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Biomedical subjects

A Hishida

Publications and source records attributed to A Hishida.

At least 127 records · Page 7Linked to original sources
PubMed1994

Reduction of albuminuria by a calcium antagonist, manidipine, in rats with passive Heymann nephritis.

We evaluated the effects of a novel calcium antagonist, manidipine, on albuminuria in rats with passive Heymann nephritis (PHN). Treatment with 0.05% manidipine significantly reduced urinary albumin excretion (62.1 +/- 7.5 vs. 46.9 +/- 8.5 mg/urinary creatinine excretion mg, P < 0.05) and attenuated lipid peroxidation of the renal cortices (0.97 +/- 0.08 vs 0.84 +/- 0.11 nM MDA/mg protein, P < 0.05) on day 14 in PHN. Manidipine affected neither the light microscopic, immunofluorescent nor electron microscopic findings. These results indicate that manidipine reduced proteinuria in rats with PHN, and that its antiproteinuric effect was associated with the reduction of lipid peroxidation.

Albuminuria↗
PubMed1994

Light chain nephropathy with remarkable accumulation of multinucleated giant cells in the kidney.

A case of light chain deposition disease with multinucleated giant cell accumulation in the kidney is described. A 54-year-old man was admitted to out hospital due to moderate renal failure. Complicated with eosinophilic pneumonia two months after admission, his renal function abruptly deteriorated and hemodialysis was started. Three-day methylprednisolone pulse therapy, however, partially recovered his renal function and hemodialysis was discontinued. His renal biopsy specimen revealed kappa light chain deposition disease with nodular mesangial expansion and subendothelial electron dense deposits. The most characteristic finding in this patient was accumulation of foreign body type multinucleated giant cells around atrophic tubules, small arteries and obsolescent glomeruli, probably associated with light chain deposition. No increase in kappa light chain was detected in his serum or concentrated urine. Such disseminated giant cell reaction, other than intra-luminal infiltration in the tubules, has not been reported in the literature and might be related to the physicochemical or structural properties of the deposited protein.

Giant Cells, Foreign-Body↗
PubMed1994

[Renal damage in liver cirrhosis: pathophysiology and management].

Acute renal failure in liver disease includes prerenal renal failure, acute tubular necrosis (ATN) and hepatorenal syndrome (HRS). Patients with liver cirrhosis are susceptible to prerenal renal failure because of gastrointestinal bleeding, diuretics and paracentesis etc. ATN is more common in patients with obstructive jaundice but it also develops as a result of prolonged prerenal renal failure. HRS is a functional form of oliguric acute renal failure, occurring in patients with advanced liver disease in the absence of known cause of renal failure. Intrarenal vasoconstriction, attributable to a decrease in effective arterial blood volume, induced by peripheral arterial vasodilation, is proposed to play a causative role. Central hemodynamic monitoring is useful to distinguish HRS from other reversible conditions with renal failure in liver disease.

Acute Kidney Injury↗
PubMed1993

Intra-GBM site of the functional filtration barrier for endogenous proteins in rats.

The passage of various endogenous proteins [such as albumin, transferrin, immunoglobulin G (IgG), and immunoglobulin M (IgM)] across GBM was studied in vivo in normal Munich-Wistar rats. Glomeruli were fixed by three different methods: in situ drip-fixation, perfusion- and immersion-fixation; then they were processed for immunogold electron microscopy. The most reproducible results were obtained with in situ drip-fixation. Albumin, transferrin and IgG penetrated into GBM, but IgM did not. Morphometry revealed that density of albumin increased towards the inner 1/5 to 1/3 of GBM (junction of lamina rara interna and lamina densa) and decreased towards the subepithelial region of GBM, whereas density of IgG and transferrin was the highest at the subendothelial site and declined towards the subepithelial side of GBM. These findings suggest that central and/or outer zone of GBM constitute the main filtration barrier for albumin, and that subendothelial zone may contribute also to the charge-selective barrier. It is also suggested that the subendothelial zone acts more effectively as a filtration barrier for IgG and transferrin than for albumin. In the outer zone of GBM, which roughly corresponds to lamina rara externa visualized by conventional electron microscopy, the relative density of IgG and transferrin was higher than that of albumin. Since the pI of albumin was lower than that of IgG and transferrin, this finding suggests that subepithelial zone of GBM also acts as a charge-selective barrier. In conclusion, the main GBM filtration barrier for albumin might be the central and outer zones of GBM, and that for transferrin and IgG might be the entire width of GBM.(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗
PubMed1993

Specific increases in urinary excretion of anti-DNA antibodies in lupus mice induced by lysozyme administration: further evidence for DNA-anti-DNA immune complexes in the pathogenesis of nephritis.

We previously reported that lysozyme electrostatically inhibits the fibronectin-mediated DNA binding to the glomerular basement membrane (GBM) and reduces in situ DNA-anti-DNA complex formation in the GBM in NZB/W F1 mice [1]. In this study, we further noticed significant increases in urinary excretion of anti-DNA antibodies and immune complexes (IC) in lysozyme-treated NZB/W F1 mice. Their clearance ratios of IgG anti-DNA antibody to whole IgG were markedly high compared with those of saline-treated animals. A large number of IgG and C3 positive granules were observed in the tubular cells of NZB/W F1 mice treated with lysozyme. On the contrary, nil or only small amounts of anti-DNA antibodies were detected in the urine of NZB/W F1 mice without lysozyme administration despite a large amount of proteinuria, suggesting entrapment of the antibodies in lupus glomeruli. Lysozyme neither inhibited the binding of anti-DNA antibodies to DNA or heparan sulphate nor did it displace anti-DNA antibodies and IC from the kidney homogenates of lupus mice. It thus appears that the inhibition of DNA binding to the GBM due to lysozyme reduced the entrapment of anti-DNA antibodies in the GBM, resulting in urinary excretion of the antibodies.

Animals↗
PubMed1993

Interstrain differences in murine daunomycin-induced nephrosis.

Examining 8 inbred murine strains [A/J, BALB/c, SM/J, C3H/J, SWR/J, C57BL/6J (B6), DBA-2, B10D2/old (B10D2/o)] for urinary albumin excretion after a single daunomycin (DM) injection (20 mg/kg), we found strain specificity in susceptibility to DM nephrosis. This specificity did not relate to the serum disappearance rate of this drug. A/J and BALB/c were highly susceptible to the nephrosis while C57BL/6J, DBA-2 and B10D2/o were completely resistant to it. Chronological observation revealed that A/J mice had significant proteinuria at 2 weeks after injection, and it persisted for the remaining 4 weeks of this experiment, while C57BL/6J showed no increase over the experimental period. Using segregants obtained from an A/J and B6 backcross, it has been shown that susceptibility is inherited as an autosomal recessive trait and involves approximately three genes. Neither a C5 deficiency, H-2 type nor coat color gene (c-locus) was related to this susceptibility. This strain difference in nephrotoxicity would be a promising way to investigate its subcellular mechanism.

Albuminuria↗
PubMed1993

Interstitial inflammatory and chronic tubulointerstitial lesions in lupus nephritis: comparison with those in IgA nephropathy.

The significance of interstitial inflammatory and chronic tubulointerstitial lesions was studied in relation to the severity of glomerular lesions in 62 patients with lupus nephritis and 88 with IgA nephropathy. Severe interstitial inflammatory and chronic tubulointerstitial lesions were found in patients with severe glomerular lesions in both lupus nephritis and IgA nephropathy. In such cases, the serum creatinine levels at biopsy were high and the renal prognosis was poor regardless of the underlying disease (lupus nephritis or IgA nephropathy). No IgA nephropathy patients with nil or mild glomerular lesions had moderate or severe interstitial inflammatory and/or chronic tubulointerstitial lesions. In contrast, predominantly severe interstitial inflammatory lesions were found in 36% of lupus nephritis patients with nil or mild glomerular lesions. The prevalence of interstitial immune complexes deposition was markedly high in those with predominant interstitial inflammatory lesions. However, the severity of chronic tubulointerstitial lesions was mild and renal function did not deteriorate in the mean follow-up periods of 68.6 months. It is suggested that, besides the tubulointerstitial lesions attributable to the severe concomitant glomerular damage, the interstitial deposition of immune complexes per se plays a pathogenic role in the interstitial inflammatory lesions in lupus nephritis. Its prognostic significance, however, was considered to be minor.

Adult↗
PubMed1993

Reversible acute renal failure in idiopathic nephrotic syndrome.

Acute renal insufficiency developed in four idiopathic nephrotic patients with minimal change or mild proliferative glomerulonephritis. The reduction in glomerular filtration rate (CInulin) was not in proportion to the renal plasma flow (CPAH) as evidenced by a low filtration fraction. Diuretic therapy failed to reverse renal insufficiency, and renal biopsy showed no evidence of interstitial nephritis, acute tubular necrosis or interstitial edema. Corticosteroid therapy induced a recovery of renal function with a decrease in proteinuria. These observations suggest that acute renal insufficiency in the idiopathic nephrotic syndrome might be caused by impaired glomerular permeability.

Acute Kidney Injury↗
PubMed1993

Biloma during steroid therapy for minimal change nephrotic syndrome.

A 27-year-old man, who had been on steroid therapy for 2 months for his nephrotic syndrome, suddenly developed intra-abdominal bile collection (biloma). He had no previous history of abdominal surgery, trauma, or any disease of the hepatobiliary system. The cause of the biloma formation was due, probably, to cholecystitis in the absence of calculi and a pinhole size perforation in the wall of gall bladder. It was assumed to be closely related to the high-dose steroid therapy over a prolonged period, which would likely suppress the repair process of the locally damaged biliary system.

Abdominal Pain↗
PubMed1993

Spontaneous bacterial peritonitis in an adult patient with nephrotic syndrome.

Most cases of spontaneous bacterial peritonitis (SBP) in association with nephrotic syndrome are children. The complication of SBP in adults with nephrotic syndrome is extremely rare. Herein, we report a 25-year-old man with nephrotic syndrome and chronic renal failure who suffered from SBP. Citrobacter freundii was isolated from ascites. Irreversible deterioration of renal function followed the development of SBP, though the peritonitis was cured with antibiotic treatment. This case suggests that SBP is a rare, but serious complication of adult nephrotic syndrome with ascites.

Adult↗
PubMed1993

Glomerular alterations in experimental oliguric and nonoliguric acute renal failure.

Studies were performed in oliguric and nonoliguric forms of uranyl acetate (UA)-induced and ischemic acute renal failure (ARF) to examine whether a reduction in GFR is correlated with glomerular morphologic alterations. UA-induced nonoliguric and oliguric ARF were induced in rabbits by i.v. injections of 0.9 and 2 mg/kg, respectively. A 60-min renal artery clamping produced nonoliguric ARF in previously uninephrectomized rats, but oliguric ARF in the clamped kidneys of sham-nephrectomized animals. A decline in the whole-kidney CIn rate was more marked in oliguric ARF kidneys of both models than in nonoliguric ARF kidneys. Also, tubular damage was more pronounced in oliguric kidneys when compared with nonoliguric kidneys. Scanning electron microscopic observations revealed glomerular alterations in oliguric and nonoliguric kidneys in both models, evidenced by a flattening and spreading of podocyte cell bodies associated with loss of epithelial foot processes and a reduction in the density and diameter of endothelial fenestrae. There was no significant difference in these glomerular changes between oliguric and nonoliguric kidneys. The findings suggest that less reduction in the whole-kidney GFR in nonoliguric ARF kidneys is ascribed largely to less pronounced tubular damage rather than to less severe glomerular morphologic alterations.

Acute Kidney Injury↗
PubMed1992

Bucillamine (a new therapeutic agent for rheumatoid arthritis) induced nephrotic syndrome: a report of two cases and review of the literature.

Two cases of nephrotic syndrome during bucillamine treatment were encountered in 1989 in our hospital; both patients had suffered from rheumatoid arthritis for 2 years. They had received 200 mg bucillamine orally per day for 3-4 months before the onset of the nephrotic syndrome. Discontinuation of bucillamine led to complete remission of the nephrotic syndrome within 1 year. Bucillamine is a new therapeutic agent for rheumatoid arthritis developed in 1982 in Japan. Since 1985, 14 cases of nephrotic syndrome, including the two cases reported here have been reported. We review these cases and discuss the pathogenesis.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1992

Acute aortic thrombosis associated with spinal cord infarction in nephrotic syndrome.

Acute aortic thrombosis associated with spinal cord infarction in a 47-year-old man with nephrotic syndrome is described. He was admitted to our hospital presenting with the nephrotic syndrome. Renal biopsy revealed mild mesangial proliferative glomerulonephritis. The urinary protein excretion rate transiently decreased after the start of treatment with prednisolone, but it increased again and was followed by the development of the signs and symptoms of spinal cord infarction, which was diagnosed by magnetic resonance signal abnormalities, and then symptoms of ischemia in the lower limbs. Digital subtraction angiography revealed an obstruction at the bifurcation of the abdominal aorta. Emergency thrombectomy was performed, and the arterial blood flow was reestablished. Laboratory data on the fibrinocoagulation system showed a hypercoagulable state. In this case, fibrinocoagulation abnormalities due to the nephrotic syndrome led to the hypercoagulable state, and dehydration might have triggered the thrombotic complication.

Acute Disease↗