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Bilateral Polyadenomatous Kidneys; Adenomatosis of the Kidneys Simulating Polycystic Disease
THE JOURNAL OF UROLOGY
Vol. 72, No. 6, December 1954 Printed in U.S.A.
BILATERAL POLYADENOMATOUS KIDNEYS; ADENOMATOSIS OF THE KIDNEYS SIMULATING POLYCYSTIC DISEASE HERMAN J. MEISEL
From the Veterans Administration Hospital, Fort Howard, lVId.
In the American Journal of 111edical Sciences for December 1890, an article appeared by Edward Keyes,1 one of the founders of modern Urology, entitled "Adenoma of the Kidney; Successful Nephrectomy." This is a vivid description of a 49 year old white man suffering from severe gross hematuria and anemia. Under chloroform anesthesia a large right kidney was palpated. This completed Dr. Keyes' investigation, since roentgenography and ureteral catheterization were then unknown. When it is also noted that the field of renal surgery was unexplored and transfusion was impractical, the courage and perspicacity of such pioneering urologists are to be admired. Nephrectomy was sucessfully performed later. The excised kidney contained an enormous number of adenomas from 2 mm. to 1.5 cm. in diameter. Dr. Keyes' report is the only instance found, in a search of the literature since 1890, which resembles the case to be presented. CASE REPORT
A 30 year old, single, white man, a crane operator (R-31,300), was admitted to the Veterans Administration Hospital, Fort Howard, Md. on October 14, 1951, with a complaint of painless, gross total hematuria for 24 hours. No other urinary symptoms were present. No history of genito-urinary disease was elicited. It had been noted, however, since childhood, that the left testis was not present in the scrotum. The past history and family history were not pertinent. No evidence of genito-urinary abnormalities in his parents or his three siblings was revealed after careful questioning. The patient was intelligent and healthy. The temperature was 98.6F, the pulse 84 and the respirations 20. The blood pressure was 158/110. The lungs were clear. The heart was not enlarged but the heart sounds were loud and forceful. There were no murmurs. In each flank there was a large, firm, irregular, nontender mass which was easily ballottable. On the right, the mass extended from the flank to the midline, and from the costal margin well down into the right lower quadrant. It measured approximately 25 cm. vertically and 10 cm. transversely. The mass on the left was similar in all respects except that it was slightly smaller, 20 cm. by 8 cm. These masses were thought to be typical polycystic kidneys. The right testis was normal, but the left testis could not be palpated in the scrotum, inguinal canal or perineum. There was a well healed right inguinal scar. The prostate was normal. The remainder of the examination was normal. Reviewed in the Veterans Administration and published with the approval of the Chief Medical Director. The statements and conclusions published by the authors are the result of their own study and do not necessarily reflect the opinion or policy of the Veterans Administration. Read at annual meeting, Mid-Atlantic Section of the American Urological Association, Washington, D. 0., April 22, 1954. 1 Keyes, E. L.: Am. J. Med. Sc., 100: 549-558, 1890. 1140
RENAL ADENOMATOSIS
1141
The roentgenogram of the chest was within normal limits. The serological test for syphilis was negative. The voided urine was grossly bloody and microscopically contained many erythrocytes. The specific gravity of the urine was 1.020, test for albumin was 3 plus, and aerobic and anaerobic cultures were sterile. The hemoglobin was 12.5 gm. per cent; the red blood cell count was 4 million per cmm. and the white blood cell count was 11,650 per cmm., of which 71 per cent were polymorphonuclears, 27 per cent lymphocytes and 1 per cent each were monocytes and eosinophils. The urea nitrogen was 10.3 mg. per cent and the carbon-dioxide combining power 40 volumes per cent. At cystoscopy, shortly after admission, the lower urinary tract was found to be normal. Efflux from the left ureter, however, was grossly bloody. Indigo carmine appeared in four plus concentration from the right kidney within five minutes;
Fm. L Retrograde pyelograms
on the left, evaluation could not be made because of admixture of the dye with blood. The retrograde pyelograms (fig. 1) were interpreted as showing typical bilateral polycystic kidneys. A small filling defect in the left upper calyx was thought to be due to blood clot. The excretory urogram confirmed these findings. It was felt that the patient had bilateral polycystic kidneys with good function, and that the source of the bleeding was an erosion or rupture of a cyst into the left renal pelvis. Therefore, a conservative policy was carried out. Bed rest, replacement of blood, and vitamin therapy including vitamin K were instituted. During the 45 days after admission, hematuria in varying amounts was almost continuous. Several episodes of cessation of hematuria were accompanied by left renal pain indicative of left ureteral blockage. With the passage of clots, the pain subsided and hematuria recurred. On November 26 an attempt was made to control bleeding by lavage of the left renal pelvis with dilute silver nitrate solution. ·vvhen this also failed, it was felt that surgical exploration and possible application of Rovsing's procedure were justified. On November 29 exposure was secured through a flank incision. The kidney was four times as large as normal with its surface everywhere studded with firm, rubbery, whitish nodules of varied size. Incision of one of these nodules revealed the same white, rubbery tissue, a portion of which, taken for frozen section, was reported to be "adenoma." Since
1142
HERMAN J. MEISEL
Fm. 2. A, left kidney, external surface; B, cut surface. Note filling defect in upper calyx
the nature and extent of the disease precluded conservative procedure, nephrectomy was performed without difficulty. The postoperative course was without event. Hematuria ceased immediately. The blood urea nitrogen rose to 46 mg. per 100 cc but at the time of discharge had fallen to 33 mg. per 100 cc. Follow-up examinations have been done at frequent intervals. Hematuria has not recurred. The blood urea nitrogen has stabilized at 20~25 mg. per 100 cc. The urine has been negative on routine examination and culture. The phenolsulfonphthalein output is 70 per cent in 2 hours. Urinary concentration however is fixed at a specific gravity of 1.008 to 1.010. The right kidney remains large, hard, and irregular to palpation. Although it undoubtedly duplicates the lesion in its excised fellow, it satisfactorily maintains life. The patient performs a full day of sedentary work and, despite contrary advice, has married. The kidney (fig. 2) weighed 800 gm. and measured 22 by 9 by 5 cm. Its surface was studded with nodules varying in size from 3 mm. to 2 cm. and, in color, from whitish yellow to dark red and hemorrhagic. On cut section (fig. 2) almost the entire parenchyma was replaced by discrete yellow nodules. The nodules were firm and rubbery, though some showed central necrosis. In the upper calyx there was a dark red protruding mass. Near the hilum of the kidney small areas of normal renal tissue about one cm. across could be recognized. Microscopically (fig. 3), the nodules were all renal adenomas varying in structure. Some were papillary and some solid. Several showed invasion of their fibrous capsules while others showed calcification or necrosis. The mass protrud-
RENAL ADENOMATOSIS
1143
Fm. 3. Typical microscopic section
ing into the upper calyx was a necrotic ruptured adenoma. The pelvic mucosa showed squamous metaplasia and pyelitis cystica. DISCUSSION
Adenoma of the kidney was first accurately described by Sturm2 in 1875. The many papers which have since appeared can roughly be divided into two groups. The "clinical" papers report large benign adenoma of the kidney diagnosed during life and requiring surgical treatment. By 1944 Higgins 3 could find only 27 such cases including one of his own. In 1953 the latest reviewers, Childs and Waterfall 4 found 33 reports in the literature and added two of their own. The other, and larger, group of papers deal with "nonclinical adenomas" i.e., those which cannot be diagnosed during life, which are found at autopsy, or in a kidney excised for some other disease. The greatest interest and diversity of opinion appear in the discussion of the histogenesis of this latter group. Most recent students, Ewing, 5 Cristol, McDonald and Emmett, 6 Fuchsman and Angrist, 7 and Gordon,8 state that these small adenomas occur in kidneys which have been previously scarred because of localized vascular occlusions on an Sturm, P.: Arch. f. Heilk., 16: 193-237, 1875. Higgins, C. C.: Am. J. Surg., 65: 3-14, 1944. 4 Childs, P. and Waterfall, W. B.: Brit. J. Urol., 25: 187-194, 1953. 5 Ewing, J.: Neoplastic Diseases. Philadelphia: W. B. Saunders Co., 4th ed., pp. 700-829. 6 Cristol, D. S., McDonald, J. R. and E=ett, J. L.: J. Urol., 55: 18-27, 1946. 7 Fuchsman, J. J. and Angrist, A.: J. Urol., 59: 167-173, 1948. 8 Gordon, B. S.: J. Urol., 59: 1019-1021, 1948. 2
3
1144
HERMAN J, MEISEL
arteriosclerotic basis. There is postulated first necrosis of tubules due to a small vascular lesion. A tubule becomes fragmented into isolated segments. Apparently the ends of a segment are sealed forming a small cyst, within which the tubular cells then proliferate forming an adenomatous nodule. This theory is fortified by the facts that these tumors are found most often in people over 50 years of age and that they occur in the subcapsular areas where endarteritis would be most evident. They also occur often in association with microscopic cysts presumably also formed by tubular necrosis. Turley and Steel,9 however, from a careful morphological study of similar material concluded, in their case of multiple miliary adenomas, that the tumors must arise from the glomeruli. l\![ost unfashionable at the moment is the theory of congenital origin. Albarran10 stated that the precursors of adenomas were islands of imperfectly developed or displaced tubules originating in some aberration of fusion of the nephrogenic and wolffian elements. This latter hypothesis would seem most adequately to fit the present case. The youth of the patient, the diffuse distribution throughout both kidneys, the lack of vascular changes and the lack of correspondence to vascular distribution, tend to confirm the congenital origin of this disease in this patient. It is felt by many that adenoma may become malignant. Cristol, McDonald and Emmett 6 reported incidental adenomas in 34 per cent of kidneys excised for carcinoma. Others have found adenomas with invasion of the capsule, and have described gradations of cellular architecture from benign to malignant within the same tumor. In the present case no evidence of malignant degeneration was found and after 2 years of observation there is no clinical evidence of malignant disease. Histologically, adenomas have been classified into three types. The tubular type exhibits long, branching, irregular channels; the alveolar type contains polyhedral cells, arranged more or less uniformly in alveoli; and the papillary adenoma is made up of infolding, branch-like outgrowths often appearing to arise from the epithelium of a surrounding cyst wall. The present case shows all these types in different adenomas and often within the same nodules. Bilateral involvement of the kidneys by primary neoplasm is frequent in the instances of nonclinical multiple miliary type of adenomas found at autopsy. Less than 30 cases of primary malignant involvement of both kidneys have been reported. 11 • 12 , 13 Several cases of diffuse bilateral involvement of the kidneys by malignant or granulomatous lesions such as lymphosarcoma, leukemia, roundcell sarcoma and sarcoid have been reported. 12 • 13 • 14 Unfortunately most of these were autopsy cases and did not have pyelographic study. In a rather careful search of the literature, only one instance was found in which pyelographic findings indicative of polycystic kidneys were found to be due to diffuse involvement 'Turley, L.A. and Steel, J.: J.A.M.A., 82: 857-859, 1924. Albarran, J.: Quoted by Cristal, McDonald, and Emmett. 6 11 Eisendrath, D. E. and Rolnick, H. C.: Textbook of Urology. Philadelphia: J.B. Lipincott Co., 1938. 12 Forsythe, W. E.: J. Urol., 47: 784-791, 1942. 13 Flynn, J.E. and Bowers, J.M.: J. Urol., 58: 106-111, 1947. 14 Fischer, G. S.: Grace Hosp. Bull., 26: 11-24, 1948. 10
RENAL ADENOMATOSIS
1145
by tumor, in this case, lymphoblastoma (Fischer). 4 It would seem that pyelography, if done more often in diffuse neoplastic disease with renal involvement, might reveal more cases simulating polycystic disease. It is certainly obvious that diffuse neoplastic renal involvement could distort and elongate calyces in similar fashion, and as easily as, cysts. It is also notable that the clinical findings of hypertension, fixed urinary specific gravity, elevated blood urea nitrogen, all consistent with polycystic kidneys, were present in our case. An accurately descriptive name for this disease was not at hand. It was felt that a parallel could be drawn with the nomenclature of renal cysts. Thus a solitary cyst could be compared with a solitary adenoma and multiple cysts with multiple adenoma. The special appellation for polycystic disease of the kidneys, therefore, logically suggested the parallel term of polyadenomatous kidneys, which ·was thus adopted as the title of this paper. CONCLUSION
An instance of bilateral diffuse adenomatosis of the kidneys has been presented. Only one other similar case has been recorded by Keyes in 1890 and, as far as is known, this was unilateral. The distinctive name of bilateral polyadenomatous kidneys has been suggested. The clinical, urinary and pyelographic changes in this case simulated bilateral polycystic renal disease very closely.
Vol. 72, No. 6, December 1954 Printed in U.S.A.
BILATERAL POLYADENOMATOUS KIDNEYS; ADENOMATOSIS OF THE KIDNEYS SIMULATING POLYCYSTIC DISEASE HERMAN J. MEISEL
From the Veterans Administration Hospital, Fort Howard, lVId.
In the American Journal of 111edical Sciences for December 1890, an article appeared by Edward Keyes,1 one of the founders of modern Urology, entitled "Adenoma of the Kidney; Successful Nephrectomy." This is a vivid description of a 49 year old white man suffering from severe gross hematuria and anemia. Under chloroform anesthesia a large right kidney was palpated. This completed Dr. Keyes' investigation, since roentgenography and ureteral catheterization were then unknown. When it is also noted that the field of renal surgery was unexplored and transfusion was impractical, the courage and perspicacity of such pioneering urologists are to be admired. Nephrectomy was sucessfully performed later. The excised kidney contained an enormous number of adenomas from 2 mm. to 1.5 cm. in diameter. Dr. Keyes' report is the only instance found, in a search of the literature since 1890, which resembles the case to be presented. CASE REPORT
A 30 year old, single, white man, a crane operator (R-31,300), was admitted to the Veterans Administration Hospital, Fort Howard, Md. on October 14, 1951, with a complaint of painless, gross total hematuria for 24 hours. No other urinary symptoms were present. No history of genito-urinary disease was elicited. It had been noted, however, since childhood, that the left testis was not present in the scrotum. The past history and family history were not pertinent. No evidence of genito-urinary abnormalities in his parents or his three siblings was revealed after careful questioning. The patient was intelligent and healthy. The temperature was 98.6F, the pulse 84 and the respirations 20. The blood pressure was 158/110. The lungs were clear. The heart was not enlarged but the heart sounds were loud and forceful. There were no murmurs. In each flank there was a large, firm, irregular, nontender mass which was easily ballottable. On the right, the mass extended from the flank to the midline, and from the costal margin well down into the right lower quadrant. It measured approximately 25 cm. vertically and 10 cm. transversely. The mass on the left was similar in all respects except that it was slightly smaller, 20 cm. by 8 cm. These masses were thought to be typical polycystic kidneys. The right testis was normal, but the left testis could not be palpated in the scrotum, inguinal canal or perineum. There was a well healed right inguinal scar. The prostate was normal. The remainder of the examination was normal. Reviewed in the Veterans Administration and published with the approval of the Chief Medical Director. The statements and conclusions published by the authors are the result of their own study and do not necessarily reflect the opinion or policy of the Veterans Administration. Read at annual meeting, Mid-Atlantic Section of the American Urological Association, Washington, D. 0., April 22, 1954. 1 Keyes, E. L.: Am. J. Med. Sc., 100: 549-558, 1890. 1140
RENAL ADENOMATOSIS
1141
The roentgenogram of the chest was within normal limits. The serological test for syphilis was negative. The voided urine was grossly bloody and microscopically contained many erythrocytes. The specific gravity of the urine was 1.020, test for albumin was 3 plus, and aerobic and anaerobic cultures were sterile. The hemoglobin was 12.5 gm. per cent; the red blood cell count was 4 million per cmm. and the white blood cell count was 11,650 per cmm., of which 71 per cent were polymorphonuclears, 27 per cent lymphocytes and 1 per cent each were monocytes and eosinophils. The urea nitrogen was 10.3 mg. per cent and the carbon-dioxide combining power 40 volumes per cent. At cystoscopy, shortly after admission, the lower urinary tract was found to be normal. Efflux from the left ureter, however, was grossly bloody. Indigo carmine appeared in four plus concentration from the right kidney within five minutes;
Fm. L Retrograde pyelograms
on the left, evaluation could not be made because of admixture of the dye with blood. The retrograde pyelograms (fig. 1) were interpreted as showing typical bilateral polycystic kidneys. A small filling defect in the left upper calyx was thought to be due to blood clot. The excretory urogram confirmed these findings. It was felt that the patient had bilateral polycystic kidneys with good function, and that the source of the bleeding was an erosion or rupture of a cyst into the left renal pelvis. Therefore, a conservative policy was carried out. Bed rest, replacement of blood, and vitamin therapy including vitamin K were instituted. During the 45 days after admission, hematuria in varying amounts was almost continuous. Several episodes of cessation of hematuria were accompanied by left renal pain indicative of left ureteral blockage. With the passage of clots, the pain subsided and hematuria recurred. On November 26 an attempt was made to control bleeding by lavage of the left renal pelvis with dilute silver nitrate solution. ·vvhen this also failed, it was felt that surgical exploration and possible application of Rovsing's procedure were justified. On November 29 exposure was secured through a flank incision. The kidney was four times as large as normal with its surface everywhere studded with firm, rubbery, whitish nodules of varied size. Incision of one of these nodules revealed the same white, rubbery tissue, a portion of which, taken for frozen section, was reported to be "adenoma." Since
1142
HERMAN J. MEISEL
Fm. 2. A, left kidney, external surface; B, cut surface. Note filling defect in upper calyx
the nature and extent of the disease precluded conservative procedure, nephrectomy was performed without difficulty. The postoperative course was without event. Hematuria ceased immediately. The blood urea nitrogen rose to 46 mg. per 100 cc but at the time of discharge had fallen to 33 mg. per 100 cc. Follow-up examinations have been done at frequent intervals. Hematuria has not recurred. The blood urea nitrogen has stabilized at 20~25 mg. per 100 cc. The urine has been negative on routine examination and culture. The phenolsulfonphthalein output is 70 per cent in 2 hours. Urinary concentration however is fixed at a specific gravity of 1.008 to 1.010. The right kidney remains large, hard, and irregular to palpation. Although it undoubtedly duplicates the lesion in its excised fellow, it satisfactorily maintains life. The patient performs a full day of sedentary work and, despite contrary advice, has married. The kidney (fig. 2) weighed 800 gm. and measured 22 by 9 by 5 cm. Its surface was studded with nodules varying in size from 3 mm. to 2 cm. and, in color, from whitish yellow to dark red and hemorrhagic. On cut section (fig. 2) almost the entire parenchyma was replaced by discrete yellow nodules. The nodules were firm and rubbery, though some showed central necrosis. In the upper calyx there was a dark red protruding mass. Near the hilum of the kidney small areas of normal renal tissue about one cm. across could be recognized. Microscopically (fig. 3), the nodules were all renal adenomas varying in structure. Some were papillary and some solid. Several showed invasion of their fibrous capsules while others showed calcification or necrosis. The mass protrud-
RENAL ADENOMATOSIS
1143
Fm. 3. Typical microscopic section
ing into the upper calyx was a necrotic ruptured adenoma. The pelvic mucosa showed squamous metaplasia and pyelitis cystica. DISCUSSION
Adenoma of the kidney was first accurately described by Sturm2 in 1875. The many papers which have since appeared can roughly be divided into two groups. The "clinical" papers report large benign adenoma of the kidney diagnosed during life and requiring surgical treatment. By 1944 Higgins 3 could find only 27 such cases including one of his own. In 1953 the latest reviewers, Childs and Waterfall 4 found 33 reports in the literature and added two of their own. The other, and larger, group of papers deal with "nonclinical adenomas" i.e., those which cannot be diagnosed during life, which are found at autopsy, or in a kidney excised for some other disease. The greatest interest and diversity of opinion appear in the discussion of the histogenesis of this latter group. Most recent students, Ewing, 5 Cristol, McDonald and Emmett, 6 Fuchsman and Angrist, 7 and Gordon,8 state that these small adenomas occur in kidneys which have been previously scarred because of localized vascular occlusions on an Sturm, P.: Arch. f. Heilk., 16: 193-237, 1875. Higgins, C. C.: Am. J. Surg., 65: 3-14, 1944. 4 Childs, P. and Waterfall, W. B.: Brit. J. Urol., 25: 187-194, 1953. 5 Ewing, J.: Neoplastic Diseases. Philadelphia: W. B. Saunders Co., 4th ed., pp. 700-829. 6 Cristol, D. S., McDonald, J. R. and E=ett, J. L.: J. Urol., 55: 18-27, 1946. 7 Fuchsman, J. J. and Angrist, A.: J. Urol., 59: 167-173, 1948. 8 Gordon, B. S.: J. Urol., 59: 1019-1021, 1948. 2
3
1144
HERMAN J, MEISEL
arteriosclerotic basis. There is postulated first necrosis of tubules due to a small vascular lesion. A tubule becomes fragmented into isolated segments. Apparently the ends of a segment are sealed forming a small cyst, within which the tubular cells then proliferate forming an adenomatous nodule. This theory is fortified by the facts that these tumors are found most often in people over 50 years of age and that they occur in the subcapsular areas where endarteritis would be most evident. They also occur often in association with microscopic cysts presumably also formed by tubular necrosis. Turley and Steel,9 however, from a careful morphological study of similar material concluded, in their case of multiple miliary adenomas, that the tumors must arise from the glomeruli. l\![ost unfashionable at the moment is the theory of congenital origin. Albarran10 stated that the precursors of adenomas were islands of imperfectly developed or displaced tubules originating in some aberration of fusion of the nephrogenic and wolffian elements. This latter hypothesis would seem most adequately to fit the present case. The youth of the patient, the diffuse distribution throughout both kidneys, the lack of vascular changes and the lack of correspondence to vascular distribution, tend to confirm the congenital origin of this disease in this patient. It is felt by many that adenoma may become malignant. Cristol, McDonald and Emmett 6 reported incidental adenomas in 34 per cent of kidneys excised for carcinoma. Others have found adenomas with invasion of the capsule, and have described gradations of cellular architecture from benign to malignant within the same tumor. In the present case no evidence of malignant degeneration was found and after 2 years of observation there is no clinical evidence of malignant disease. Histologically, adenomas have been classified into three types. The tubular type exhibits long, branching, irregular channels; the alveolar type contains polyhedral cells, arranged more or less uniformly in alveoli; and the papillary adenoma is made up of infolding, branch-like outgrowths often appearing to arise from the epithelium of a surrounding cyst wall. The present case shows all these types in different adenomas and often within the same nodules. Bilateral involvement of the kidneys by primary neoplasm is frequent in the instances of nonclinical multiple miliary type of adenomas found at autopsy. Less than 30 cases of primary malignant involvement of both kidneys have been reported. 11 • 12 , 13 Several cases of diffuse bilateral involvement of the kidneys by malignant or granulomatous lesions such as lymphosarcoma, leukemia, roundcell sarcoma and sarcoid have been reported. 12 • 13 • 14 Unfortunately most of these were autopsy cases and did not have pyelographic study. In a rather careful search of the literature, only one instance was found in which pyelographic findings indicative of polycystic kidneys were found to be due to diffuse involvement 'Turley, L.A. and Steel, J.: J.A.M.A., 82: 857-859, 1924. Albarran, J.: Quoted by Cristal, McDonald, and Emmett. 6 11 Eisendrath, D. E. and Rolnick, H. C.: Textbook of Urology. Philadelphia: J.B. Lipincott Co., 1938. 12 Forsythe, W. E.: J. Urol., 47: 784-791, 1942. 13 Flynn, J.E. and Bowers, J.M.: J. Urol., 58: 106-111, 1947. 14 Fischer, G. S.: Grace Hosp. Bull., 26: 11-24, 1948. 10
RENAL ADENOMATOSIS
1145
by tumor, in this case, lymphoblastoma (Fischer). 4 It would seem that pyelography, if done more often in diffuse neoplastic disease with renal involvement, might reveal more cases simulating polycystic disease. It is certainly obvious that diffuse neoplastic renal involvement could distort and elongate calyces in similar fashion, and as easily as, cysts. It is also notable that the clinical findings of hypertension, fixed urinary specific gravity, elevated blood urea nitrogen, all consistent with polycystic kidneys, were present in our case. An accurately descriptive name for this disease was not at hand. It was felt that a parallel could be drawn with the nomenclature of renal cysts. Thus a solitary cyst could be compared with a solitary adenoma and multiple cysts with multiple adenoma. The special appellation for polycystic disease of the kidneys, therefore, logically suggested the parallel term of polyadenomatous kidneys, which ·was thus adopted as the title of this paper. CONCLUSION
An instance of bilateral diffuse adenomatosis of the kidneys has been presented. Only one other similar case has been recorded by Keyes in 1890 and, as far as is known, this was unilateral. The distinctive name of bilateral polyadenomatous kidneys has been suggested. The clinical, urinary and pyelographic changes in this case simulated bilateral polycystic renal disease very closely.