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Biomedical subjects

F Marumo

Publications and source records attributed to F Marumo.

730 records · Page 41Linked to original sources
PubMedDate not supplied

Massive pulmonary hemorrhage in polyarteritis nodosa (PN); report of a case.

We report a case of massive pulmonary hemorrhage which emerged in the course of polyarteritis nodosa (PN). Pulmonary hemorrhage was the major manifestation which determined the mortality of this patient, though severe renal failure concurrently developed. The diagnosis of PN should be considered in all cases of pulmonary hemorrhage coexisting with renal failure. As pulmonary hemorrhage can be life-threatening, early diagnosis is essential for the prompt start of adequate therapy.

Acute Kidney Injury↗
PubMedDate not supplied

Lactic acidosis with hypoglycemia and hyperammonemia observed in two uremic patients during calcium hopantenate treatment.

Calcium hopantenate (HOPA), a drug for treating symptoms of cerebrovascular disease, is a derivative of gamma-amino butyric acid and is also an analog of pantothenic acid. It is speculated that calcium hopantenate may affect lactate generation, glucose metabolism, and ammonia disposal through the inhibition of pantothenic acid metabolism. We report two uremic patients with complaints of consciousness disturbance with lactic acidosis, hypoglycemia and hyperammonemia. HOPA is mainly excreted with urine. Severe accumulation of HOPA, documented at the onset of unconsciousness in our uremic cases, might be responsible for marked inhibition of pantothenic acid metabolism.

Acidosis, Lactic↗
PubMedDate not supplied

Hepatic involvement in graft-versus-host disease associated with blood transfusion.

A 73-year-old man developed graft-versus-host disease (GVHD) after blood transfusion; he developed hepatitis, fever, rash, and pancytopenia. Although similar cases have been previously reported, the spectra of their liver injury was not clarified. The clinical and pathological findings of this case and a review of earlier reports suggest a possible predominance of hepatocellular injury in cases of GVHD after blood transfusion, which is in contrast to the prevalence of cholestatic liver disease in GVHD following bone marrow transplantation.

Aged↗
PubMedDate not supplied

Vitiligo and chronic photosensitivity in human immunodeficiency virus infection.

A 56-year-old man was admitted with hemiparesis and shortness of breath. He was positive to human immunodeficiency virus (HIV) antibody and was diagnosed as acquired immunodeficiency syndrome (AIDS) with Kaposi's sarcoma and pneumocystis carinii pneumonia. He developed chronic photosensitivity and vitiligo preceding the onset of the AIDS-related complex (ARC). Association of the two skin lesions with HIV infection is very rare. Although the role of HIV infection in these skin lesions is not significant, the immunological responses in the early course of HIV infection may have contributed to the development of both of these skin lesions.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Localization and expression of a collecting duct water channel, aquaporin, in hydrated and dehydrated rats.

The cellular and subcellular localization and expression of a kidney collecting duct water channel, aquaporin (AQP)-CD, were examined in the kidneys of hydrated and dehydrated rats by immunostaining, Northern blot analysis, and radioimmunoassay. In hydrated rat kidneys, AQP-CD was selectively found in the collecting duct principal cells and inner medullary collecting duct cells, but not in the intercalated cells. At a light microscopic level, AQP-CD was diffusely present in a granular pattern throughout the cytoplasm of the collecting duct cells with a preferential accumulation in subapical regions. By immunoelectron microscopy, AQP-CD was frequently demonstrated along membranes of small vesicles in the subapical cytoplasm and occasionally along the basolateral membranes of these cells. However, immunolabeling was sparse on the apical membranes. In dehydrated rats, AQP-CD immunostaining was intensified in the subapical cytoplasm of the collecting duct cells, along with increases in the number and size of AQP-CD-bearing vesicles in the subapical regions and with increment of labeling along the apical membranes. The increase in the amount of AQP-CD in the collecting duct cells of dehydrated rat kidneys was quantitatively confirmed by elevation of AQP-CD at mRNA and protein levels. The AQP-CD localization is consistent with the predicted site of the antidiuretic hormone (ADH)-regulated water channel in the collecting ducts and the increase in AQP-CD at mRNA and protein levels by dehydration may account for high concentration of urine in dehydrated subjects.

Animals↗
PubMedDate not supplied

Endothelin production in the rabbit collecting ducts of acute renal failure models. An immunohistochemical study.

Endothelin 1 (ET-1) production was examined in the rabbit nephron in acute renal failure (ARF) induced by uranyl acetate administration or by clamping the renal artery. Uranyl acetate dissolved in saline was injected intravenously at a dose of 0.8 mg/kg (n = 12). In the ischemic kidney experiment, 60 min of left renal artery clamping was carried out 1 week after removing the right kidney (n = 8). Plasma and urine concentrations of ET-1 were measured 0, 24, and 48 h after treatment, and immunohistochemical studies of renal tissues obtained 48 h after the experiments were carried out using ET-1 monoclonal antibody. The fractional excretion of ET-1 increased from 10 to 89% at 48 h in the uranyl acetate treated group and from 6 to 15% at 24 h in the renal artery clamping group, suggesting the existence of ET-1 secretion from the nephron in both types of ARF. By immunohistochemical examination, strong ET-1 expression was noted only in the collecting ducts. No staining was observed in other parts of the nephron in both types of ARF. The present study indicates that the increased expression of ET-1 probably reflects production by the collecting ducts in both rabbit ARF models.

Acute Kidney Injury↗
PubMedDate not supplied

Enhanced renal susceptibility to ischemia-reperfusion injury in the rat with obstructive jaundice.

BACKGROUND/AIMS: To investigate the susceptibility of kidneys to ischemia-reperfusion injury under obstructive jaundice. MATERIALS AND METHODS: Bile ducts of male rats were ligated for five days, right kidneys were removed, and vascular clamps were placed across left renal arteries for 30 minutes. RESULTS: Twenty-four hours later, ischemia-reperfusion produced renal injury in jaundiced rats as shown by increased serum creatinine and urea nitrogen levels. Histological observation showed tubular damages. These changes were minimal after ischemia-reperfusion in control rats. Renal thiobarbituric acid reactive substance contents were increased after bile duct ligation, which did not change after ischemia-reperfusion. On the other hand, ischemia-reperfusion produced a significant increase in renal thiobarbituric acid reactive substance contents in control rats. Renal glutathione contents were increased two fold after bile duct ligation and they were significantly decreased by ischemia-reperfusion. CONCLUSIONS: Kidneys in obstructive jaundice appear to be susceptible to ischemia-reperfusion injury. Although protective roles of GSH is suggested, the role of oxygen radicals in this type of renal injury remains to be further elucidated.

Animals↗