International Urology and Nephrology 24 (6), pp. 607--611 (1992)
Renal Cell Carcinoma in Chronic Renal Failure without Dialysis Treatment I. SASAGAWA,* T. NAKADA,* Y. TERASAWA,** H. TAKAHASHI*** *Department of Urology, Yamagata University School of Medicine, Yamagata; **Department of Internal Medicine and ***Kidney Center, Sendai Shakai-Hoken Hospital, Sendai, Japan (Accepted April 11, 1992) We report a case of renal cell carcinoma in chronic renal failure without dialysis treatment. The literature is reviewed, and the relationship between renal cell carcinoma and uraemia is discussed.
Introduction
Since Dunnill et al. [I ] reported renal cell carcinoma in long-term dialysis patients, the relationship between dialysis treatment and renal cell carcinoma has been emphasized. However, reports on renal tumours in chronic renal failure without chronic dialysis are very limited [2]. Herein we report a case of renal cell carcinoma in chronic renal insufficiency without haemodialysis.
Case report
A 55-year-old Japanese woman was admitted to our hospital for health check. Her previous history revealed hypertension at the age of 49 years and renal insufficiency at 54 years. On physical examination, chest and abdomen were normal. Blood pressure was 160/90 mm Hg. A haemogram disclosed lenkocytes of 8200/mm ~ (normal: 4000--9000), erythrocytes 242 x 104/mm3 (normal: 430-570 x 10~), haemoglobin 7.2 g/dl (normal: 14.0-18.0), haematocrit 23 % (normal: 40-54 %) and platelet 26.1 x 104/mm3 (normal: 13-34• 104/mm3). Serum sodium was 132 mEq/1 (normal: 135-146), potassium 4.8 mEq/1 (normal: 3.2-4.5), chloride 104 mEq/1 (normal: 96-110). Blood nitrogen, serum creatinine and uric acid were elevated at 76 mg/dl (normal: 9-25), 7.3 mg/dl (normal: 0.5-1.5) and 9.0 mg/dl (normal: 2.0-7.6), respectively. Fasting blood sugar was 107 mg/dl (normal: 70-110). Liver function was normal. Urinalysis revealed about 1.0 g protein/24 h, about 2.0 glucose/24 h, 0-5 white and 5-10 red blood cells per high-power field. Ultrasonograms revealed a solid mass, measuring 30 x 20 mm, in the midupper portion of the left kidney (Fig. 1). Abdominal computerized tomograms showed bilateral contracted kidneys and a round mass involving the upper pole VSP, Utrecht Akad~miai Kiad6, Budapest
608
Sasayawa et aLt Renal cell carcinoma
Fig. 1. Longitudinal ultrasonogram of the left kidney: An inhomogeneous solid mass with echogenicity similar to normal parenchyma (arrow)
Fig. 2. Abdominal computerized tomogram: A round exophytic mass involving the upper pole of the left kidney o f the left kidney (Fig. 2). Selective renal angiograms revealed an exophytic mass in the upper portion of the left kidney (Fig. 3). Left nephrectomy was performed. At operation, a solid mass measuring 30 • 30 • 35 m m invaded the perinephric fat but was confined to Gerota's fascia. Histological diagnosis was clear cell adenocarcinoma of the kidney, but cystic formation was not observed (Fig. 4). International Urology and Nephrology 24, 1992
S a s a g a w a et aL : R e n a l cell carcinoma
609
Fig. 3. Selective renal angiogram, late venous phase: A protrusive lesion in the lateral aspect of the upper pole of the left kidney (arrow)
Postoperatively, the patient received no treatment for renal cell carcinoma. Four years after the operation the patient is alive and apparently tumour-free.
Discussion
Although renal cell carcinoma is four times as common among dialysis patients, it is not more prevalent among the azotaemic population than among the general population [3]. However, Matas et al. [4] reported 10 tumours in 646 uraemic patients after the onset of chronic renal failure. According to ChungPark et al. [5], review of 176 reported cases of acquired cystic disease of the kidneys and renal tumours disclosed that 18 patients had never received dialysis treatment. Uraemic patients without dialysis treatment are considered to be more prone to develop cancer than those without renal disease. International Urology and Nephrology 24, 1992
610
Sasagawa et al. : Renal cell carcinoma
Fig. 4. The tumour consists o f rounded or polygonal cells with abundant cytoplasm. H. E., • 140 Recently, a renal growth factor called renotropin has been isolated from animals [6]. This is normally excreted in the urine, but dialysis does not remove it from the circulation [7]. Retention of renotropin may induce excessive epithelial cell proliferation and tumour formation in end-stage kidney. Hughson et al. [8] suggested that renal cell carcinomas occur with increased incidence in acquired cystic disease. Experimentally, an association between cysts and neoplasms of the renal cortex has been shown [9]. Acquired cystic disease of the kidney is considered to be a premalignant state. However, tumours are sometimes found in areas of the kidney not involved by cystic formation [10]. In our case, too, cystic formation was not observed in the kidney. These facts suggest that chronic renal failure patients have an increased malignant potential of the kidney even if they neither receive dialysis treatment nor have acquired cystic disease o f the kidney. Although reports on renal cell carcinoma in chronic renal failure without dialysis therapy are limited, regular follow-up should be performed in all patients with chronic renal failure before the initiation of dialysis treatment.
References 1. Dunnill, M. S., Millard, P. R., Oliver, D. : Acquired cystic disease of the kidneys. A hazard of long-term intermittent maintenance hemodialysis. J. Clin. PathoL, 30, 868 (1977). 2. Chung-Park, M., Ricanati, E., Lankerani, M., Kedia, K. : Acquired renal cysts and multiple renal cell and urothelial tumors. Am. J. Clin. PathoL, 79, 238 (1983). 3. Gardner, K. D. Jr., Evan, A. P. : Cystic kidneys. An enigma evolves. Am. J. Kidney Dis., 3, 403 (1984). International Uroloqy and Nephroloyy 24, 1992
Sasagawa et al. : Renal cell carcinoma
611
4. Matas, A. J., Simmons, R. L., Kjellstrand, C. M., Buselmeier, T. J., Najarian, J. S. : Increased incidence of malignancy during chronic renal failure. Lancet, i, 883 (1975). 5. Chung-Park, M., Parveen, T., Lain, M. : Acquired cystic disease of the kidneys and renal cell carcinoma in chronic renal insufficiency without dialysis treatment. Neplwon, 53, 157 (1989). 6. Preuss, H. G. : Compensatory renal growth symposium. An introduction. Kidney Int., 23, 571 (1983). 7. Harris, R. H., Hise, M. K., Best, C. F.: Renotropic factors in urine. Kidney Int., 23, 616 (1983). 8. Hughson, M. D., Hennigar, G. R., McManus, J. F. A. : Atypical cysts, acquired renal cystic disease, and renal cell tumors in end stage dialysis kidneys. Lab. Invest., 42, 475 (1980). 9. Lee, S., Mauer, S. M., Brown, D. M. : Renal transplantation in diabetes rnellitus in rats. J. Exp. Med., 138, 793 (1974). 10. Fayemi, A. O., Ali, M. : Acquired renal cysts and tumors superimposed on chronic primary kidney disease. PathoL Res. Pract., 168, 73 (1980).
International Urology and Nt;ohrolo#y 24, 1992
Renal Cell Carcinoma in Chronic Renal Failure without Dialysis Treatment I. SASAGAWA,* T. NAKADA,* Y. TERASAWA,** H. TAKAHASHI*** *Department of Urology, Yamagata University School of Medicine, Yamagata; **Department of Internal Medicine and ***Kidney Center, Sendai Shakai-Hoken Hospital, Sendai, Japan (Accepted April 11, 1992) We report a case of renal cell carcinoma in chronic renal failure without dialysis treatment. The literature is reviewed, and the relationship between renal cell carcinoma and uraemia is discussed.
Introduction
Since Dunnill et al. [I ] reported renal cell carcinoma in long-term dialysis patients, the relationship between dialysis treatment and renal cell carcinoma has been emphasized. However, reports on renal tumours in chronic renal failure without chronic dialysis are very limited [2]. Herein we report a case of renal cell carcinoma in chronic renal insufficiency without haemodialysis.
Case report
A 55-year-old Japanese woman was admitted to our hospital for health check. Her previous history revealed hypertension at the age of 49 years and renal insufficiency at 54 years. On physical examination, chest and abdomen were normal. Blood pressure was 160/90 mm Hg. A haemogram disclosed lenkocytes of 8200/mm ~ (normal: 4000--9000), erythrocytes 242 x 104/mm3 (normal: 430-570 x 10~), haemoglobin 7.2 g/dl (normal: 14.0-18.0), haematocrit 23 % (normal: 40-54 %) and platelet 26.1 x 104/mm3 (normal: 13-34• 104/mm3). Serum sodium was 132 mEq/1 (normal: 135-146), potassium 4.8 mEq/1 (normal: 3.2-4.5), chloride 104 mEq/1 (normal: 96-110). Blood nitrogen, serum creatinine and uric acid were elevated at 76 mg/dl (normal: 9-25), 7.3 mg/dl (normal: 0.5-1.5) and 9.0 mg/dl (normal: 2.0-7.6), respectively. Fasting blood sugar was 107 mg/dl (normal: 70-110). Liver function was normal. Urinalysis revealed about 1.0 g protein/24 h, about 2.0 glucose/24 h, 0-5 white and 5-10 red blood cells per high-power field. Ultrasonograms revealed a solid mass, measuring 30 x 20 mm, in the midupper portion of the left kidney (Fig. 1). Abdominal computerized tomograms showed bilateral contracted kidneys and a round mass involving the upper pole VSP, Utrecht Akad~miai Kiad6, Budapest
608
Sasayawa et aLt Renal cell carcinoma
Fig. 1. Longitudinal ultrasonogram of the left kidney: An inhomogeneous solid mass with echogenicity similar to normal parenchyma (arrow)
Fig. 2. Abdominal computerized tomogram: A round exophytic mass involving the upper pole of the left kidney o f the left kidney (Fig. 2). Selective renal angiograms revealed an exophytic mass in the upper portion of the left kidney (Fig. 3). Left nephrectomy was performed. At operation, a solid mass measuring 30 • 30 • 35 m m invaded the perinephric fat but was confined to Gerota's fascia. Histological diagnosis was clear cell adenocarcinoma of the kidney, but cystic formation was not observed (Fig. 4). International Urology and Nephrology 24, 1992
S a s a g a w a et aL : R e n a l cell carcinoma
609
Fig. 3. Selective renal angiogram, late venous phase: A protrusive lesion in the lateral aspect of the upper pole of the left kidney (arrow)
Postoperatively, the patient received no treatment for renal cell carcinoma. Four years after the operation the patient is alive and apparently tumour-free.
Discussion
Although renal cell carcinoma is four times as common among dialysis patients, it is not more prevalent among the azotaemic population than among the general population [3]. However, Matas et al. [4] reported 10 tumours in 646 uraemic patients after the onset of chronic renal failure. According to ChungPark et al. [5], review of 176 reported cases of acquired cystic disease of the kidneys and renal tumours disclosed that 18 patients had never received dialysis treatment. Uraemic patients without dialysis treatment are considered to be more prone to develop cancer than those without renal disease. International Urology and Nephrology 24, 1992
610
Sasagawa et al. : Renal cell carcinoma
Fig. 4. The tumour consists o f rounded or polygonal cells with abundant cytoplasm. H. E., • 140 Recently, a renal growth factor called renotropin has been isolated from animals [6]. This is normally excreted in the urine, but dialysis does not remove it from the circulation [7]. Retention of renotropin may induce excessive epithelial cell proliferation and tumour formation in end-stage kidney. Hughson et al. [8] suggested that renal cell carcinomas occur with increased incidence in acquired cystic disease. Experimentally, an association between cysts and neoplasms of the renal cortex has been shown [9]. Acquired cystic disease of the kidney is considered to be a premalignant state. However, tumours are sometimes found in areas of the kidney not involved by cystic formation [10]. In our case, too, cystic formation was not observed in the kidney. These facts suggest that chronic renal failure patients have an increased malignant potential of the kidney even if they neither receive dialysis treatment nor have acquired cystic disease o f the kidney. Although reports on renal cell carcinoma in chronic renal failure without dialysis therapy are limited, regular follow-up should be performed in all patients with chronic renal failure before the initiation of dialysis treatment.
References 1. Dunnill, M. S., Millard, P. R., Oliver, D. : Acquired cystic disease of the kidneys. A hazard of long-term intermittent maintenance hemodialysis. J. Clin. PathoL, 30, 868 (1977). 2. Chung-Park, M., Ricanati, E., Lankerani, M., Kedia, K. : Acquired renal cysts and multiple renal cell and urothelial tumors. Am. J. Clin. PathoL, 79, 238 (1983). 3. Gardner, K. D. Jr., Evan, A. P. : Cystic kidneys. An enigma evolves. Am. J. Kidney Dis., 3, 403 (1984). International Uroloqy and Nephroloyy 24, 1992
Sasagawa et al. : Renal cell carcinoma
611
4. Matas, A. J., Simmons, R. L., Kjellstrand, C. M., Buselmeier, T. J., Najarian, J. S. : Increased incidence of malignancy during chronic renal failure. Lancet, i, 883 (1975). 5. Chung-Park, M., Parveen, T., Lain, M. : Acquired cystic disease of the kidneys and renal cell carcinoma in chronic renal insufficiency without dialysis treatment. Neplwon, 53, 157 (1989). 6. Preuss, H. G. : Compensatory renal growth symposium. An introduction. Kidney Int., 23, 571 (1983). 7. Harris, R. H., Hise, M. K., Best, C. F.: Renotropic factors in urine. Kidney Int., 23, 616 (1983). 8. Hughson, M. D., Hennigar, G. R., McManus, J. F. A. : Atypical cysts, acquired renal cystic disease, and renal cell tumors in end stage dialysis kidneys. Lab. Invest., 42, 475 (1980). 9. Lee, S., Mauer, S. M., Brown, D. M. : Renal transplantation in diabetes rnellitus in rats. J. Exp. Med., 138, 793 (1974). 10. Fayemi, A. O., Ali, M. : Acquired renal cysts and tumors superimposed on chronic primary kidney disease. PathoL Res. Pract., 168, 73 (1980).
International Urology and Nt;ohrolo#y 24, 1992
