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Biomedical subjects

A Hishida

Publications and source records attributed to A Hishida.

At least 145 records · Page 8Linked to original sources
PubMed1992

Intraglomerular fibronectin in rat experimental glomerulonephritis.

To clarify the mechanisms of glomerular pericapillary fibronectin deposition in human membranous nephropathy and mesangial proliferative glomerulonephritis, intraglomerular fibronectin distribution was examined by light and electron microscopy using the experimental rat models of Heymann and nephrotoxic serum nephritis. As previously demonstrated by immunofluorescence microscopy (Pettersson and Colvin 1978; Ikeya et al. 1985, 1986), fibronectin was distributed in the mesangial areas and occasionally on percicapillary walls of normal glomeruli, while in nephrotoxic serum nephritis and Heymann nephritis, fibronectin was diffusely located along glomerular capillary walls as well as in the mesangium. By immunoelectron microscopy using the immunogold technique, fibronectin was also noted in the mesangial areas and the lamina densa of the glomerular basement membrane (GBM) in normal glomeruli. In nephrotoxic serum nephritis, fibronectin was seen around mesangial cells situated between endothelial cells and the GBM, suggesting that pericapillary fibronectin in nephrotoxic serum nephritis reflects mesangial extension. However, in Heymann nephritis, it was found uniformly in the lamina rara interna, lamina densa and lamina rara externa of the GBM, indicating no specific relation to glomerular cells. When sections of normal and both experimental nephritis kidneys were incubated with fluorescein isothiocyanate conjugated with rat plasma fibronectin, a linear pattern of fluorescein staining along the glomerular capillary walls was observed in Heymann nephritis but not in normal or nephrotoxic serum nephritic rats. The GBM in Heymann nephritis would thus appear to have an affinity for plasma fibronectin. Based on the above findings, fibronectin in the GBM of rats with Heymann nephritis may reasonably be concluded to originate from the plasma.

Animals↗
PubMed1992

Effects of desoxycorticosterone acetate (DOCA) plus saline drinking on gentamicin-mediated nephropathy in rats.

Studies were performed to examine the effect of desoxycorticosterone acetate (DOCA) treatment plus isotonic saline drinking on gentamicin (GM)-mediated nephropathy in rats. GM, 40 mg/kg/day, was subcutaneously injected for 13 days following a 5-week treatment with water drinking or DOCA (10 mg/kg/week) plus saline drinking. Twenty-four hours after the last injection of GM, renal blood flow (RBF) and Cin decreased to approximately 69% and 52% of the control values in water-drinking GM-treated rats, respectively, but was well maintained in DOCA plus saline-drinking GM-treated animals. There was no significant difference in morphologic tubular injury or the renal cortical GM content between GM-treated groups. Saline drinking alone (1% saline, 5 weeks) lessened neither GM-induced reduction in GFR nor tubular damage. Body weight loss occurred following GM injection in the water-drinking group but not in the DOCA plus saline-drinking and saline-drinking-alone groups. DOCA plus saline drinking significantly suppressed the plasma renin activity (PRA) but saline drinking alone did not. A significant inverse correlation was found between PRA and Cin in water-drinking GM-treated and untreated rats. The data suggest that the beneficial effect of DOCA plus saline drinking is associated with renin-angiotensin suppression rather than with the renal GM content or well-maintained hydration.

Acute Kidney Injury↗
PubMed1992

Factors affecting severity of renal injury and recovery of function in acute renal failure.

Severity of renal injury and recovery of function in acute renal failure (ARF) are strongly related not only to the magnitude and nature of ARF insult but also to numerous factors in the host which govern renal susceptibility to the insult and repair of renal lesion. Prior ARF affords resistance to a rechallenge with the same or different ARF insult. The mechanisms for this acquired resistance to ARF have not been well established, but suggested mechanisms include (a) increased resistance of regenerated tubular epithelial cells to a rechallenge, (b) glomerular refractoriness to vasoactive substances, (c) failure of damaged kidney to concentrate the toxic substance, (d) enhanced antioxidant enzyme activity in glomeruli, and (e) increased Na(+)-K(+)-ATPase activity in regenerated tubular epithelial cells. Controversy still exists regarding roles of these factors in the resistance to renal failure. Functional and morphologic recovery of postischemic kidney is enhanced by antecedent unilateral nephrectomy but delayed in the presence of the contralateral kidney. The mechanisms for the effect of uninephrectomy remain unsettled. Recent studies suggest contributions of changes in preglomerular vascular resistance; alterations in the environment which follow ischemia to all functioning excretory renal tissues; and altered production and release of vasoactive substances such as angiotensin, endothelin, thromboxane, and atrial natriuretic peptide.

Acute Kidney Injury↗
PubMed1992

[Effects of age, renal diseases and diabetes mellitus on the renal size reduction accompanied by the decrease of renal function].

Renal size reduction accompanied by the decrease of renal function was evaluated by ultrasonography in 30 normal controls, 45 patients with chronic renal diseases (CRD) and 22 patients with diabetic nephropathy (DN). In controls, significant positive correlation was observed between sectional areas of right kidney and creatinine clearance (Ccr) (r = 0.794, p < 0.001), suggesting that the decrease of renal function due to aging was accompanied by the renal size reduction. Significant correlation was also found between the size and Ccr in CRD (r = 0.814, p < 0.001) and DN (r = 0.640, p < 0.01). No significant difference was observed between controls and CRD in the reduction rate of renal size per unit change of Ccr, which suggested that the renal size reduction accompanied by the decrease in Ccr was the same in controls and CRD. In contrast, in DN, renal size reduction accompanied by the decrease in Ccr was smaller than controls or CRD. When renal sizes were compared in patients, whose Ccr were equal or less than 20 ml/min, renal sizes were significantly larger in DN than CRD (p < 0.001). The duration of illness from the onset of proteinuria was longer in CRD than DN (13.5 years and 4.7 years, respectively). The difference of renal sizes, however, can not be fully explained by the differences in the length of illness, since the renal size was larger in DN than CRD even when we compared the patients with the similar length of illness. In conclusion, renal size decreased with the reduction in the renal function in controls, CRD and DN.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

[Laboratory tests in acute renal failure].

This review is focused on the roles of laboratory test in acute renal failure (ARF). The roles of the laboratory test changes along with the alterations in clinical features and with the advances of treatment. Recent acute renal failure is characterized by the following three features: most of the ARF develops in hospitals, the frequency of nonoliguric ARF is increasing, and the association of other organ failure such as heart failure, liver failure or respiratory failure, increases the mortality rate. Hemodialysis is instituted in the early phase of ARF to enable the supply of enough nutriments and drugs. These features of recent ARF increases the importance of the frequent analysis of plasma creatinine in patients, who are at risk for ARF, to diagnose ARF at the onset. After the development of ARF, laboratory tests for the evaluation of other organ function is repeated. The development of new drugs increases the incidence of interstitial nephritis, and the advances in the therapeutic approach on systemic diseases (such as SLE or PN), which frequently develop ARF, alter the prognosis of these diseases. Since the early diagnosis of these diseases is important, it is necessary to develop noninvasive and reliable tests for the diagnosis of these diseases.

Acute Kidney Injury↗
PubMed1992

Manidipine attenuates a progressive renal injury in remnant kidneys of rats.

The effects of a calcium antagonist, manidipine, on the outcome of the remnant kidney model of chronic renal failure in rats were studied. After 5/6 nephrectomy (5/6 Nx), rats were assigned to one of the following groups, and fed: Nx without manidipine, group 1; diet with 0.01% manidipine, group 2. A sham 5/6 Nx group was also included as the control. Each diet contained the same calories (3.44 kcal/g) and protein (25% casein). Increased systolic blood pressure seen after 8 weeks postablation was less with manidipine in group 2. Group 2 also had significantly less proteinuria. By 12 weeks postablation, group 1 showed severe parenchymal damage, characteristic of end-stage renal pathology. These changes were prevented by manidipine. The percentage of glomeruli with severe structural damage including sclerosis and/or hyalinosis, arbitrarily defined as glomerular sclerosis index (GSI) was significantly less in group 2 (41 +/- 11%) compared with group 1 (58 +/- 10%). Tubulointerstitial injury (TII) was also less in group 2 (29.1 +/- 9.1%) compared with group 1 (45.1 +/- 10.3%). Sham-Nx control group without manidipine showed normal renal morphology (GSI, 0.2 +/- 0.6, TII, 3.8 +/- 1.0). These results indicate that manidipine attenuates the development of end-stage renal pathology in the remnant kidney model of chronic renal failure in rats. The mechanism(s) remains to be elucidated.

Animals↗
PubMed1992

Roles of hormones in plasma potassium alteration in acute respiratory acidosis in dogs.

The present study was conducted to examine the roles of hormonal factors in plasma potassium alterations in acute respiratory acidosis. Respiratory acidosis (pH, 7.07-7.10) induced by the inhalation of 10% CO2, 20% O2 and 70% N2 mixed gas caused an increase in the plasma potassium concentration beyond that of the control of 3.44 +/- 0.12 (mean +/- SE) to 4.36 +/- 0.07 mEq/l (p less than 0.01) within 180 min. The plasma norepinephrine concentration was also noted to significantly increase at the same time. Phentolamine (40 micrograms/kg/min i.v.) did not affect the degree of acidosis or acidosis-induced hyperkalemia. No significant changes in the plasma levels of epinephrine, insulin, glucagon, cortisol or aldosterone could be detected. Hormonal factors would thus appear not to be essential to potassium movement from intracellular to extracellular compartments in acute respiratory acidosis.

Acidosis, Respiratory↗
PubMed1991

Effect of Ringer infusion on ischemic acute renal failure: caution on interpreting the results of short-term studies.

The effect of a 4.5 mL/h Ringer infusion on the recovery from a unilateral 40-min renal artery occlusion was investigated in Sprague-Dawley rats. The inulin clearance measured in the experimental kidney 24 and 48 h after the insult in control animals that did not receive the Ringer infusion was 0.14 +/- 0.10 (mean +/- SE) and 0.11 +/- 0.05 mL/min, respectively. In animals that received 24 h of Ringer infusion begun at the time of the renal artery occlusion the inulin clearance was 0.81 +/- 0.07 mL/min, a value significantly higher than either of the control groups (p less than .05). If, however, the Ringer infusion was stopped at 24 h and the inulin clearance measured at 48 h, it had decreased significantly (0.27 +/- 0.09 mL/min) and was no longer greater than the control groups. Similarly, if the infusion was continued for 48 h there was no longer a significant difference between the inulin clearance (0.37 +/- 0.11), when compared with 48 h of no infusion (0.11 +/- 0.05). The histology of the different groups corresponded with the functional data. We conclude that 24 h of Ringer infusion leads to functional and histological protection when measured at 24 h; however, if measured at 48 h, protection is no longer evident. These studies suggest that caution should be exercised in extrapolating from the results of protective maneuvers in ischemic acute renal failure investigated by short-term studies.

Acute Kidney Injury↗
PubMed1991

Crystal-storing histiocytosis and crystalline tissue deposition in multiple myeloma.

Systemic distribution of crystal-storing histiocytes, increasing in number, and widespread crystalline tissue deposition were found in a 75-year-old man with a 5-year history of IgG-kappa-type multiple myeloma associated with corneal opacity and chronic renal failure. Characteristic crystalline inclusions were present not only in myeloma cells but also in cornea, epithelial cells of glomeruli, tubuli, Bowman's capsules, and choroid plexus. Histiocytes had particularly infiltrated the renal interstitium. These inclusions were positive by immunofluorescence for kappa light and gamma heavy chains. By electron microscopy, the inclusions were filled with fine crystalline hexagonal columns, each possessing a core structure. Of various factors generally considered responsible for renal failure in multiple myeloma, marked infiltration of histiocytes and the nephrotoxic effects of light chain appeared most relevant in the present case.

Aged↗
PubMed1991

[Myoglobinuria and acute renal failure].

Clinical and experimental studies on the development of myoglobinuria-associated acute renal failure (ARF) were reviewed. ARF developed in 30% of the cases of rhabdomyolysis. Rhabdomyolysis-associated ARF accounted for 5-10% of all ARF. The presence of dehydration or hypotension at the presentation of rhabdomyolysis seems to be a risk factor in the development of rhabdomyolysis-associated ARF. ARF occurred more frequently in the rhabdomyolysis caused by sepsis or burns. Glycerol-induced ARF in rats or rabbits has been studied to investigate the pathogenesis of myoglobinuria-associated ARF. The early decrease in inulin clearance (Cin) in glycerol-induced ARF was dependent upon the decrease in renal blood flow, but the decrease in Cin in the late phase could not be attributed to the decrease in renal blood flow. Diminished glomerular permeability and cast formation might play important roles in the decrease in Cin in the late phase of glycerol-induced ARF.

Acute Kidney Injury↗
PubMed1990

Role of hormonal factors in plasma K alterations in acute respiratory and metabolic alkalosis in dogs.

Studies were performed on previously nephrectomized dogs to examine roles of hormonal factors in plasma potassium alterations in acute alkalosis. Respiratory and metabolic alkalosis were induced by hyperventilation and intravenous NaHCO3 or tris(hydroxymethyl)aminomethane (Tris) infusion, respectively. Respiratory and NaHCO3-induced alkalosis provoked decreases in plasma potassium from the control value of 5.12 +/- 0.68 (SE) to 4.21 +/- 0.55 meq/l (P less than 0.01) and from 4.65 +/- 0.26 to 3.91 +/- 0.16 meq/l (P less than 0.01) within 180 min, respectively. In contrast, Tris-induced alkalosis elicited an increase in plasma potassium from the control value of 4.56 +/- 0.30 to 5.31 +/- 0.30 meq/l (P less than 0.01). Hypokalemia in respiratory alkalosis was associated with a decrease in the plasma norepinephrine concentration from the control level of 377 +/- 104 to 155 +/- 41 pg/ml (P less than 0.05) but not with changes in plasma levels of epinephrine, insulin, glucagon, cortisol, and aldosterone. However, this hypokalemia was not affected by phentolamine. Also, somatostatin did not modify the hypokalemic response. NaHCO3-induced hypokalemia was associated with a decline in the plasma aldosterone and norepinephrine concentrations. The decline in plasma norepinephrine in NaHCO3-induced alkalosis followed the decrease in plasma potassium. In Tris-induced alkalosis, plasma insulin increased but norepinephrine decreased. The findings do not suggest fundamental roles of the hormonal factors in the plasma potassium alterations in bilaterally nephrectomized dogs with acute alkalosis.

Acid-Base Equilibrium↗
PubMed1990

[A case of progressive systemic sclerosis with Sjögren's syndrome complicated by nephrotic syndrome caused by bucillamine].

A 53-year-old woman was admitted with complaints of edema in the lower legs. The patient had developed polyarthralgia in 1982 and had been treated with D-penicillamine and prednisolone under the diagnosis of rheumatoid arthritis. She then had developed sclerosis of skin as well as dry eyes and dry mouth. In November 1987, bucillamine treatment had started and proteinuria had appeared in February 1988. Her blood showed hypoproteinemia and was positive for anti-Scl-70 antibody test and for anti-SS-A antibody test. The skin biopsy and labial salivary gland biopsy revealed the increased collagen fibers in the subcutaneous tissue and the round cell infiltration around the salivary ducts. We diagnosed her as progressive systemic sclerosis (PSS) with Sjögren's syndrome (SjS) complicated by nephrotic syndrome. Subsequently a renal biopsy was performed. There were the granular deposition of IgG and complements in the glomerular capillary wall and electron dense deposits in the subepithelial region. These findings suggested that she had membranous nephropathy. Since such a renal lesion was rarely observed in PSS and SjS, it was highly probable that bucillamine induced the nephropathy. The bucillamine treatment was discontinued about 2 months after the nephrotic syndrome had developed. However, the nephrotic syndrome has continued for additional 8 months. Thus it is concluded that the renal damage is one of the important side effect caused by bucillamine.

Anti-Inflammatory Agents, Non-Steroidal↗