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      Call for Papers: Green Renal Replacement Therapy: Caring for the Environment

      Submit here before July 31, 2024

      About Blood Purification: 3.0 Impact Factor I 5.6 CiteScore I 0.83 Scimago Journal & Country Rank (SJR)

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      Pentoxifylline ameliorates renal tumor necrosis factor expression, sodium retention, and renal hypertrophy in diabetic rats.

      Author(s): 1 ,
      Publication date (Electronic):
      Journal: American journal of nephrology

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          Abstract

          Diabetic nephropathy contributes substantially to cardiovascular morbidity and mortality associated with diabetes. Urinary tumor necrosis factor (TNF) excretion is increased during diabetes and serves as an important mediator of pathological changes during the initial stages of diabetic nephropathy, including sodium retention and renal hypertrophy. We tested the hypothesis that pentoxifylline (PTF), an agent that inhibits TNF synthesis, could prevent sodium retention and renal hypertrophy during diabetes.

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          Long-term prevention of renal insufficiency, excess matrix gene expression, and glomerular mesangial matrix expansion by treatment with monoclonal antitransforming growth factor-beta antibody in db/db diabetic mice.

          F Ziyadeh, B. B. Hoffman, D Han … (2000)
          Emerging evidence suggests that transforming growth factor-beta (TGF-beta) is an important mediator of diabetic nephropathy. We showed previously that short-term treatment with a neutralizing monoclonal anti-TGF-beta antibody (alphaT) in streptozotocin-diabetic mice prevents early changes of renal hypertrophy and increased matrix mRNA. To establish that overactivity of the renal TGF-beta system mediates the functional and structural changes of the more advanced stages of nephropathy, we tested whether chronic administration of alphaT prevents renal insufficiency and glomerulosclerosis in the db/db mouse, a model of type 2 diabetes that develops overt nephropathy. Diabetic db/db mice and nondiabetic db/m littermates were treated intraperitoneally with alphaT or control IgG, 300 microgram three times per week for 8 wk. Treatment with alphaT, but not with IgG, significantly decreased the plasma TGF-beta1 concentration without decreasing the plasma glucose concentration. The IgG-treated db/db mice developed albuminuria, renal insufficiency, and glomerular mesangial matrix expansion associated with increased renal mRNAs encoding alpha1(IV) collagen and fibronectin. On the other hand, treatment with alphaT completely prevented the increase in plasma creatinine concentration, the decrease in urinary creatinine clearance, and the expansion of mesangial matrix in db/db mice. The increase in renal matrix mRNAs was substantially attenuated, but the excretion of urinary albumin factored for creatinine clearance was not significantly affected by alphaT treatment. We conclude that chronic inhibition of the biologic actions of TGF-beta with a neutralizing monoclonal antibody in db/db mice prevents the glomerulosclerosis and renal insufficiency resulting from type 2 diabetes.
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            Transforming growth factor beta contributes to progressive diabetic nephropathy

            T. E. Andreoli, W B Reeves (2000)
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              Salt. A perpetrator of hypertensive target organ disease?

              F G Messerli, R Schmieder, Jacquelyn Weir (1997)
              Experimental and clinical data suggest salt intake to be an important factor in the pathogenesis of essential hypertension. However, the relationship between dietary sodium and blood pressure has been found to be relatively weak, perhaps because causal blood pressure levels fluctuate considerably. We hypothesized that a closer correlation could be expected between salt intake and the degree of hypertensive target organ disease. We reviewed the literature for studies dealing with 24-hour urinary sodium excretion (as a measure of salt intake) and hypertensive target organ disease as assessed by left ventricular structure and function, microproteinuria, cerebrovascular disease, and arterial compliance. Salt intake as assessed by 24-hour urinary sodium excretion was found to be a close independent determinant of left ventricular mass in 9 different studies worldwide. A reduction in dietary sodium has been shown to reduce left ventricular hypertrophy. There is clinical and experimental evidence, particularly in salt-sensitive patients, that salt intake directly affects hypertensive renal disease, cerebrovascular disease, and compliance of large arteries. The close and partially independent correlation between salt intake and hypertensive target organ disease suggests dietary sodium to be a direct perpetrator of cardiovascular disease.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Am. J. Nephrol.
                Title: American journal of nephrology
                ISSN: 0250-8095
                ISSN (Print): 0250-8095
                Publication date (Electronic):
                Volume: 24
                Issue: 3
                Affiliations
                [1 ] Department of Pharmacology and Toxicology, Dartmouth Medical School, Hanover, NH, USA.
                Article
                Publisher Item ID: 79121
                DOI: 10.1159/000079121
                PubMed ID: 15205554
                SO-VID: 1c36e6ff-6f53-4219-8934-4aad09c30015
                Copyright © Copyright 2004 S. Karger AG, Basel
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