Pathophysiology and treatment of edema in patients with the nephrotic syndrome
- Jai Radhakrishnan, MD, MS
Jai Radhakrishnan, MD, MS
- Professor of Medicine
- Columbia University Medical Center
- Section Editors
- Richard J Glassock, MD, MACP
Richard J Glassock, MD, MACP
- Editor-in-Chief — Nephrology
- Section Editor — Glomerular Diseases
- Emeritus Professor
- The David Geffen School of Medicine at UCLA
- Fernando C Fervenza, MD, PhD
Fernando C Fervenza, MD, PhD
- Section Editor — Glomerular Diseases
- Professor of Medicine
- Mayo Clinic College of Medicine
Edema is one of the major clinical manifestations of the nephrotic syndrome. The pathophysiology and treatment of edema in patients with the nephrotic syndrome will be reviewed here. More general issues such as the clinical manifestations, diagnosis, and general principles of the treatment of edema are discussed elsewhere as is the mechanism of hypoalbuminemia in the nephrotic syndrome. (See "Clinical manifestations and diagnosis of edema in adults" and "General principles of the treatment of edema in adults" and "Overview of heavy proteinuria and the nephrotic syndrome", section on 'Hypoalbuminemia'.)
UNDERFILLING VERSUS RENAL SODIUM RETENTION
Two major factors, both of which lead to retention, have been thought to be responsible for the development of edema in patients with the nephrotic syndrome; it is likely that both contribute to a variable degree in individual patients [1,2]:
●Primary sodium retention that is directly induced by the renal disease (overfill hypothesis)
●Secondary sodium retention in which the low plasma oncotic pressure due to hypoalbuminemia promotes the movement of fluid from the vascular space into the interstitium, leading to underfilling of the vasculature and activation of the renin-angiotensin-aldosterone system (underfill hypothesis)
The clinical importance of distinguishing between these mechanisms is the ability to tolerate diuretic therapy. Diuretics are well tolerated in patients with renal sodium retention but, if underfilling is the primary mechanism, can lead to worsening hypovolemia as evidenced clinically by an elevation in serum creatinine. As will be described below, most patients tolerate diuretic therapy at least initially.To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:
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- UNDERFILLING VERSUS RENAL SODIUM RETENTION
- Starling's law
- - Application to nephrotic syndrome
- Evidence supporting underfilling
- Evidence supporting primary renal sodium retention
- - Volume regulatory hormones
- - Response to glucocorticoids in minimal change disease
- Varying mechanisms in childhood minimal change disease
- Hypoalbuminemia in other edematous disorders
- Diuretics and sodium restriction
- Angiotensin inhibition
- INFORMATION FOR PATIENTS
- SUMMARY AND RECOMMENDATIONS