A 28-year-old man presents with sudden onset hematuria, mild hypertension (BP 145/92 mmHg), and mild proteinuria. Serum creatinine is 1.2 mg/dL. Serological workup shows elevated anti-streptolysin O (ASO) titre and low C3 levels. Kidney biopsy confirms post-streptococcal glomerulonephritis (PSGN). What is the drug of choice for management of hypertension in this patient?

Explanation

## Drug of Choice for Hypertension in PSGN ### Rationale for ACE Inhibitor (Lisinopril) **Key Point:** ACE inhibitors are the first-line antihypertensive agents in acute nephritic syndrome, particularly post-streptococcal glomerulonephritis, because they provide dual renal protection: blood pressure reduction AND reduction of intraglomerular pressure via efferent arteriolar vasodilation. **High-Yield:** In PSGN with preserved renal function (creatinine <1.5 mg/dL), ACE inhibitors reduce proteinuria and slow progression of renal disease. They are preferred over other antihypertensives in all forms of nephritic syndrome with proteinuria. **Clinical Pearl:** PSGN is self-limited in most cases, but hypertension management is critical to prevent acute kidney injury and progression. ACE inhibitors are superior because they: - Lower systemic and glomerular capillary pressure - Reduce proteinuria - Have renoprotective effects independent of blood pressure lowering - Do not cause metabolic side effects (unlike thiazides) ### Comparison of Antihypertensive Options in Nephritic Syndrome | Agent | Mechanism | Renal Effect | Use in PSGN | |-------|-----------|--------------|-------------| | **ACE Inhibitor (Lisinopril)** | Blocks angiotensin II | ↓ Efferent vasoconstriction, ↓ GFR initially then stabilizes | **First-line** | | Calcium channel blocker (Amlodipine) | Vasodilation | Non-selective; dilates afferent > efferent | Second-line; less renoprotective | | Beta-blocker (Labetalol) | α/β blockade | Reduces cardiac output; no direct renal benefit | Reserved for specific scenarios (e.g., hypertensive emergency) | | Thiazide diuretic (HCTZ) | Inhibits Na-Cl reabsorption | Hypokalemia, hyperglycemia, hyperuricemia; worsens metabolic profile | **Contraindicated** in acute nephritic syndrome | **Tip:** Remember that in acute nephritic syndrome, avoid diuretics (including thiazides) unless there is volume overload with pulmonary edema, because these patients often have mild-to-moderate volume expansion and diuretics may worsen renal perfusion.