Hisayuki Sugimoto

Characteristics of Patients on Hemodialysis Therapy for More Than 30 Years

Abstract:  Since its experimental introduction in 1960, hemodialysis has become a widely performed and relatively safe procedure. Therapeutic strategies have been developed, and the numbers of long‐term survivors of hemodialysis therapy have been increasing. Hemodialysis therapy was introduced at Sangenjaya Hospital in October 1970, and the 16 patients who have survived for more than 30 years on hemodialysis therapy since its introduction at the hospital were enrolled in this study to investigate the characteristics of long‐term hemodialysis patients. For comparison, 50 patients on hemodialysis for less than 30 years were also studied (21 patients with <10 years hemodialysis, 13 with 10–20 years hemodialysis and 16 with 20–30 years hemodialysis). Background information (age, gender, and cause of renal disease), dialysis dose (single pool [sp.] Kt/V), mineral metabolism (serum phosphate), anemia management (serum hemoglobin), and nutrition (serum albumin and reduced interdialytic weight gain) were assessed. Hemodialysis was instituted at 28.7 ± 6.4 years of age. The primary cause of end‐stage renal disease was chronic glomerulonephritis in all of the patients except one, and in that patient it was polycystic kidney disease. As an index of the dialysis dose, sp. Kt/V was 1.2 ± 0.11. As an index of mineral metabolism, serum phosphate was 5.4 ± 0.9 mg/dL. As an index of anemia management, serum hemoglobin was 10.2 ± 1.2 g/dL. As indexes of nutrition, serum albumin was 4.0 ± 0.2 g/dL and interdialytic weight gain was 4.43 ± 1.36%. The sp. Kt/V‐value, serum phosphate, serum hemoglobin and interdialytic weight gain did not differ between the four different hemodialysis duration groups. Serum albumin was lower in the >30 group (4.0 ± 0.2 g/dL) than in the <10 group (4.2 ± 0.3 g/dL) (P = 0.046). As the duration of hemodialysis has increased, the age at hemodialysis induction has become younger. The cause of the renal failure was chronic glomerulonephritis in most of the cases. None had diabetic nephropathy. Improvement of the prognosis of patients with diabetic nephropathy is required. Most of the indexes of these patients nearly satisfied the recommended values.

Spontaneous rupture of hepatocellular carcinoma: An approach with delayed hepatectomy

Two cirrhotic patients with ruptured hepatocellular carcinoma (HCC), presenting with hemoperitoneum, were successfully treated by elective hepatectomy. Both of these patients, a 67-year-old female and a 76-year-old male, had first been taken to other primary hospitals by ambulance due to hypovolemic shock. They were then found to have a mass of approximately 5 cm in the cirrhotic liver. In the initial management, however, neither any direct hemostasis by surgery nor indirect measures such as transcatheter hepatic arterial embolization were performed in either case. Instead, conservative treatment consisting mainly of fresh blood and plasma transfusions were continued for more than a month until the liver function stabilized. In both hepatectomies, the use of a microwave tissue coagulator resulted in minimal intra-operative blood loss and an appreciably excellent post-operative course. These cases point to the effectiveness of a “wait and see” policy for selected patients with ruptured HCC.

Does H2-receptor antagonist alter the renal function of cyclosporine-treated kidney grafts?

Histamine-type 2 antagonists (H2-blockers) as represented by cimentidine have been shown to adversely affect renal allograft function, particularly when coadministered with cyclosporine, currently a major immunosuppressant. To determine whether or not a newer and more powerful H2-blocker, famotidine, would produce similar adverse effects, we assessed seven cyclosporine-treated renal allograft recipients with regard to changes in their renal function on or off the H2-blocker over a one-week period. Neither the administration nor withdrawal of famotidine (20–40 mg/day) resulted in any significant changes in serum creatine, BUN, urine output or cyclosporine trough levels, suggesting that famotidine can be safely administered as an H2-blocker to cyclosporine-treated renal allograft recipients.

IDENTIFICATION OF INFLAMMATORY CELLS INFILTRATING RENAL ALLOGRAFTS

Eight nephrectomies and 13 biopsies of renal allografts (living 15, cadaveric 6) were investigated on the origin of inflammatory cells in the graft tissues by the use of an immunohistologic method (ABC method). Various monoclonal antibodies and heterosera were used to identify different leukocyte subsets. In all specimens the most predominant inflammatory cells were T cells. Other cells decreased in the following order; B cells, neutrophils and monocytes, and natural killer cells. In T cell subsets Leu 2a‐positive cells (suppressor/ cytotoxic T cells) predominated over Leu 3a‐positive cells (helper/inducer T cells) in 4 nephrectomies (living 1, cadaveric 3) and 12 biopsies (living 11, cadaveric 1). Among these 16 cases, 7 were undergoing acute rejection in various degrees, and 9 were without clinical rejection. In the former 7 cases only one was suffering from another disease. In contrast, Leu 3a‐positive cells predominated over Leu 2a‐positive cells in 1 biopsy (living) and 4 nephrectomies (living 2, cadaveric 2). Four of these 5 cases concurrently had other diseases in addition to acute rejection. Two cases underwent acute tubular necrosis (cadaveric graft nephrectomies) and 2 underwent chronic rejection and crescentic glomerulonephritis (living graft nephrectomies). The one remaining case was without clinical rejection.

Renal Allografts With Glomerulonephritic Change and Proteinuria

Eight cases of renal allografts with glomerulonephritic change and proteinuria were classified into three groups according to the morphological features of the glomerular lesions. Group I (3 cases): By light microscope, remarkable reduplication of glomerular basement membrane (GBM), widening of mesangial region, and slight increase in mesangial cells, were observed. Electron microscopy revealed thickening of subendothelial space by deposition of electron‐lucent material, mesangial interposition, and dense deposits in various regions (mainly in the subendothelial space). Group II (3 cases): By light microscope, crescent formation and reduplication of GBM were observed, while by electron microscope, changes of GBM similar to group I, but less remarkable, were seen. Group III (2 cases): Light microscope revealed spike formation in one case, but not in the other. With an electron microscope, subepithelial dense deposits were observed in both cases. Thickening of subendothelial space by deposition of electron‐lucent material was noted in one case, while thickening of lamina densa was observed in the other case. Morphological change caused by rejection was observed in all eight cases, with six cases showing massive proteinuria and the other two showing slight proteinuria.