Hypertension in Chronic Glomerulonephritis

Area of Science:

• Nephrology
• Cardiovascular Medicine

Background:

• Chronic glomerulonephritis (GN) significantly elevates hypertension risk.
• Hypertension in GN is primarily volume-dependent, independent of renal function decline.
• Renal damage and ischemia in GN activate the intrarenal renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system, contributing to elevated blood pressure.

Purpose of the Study:

• To review the mechanisms of hypertension in chronic GN.
• To discuss current KDIGO guidelines for blood pressure targets in CKD patients.
• To evaluate therapeutic strategies for managing hypertension and proteinuria in chronic GN.

Main Methods:

• Literature review of studies on chronic glomerulonephritis and hypertension.
• Analysis of KDIGO guidelines for blood pressure management in chronic kidney disease.
• Synthesis of evidence on the role of RAAS, sympathetic nervous system, and therapeutic interventions.

Main Results:

• Hypertension in chronic GN is linked to volume overload, salt sensitivity, arteriolosclerosis, and RAAS/sympathetic overactivity.
• KDIGO guidelines suggest BP targets of ≤140/90 mmHg for CKD without albuminuria and ≤130/80 mmHg for those with albuminuria (≥30mg/24h).
• RAAS blockade is recommended for patients with albuminuria; combination therapy with calcium channel blockers and diuretics may improve BP control and reduce proteinuria.

Conclusions:

• Hypertension in chronic GN is multifactorial, involving volume, RAAS, and sympathetic tone.
• Tailored BP targets and RAAS-blocking agents are crucial for managing hypertension in chronic GN.
• Combination therapy offers a promising approach to achieve BP goals and mitigate proteinuria in this patient population.