Nephrotic syndrome is characterized by proteinuria, hypoalbuminemia, edema, and dyslipidemia. Edema is a key feature and a primary reason patients seek medical attention. The management of nephrotic edema is crucial, as it can lead to serious complications such as pulmonary congestion, cardiovascular risk, and infections. Two main hypotheses explain edema development: the underfill hypothesis, which suggests fluid loss due to hypoalbuminemia, and the overfill hypothesis, which posits fluid retention due to sodium reabsorption in the kidneys. Recent studies indicate that sodium reabsorption in the kidneys is mediated by serine proteases activating ENaC channels. Diuretic therapy remains the primary treatment, with loop diuretics being the first-line option. However, diuretic resistance is common, and combination therapy may be necessary. ENaC blockers are emerging as potential add-on treatments. Despite limited data, ENaC blockers may offer benefits in reducing sodium reabsorption. Diuretic resistance is defined as failure to achieve decongestion despite maximum doses. Factors contributing to resistance include poor compliance, high sodium intake, and kidney dysfunction. Diuretic resistance can be managed by using different diuretic classes or adding ENaC blockers. Loop diuretics are preferred for their efficacy and safety, but they can cause side effects such as hypokalemia. Thiazide diuretics are less effective but have fewer side effects. Potassium-sparing diuretics may help counteract hypokalemia. Vasopressin receptor antagonists and SGLT2 inhibitors are also being explored for their potential in treating nephrotic edema. The choice of diuretic depends on the underlying mechanism of edema, with careful monitoring of electrolytes and renal function. The management of nephrotic edema remains challenging, and further research is needed to develop more effective treatments.Nephrotic syndrome is characterized by proteinuria, hypoalbuminemia, edema, and dyslipidemia. Edema is a key feature and a primary reason patients seek medical attention. The management of nephrotic edema is crucial, as it can lead to serious complications such as pulmonary congestion, cardiovascular risk, and infections. Two main hypotheses explain edema development: the underfill hypothesis, which suggests fluid loss due to hypoalbuminemia, and the overfill hypothesis, which posits fluid retention due to sodium reabsorption in the kidneys. Recent studies indicate that sodium reabsorption in the kidneys is mediated by serine proteases activating ENaC channels. Diuretic therapy remains the primary treatment, with loop diuretics being the first-line option. However, diuretic resistance is common, and combination therapy may be necessary. ENaC blockers are emerging as potential add-on treatments. Despite limited data, ENaC blockers may offer benefits in reducing sodium reabsorption. Diuretic resistance is defined as failure to achieve decongestion despite maximum doses. Factors contributing to resistance include poor compliance, high sodium intake, and kidney dysfunction. Diuretic resistance can be managed by using different diuretic classes or adding ENaC blockers. Loop diuretics are preferred for their efficacy and safety, but they can cause side effects such as hypokalemia. Thiazide diuretics are less effective but have fewer side effects. Potassium-sparing diuretics may help counteract hypokalemia. Vasopressin receptor antagonists and SGLT2 inhibitors are also being explored for their potential in treating nephrotic edema. The choice of diuretic depends on the underlying mechanism of edema, with careful monitoring of electrolytes and renal function. The management of nephrotic edema remains challenging, and further research is needed to develop more effective treatments.