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World J Nephrol. Sep 25, 2026; 15(3): 121561
Published online Sep 25, 2026. doi: 10.5527/wjn.121561
Table 1 Blood pressure phenotypes, mechanisms, and emergency department management in renal diseases
Renal disease
BP phenotype
Key pathophysiology
ED diagnostic clues
Immediate ED management
Ref.
CKDPersistent HTN (± refractory)Na+/water retention; RAAS activationKnown CKD, Cr (increase), anemiaGradual BP reduction (≤ 25%); start IV CCB (nicardipine); avoid overcorrectionDylewska et al[4], Jeon et al[7], Nakazawa et al[43]
AKIVariable: HTN or hypotensionVolume overload or hypoperfusionRapid Cr (increase), oliguriaTreat cause: Fluids (if hypovolemic) or diuretics; avoid nephrotoxinsYu et al[2], Lehman et al[3], Badin et al[13]
GNSevere HTNInflammation + RAAS activationHematuria, proteinuria, edemaIV antihypertensives; consider immunologic workupIhm[25], Tizki et al[26]
Nephrotic syndromeMild-moderate HTNHypoalbuminemia to edemaMassive proteinuria, edemaDiuretics; cautious BP controlBovée et al[18], Pugh et al[19], Ihm[25], Kidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group[27]
RASResistant HTNRenal ischemia to RAAS overactivationAbdominal bruit, flash pulmonary edemaAvoid ACEI if bilateral; imaging referralShen et al[38]
Uremia (ESRD)Severe HTN or hypotensionToxin accumulationUremic symptomsUrgent dialysis indicationLacson and Lazarus[6], Davenport[20], Flythe and Bansal[21]
Obstructive uropathyHTN (early) to hypotension (late)Back pressure + renal dysfunctionHydronephrosis (US)Relieve obstruction (catheter, stent)Kittanamongkolchai et al[41], Chalisey and Karim[42]
Sepsis-associated AKIHypotensionVasodilation + capillary leakInfection signs, lactate (increase)Early fluids + vasopressorsTsuchida et al[35]


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