This suggests our hypothesis presented in Figure 1, namely, (1) during the peak phase of APSGN, ERPF decreases due to endothelial cell swelling, leading to transient activation of the RAAS; (2) sodium and water are reabsorbed from the renal tubules, causing fluid overload (elevated BNP, IVCd, CTR); (3) the renal tubules are flooded with sodium and water, causing hypertension (increased BNP, IVCd, CTR); (4) APSGN is a self-limited acute disease that resolves as the endothelial cell swelling subsides; and (5) a temporary increase in ERPF occurs during recovery, leading to a diuretic phase. Here, NPPB is linked to hypertensive disorder.