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investigated the renoprotective properties of adiponectin in podocyte apoptosis through targeted activation of caspase-8 (POD-ATTAC) mice generated by induction of caspase-8-mediated apoptosis in podocytes after injection of a construct-specific agent. POD-ATTAC mice exhibited kidney damage that recovered after the initial induction. Ad −/− POD-ATTAC mice had more severe albuminuria and ablated podocytes failed to recover. Adiponectin-overexpressing POD-ATTAC mice maintained normal GFR, had reduced renal interstitial fibrosis and exhibited a greater recovery from podocyte injury and albuminuria. These findings imply that adiponectin aids in restoring podocytes and renal function but the initial protection of podocytes from apoptosis may be minimal.

Nakamaki et al . (2011) examined streptozotocin-induced diabetic rats that received injections of an adenovirus to cause overexpression of adiponectin (Ad-Adipo) or control protein (Ad-lacZ). Ad-Adipo rats exhibited reduced proteinuria compared with Ad-lacZ rats. In addition, Ad-Adipo rats had decreased transforming growth factor β1 (TGF-β1) levels in the renal cortex. Taking into account the involvement of TGF-β1 in the pathogenesis of diabetic nephropathy, contributing to cellular hypertrophy and increased synthesis of collagen, adiponectin may inhibit the adverse TGF-β1-mediated changes in renal physiology, that result in development of proteinuria. Nakamaki et al . (2011) also demonstrated that Ad-Adipo rats had increased levels of nephrin-mRNA in renal cortex. Nephrin is a protein found in podocytes and is crucial for the proper function of the glomerular filtration barrier, whereas downregulation of nephrin contributes to the development of proteinuria in diabetic nephropathy. Thus, the upregulation of nephrin levels in renal cortex appears to constitute a pathway through which adiponectin can reduce albuminuria, at least in diabetic nephropathy. Furthermore, this study showed that Ad-Adipo rats had decreased proinflammatory endothelin-1, plasminogen activator inhibitor-1 and inducible nitric oxide synthase (iNOS) mRNA levels and increased vasodilatory endothelial nitric oxide synthase (eNOS) mRNA levels in renal cortex. Therefore, adiponectin appears to reduce endothelial dysfunction in diabetic nephropathy.

Ohashi et al . (2007) reported that adiponectin can attenuate the adverse effects of partial nephrectomy on renal structure and function, eventually reducing the albuminuria associated with this procedure. Partial nephrectomy results in hypertrophy of the remaining nephrons, podocyte injury, glomerular fibrosis and development of proteinuria through adaptive glomerular hyperfiltration, oxidative stress and inflammation. In the relevant study, subtotal nephrectomy was performed in Ad −/− mice and WT mice. Ad −/− mice exhibited more severe glomerular hypertrophy, glomerular infiltration of macrophages, glomerular and tubulointerstitial fibrosis and decreased nephrin-mRNA levels in the remnant kidney, and increased albuminuria compared with WT mice. Exogenous adiponectin replenishment of Ad −/− mice resulted in reduction in albuminuria and reversal of the adverse changes in renal structure of Ad −/− mice mentioned earlier. Therefore, adiponectin appears to attenuate albuminuria through activation of anti-inflammatory, antifibrotic and antioxidative pathways. Moreover, in this study immunohistochemical analysis revealed abundant immunostaining for adiponectin in the glomeruli and interstitium of the remnant kidney of WT mice after subtotal nephrectomy, but limited glomerular and tubulointerstitial immunostaining for adiponectin in nonoperated WT mice. This finding indicates that adiponectin possibly accumulates in the glomeruli and interstitium of the remnant kidney to counteract this renal injury, in response to an as yet unknown signal from the injured kidney. Further studies are needed to elucidate this issue.


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