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K Hironaka

Publications and source records attributed to K Hironaka.

53 records · Page 3Linked to original sources
PubMed1993

Immune complex glomerulonephritis in a pregnant woman with congenital C9 deficiency.

A 27-year-old woman developed proteinuria, hypertension, and peripheral edema during the ninth month of her first pregnancy. The clinical and serological features were compatible with a diagnosis of toxemia of pregnancy, except for the presence of hypocomplementemia. The patient had glomerulonephritis characterized by large electron-dense deposits, predominantly in the mesangium. Immunofluorescence studies revealed striking accumulations of Clq and C3, and the presence of small amounts of IgG and IgM in the mesangium. Serum and plasma levels of complement components were normal, except for the C9 component. Family studies demonstrated that the C9 deficiency was inherited.

Adult↗
PubMed1993

[Two cases of hypercalcemic nephropathy associated with primary hyperparathyroidism].

We present two cases of hypercalcemic nephropathy associated with primary hyperparathyroidism. Case 1 is a 37-year-old man who had repeated bone fractures and recurrent ureteral stones, which led to the diagnosis of primary hyperparathyroidism. Case 2 is a 35-year-old man in whom parathyroid carcinoma was discovered because of secondary nephrogenic diabetes insipidus, resulting from severe hypercalcemia. Both patients developed mild renal dysfunction during the course of hyperparathyroidism. In the renal biopsy materials obtained from case 1, the renal interstitium showed chronic inflammatory changes. The tubules were partly damaged (focal necrosis). Deposition of calcium was sometimes noted within the mitochondria of the tubular epithelial cells. Some glomeruli showed glomerular sclerosis. In biopsy materials obtained from case 2 after resection of the carcinoma, similar histological features were observed, but tubular atrophy and necrosis were advanced. Polyuria and hypercalcemia were ameliorated after resection. These findings indicate that severe hypercalcemia might induce tubular dysfunction as well as organized changes.

Adult↗
PubMed1993

Ultrastructural changes of extracellular matrices in diabetic nephropathy revealed by high resolution scanning and immunoelectron microscopy.

BACKGROUND: Diabetic nephropathy is invariably associated with proteinuria. EXPERIMENTAL DESIGN: To delineate the mechanism(s) of proteinuria in diabetic nephropathy, ultrastructural changes of the glomerular basement membranes (GBMs) were studied by high resolution scanning and immunoelectron microscopy. Acellular glomeruli from diabetic and age-matched control human subjects were prepared by detergent method and subjected to conductive staining, the technique in which the tissues are impregnated with metals rather than surface-coated with metallic alloys for visualization by electron microscopy. Subsequent to conductive staining, the tissues were examined by in-lens field emission scanning electron microscopy. RESULTS: Thirty glomeruli, each from the control and diabetic groups, were examined by scanning microscopy. In diabetic GBMs, a loose meshwork structure consisting of numerous pores of approximately 8 nm in diameter and distinct strands was observed. In contrast, meshwork structure was not readily discernible in controls and a few pores were observed. Five glomerular capillary loops, each from control and diabetic groups, were examined by immunoelectron microscopy. In controls, heparan sulfate-proteoglycan was localized in the lamina rara interna and externa, and type-IV collagen was distributed throughout the whole width of the GBM. In diabetic GBMs, a relative loss of staining of heparan sulfate-proteoglycan, both in the lamina rara interna and externa of the GBM, was observed. Type IV collagen was distributed in all layers of the thickened GBM, and the absolute number of the immunogold particles was increased. However, immunogold particle density of type IV collagen per unit area was decreased as compared with the control. CONCLUSIONS: These ultrastructural and immunoelectron microscopic changes in the GBM may explain the loss of charge as well as size selectivities of the glomerulus, as observed in diabetic nephropathy associated with proteinuria.

Aged↗
PubMed1992

Glomerular extracellular matrices in rat diabetic glomerulopathy by scanning electron microscopy.

Characteristic pathological changes in the glomeruli in diabetic nephropathy include expansion of the mesangial matrix and thickening of the glomerular basement membrane (GBM). Using an acellular digestion technique combined with scanning electron microscopy, the three-dimensional ultrastructural changes in glomerular extracellular matrices were studied in rats with diabetic glomerulopathy. Diabetes was induced by the intravenous injection of streptozotocin and morphological analyses were performed 3, 6 and 11 months after the injection. Expansion of mesangial area and GBM thickening became evident with time. After treatment with the series of detergents, all cellular components were completely removed leaving the extracellular matrices intact. In normal controls, the mesangial matrix appeared as fenestrated septa with oval or round stomata between the glomerular capillaries. In diabetic glomerulopathy, expansion of mesangial matrix and narrowing of the mesangial fenestrae were observed. These changes in the mesangial matrices seem to play a vital role in the progression of glomerulosclerosis in rat diabetes. A subendothelial thin layer of the GBM was continuous with the mesangial matrix. One cause of GBM thickening in streptozotocin diabetes may be expansion of the mesangial matrix into the peripheral GBM.

Animals↗
PubMed1992

A case of nephrotic syndrome and renal dysfunction in a pregnant woman with diabetes mellitus.

A 29-year-old diabetic woman who developed severe anaemia, nephrotic syndrome, and hypertension before the 28th week of gestation, had residual evidence of toxaemia and renal dysfunction more than 1 month following delivery. The histopathological findings of renal biopsy specimens were considered most consistent with toxaemia of pregnancy complicated by diabetic glomerulosclerosis. We consider that rapid acceleration of renal dysfunction may have been induced by: (1) poor control of diabetes before pregnancy; (2) glomerular hyperfiltration of the remnant nephrons throughout pregnancy; (3) hypercoagulopathy associated with pregnancy; (4) appearance of hypertension following these three conditions.

Adult↗
PubMed1990

Three-dimensional architecture of rat glomerular basement membrane by ultra-high resolution scanning electron microscopy.

We demonstrated the ultrastructure of rat glomerular basement membrane (GBM) by ultra-high resolution scanning electron microscopy. GBM prepared by sonication methods and conductive-staining could be observed without metal coating at magnifications as high as 400,000 times. The GBM showed an irregular meshwork structure composed of various strands and pores. The width of the strands ranged from 6 to 15 nm, and the diameter of pores ranged from 6 to 50 nm. The present study confirmed our molecular sieve theory of the basement membrane.

Animals↗
PubMed1985

Enzyme immunoassay for elcatonin, a synthetic analogue of eel calcitonin, in plasma.

An enzyme immunoassay for the direct measurement of elcatonin, a synthetic analogue of eel calcitonin with hypocalcemic activity, in rat and dog plasma was developed. Elcatonin was conjugated to beta-galactosidase using an N-succinimidyl ester, and the product was used as the tracer. The antibody-bound tracer was precipitated using a second antibody. The nonequilibrated procedure gave better sensitivity and precision than the equilibrated procedure. The nonequilibrated method was sensitive at quantifiable concentrations as low as 0.2 ng/mL using 0.1 mL of plasma and was also reproducible, with RSD values generally less than +/- 10%. Plasma levels in rats and dogs were determined by this competitive enzyme immunoassay after intramuscular or intravenous injection of 40 U/kg (8 micrograms/kg) of elcatonin.

Animals↗
PubMed1983

[Assessment of urinary ferritin, CEA and beta 2-MG determinations in patients with urinary tract malignancies].

Ferritin, carcinoembryonic antigen (CEA) and beta 2-microglobulin (beta 2-MG) levels in urine from 45 patients with cancer (4 with renal adenocarcinoma, 7 with renal pelvic and ureteral cancer and 34 with bladder cancer) at various stages were clinically evaluated for their significance as parameter of urinary tract malignancies as compared to urinary fibrin/fibrinogen degradation products (FDP) and urine cytology. Ferritin levels for the poorly-differentiated and advanced stage groups were higher than those for the well-differentiated and early stage groups, and were especially high in 5 of the 7 patients with renal pelvic and ureteral cancer and all of the 7 patients with bladder cancer involving the upper urinary tract. These data suggest that determination of urinary ferritin is useful in the detection of urinary tract cancer involving the upper urinary tract. The upper limits of CEA levels were determined respectively according to white blood cell counts in urine. Although, CEA levels were elevated in the poorly-differentiated group and the advanced stage group compared to the well-differentiated and early stage groups, the values were positive in only 12 out of 52 cases (23.1%). These values seemed to be low compared to other reports. beta 2-MG levels increased significantly in the poorly-differentiated and advanced stage groups. However, most cases in the above groups were complicated with pyelonephritis or renal impairment. It is suggested that the urinary beta 2-MG secretion from cancer itself is not so significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Carcinoembryonic Antigen↗
PubMed1983

[Assessment of serum ferritin, CEA, beta 2-MG and PAP determinations in patients with urinary tract malignancies].

Ferritin, carcinoembryonic antigen (CEA), beta 2-microglobulin (beta 2-MG) and prostatic acid phosphatase (PAP) levels in serum from 77 patients with cancer (6 with renal adenocarcinoma, 9 with renal pelvic and ureteral cancer, 29 with bladder cancer and 33 with prostatic cancer) at various stages were clinically evaluated for their significance as a parameter of urinary tract malignancies. Although, ferritin, CEA and beta 2-MG levels in the poorly-differentiated and advanced stage groups of renal adenocarcinoma, renal pelvic and ureteral cancer, and bladder cancer were higher than those in the well-differentiated and early stage groups, those in most cases were within normal ranges. These proteins were not considered suitable for the screening test. Ferritin and beta 2-MG levels increased with advancement of the performance status (P.S.) proposed by Koyama and Saito; however, the latter was affected greatly by renal impairment. In prostatic cancer, PAP and ferritin levels were remarkably high in the poorly-differentiated group (PAP mean +/- S.E.: 57.6 +/- 22.5 ng/ml, ferritin 883 +/- 319 ng/ml) and the advanced stage group (27.2 +/- 10.5 ng/ml, 398 +/- 152 ng/ml) compared to the well-differentiated group (7.87 +/- 3.61 ng/ml, 88.5 +/- 25.8 ng/ml) and the early stage group (2.24 +/- 0.54 ng/ml, 186 +/- 91.7 ng/ml). PAP and ferritin levels of the untreated cases were positive in 10 out of 18 cases (55.6%) and 7 out of 18 cases (38.9%), respectively, and those of the relapsing cases were positive in 4 out of 7 cases (57.1%) and 6 out of 7 cases (85.7%), respectively. However, CEA and beta 2-MG levels were negative in most cases. Furthermore, increments of PAP and ferritin levels, especially that of the ferritin level, were significantly related to advancement of P.S., and high ferritin levels were obtained in all cases of P.S. 3 and 4. Therefore, determination of PAP and ferritin seems to be useful in monitoring prostatic cancer, and the latter to be useful in early detection of relapsing cases.

Acid Phosphatase↗
PubMedDate not supplied

Nondiabetic renal disease complicating diabetic nephropathy.

The clinicopathological and laboratory findings for 35 diabetic patients who had undergone renal biopsy from 1982 to 1990 were reviewed. Ten of these patients (28.6%) were found to have nondiabetic renal diseases. Five of those patients (14.3%) suffered from nondiabetic renal disease complicated by diabetic nephropathy. Nondiabetic renal diseases included IgA nephropathy, idiopathic membranous nephropathy, membranoproliferative glomerulonephritis (types I and III), minimal change disease, and toxemia of pregnancy. The diagnosis of nondiabetic renal diseases complicated by diabetes is important for the treatment of renal disease. Urinary abnormalities and/or deterioration in renal function inconsistent with the natural history of diabetic nephropathy were suggestive of the presence of nondiabetic renal disease.

Adult↗
PubMedDate not supplied

Ultrastructure of glomerular basement membrane in active heymann nephritis rats revealed by tissue-negative staining method.

Recently, we have developed a tissue-negative staining method, and successfully visualized fine meshwork structure of the glomerular basement membrane (GBM). To clarify the mechanism of proteinuria in active Heymann nephritis, we performed tissue-negative staining and investigated the ultrastructural alterations of the GBM. Active Heymann nephritis, the animal model of human membranous nephropathy, was induced in Lewis rats by the injection of proximal tubular brush border antigen, i.e. Fx1A. Urinary protein excretion was measured and histological studies were performed over 15 weeks following the Fx1A injection. Proteinuria developed at 10 weeks after injection (38.2 +/- 7.4 mg/day) and progressively increased (160.2 +/- 20.6 mg/day at 15 weeks). Capillary fine deposits of IgG and C3 were seen by immunofluorescence, and subepithelial electron dense deposits (EDD) by transmission electron microscopy (TEM). Using the tissue-negative staining method, regular meshwork structure consisted of fine fibrils and pores (2.5 +/- 0.7 nm in short dimension) was observed in the GBM of control rats. At 10 and 15 weeks after injection, the GBM, directly facing the endothelial side of EDD, contained enlarged pores and nephrotic tunnels. Mean values of the short dimension of enlarged pores were 2.9 +/- 0.5 nm at 10 weeks and 3.1 +/- 0.4 nm at 15 weeks, which were significantly larger than that of control rats (p < 0.01). The rest area of the GBM, including newly produced GBM covering the epithelial side of EDD, had no significant difference in size of the pores from control GBM and no tunnels. Although there was no significant difference in the size of enlarged pores between 10 and 15 weeks, the percentage area of GBM with impaired size barrier increased at 15 weeks (51.4 +/- 8.1%) compared with 10 weeks (24.0 +/- 8.3%) and related to severity of proteinuria. The density of the tunnels also increased at 15 weeks. In conclusion, immune deposits may affect the GBM biosynthesis and induce the defect of size barrier of the GBM, which is responsible for proteinuria in active Heymann nephritis.

Animals↗