# Coexistence of Intravascular Excess Fluid and Reduced Renal Blood Flow in the Acute Phase of Acute Post-Streptococcal Glomerulonephritis

## TL;DR

This study shows that acute post-streptococcal glomerulonephritis involves fluid overload and reduced kidney blood flow, resembling prerenal kidney injury.

## Contribution

The study identifies a paradoxical coexistence of fluid overload and reduced renal blood flow in APSGN, supporting prerenal-like pathophysiology.

## Key findings

- BNP levels peaked during the acute phase of APSGN, indicating fluid overload.
- FENa was low during the acute phase despite high BNP, suggesting prerenal-like sodium retention.
- FENa increased during recovery as BNP levels decreased.

## Abstract

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.

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.

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.

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.