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      The Level of Serum Albumin Is Associated with Renal Prognosis in Patients with Diabetic Nephropathy

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          Although hypoalbuminemia is frequently found in most patients with diabetic nephropathy (DN), its relationship to the severity and progression of DN remains largely unknown. Our aim was to investigate the association between the serum albumin levels and clinicopathological features and renal outcomes in patients with type 2 diabetes mellitus (T2DM) and biopsy-proven DN.

          Materials and Methods

          A total of 188 patients with T2DM and biopsy-proven DN followed up for at least one year were enrolled. The patients were divided into four groups based on the albumin levels: normal group: ≥35 g/L ( n = 87); mild group: 30-35 g/L ( n = 34); moderate group: 25-30 g/L ( n = 36); and severe group: <25 g/L ( n = 31). The renal outcome was defined by progression to end-stage renal disease. The impact of the serum albumin level on renal survival was estimated using Cox regression analysis.


          Among the cases, the serum albumin level had a significant correlation with proteinuria, renal function, and glomerular lesions. A multivariate Cox regression analysis indicated that the severity of hypoalbuminemia remained significantly associated with an adverse renal outcome, independent of clinical and histopathological features. In reference to the normal group, the risk of progression to ESRD increased such that the hazard ratio (HR) for the mild group was 2.09 (95% CI, 0.67-6.56, p = 0.205), 6.20 (95% CI, 1.95-19.76, p = 0.002) for the moderate group, and 7.37 (95% CI, 1.24-43.83, p = 0.028) for the severe group.


          These findings suggested that hypoalbuminemia was associated with a poorer renal prognosis in patients with T2DM and DN.

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          Most cited references 34

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          Pathologic classification of diabetic nephropathy.

          Although pathologic classifications exist for several renal diseases, including IgA nephropathy, focal segmental glomerulosclerosis, and lupus nephritis, a uniform classification for diabetic nephropathy is lacking. Our aim, commissioned by the Research Committee of the Renal Pathology Society, was to develop a consensus classification combining type1 and type 2 diabetic nephropathies. Such a classification should discriminate lesions by various degrees of severity that would be easy to use internationally in clinical practice. We divide diabetic nephropathy into four hierarchical glomerular lesions with a separate evaluation for degrees of interstitial and vascular involvement. Biopsies diagnosed as diabetic nephropathy are classified as follows: Class I, glomerular basement membrane thickening: isolated glomerular basement membrane thickening and only mild, nonspecific changes by light microscopy that do not meet the criteria of classes II through IV. Class II, mesangial expansion, mild (IIa) or severe (IIb): glomeruli classified as mild or severe mesangial expansion but without nodular sclerosis (Kimmelstiel-Wilson lesions) or global glomerulosclerosis in more than 50% of glomeruli. Class III, nodular sclerosis (Kimmelstiel-Wilson lesions): at least one glomerulus with nodular increase in mesangial matrix (Kimmelstiel-Wilson) without changes described in class IV. Class IV, advanced diabetic glomerulosclerosis: more than 50% global glomerulosclerosis with other clinical or pathologic evidence that sclerosis is attributable to diabetic nephropathy. A good interobserver reproducibility for the four classes of DN was shown (intraclass correlation coefficient = 0.84) in a test of this classification.
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            Innate immunity in diabetes and diabetic nephropathy.

            The innate immune system includes several classes of pattern recognition receptors (PRRs), including membrane-bound Toll-like receptors (TLRs) and nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs). These receptors detect pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) in the extracellular and intracellular space. Intracellular NLRs constitute inflammasomes, which activate and release caspase-1, IL-1β, and IL-18 thereby initiating an inflammatory response. Systemic and local low-grade inflammation and release of proinflammatory cytokines are implicated in the development and progression of diabetes mellitus and diabetic nephropathy. TLR2, TLR4, and the NLRP3 inflammasome can induce the production of various proinflammatory cytokines and are critically involved in inflammatory responses in pancreatic islets, and in adipose, liver and kidney tissues. This Review describes how innate immune system-driven inflammatory processes can lead to apoptosis, tissue fibrosis, and organ dysfunction resulting in insulin resistance, impaired insulin secretion, and renal failure. We propose that careful targeting of TLR2, TLR4, and NLRP3 signalling pathways could be beneficial for the treatment of diabetes mellitus and diabetic nephropathy.
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              Study of the molecular mechanism of decreased liver synthesis of albumin in inflammation.

              Hypoalbuminemia in inflammatory disorders is not an infrequent finding. However, little is known about albumin synthesis in these patients. In the present study we have measured the albumin synthesis in four patients with inflammatory diseases using the [14C]carbonate technique. Because inflammation causes a decreased albumin synthesis and this decreased synthesis could not be related to a reduced amino acid supply, we have also examined the possible molecular mechanisms of reduced albumin synthesis during inflammation using in vivo and in vitro experiments in rats. In rats with turpentine-induced inflammation, serum albumin concentration and liver albumin mRNa level were markedly decreased. These changes could not be reproduced by administration of fibrinogen-, or fibrin-degradation products, or several hormones, such as corticosteroids, growth hormone, and adrenaline. However, monocytic products, especially interleukin 1, postulated to be important mediators of the inflammatory response, reduced albumin synthesis and liver albumin messenger RNA content but not total protein synthesis in rats in vivo and in primary cultures of rat hepatocytes. These findings suggest that monocytic products play an important role in reduced albumin synthesis during inflammation.

                Author and article information

                J Diabetes Res
                J Diabetes Res
                Journal of Diabetes Research
                17 February 2019
                : 2019
                Division of Nephrology, West China Hospital of Sichuan University, Chengdu 610041, China
                Author notes

                Academic Editor: Raffaella Mastrocola

                Copyright © 2019 Junlin Zhang et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Funded by: National Natural Science Foundation of China
                Award ID: 81670662
                Research Article


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