JMA journal · 2025
Coexistence of Intravascular Excess Fluid and Reduced Renal Blood Flow in the Acute Phase of Acute Post-Streptococcal Glomerulonephritis.
СтатьяНазвание и аннотация: Перевод в очереди
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Majima Hisakazu, Uemura Osamu, Hattrori Toshihiko, Fujita Naoya, Ushijima Katsumi, Miyoshi Masamichi, Yamada Takuji, Yamamoto Masaki, Matsukuma Eiji, Nagai Takuhito, Gotoh Yoshimitsu
Аннотация
INTRODUCTION: Acute post-streptococcal glomerulonephritis (APSGN) is traditionally classified as an intrinsic form of acute kidney injury (AKI). However, previous reports suggest that its pathophysiology may resemble prerenal AKI, particularly regarding low fractional excretion of sodium (FENa) in the acute phase. This study aimed to evaluate the paradoxical coexistence of reduced renal blood flow and fluid overload in APSGN.
METHODS: We retrospectively analyzed patients with APSGN (≤15 years old) hospitalized between 2010 and 2019 who exhibited ≥5% weight gain and brain natriuretic peptide (BNP) ≥100 pg/mL. The acute phase was divided into three periods: peak (3 days), early recovery (2 days), and late recovery (up to 30 days). Patients with FENa and BNP recorded in at least two periods were included.
RESULTS: Among 10 patients (median age: 7 years, interquartile range: 5-7), BNP levels peaked during the acute phase and decreased in the recovery phases. Conversely, FENa was low during the peak phase but increased during recovery, despite decreasing BNP levels.
CONCLUSIONS: In APSGN, FENa remained paradoxically low during the peak phase despite fluid overload (indicated by high BNP). These findings suggest that the acute phase of APSGN involves transient renal hypoperfusion and renin-angiotensin-aldosterone system activation, leading to sodium retention and volume overload. This mechanism supports the hypothesis that APSGN exhibits characteristics of prerenal AKI in its early stage.
METHODS: We retrospectively analyzed patients with APSGN (≤15 years old) hospitalized between 2010 and 2019 who exhibited ≥5% weight gain and brain natriuretic peptide (BNP) ≥100 pg/mL. The acute phase was divided into three periods: peak (3 days), early recovery (2 days), and late recovery (up to 30 days). Patients with FENa and BNP recorded in at least two periods were included.
RESULTS: Among 10 patients (median age: 7 years, interquartile range: 5-7), BNP levels peaked during the acute phase and decreased in the recovery phases. Conversely, FENa was low during the peak phase but increased during recovery, despite decreasing BNP levels.
CONCLUSIONS: In APSGN, FENa remained paradoxically low during the peak phase despite fluid overload (indicated by high BNP). These findings suggest that the acute phase of APSGN involves transient renal hypoperfusion and renin-angiotensin-aldosterone system activation, leading to sodium retention and volume overload. This mechanism supports the hypothesis that APSGN exhibits characteristics of prerenal AKI in its early stage.