Hisato Sakamoto

A highly sensitive radioimmunoassay of atrial natriuretic peptide (ANP) in human plasma and urine

A highly sensitive radioimmunoassay has been established for measurement of human plasma and urine concentrations of atrial natriuretic peptide (ANP) and requires no extraction or concentration process such as Sep-Pak C-18 cartridge treatment. An antiserum was prepared from rabbits immunized with alpha-human ANP (alpha-hANP) coupled with bovine-thyroglobulin. The sensitivity of this method was 0.3 pg/tube of synthetic alpha-hANP utilized as authentic standard. Recovery of alpha-hANP spiked to plasma and urine was 97.7 +/- 15.4% and 97.1 +/- 9.5% (mean +/- SD), respectively. Plasma and urinary ANP concentrations versus assay data showed satisfactory linearity. In 124 healthy subjects, the plasma ANP-concentration was 31.7 +/- 12.0 pg/ml. Two different molecular forms of ANP in plasma and a single form in urine were found by gel permeation chromatography.

Effective Antibiotic Treatment of Methicillin-Resistant Staphylococcus aureus-Associated Glomerulonephritis

Background: A new type of glomerulonephritis following a methicillin-resistant Staphylococcus aureus (MRSA) infection has been reported. The purpose of this study is to elucidate the clinicopathological features and the responsiveness to treatment of the disease. Methods: We studied the treatment of 8 patients with glomerulonephritis related to MRSA infection. We observed the eight cases and analyzed clinical features, laboratory findings and histopathological data. Results: On admission, all patients had no renal abnormalities. One to four months after suffering from MRSA infection, severe proteinuria and hematuria developed. Renal biopsy specimens revealed moderate to severe mesangial proliferative glomerulonephritis with various degrees of crescent formation. Immunofluorescence studies showed IgA and C3. Antibiotic therapy was performed in six cases, resulting in successfully reducing the proteinuria in parallel with the decreased activity of MRSA infection in five cases. The other 2 cases received corticosteroid treatment after complete cessation of MRSA infection, but they had a relapse of MRSA infection and later died from sepsis. Conclusions: These results suggested that MRSA-associated glomerulonephritis might respond to antibiotic treatment in most cases. This also indicated that special care must be taken in the application of steroid therapy for the glomerulonephritis with crescents, even though the MRSA infection has gone into an inactive state.

Functional coupling of chloride–proton exchanger ClC-5 to gastric H+,K+-ATPase

Summary It has been reported that chloride–proton exchanger ClC-5 and vacuolar-type H+-ATPase are essential for endosomal acidification in the renal proximal cells. Here, we found that ClC-5 is expressed in the gastric parietal cells which secrete actively hydrochloric acid at the luminal region of the gland, and that it is partially localized in the intracellular tubulovesicles in which gastric H+,K+-ATPase is abundantly expressed. ClC-5 was co-immunoprecipitated with H+,K+-ATPase in the lysate of tubulovesicles. The ATP-dependent uptake of 36Cl− into the vesicles was abolished by 2-methyl-8-(phenylmethoxy)imidazo[1,2-a]pyridine-3-acetonitrile (SCH28080), an inhibitor of H+,K+-ATPase, suggesting functional expression of ClC-5. In the tetracycline-regulated expression system of ClC-5 in the HEK293 cells stably expressing gastric H+,K+-ATPase, ClC-5 was co-immunoprecipitated with H+,K+-ATPase, but not with endogenous Na+,K+-ATPase. The SCH28080-sensitive 36Cl− transporting activity was observed in the ClC-5-expressing cells, but not in the ClC-5-non-expressing cells. The mutant (E211A-ClC-5), which has no H+ transport activity, did not show the SCH28080-sensitive 36Cl− transport. On the other hand, both ClC-5 and its mutant (E211A) significantly increased the activity of H+,K+-ATPase. Our results suggest that ClC-5 and H+,K+-ATPase are functionally associated and that they may contribute to gastric acid secretion.

Atrial natriuretic peptide is only a minor diuretic factor in dehydrated subjects immersed to the neck in water

SummaryTo determine if the atrial natriuretic peptide (ANP) is an important factor for inducing diuresis during head-out water immersion even in dehydrated subjects, six healthy volunteers were immersed up to the neck in water at 34.5° C for three hrs. Significant diuresis and natriuresis occurred, but urine osmolality decreased and negative

Tubulointerstitial Nephritis and Uveitis Syndrome With Autoantibody Directed to Renal Tubular Cells

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The absence of any effect of .ALPHA.-human atrial natriuretic peptide on sodium transport and osmotic water flow in the toad bladder.

was restored in a positive direction toward zero, even though subjects were still in a state of considerable dehydration. Plasma renin activity and plasma angiotensin I and II concentrations decreased but that of plasma aldosterone remained unchanged during water immersion, and plasma ANP did not increase thoughout the examination. On the basis of the data of the present study, the factor inducing diuresis during head-out water immersion in hydrated subjects appears to differ from that in dehydrated subjects, and the main factor inducing diuresis during water immersion in dehydrated subjects may be the suppression of vasopressin release and not ANP.

Atrial natriuretic peptide secretion in response to volume expansion and contraction in normal man.

症例は29才,女性. 14年間のfurosemide服用歴と浮腫増悪に対する習慣性の食塩制限を認めた.低K血症性アルカローシスの精査で入院.レニン・アルドステロン系の亢進,正常血圧, JG細胞過形成等からBartter症候群類似の病態を示したが,約420mEqのK欠乏にもかかわらず,ネフロン希釈部のCl再吸収は正常で, K欠乏補正後も不可逆性の濃縮障害を示した.腎組織はJG細胞過形成,間質の線維化,円形細胞浸潤,遠位尿細管基底膜肥厚を示した.本例は利尿薬長期服用,食塩制限, K欠乏により不可逆性濃縮障害を伴つたpseudo-Bartter症候群と考えられた.なお, Bartter症候群の鑑別に利尿薬中止後の希釈能検索の重要性が示唆された.