Abstract
Oedema is a defining element of the nephrotic syndrome. Its’ management varies considerably between clinicians, with no national or international clinical guidelines, and hence variable outcomes. Oedema may have serious sequelae such as immobility, skin breakdown and local or systemic infection. Treatment of nephrotic oedema is often of limited efficacy, with frequent side-effects and interactions with other pharmacotherapy. Here, we describe the current paradigms of oedema in nephrosis, including insights into emerging mechanisms such as the role of the abnormal activation of the epithelial sodium channel in the collecting duct. We then discuss the physiological basis for traditional and novel therapies for the treatment of nephrotic oedema. Despite being the cardinal symptom of nephrosis, few clinical studies guide clinicians to the rational use of therapy. This is reflected in the scarcity of publications in this field; it is time to undertake new clinical trials to direct clinical practice.
Highlights
Interstitial oedema is present in all individuals with nephrotic syndrome and can be profound, accounting for as much as an additional 30% to an individual’s total body weight (Doucet et al, 2007)
We have focused on the putative mechanisms of salt and water retention in nephrotic syndrome; mechanisms other than renal sodium retention may be important in causing interstitial oedema
With increased understanding of the underlying pathophysiology of interstitial oedema in nephrotic syndrome we are in a better position to better treat individuals suffering with the complications that severe interstitial oedema brings
Summary
Interstitial oedema is present in all individuals with nephrotic syndrome and can be profound, accounting for as much as an additional 30% to an individual’s total body weight (Doucet et al, 2007). Both result in sodium and water retention and increased interstitial fluid volume presenting as oedema. Systemic infusion of synthetic ANP or ANP extract in experimental studies in nephrotic individuals had a diminished natriuretic and diuretic response compared to healthy controls (Koepke and DiBona, 1987; Perico et al, 1989) despite the prediction from animal models for the opposite (Wang et al, 2006).
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