoperative six-hour scan showed mild hydronephrosis which later resolved (Fig. 1). In six of seven animals, no parenchymal changes were detected by ultrasound initially or on subsequent examination. The characteristic normal echo pattern of the renal parenchyma was unchanged. The cortex remained more echogenic than the medulla and less echogenic than the renal sinus (3). The amplitude of the cortical echoes and the thickness of the cortex remained unchanged (Fig. 1). The relatively sonolucent, triangular pyramids also showed no alterations throughout the course of ATN. In one animal, the initial six-hour scan showed sparsely distributed cortical echoes (Fig. 2, a). The corticomedullary boundary was distinct, and the medullary pyramids were normally sonolucent and unremarkable. There was mild hydronephrosis. The 96-hour (four-day) scan displayed a localized anechoic area in the cortex (Fig. 2, b), corresponding to an area of cortical necrosis in the pathology specimen (Fig. 2, c). The cortical echoes remained
LTRASOUND
U
RESULTS
Seven adult mongrel dogs weighing 17-24 kg were anesthetized with sodium thiamylal (4 %, 40 mg/ml) for induction and halothane (Fluothane's) (0.5-1 %) for maintenance. Prior to surgery, 200-300 ml of Ringer's lactate was administered intravenously. Through a midline laparotomy, the left kidney, vascular structures, and ureters were removed and maintained at 37°C. Renal vessels were clamped for 40 minutes in the first dog, and for 60 minutes in the remaining dogs. The kidney was then excised, flushed with Ringer's lactate containing 10,000 units of heparin at 4°C, and transplanted into the right iliac fossa of the same dog. The right kidney was excised during this operation. Furosemide (10 mg) was given before crossclamping and 20 mg after autotransplantation. The abdomen was closed in a routine manner, and 250 ml of Ringer's lactate was administered intravenously for the next six hours. Serum creatinine values were obtained daily. As the implanted kidney was from the recipient, the possibility of rejection was obviated.
1 From the Departments of Diagnostic Radiology (H.H., W.R.E., B.L.M.), Surgical Research (L.H.T.), and General Surgery (G.S.S.), Henry Ford Hospital, Detroit, Michigan. Received April 18, 1979; accepted and revision requested May 30; revision received June 29. This work was partially supported by a Henry Ford Hospital Grant from the Ford Foundation No. 730-0786. sb
443
444
HEDVIG HRICAK AND OTHERS
November 1979
Fig. 1. a. Longitudinal scan six hours after transplantation. The central renal sinus echoes ($) are separated slightly , indicating hydronephrosis. The renal cortex (C) shows homogeneously distributed echoes of medium strength . The renal cortex measures 9 mm. The corticomedullary boundary is distinct. Arcuate vessels are indicated by the arrowhead . b. Longitudinal scan three days after transplantation. The axis of orientation is slightly different from Figure 1, a. The serum creatinine level is 3.6 mg/dl. Acute renal failure . There is no evidence of hydronephrosis. The cortical thickness remains the same, and the central sinus echoes. characteristics of the cortical echoes remain normal. $ c. Oblique scan. The serum creatinine level is 4.0 mg/dl. Sonographically, the kidney appears normal. d. After the Figure 1, c scan was obtained, the dog was killed. Photomicrograph of the renal cortex shows diffuse tubular dilatation with flattening and degenerative -regenerative changes of the tubular epithelium. There is nuclear debris within the lumen of the tubules and minimal interstitial edema. Changes are consistent with acute tubular necrosis. (X 128)
=
sparsely distributed; on pathological correlation, there was interstitial edema throughout the cortex (Fig. 2, d). The corticomedullary junction was distinctly seen except in the area of necrosis. The size and echogenecity of the medullary pyramids remained the same and hydronephrosis became less pronounced. The central sinus echoes showed the same high amplitude as those on the initial study. DISCUSSION Acute tubular necrosis is a common cause of acute post-transplant renal failure (9). Atter renal transplantation, some degree of ATN has been reported in as many as 50 % of the recipients of cadaver kidneys (4). The incidence of ATN following renal transplantation is higher in cadaver transplants than in donor-related kidney transplants (9). ATN is more frequent in kidneys that undergo warm ischemia or prolonged preservation (16), have multiple renal arteries (12), or are obtained from elderly donors (12). The label "ATN" is actually a misnomer, since there is seldom actual tubular necrosis. There are usually
hydropic changes within the tubules. If necrosis is present, it is focal and not extensive (12). Clinically, ATN may present with a variety of different patterns. Urine volumes may be good initially followed by oliguria or anuria, or there may be a low urine output from the time of transplantation. The serum creatinine level is always elevated. Uncomplicated ATN is usually reversible and can be treated by immediate use of diuretics and satisfactory hydration (9, 12). It is important to recognize uncomplicated ATN and distinguish it from acute rejection, because therapy for the two conditions is different. Antirejection therapy includes increased dosage of steroids, while in the treatment of ATN the dosage of azothioprine should be reduced to 1.5 kg (12). On the basis of clinical information and laboratory findings, it is often impossible to distinguish ATN from acute rejection. Radionuclides provide useful functional and anatomic information about renal transplantation, and the differentiation between ATN and rejection can be suggested, but it should be emphasized that this cannot always be done conclusively (4) (TABLE I).
445
Ev ALUA TION OF RENAL FAILURE BY ULTRASOUND
Vol. 133
Ultrasound
Fig. 2. a. Longitudinal section six hours after transplantation. Hydronephrosis is causing separation of the central sinus (S) echoes. The cortical echoes (C) are of medium strength and sparsely distributed . Arcuate arteries are seen at the corticomedullary junction (arrowhead) and the pyramids (P) are visible. b. Longitudinal scan four days following transplantation. Acute renal failure . The serum creatinine level is 3 mg/dl. Hydronephrosis is less prominent. Cortical echoes remain sparsely distributed, and there is a localized anechoic area (arrowhead) along the inferior part of the kidney , representing cortical necrosis. c. Photograph of a transplant specimen, showing diffuse swelling of the cortex with an area of hemorrhage representing the cortical infarct. d. Photomicrograph of a transplant specimen shows mild tubular dilatation with mild flattening of the tubular epithelium and interstitial edema. There is nuclear debris within the tubular lumen. Occasional tubules show tubular epithelial necrosis.
Sonographically, in most cases. there were no changes seen within the renal parenchyma throughout the course of ATN (Fig. 3. a and b). In one animal, cortical echoes were sparsely distributed. corresponding to interstitial edema seen on pathological specimens, with the localized, TABLE
Radionuclide 99mTc_
Sulfur colloid 99mTc_
DTPA (flow study)
I:
anechoic area within the cortex corresponding to the area of cortical necrosis. In contrast , patients and experimental animals with acute rejection demonstrated a number of sonographic parenchymal changes. some of which were always
USEFULNESS OF RADIONUCLIDES IN DIFFERENTIATING BETWEEN ATN AND REJECTION
Normal
ATN
Rejection
Activity= none-minimal
Activity= none-moderate
Activity= moderate-marked
Aorto-renal transit time= 2-8 sec.
MiId-moderate prolongation, transit time= 8-12 sec .
Moderate-marked prolongation, transit time= 10-16 sec. No activity in transplant=vascular occlusion
131 1
OIH
Rapid accumulation, normal radionuclide progression
Rapid-lair accumulation, marked parenchymal retention
Poor accumulation, mild, parencymal retention
446
HEDVIG HRICAK AND OTHERS
November 1979
3a,b
3c ,d
Fig. 3.
a.
Longitudinal scan six hours after transplantation shows a normal kidney. C
= renal sinus; arrowhead indicates the arcuate vessels.
= renal cortex , P = pyramids, S
b. Longitudinal scan in a slightly different axis than Figure 3, a four days after transplantation. The serum creatinine level is 4 mg/dl. Sonographically, the kidney appears normal; the medullary pyramids show no change from the base-line study. ATN was proved pathologically. c . Oblique scan six hours after transplantation shows a normal kidney. C = renal cortex, P = pyramids; arrowhead indicates the arcuate vessels. d. Oblique scan four days after transplantation. The serum creatinine level is 1.8 mg/dl. Rejection was proved at biopsy. The medullary pyramids (P) are enlarged and more prominent than on the initial study. In our experience, enlargement of the medullary pyramids is the earliest, consistent sign of rejection.
present (2, 7). Those changes consisted of prominent pyramids (Fig. 3, c and d), swollen enlarged kidney, increased cortical thickness , decreased or increased echogenicity of the cortex, indistinct corticomedullary boundaries, decrease in the amplitude of the renal sinus echoes, and in a few cases perirenal fluid collection as a result of renal rupture (2, 7). During rejection sonograms are always abnormal. In summary, in acute post-transplant renal failure, when radionuclide study is equivocal, differentiation between ATN and rejection can be made by ultrasound.
Department of Diagnostic Radiology Henry Ford Hospital 2799 W. Grand Blvd. Detroit , Mich. 48202
ACKNOWLEDGMENTS: We would like to thank Mrs. Annie Jeffries for her help in laboratory work and Mrs. Mary Tobey for her assistance in the preparation of the manuscript.
REFERENCES 1. Bartrum RJ, Smith EH, D'Orsi CJ, et al: Evaluation of renal transplants with ultrasound. Radiology 118:405-410, Feb 1976 2. Conrad MR, Dickerman R, Love IL, et al: New observations in renal transplants using ultrasound. Am J RoentgenoI131:851 -855, Nov 1978 3. Cook JH, Rosenfield AT, Taylor KJW: Ultrasonic demonstration of intrarenal anatomy. Am J RoentgenoI129:831-835, Nov 1977 4. Delmonico FL, McKusick KA, Cosimi AB, et al: Differentiation between renal allograft rejection and acute tubular necrosis by renal scan. Am J RoentgenoI128:625-628, Apr 1977 5. Dunnill MS: A review of the pathology and pathogenesis of acute renal failure due to acute tubular necrosis. J Clin PathoI27:2-13, Jun 1974
Vol. 133
Ev ALUA TION OF RENAL FAILURE BY ULTRASOUND
6. Hricak H, Toledo-Pereyra LH, Eyler WR, et al: The role of ultrasound in kidney allograft rejection. Radiology 132:667-672, Sep
1979 7. Kjellstrand CM, Casali RE, Simmons RL, et al: Etiology and prognosis in acute post-transplantrenal failure. Am J Moo 61:190-199, Aug 1976 8. Koehler PR, Kanemoto HH, Maxwell JG: Ultrasonic "B" scanning in the diagnosis of complications in renal transplant patients.
447
Ultrasound
Radiology 119:661-664, Jun 1976 9. Najarian JS, Simmons RL: Transplantation. Philadelphia, Lea & Febiger, 1972, pp 462-469 10. Petrek J, Tilney NL, SmithEH, et al: Ultrasound in renal transplantation. Ann Surg 185:441-447, Apr 1977 11. Toledo-Pereyra LH, Simmons RL, Olson LC, et al: Perfusion time and the survival of cadaver transplants. Surgery 79:377-383, Apr 1976
Evaluation of Acute Post-Transplant Renal Failure by Ultrasound 1 Hedvig Hricak, M.D., Luis H. Toledo-Pereyra, M.D., Ph.D., William R. Eyler, M.D., Beatrice L. Madrazo, M.D., and Guat 5. 5y, M.D.
Autotransplantation of the kidney was performed in seven adult mongrel dogs. A model of acute tubular necrosis (ATN) was developed by subjecting the kidney to warm ischemia (37°C) for 40 to 60 minutes. Serial ultrasound examinations were performed every 12 hours until the animal died or was killed. Sonographic findings were correlated with laboratory and histological data. Throughout the course of ATN, the characteristic normal echo pattern of the kidney remained unchanged in six of seven dogs. In one animal there were changes in the renal cortex, while the medullary pyramids showed no alteration from the base-line study. This contrasts with extensive abnormalities found during rejection. INDEX TERMS:
Kidneys, failure. Kidneys, necrosis • Kidneys, transplantation, 8 [1] .455 • Kidneys, ultrasound stud-
ies,8[1].1298 Radiology 133:443-447, November 1979
is a valuable noninvasive procedure in the monitoring of the renal transplant patient. It is used to demonstrate hydronephrosis, to detect perirenal fluid collections (1, 10), and recently to assess transplant rejection (2, 7). Immediately after transplantation, acute tubular necrosis (ATN) is a frequent complication which can be confused with rejection both clinically and by laboratory parameters (9, 12). To our knowledge, there are no studies describing sonographic parenchymal changes during ATN. Using a canine kidney as the model, this study was undertaken to evaluate parenchymal changes following post-transplant tubular necrosis.
An ultrasound examination was performed four to six hours after surgery, then every 12 hours until the animal died or was killed. Picker 80-L analog and digital units and a 5-MHz focused transducer were used. The sonograms were evaluated by two authors, first independently and then together. Observations were made regarding kidney size, cortical thickness, the distribution of the echoes throughout the cortex, distinction of the corticomedullary boundary, appearance of the medullary pyramids, and amplitude of the echoes within the renal sinus.
MATERIALS AND METHODS
Acute tubular necrosis was diagnosed by laboratory and pathological examination in all seven dogs. In two cases the immediate postoperative six-hour scan showed mild hydronephrosis which later resolved (Fig. 1). In six of seven animals, no parenchymal changes were detected by ultrasound initially or on subsequent examination. The characteristic normal echo pattern of the renal parenchyma was unchanged. The cortex remained more echogenic than the medulla and less echogenic than the renal sinus (3). The amplitude of the cortical echoes and the thickness of the cortex remained unchanged (Fig. 1). The relatively sonolucent, triangular pyramids also showed no alterations throughout the course of ATN. In one animal, the initial six-hour scan showed sparsely distributed cortical echoes (Fig. 2, a). The corticomedullary boundary was distinct, and the medullary pyramids were normally sonolucent and unremarkable. There was mild hydronephrosis. The 96-hour (four-day) scan displayed a localized anechoic area in the cortex (Fig. 2, b), corresponding to an area of cortical necrosis in the pathology specimen (Fig. 2, c). The cortical echoes remained
LTRASOUND
U
RESULTS
Seven adult mongrel dogs weighing 17-24 kg were anesthetized with sodium thiamylal (4 %, 40 mg/ml) for induction and halothane (Fluothane's) (0.5-1 %) for maintenance. Prior to surgery, 200-300 ml of Ringer's lactate was administered intravenously. Through a midline laparotomy, the left kidney, vascular structures, and ureters were removed and maintained at 37°C. Renal vessels were clamped for 40 minutes in the first dog, and for 60 minutes in the remaining dogs. The kidney was then excised, flushed with Ringer's lactate containing 10,000 units of heparin at 4°C, and transplanted into the right iliac fossa of the same dog. The right kidney was excised during this operation. Furosemide (10 mg) was given before crossclamping and 20 mg after autotransplantation. The abdomen was closed in a routine manner, and 250 ml of Ringer's lactate was administered intravenously for the next six hours. Serum creatinine values were obtained daily. As the implanted kidney was from the recipient, the possibility of rejection was obviated.
1 From the Departments of Diagnostic Radiology (H.H., W.R.E., B.L.M.), Surgical Research (L.H.T.), and General Surgery (G.S.S.), Henry Ford Hospital, Detroit, Michigan. Received April 18, 1979; accepted and revision requested May 30; revision received June 29. This work was partially supported by a Henry Ford Hospital Grant from the Ford Foundation No. 730-0786. sb
443
444
HEDVIG HRICAK AND OTHERS
November 1979
Fig. 1. a. Longitudinal scan six hours after transplantation. The central renal sinus echoes ($) are separated slightly , indicating hydronephrosis. The renal cortex (C) shows homogeneously distributed echoes of medium strength . The renal cortex measures 9 mm. The corticomedullary boundary is distinct. Arcuate vessels are indicated by the arrowhead . b. Longitudinal scan three days after transplantation. The axis of orientation is slightly different from Figure 1, a. The serum creatinine level is 3.6 mg/dl. Acute renal failure . There is no evidence of hydronephrosis. The cortical thickness remains the same, and the central sinus echoes. characteristics of the cortical echoes remain normal. $ c. Oblique scan. The serum creatinine level is 4.0 mg/dl. Sonographically, the kidney appears normal. d. After the Figure 1, c scan was obtained, the dog was killed. Photomicrograph of the renal cortex shows diffuse tubular dilatation with flattening and degenerative -regenerative changes of the tubular epithelium. There is nuclear debris within the lumen of the tubules and minimal interstitial edema. Changes are consistent with acute tubular necrosis. (X 128)
=
sparsely distributed; on pathological correlation, there was interstitial edema throughout the cortex (Fig. 2, d). The corticomedullary junction was distinctly seen except in the area of necrosis. The size and echogenecity of the medullary pyramids remained the same and hydronephrosis became less pronounced. The central sinus echoes showed the same high amplitude as those on the initial study. DISCUSSION Acute tubular necrosis is a common cause of acute post-transplant renal failure (9). Atter renal transplantation, some degree of ATN has been reported in as many as 50 % of the recipients of cadaver kidneys (4). The incidence of ATN following renal transplantation is higher in cadaver transplants than in donor-related kidney transplants (9). ATN is more frequent in kidneys that undergo warm ischemia or prolonged preservation (16), have multiple renal arteries (12), or are obtained from elderly donors (12). The label "ATN" is actually a misnomer, since there is seldom actual tubular necrosis. There are usually
hydropic changes within the tubules. If necrosis is present, it is focal and not extensive (12). Clinically, ATN may present with a variety of different patterns. Urine volumes may be good initially followed by oliguria or anuria, or there may be a low urine output from the time of transplantation. The serum creatinine level is always elevated. Uncomplicated ATN is usually reversible and can be treated by immediate use of diuretics and satisfactory hydration (9, 12). It is important to recognize uncomplicated ATN and distinguish it from acute rejection, because therapy for the two conditions is different. Antirejection therapy includes increased dosage of steroids, while in the treatment of ATN the dosage of azothioprine should be reduced to 1.5 kg (12). On the basis of clinical information and laboratory findings, it is often impossible to distinguish ATN from acute rejection. Radionuclides provide useful functional and anatomic information about renal transplantation, and the differentiation between ATN and rejection can be suggested, but it should be emphasized that this cannot always be done conclusively (4) (TABLE I).
445
Ev ALUA TION OF RENAL FAILURE BY ULTRASOUND
Vol. 133
Ultrasound
Fig. 2. a. Longitudinal section six hours after transplantation. Hydronephrosis is causing separation of the central sinus (S) echoes. The cortical echoes (C) are of medium strength and sparsely distributed . Arcuate arteries are seen at the corticomedullary junction (arrowhead) and the pyramids (P) are visible. b. Longitudinal scan four days following transplantation. Acute renal failure . The serum creatinine level is 3 mg/dl. Hydronephrosis is less prominent. Cortical echoes remain sparsely distributed, and there is a localized anechoic area (arrowhead) along the inferior part of the kidney , representing cortical necrosis. c. Photograph of a transplant specimen, showing diffuse swelling of the cortex with an area of hemorrhage representing the cortical infarct. d. Photomicrograph of a transplant specimen shows mild tubular dilatation with mild flattening of the tubular epithelium and interstitial edema. There is nuclear debris within the tubular lumen. Occasional tubules show tubular epithelial necrosis.
Sonographically, in most cases. there were no changes seen within the renal parenchyma throughout the course of ATN (Fig. 3. a and b). In one animal, cortical echoes were sparsely distributed. corresponding to interstitial edema seen on pathological specimens, with the localized, TABLE
Radionuclide 99mTc_
Sulfur colloid 99mTc_
DTPA (flow study)
I:
anechoic area within the cortex corresponding to the area of cortical necrosis. In contrast , patients and experimental animals with acute rejection demonstrated a number of sonographic parenchymal changes. some of which were always
USEFULNESS OF RADIONUCLIDES IN DIFFERENTIATING BETWEEN ATN AND REJECTION
Normal
ATN
Rejection
Activity= none-minimal
Activity= none-moderate
Activity= moderate-marked
Aorto-renal transit time= 2-8 sec.
MiId-moderate prolongation, transit time= 8-12 sec .
Moderate-marked prolongation, transit time= 10-16 sec. No activity in transplant=vascular occlusion
131 1
OIH
Rapid accumulation, normal radionuclide progression
Rapid-lair accumulation, marked parenchymal retention
Poor accumulation, mild, parencymal retention
446
HEDVIG HRICAK AND OTHERS
November 1979
3a,b
3c ,d
Fig. 3.
a.
Longitudinal scan six hours after transplantation shows a normal kidney. C
= renal sinus; arrowhead indicates the arcuate vessels.
= renal cortex , P = pyramids, S
b. Longitudinal scan in a slightly different axis than Figure 3, a four days after transplantation. The serum creatinine level is 4 mg/dl. Sonographically, the kidney appears normal; the medullary pyramids show no change from the base-line study. ATN was proved pathologically. c . Oblique scan six hours after transplantation shows a normal kidney. C = renal cortex, P = pyramids; arrowhead indicates the arcuate vessels. d. Oblique scan four days after transplantation. The serum creatinine level is 1.8 mg/dl. Rejection was proved at biopsy. The medullary pyramids (P) are enlarged and more prominent than on the initial study. In our experience, enlargement of the medullary pyramids is the earliest, consistent sign of rejection.
present (2, 7). Those changes consisted of prominent pyramids (Fig. 3, c and d), swollen enlarged kidney, increased cortical thickness , decreased or increased echogenicity of the cortex, indistinct corticomedullary boundaries, decrease in the amplitude of the renal sinus echoes, and in a few cases perirenal fluid collection as a result of renal rupture (2, 7). During rejection sonograms are always abnormal. In summary, in acute post-transplant renal failure, when radionuclide study is equivocal, differentiation between ATN and rejection can be made by ultrasound.
Department of Diagnostic Radiology Henry Ford Hospital 2799 W. Grand Blvd. Detroit , Mich. 48202
ACKNOWLEDGMENTS: We would like to thank Mrs. Annie Jeffries for her help in laboratory work and Mrs. Mary Tobey for her assistance in the preparation of the manuscript.
REFERENCES 1. Bartrum RJ, Smith EH, D'Orsi CJ, et al: Evaluation of renal transplants with ultrasound. Radiology 118:405-410, Feb 1976 2. Conrad MR, Dickerman R, Love IL, et al: New observations in renal transplants using ultrasound. Am J RoentgenoI131:851 -855, Nov 1978 3. Cook JH, Rosenfield AT, Taylor KJW: Ultrasonic demonstration of intrarenal anatomy. Am J RoentgenoI129:831-835, Nov 1977 4. Delmonico FL, McKusick KA, Cosimi AB, et al: Differentiation between renal allograft rejection and acute tubular necrosis by renal scan. Am J RoentgenoI128:625-628, Apr 1977 5. Dunnill MS: A review of the pathology and pathogenesis of acute renal failure due to acute tubular necrosis. J Clin PathoI27:2-13, Jun 1974
Vol. 133
Ev ALUA TION OF RENAL FAILURE BY ULTRASOUND
6. Hricak H, Toledo-Pereyra LH, Eyler WR, et al: The role of ultrasound in kidney allograft rejection. Radiology 132:667-672, Sep
1979 7. Kjellstrand CM, Casali RE, Simmons RL, et al: Etiology and prognosis in acute post-transplantrenal failure. Am J Moo 61:190-199, Aug 1976 8. Koehler PR, Kanemoto HH, Maxwell JG: Ultrasonic "B" scanning in the diagnosis of complications in renal transplant patients.
447
Ultrasound
Radiology 119:661-664, Jun 1976 9. Najarian JS, Simmons RL: Transplantation. Philadelphia, Lea & Febiger, 1972, pp 462-469 10. Petrek J, Tilney NL, SmithEH, et al: Ultrasound in renal transplantation. Ann Surg 185:441-447, Apr 1977 11. Toledo-Pereyra LH, Simmons RL, Olson LC, et al: Perfusion time and the survival of cadaver transplants. Surgery 79:377-383, Apr 1976
