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Adiponectin is markedly increased in patients with nephrotic series of proteins spanning from TNF- and angiotensin- syndrome and is related to metabolic risk factors. ogen to plasminogen activator inhibitor type-1 and leptin. Background. Adiponectin (ADPN), the gene product of These proteins impinge upon important body functions apM1, is the most abundant secretory protein of the adipose ranging from inflammation, hematopoiesis, and immu- tissue in human plasma. Altered regulation (reduced synthesis) nomodulation, to sympathetic activity (1). Of particular of this substance may be relevant to endothelial dysfunction and cardiovascular complications in patients with ESRD. interest is the emerging hypothesis that disordered endo- Methods. We investigated the relationship between plasma crine function of the adipocyte may contribute to cardio- ADPN, glomerular filtration rate (GFR) (plasma iohexol clear- vascular disease (2), a concept supported by the observa- ance), and metabolic risk factors in 16 patients with nephrotic tion that high fat mass is associated to raised plasma syndrome, in 25 patients with chronic nephropathies without concentration of vasculotoxic cytokines, such as TNF, nephrotic syndrome, and in 31 healthy subjects. Results. Plasma ADPN was much higher (P 0.01) in pa- and to high circulating levels of leptin, which is a recog- tients with nephrotic syndrome (24.4 14.9 g/mL) than in nized sympathetic trigger and a predictor of cardiovascu- patients with chronic nephropathies without nephrotic syndrome lar events (3). Adiponectin (ADPN) is the most abundant (12.3 7.2 g/mL) and healthy subjects (5.9 2.6 g/mL). In adipose tissue protein in human plasma (4). ADPN is a the aggregate 24-hour, proteinuria (r 0.53, P 0.01) and particularly interesting compound because it may have serum cholesterol (r 0.53, P 0.01) were strong and direct correlates of plasma ADPN, while serum albumin correlated a protective influence on the cardiovascular system. In- inversely (r 0.46, P 0.01) with this protein. Proteinuria deed, it suppresses the attachment of monocytes to endo- appeared to be an important confounder of the relationship thelial cells and modulates the endothelial response to between ADPN and the GFR because in the whole patient inflammatory stimuli (5) The potential protective role population (with and without nephrotic syndrome), this rela- tionship emerged only after data adjustment for 24-hour pro- of adiponectin in human diseases is supported by the teinuria (partial r0.31, P 0.05), while no such relationship observation that plasma ADPN is low in patients with was demonstrable on crude data analysis (r 0.03, P 0.87). coronary artery disease (5) and in patients with type 2 Conclusions. ADPN is markedly increased in patients with diabetes mellitus (6). nephrotic syndrome, and proteinuria is strongly related to cir- Renal insufficiency is a notorious trigger of cardiovas- culating ADPN in patients with nephrotic and non-nephrotic renal diseases. The relationships between plasma ADPN, se- cular complications because, in this condition, endothe- rum cholesterol, and serum albumin suggest that this adipocyte lial dysfunction and atherosclerosis are almost universal. protein may serve to mitigate endothelial damage triggered by Preliminary observations in our laboratory indicated that dyslipidemia and other risk factors in patients with chronic ADPN is inversely related to creatinine clearance (7); renal diseases. this finding has been recently confirmed in a large survey in patients with dyslipidemia (8). Furthermore, we have also shown that ADPN is markedly increased in patients In the last decade substantial evidence has been ac- with ESRD (9). However, it is unknown whether the crued showing that the adipose tissue produces a large increase in plasma ADPN observed in patients with renal diseases depends purely on accumulation of this protein † Deceased. or represents a counter-regulatory response to the sev- eral metabolic and hemodynamic risk factors of renal