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Biomedical subjects

A Hishida

Publications and source records attributed to A Hishida.

At least 109 records · Page 6Linked to original sources
PubMed1996

Point mutation in the alpha-galactosidase A gene of atypical Fabry disease with only nephropathy.

A point mutation in exon 6 of the alpha-galactosidase A gene (alpha-GAL A) was found in a Japanese hemizygous male without typical manifestations of Fabry disease other than renal involvement. This 45-year-old man developed moderate proteinuria and was diagnosed with Fabry disease on the basis of renal histologic findings and prominent decreases in alpha-GAL A activity in his plasma, urine, leukocytes, and skin fibroblasts. Determination of the cDNA sequence of his alpha-GAL A gene revealed substitution of a G to A in codon 301, resulting in a glutamine rather than an arginine residue. Our case is unique in that this patient only demonstrated renal manifestations while all other reported patients with atypical Fabry disease, including a case with the identical point mutation, present with a cardiomyopathy. Direct DNA sequencing of exon 6 and measurement of alpha-GAL A activity among the patient's family confirmed that the mutation was transmitted from his mother.

Biopsy↗
PubMed1995

Colonic dilatation due to dialysis-related amyloidosis.

A 66-year-old woman with chronic renal failure who had undergone hemodialysis for 15 years developed severe dilatation of the ascending and transverse colon. She had received right carpal tunnel release 5 years before this episode. The follow-up study of upper gastrointestinal series disclosed marked dilatation of the ascending and transverse colon with the retention of gastrografin persisted for 5 days, whereas colonic fiberscope showed no obstructive lesion. Pathologic study of biopsy specimens obtained from the colon demonstrated amyloid deposition. Avidin-biotin peroxidase complex method showed that these deposits strongly reacted with the antibody to human beta 2-microglobulin, but did not react with AA, lambda, and kappa antibodies. This case suggests that dialysis-related amyloidosis can cause intestinal pseudo-obstruction.

Aged↗
PubMed1995

Role of thromboxane A2 and prostacyclin in uninephrectomy-induced attenuation of ischemic renal injury.

Contralateral uninephrectomy attenuates unilateral renal ischemic injury. The present work was performed to elucidate whether the beneficial effect of uninephrectomy was mediated through the modification of the actions of thromboxane A2 (TxA2) or prostacyclin. Unilateral ischemic injury was provoked by a 60-minute left renal artery occlusion in right nephrectomized (Nx) and in sham-nephrectomized (Sham-Nx) rats. Inulin clearance (CIn) of left kidney 48 hours after ischemia was significantly higher in the Nx group than in the Sham-Nx group (0.11 +/- 0.07 vs. 0.00 +/- 0.00 ml/min/kidney, P < 0.05). Ischemia-induced tubular necrosis was also less in Nx animals. Proliferating cell nuclear antigen (PCNA) staining, a marker for cell proliferation, was found more markedly in Nx rats than in Sham-Nx animals. Forty-eight hours after ischemia, renal cortical TxB2 content was greater in Sham-Nx rats than in Nx rats (29.5 +/- 4.4 vs. 18.3 +/- 1.7 pg/mg protein, P < 0.05). No significant difference was found in the intrarenal content of 6-keto prostaglandin F1 alpha between two ischemia groups. A thromboxane synthetase inhibitor, OKY-046 (100 mg/kg/day, i.p.), significantly increased CIn 48 hours after ischemia (0.00 +/- 0.00 vs. 0.17 +/- 0.09 ml/min/kidney, P < 0.05) and attenuated ischemic tubular damage in Sham-Nx rats but not in Nx animals. Under OKY-046 treatment, no significant difference was found in postischemic CIn and ischemic tubular damage between the Nx and Sham-Nx groups. OKY-046 also increased PCNA expression in the cortex and outer stripe in Sham-Nx animals. These data suggest that less production of intrarenal TxB2 plays an important role for the uninephrectomy-induced attenuation of ischemic renal damage and for the facilitation of tubular recovery.

6-Ketoprostaglandin F1 alpha↗
PubMed1995

Endemic occurrence of glomerulonephritis associated with streptococcal impetigo.

We report here a case of type 1 mesangiocapillary glomerulonephritis as well as a case of mesangial proliferative glomerulonephritis associated with streptococcal skin infection superimposed on atopic dermatitis. Both were endemic occurrences of postinfectious glomerulonephritis developed after repeated dirty-skin treatments for atopic dermatitis performed by unauthorized individuals under unsanitary conditions. Of 20 patients who were similarly treated and subsequently admitted to our hospital because of skin infection and fever, 8 (40%) showed urinary abnormalities. Four patients had renal dysfunction with acute nephritic onset. Almost all showed a decrease in CH50 values and an increase in levels of antistreptolysin O and IgE. In the 2 cases presented here, the disease eventually regressed in association with improvement of the skin infection. Although the occurrence of postinfectious glomerulonephritis has recently become uncommon, we must take care to note urinary abnormalities as early as possible in order to prevent the progression of glomerulonephritis.

Adolescent↗
PubMed1995

[Tubulointerstitial damage attributable to acute circulatory failure: postischemic acute renal failure].

Renal damage attributable to acute circulatory failure includes prerenal azotemia, postischemic acute renal failure and bilateral renal cortical necrosis. In this review, recent findings of the pathophysiology, diagnosis, and treatment of postischemic acute renal failure are reviewed. The medullary thick ascending limb of Henle and the proximal straight tubule are extremely susceptible to ischemic damage because of the characteristic anatomical feature of the vasa recta in the medulla. Appropriate supportive treatment and initiation of dialysis early in the course of acute renal failure improve survival. However, the prognosis of acute renal failure with multiple organ failure is poor. Further studies on the precise cellular mechanism of acute renal failure may provide us with some future modes of treatment.

Acute Kidney Injury↗
PubMed1995

Effects of a calcium antagonist, manidipine, on progressive renal injury associated with mild hypertension in remnant kidneys.

The present study was conducted to determine the effects of a calcium antagonist, manidipine, on the outcome of a remnant kidney model of chronic renal failure in Fisher 344 rats. After sham operation or five-sixths nephrectomy (Nx), the rats were assigned to one of the following groups according to the administered amount of drug and were provided a specified diet for 12 weeks: group 1 (sham), diet without manidipine; group 2 (Nx), diet without manidipine; group 3 (Nx), diet with 0.0004% manidipine; group 4 (Nx), diet with 0.002% manidipine; group 5 (Nx), diet with 0.01% manidipine; group 6 (Nx), diet with 0.05% manidipine. All diet contained the same amount of calories (3.44 kcal/gm) and protein (25% casein). Systolic blood pressure and urinary protein excretion in group 2 began to increase at 8 and 4 weeks after ablation, respectively. Manidipine attenuated the increase in blood pressure in groups 4 through 6 but not in group 3. Manidipine-treated groups 3 to 5 had significantly less proteinuria than group 2. Group 6 had significantly more proteinuria than group 2. At 12 weeks after ablation, the kidneys from group 2 showed severe parenchymal damage, which is characteristic of end-stage renal pathology. These changes were ameliorated in groups 3 through 5, while group 6 had significantly more injured renal pathology than group 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Ultrasonographic evaluation of the carpal tunnel syndrome in hemodialysis patients.

The carpal tunnel syndrome (CTS) is the most frequent clinical symptom of dialysis-related amyloidosis. We examined CTS by ultrasound imaging and correlation between CTS and bone amyloidosis was sought. One hundred and forty-two wrists of 71 hemodialysis (HD) patients and 28 of 14 normal volunteers (group 1) were studied. Patients on HD were divided into 4 groups based on HD duration: Group 2, less than 5 years; group 3, 5-10 years; group 4, 10-15 years; and group 5, more than 15 years. The frequency of CTS increased gradually with HD duration: 0% in group 2, 35.3% in group 3, 36.4% in group 4 and 74.1% in group 5. The thickness of the palmar radiocarpal ligament (PRL), corresponding to the posterior wall of the carpal tunnel was significantly greater in groups 4 (p < 0.05), and 5 (p < 0.05) than in group 1 (2.25 +/- 1.30 and 3.11 +/- 1.02 in group 4 and 5 vs 1.15 +/- 0.34 mm in group 1); and the width of the carpal tunnel (CT) was significantly larger in group 5 than in group 1 (6.92 +/- 1.78 in group 5 vs 5.53 +/- 1.48 mm in group 1, p < 0.05). Wrists operated on for CTS had significantly increased PRL and CT compared to the control group and patients without CTS. Patients with CTS had wider PRL than the control and HD patients without CTS. Cystic radiolucent lesions (CRL) of carpal bones characteristic of bone amyloidosis were noted in 15 of 71 HD patients. The thickness of PRL and width of CT in HD patients with CRL exceeded those in patients without CRL. These data indicated that ultrasonographic findings of wrists were closely correlated with the degree of CTS and CRL. The usefulness of ultrasonographic evaluation of PRL thickness and CT width in the evaluation of dialysis-related amyloidosis should be evaluated.

Amyloidosis↗
PubMed1995

Natriuretic response to acute sodium chloride or sodium bicarbonate infusions in humans.

We compared the natriuretic responses to acute sodium chloride or sodium bicarbonate loading. 2.25 mEq/kg of sodium as sodium chloride, or sodium bicarbonate was infused intravenously in 1 h. Sodium chloride infusion resulted in a gradual increase in urinary sodium excretion (UNaV) for 4 h after starting the infusion, while sodium bicarbonate infusion caused a transient increase in UNaV for the first 2 h followed by a decrease. The amount of sodium excreted over 4 h in the sodium chloride and sodium bicarbonate groups were 20.7 +/- 4.7 and 34.8 +/- 2.3% of the sodium loaded, respectively (p < 0.05). This difference could not be ascribed to divergent responses in glomerular filtration rate, aldosterone, atrial natriuretic peptide, or serum albumin concentration. The difference in UNaV might be caused by the differences in renal tubular handling of chloride and bicarbonate.

Adult↗
PubMed1994

Effects of oxygen free radical scavengers on uranium-induced acute renal failure in rats.

Study was made to determine whether oxygen free radicals mediate uranium-induced acute renal failure (ARF). Superoxide dismutase (SOD), a superoxide anion scavenger, did not prevent uranium acetate (UA) (5 mg/kg, i.v.)-induced renal injury 48 h after injection. In contrast, dimethylthiourea (DMTU), a hydroxyl radical scavenger, significantly attenuated UA-induced rise in serum creatinine concentration (1.11 +/- 0.05 (DMTU) vs. 1.40 +/- 0.06 mg/dl (control), p < .05), and tubular necrosis. Dimethyl sulfoxide (DMSO), a hydroxyl radical scavenger, decreased UA-induced tubular damage. UA injection caused no increase in renal cortical malondialdehyde (MDA) content. DMTU and DMSO did not modify intrarenal MDA content. UA administration brought about significant increase in plasma renin activity but not in renal cortical renin content. Treatment with DMTU and DMSO had no effect on plasma renin activity or intrarenal renin content. It follows from these findings that DMTU and DMSO may attenuate UA-induced renal injury. Such a protective effect would not be mediated through modulation of lipid peroxidation or renin activity.

Acute Kidney Injury↗
PubMed1994

Mechanisms for protective effects of free radical scavengers on gentamicin-mediated nephropathy in rats.

Studies were performed to examine the mechanisms for the protective effects of free radical scavengers on gentamicin (GM)-mediated nephropathy. Administration of GM at 40 mg/kg sc for 13 days to rats induced a significant reduction in renal blood flow (RBF) and inulin clearance (CIn) as well as marked tubular damage. A significant reduction in urinary guanosine 3',5'-cyclic monophosphate (cGMP) excretion and a significant increase in renal cortical renin and endothelin-1 contents were also observed in GM-mediated nephropathy. Superoxide dismutase (SOD) or dimethylthiourea (DMTU) significantly lessened the GM-induced decrement in CIn. The SOD-induced increase in glomerular filtration rate was associated with a marked improvement in RBF, an increase in urinary cGMP excretion, and a decrease in renal renin and endothelin-1 content. SOD did not attenuate the tubular damage. In contrast, DMTU significantly reduced the tubular damage and lipid peroxidation, but it did not affect renal hemodynamics and vasoactive substances. Neither SOD nor DMTU affected the renal cortical GM content in GM-treated rats. These results suggest that 1) both SOD and DMTU have protective effects on GM-mediated nephropathy, 2) the mechanisms for the protective effects differ for SOD and DMTU, and 3) superoxide anions play a critical role in GM-induced renal vasoconstriction.

Acetylglucosaminidase↗
PubMed1994

Nephrogenic diabetes insipidus associated with bilateral ureteral obstruction.

Nephrogenic diabetes insipidus associated with ureteral obstruction is rare. We report a case of nephrogenic diabetes insipidus associated with ureteral obstruction caused by ileal leiomyosarcoma in a 32-year-old man. The treatment with trichlorothiazide and diclofenac sodium reduced urine output from 8 L/day to 4 L/day. Six months after nephrostomy, urine output decreased to 2.5 L/day without any drug administration. This case suggests that ureteral obstruction may cause an increase in urine output to 8 L/day and that surgical treatment for ureteral obstruction is effective in reducing urine output in nephrogenic diabetes insipidus patients with ureteral obstruction.

Adult↗
PubMed1994

Roles of hemodynamic and tubular factors in gentamicin-mediated nephropathy.

Gentamicin (GM) often causes polyuric acute renal failure (ARF) in humans and animals. GM-mediated ARF in rats was accompanied with activated renin-angiotensin system, increased renal endothelin content, and enhanced lipid peroxidation. Suppression of the renin-angiotensin activity by desoxycorticosterone acetate and saline drinking, and treatment with superoxide dismutase attenuated the GM-induced decline in whole-kidney GFR with well-maintained RBF but did not reduce the severity of tubular necrosis. On the other hand, treatment with dimethylthiourea, a hydroxyl radical scavenger, attenuated the GM-mediated decline in GFR and lessened tubular necrosis but did not ameliorate the reduction in RBF. These data suggest contributions of both vascular and tubular factors to the GM-induced decline in GFR in rats. However, relative importance of these factors probably differs with different doses of the agent.

Acute Kidney Injury↗
PubMed1994

Erythropoietin production in patients with chronic renal failure.

Studies were performed to reexamine the response of erythropoietin (Epo) production to acute hypoxic stimuli in patients with end-stage renal disease (ESRD). In the absence of acute bleeding or hypoxia, the serum Epo level in ESRD was similar to that of normal subjects despite severe anemia. In 11 dialysis patients with acute bleeding, the decrease in the Hb level from 8.9 to 5.8 g/dL provoked a significant increase in serum Epo up to 52.2 times the normal value. The increase in serum Epo was associated with a significant increase in corrected reticulocyte. Systemic hypoxemia (PaO2 < 65 mm Hg) in 8 dialysis patients provoked a significant elevation in the serum Epo level up to 24.6 times the normal level. There was an inverse relationship between serum Epo and arterial PaO2 (r = -0.715). The serum Epo level in these patients declined to or near the normal value after recovery from acute hypoxic stress. These data suggest that the ability of the Epo production is well preserved in ESRD, indicating that acute hypoxic stimuli provoke a significant increase in serum Epo.

Acute Disease↗
PubMed1994

Correlation between histologic features and glomerular permeability in membranous nephropathy and immunoglobulin A nephropathy.

We evaluated the correlation between histologic features and glomerular permselectivity based on fractional clearances of dextrans relative to inulin (FCsDex). The subjects consisted of 12 healthy volunteers, 18 patients with membranous nephropathy, and 20 patients with immunoglobulin A nephropathy. In membranous nephropathy, FCsDex measured with large dextrans (radii larger than 56 A) increased as the capillary lesion progressed. Histologic examination showed that glomerular capillary alteration was the factor most closely linked to changes in FCsDex in membranous nephropathy. Proteinuria (normalized to glomerular filtration rate) did not correlate with FCsDex. Increased FCsDex tended to normalize during prednisolone treatment in membranous nephropathy. In immunoglobulin A nephropathy, the impairment of glomerular size selectivity depended on the degree of mesangial sclerosis and tubulointerstitial injury. FCs of dextrans of 59 A were correlated with the mesangial sclerosis index (r = 0.573, p = 0.050) and the tubulointerstitial injury index (r = 0.707, p = 0.003). Proteinuria (again normalized to glomerular filtration rate) was significantly correlated with FCs of large dextrans in immunoglobulin A nephropathy (r = 0.668, p = 0.008). We conclude that glomerular size-selective barriers were impaired both in membranous nephropathy and immunoglobulin A nephropathy. However, the mechanisms of impaired size selectivity might differ, at least in part, between these nephropathies. The predominant factors responsible for the size-selective defect seemed to be glomerular capillary wall lesions in membranous nephropathy but mesangial sclerosis or tubulointerstitial damages (or both) in immunoglobulin A nephropathy.

Adolescent↗