糸球体腎炎患者におけるナトリウム排泄に関する研究

DOI Web Site PubMed

書誌事項

タイトル別名
  • Study on Sodium Excretion in Patients with Glomerulonephritis
  • シキュウタイ ジンエン カンジャ ニ オケル ナトリウム ハイセツ ニカンスル
  • With Special Reference to Postural Change
  • とくに体位変換による検討

この論文をさがす

説明

In order to investigate the sodium excretory capacity in patients with biopsy-proven primary glomerulonephritis, two-hours' static upright position was loaded after two-hours supine position. In all of the patients and of healthy control subjects, the change from supine to upright position was followed by decreases in creatinine clearance (CCr), fractional sodium excretion (FENa), and thus sodium excretion (UNaV) . However, the decreases in these values were significantly greater in the patients than in healthy subjects, suggesting that both glomerular and tubular responses to orthostasis in the patients were abnormal. In those patients with mesangial proliferatioe glomerulonephritis whose glomerular and tubular functions during supine position were normal (NP), orthostasis induced significantly greater decreases in CCr, FENa and UNaV than in healthy subjects, indicating that renal lesion such as mesangial proliferation played an important role in the abnormal postural response. In addition, it was suggested that no abnormality in renal function in NP might be disclosed unless some stress such as a postural change would be loaded. Among the factors affecting glomerular filtration and tubular sodium reabsorption, serum total protein concentration, plasma renin activity and plasma aldosterone concentration were increased after orthostasis in both NP and healthy subjects, the increases in these values being significantly greater in NP than in healthy subjects. From these results, it was concluded that: (1) In patients with glomerulonephritis, whether their renal function during supine position was impaired or not, orthostasis resulted in more sodium retention than in healthy subjects. (2) The causal sequence leading to the abnormal orthostasic antinatriuresis in NP was greater decrease in glomerular filtration which might result from the existence of the renal lesion, and greater increase in tubular sodium reabsorption mainly caused by hyperreaction of renin-angiotensin. aldosterone system, than in healthy subjects.

収録刊行物

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ