- Email: [email protected]
Diagnosis of renal tumor by gamma-glutamyl-transpeptidase
LETTER TO THE EDITOR
DIAGNOSIS OF RENAL TUMOR BY GAMMA-GLUTAMYL-TRANSPEPTIDASE To the Editor: In the article, “Diagnosis of Renal Tumor by Gamma-Glutamyl-transpeptidase (EC 2.3.2.2.)” by Richard Hautmann M.D., Rudolf Kisters, M.D., and Wolf Lutzeyer M.D., in the January issue (vol. 7, page 12) of UROLOGY, a highly significant decrease in activity of gamma-glutamyltranspeptidase (gamma-GT) in all 16 patients with malignant renal tumors has been demonstrated in both tumor tissue and urine. The authors therefore concluded that the drop in urine gamma-GT permits the diagnosis of malignant kidney tumors. These laboratory findings probably will be helpful in the differential diagnosis of renal masses since there was a significant increase in gamma-GT activity in 117 patients with benign renal diseases. However, to understand these findings and to better determine the source of urinary gamma-GT, serum levels of the enzyme in all examined patients is significant. A normal or elevated serum level of gamma-GT derived from other organs would support the authors hypothesis of renal origin of the decreased urinary enzyme and most likely exclude the possibility of changed urine levels as due to a clearance phenomenon in the cancer patients. Whereas the significant increase in urinary levels described in 117 noncancer patients could be explained by this mechanism. Since the blood stream represents a pool for enzymes of various sources, a transfer of gamma-CT derived from benign lesions back into the serum is conceivable. The authors mentioned that urine samples were taken by ureteral catheterization and the enzyme levels of both diseased and healthy kidneys were comthe results from the contralateral pared; however, normal kidneys in patients with unilateral renal disease were not shown or discussed. These data might be the strongest support for the gamma-CT drop as being specific (and diagnostic) for renal cancer. The fact that 60 out of 117 noncancer patients, although having had lesions with atrophy of renal tissue, that is, impaired excreting parenchyma (pyelonephritic atrophic or cystic kidneys), demonstrated increased urinary gamma-GT levels would, if compared with urine gamma-GT of normal contralateral kidneys, also support the possibility of the enzyme being released by the affected kidney.
UROLOGY
/ APRIL 1976 / VOLUME
VII, NUMBER 4
Furthermore, it would be helpful to know whether there was any association with liver diseases or the paraneoplastic hepatic dysfunction syndrome in the reported patients. First, gamma-GT is well recognized as a rather specific hepatocellular enzyme which appears to be elevated in the serum during various hepatopathies and consequently may have influenced the urinary levels. 100 cases of Second, since 1961 approximately renal cell carcinoma associated with hepatic dysfunction syndrome have been pub1ished.l The two major pathogenetic hypotheses include either hepatic or renal origin of the elevated serum levels of alpha-2 globulin, alkaline phosphatase, and fibrinogen degradation products.* Recently we described 1 patient with renal cell carcinoma and Stauffer’s syndrome who had persistently elevated serum gamma-GT levels3 Since Stauffer’s syndrome represents a heterogenous disorder rather than a liver-specific entity, we tended to support the hypothesis of the increased serum enzyme levels (alkaline phosphatase and gamma-GT) as due to direct secretion by the renal tumor. This was supported by another case of this syndrome in which elevated serum gamma-CT concentration returned to normal soon after radical nephrectomy. After the findings of Hautmann and coworkers, however, renal ’ carcinoma tissue as a source for high serum gammaGT levels is unlikely to be responsible. Giinther H. Jacobi, M.D. Department of Internal Medicine, University of Texas Southwestern Medical School Dallas. Texas 75235 Thomas Philipp, M D Department of Internal Medicine, University of Maim Medical School Mainz, West Germany
References 1. STAUFFER, M. H.:
Gastroenterology
Nephrogenic hepatosplenomegaly, 40: 694 (1961).
2. JACOBI, 6. H.:
Nonurologic manifestations of renal cell cell carcinoma, Aktuelle Urol. 6: 177 (1975). 3. JACOBI, G. H., and PHILIPP, T.: Stauffer’s syndrome, diagnostic help in hypernephroma, Clin. Nephrol. 4: 113 (1975).
449
DIAGNOSIS OF RENAL TUMOR BY GAMMA-GLUTAMYL-TRANSPEPTIDASE To the Editor: In the article, “Diagnosis of Renal Tumor by Gamma-Glutamyl-transpeptidase (EC 2.3.2.2.)” by Richard Hautmann M.D., Rudolf Kisters, M.D., and Wolf Lutzeyer M.D., in the January issue (vol. 7, page 12) of UROLOGY, a highly significant decrease in activity of gamma-glutamyltranspeptidase (gamma-GT) in all 16 patients with malignant renal tumors has been demonstrated in both tumor tissue and urine. The authors therefore concluded that the drop in urine gamma-GT permits the diagnosis of malignant kidney tumors. These laboratory findings probably will be helpful in the differential diagnosis of renal masses since there was a significant increase in gamma-GT activity in 117 patients with benign renal diseases. However, to understand these findings and to better determine the source of urinary gamma-GT, serum levels of the enzyme in all examined patients is significant. A normal or elevated serum level of gamma-GT derived from other organs would support the authors hypothesis of renal origin of the decreased urinary enzyme and most likely exclude the possibility of changed urine levels as due to a clearance phenomenon in the cancer patients. Whereas the significant increase in urinary levels described in 117 noncancer patients could be explained by this mechanism. Since the blood stream represents a pool for enzymes of various sources, a transfer of gamma-CT derived from benign lesions back into the serum is conceivable. The authors mentioned that urine samples were taken by ureteral catheterization and the enzyme levels of both diseased and healthy kidneys were comthe results from the contralateral pared; however, normal kidneys in patients with unilateral renal disease were not shown or discussed. These data might be the strongest support for the gamma-CT drop as being specific (and diagnostic) for renal cancer. The fact that 60 out of 117 noncancer patients, although having had lesions with atrophy of renal tissue, that is, impaired excreting parenchyma (pyelonephritic atrophic or cystic kidneys), demonstrated increased urinary gamma-GT levels would, if compared with urine gamma-GT of normal contralateral kidneys, also support the possibility of the enzyme being released by the affected kidney.
UROLOGY
/ APRIL 1976 / VOLUME
VII, NUMBER 4
Furthermore, it would be helpful to know whether there was any association with liver diseases or the paraneoplastic hepatic dysfunction syndrome in the reported patients. First, gamma-GT is well recognized as a rather specific hepatocellular enzyme which appears to be elevated in the serum during various hepatopathies and consequently may have influenced the urinary levels. 100 cases of Second, since 1961 approximately renal cell carcinoma associated with hepatic dysfunction syndrome have been pub1ished.l The two major pathogenetic hypotheses include either hepatic or renal origin of the elevated serum levels of alpha-2 globulin, alkaline phosphatase, and fibrinogen degradation products.* Recently we described 1 patient with renal cell carcinoma and Stauffer’s syndrome who had persistently elevated serum gamma-GT levels3 Since Stauffer’s syndrome represents a heterogenous disorder rather than a liver-specific entity, we tended to support the hypothesis of the increased serum enzyme levels (alkaline phosphatase and gamma-GT) as due to direct secretion by the renal tumor. This was supported by another case of this syndrome in which elevated serum gamma-CT concentration returned to normal soon after radical nephrectomy. After the findings of Hautmann and coworkers, however, renal ’ carcinoma tissue as a source for high serum gammaGT levels is unlikely to be responsible. Giinther H. Jacobi, M.D. Department of Internal Medicine, University of Texas Southwestern Medical School Dallas. Texas 75235 Thomas Philipp, M D Department of Internal Medicine, University of Maim Medical School Mainz, West Germany
References 1. STAUFFER, M. H.:
Gastroenterology
Nephrogenic hepatosplenomegaly, 40: 694 (1961).
2. JACOBI, 6. H.:
Nonurologic manifestations of renal cell cell carcinoma, Aktuelle Urol. 6: 177 (1975). 3. JACOBI, G. H., and PHILIPP, T.: Stauffer’s syndrome, diagnostic help in hypernephroma, Clin. Nephrol. 4: 113 (1975).
449