Haemodialysis per se did not have a significant effect on endothelial function or large artery mechanical vessel wall properties in patients on maintenance dialysis therapy.

The results show that the administration of RF-bic solution was superior in normalizing acidosis of patients without the risk of alkalosis. The data also suggest that the use of RF-bic during CVVH reduces cardiovascular events in critically ill patients with acute renal failure, particularly those with previous cardiovascular disease or heart failure.

High doses of iron sucrose (Venofer((R)) at a dose of 250 mg/month) was equally effective in maintaining haemoglobin and equally well tolerated as low doses of iron gluconate (Ferrlecit((R)) at a dose of 62.5 mg once per week) in stable, rHuEpo treated haemodialysis patients.

In this retrospective cross-sectional study, even patients with slightly elevated serum creatinine levels of 1.3 to 1.4 mg/dL had a significantly reduced long-term outcome after PCI. Thus, even mild chronic renal failure appears to be associated with markedly increased risk after a PCI, with implications to the high number of patients concerned.

Thickening of the tubular basement membrane is one of the hallmarks of the polycystic kidney disease (PKD). The present study was conducted to investigate the potential role of the matrix metalloproteinase-2 (MMP-2) and its specific tissue inhibitors (TIMP-1 and TIMP-2) in the accumulation of matrix components in PKD. As a model of PKD, two-month-old heterozygous Han:SPRD rats, which are at an early stage of cystogenesis, were used. MMP-2, but not MMP-9 (gelatinase B) nor MMP-3 (stromelysin) could be detected in proximal tubules of the normal rat kidney. The presence of the inhibitors TIMP-1 and TIMP-2 was confirmed on the mRNA level. In tubules from PKD rats MMP-2 activity was lower (31 +/- 8 vs. 58 +/- 7 U/prep., N = 9, P < 0.05), mRNA of MMP-2 was reduced 4.2 +/- 0.6-fold (N = 4, P < 0.05) and enzyme protein was depressed 3.8 +/- 0.8-fold (N = 4, P < 0.05). By contrast, TIMP-1 mRNA was 9.0 +/- 1.1-fold and TIMP-2 mRNA 3.8 +/- 0.7-fold (N = 4, P < 0.05) elevated over controls. Cyst fluid from homozygous rats contained MMP-2 protein and activity. These findings indicate that tubular MMP-2 activity is reduced in PKD, due to down-regulation of MMP-2, up-regulation of TIMP-1 and TIMP-2, and luminal secretion of the enzyme. It is conceivable that these alterations relate to the enhanced matrix accumulation observed in the evolution of PKD.

Gadobutrol is effectively removed by three hemodialysis sessions using a low-flux polysulfone membrane. Our study documents initial evidence that gadobutrol can be used safely in hemodialysis patients.

The obese Zucker rat is an autosomal recessive model of obesity and hyperlipidaemia with many similarities to human non-insulin-dependent diabetes mellitus (NIDDM) [1][2][3]. These metabolic abnormalities precede the development of albuminuria and mesangial matrix expansion followed by segmental glomerulosclerosis [4,5]. Accumulation of matrix components within the mesangium has been demonstrated for collagen IV, fibronectin, laminin and proteoglycans [6][7][8].The turnover of extracellular matrix is dependent on a balance between its synthesis and degradation, and consequently enhanced matrix deposition may be either due to increased synthesis and/or reduced activity of proteinases responsible for the remodelling of the matrix components. Several lines of evidence suggest the involvement of metalloproteinases Diabetologia (1997Diabetologia ( ) 40: 1035Diabetologia ( -1043 Differential regulation of glomerular gelatinase B (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in obese Zucker rats Summary The obese Zucker rat represents a model of obesity combined with insulin resistance and hyperlipidaemia, which over a period of several months develops spontaneous glomerulosclerosis. The present study addressed the question as to whether glomerular sclerosis was associated with alterations in the degradation of matrix components. In the early phase (up to 6 months) glomeruli from obese rats displayed increased total collagen content (+ 64 %) and decreased gelatinolytic activity (− 34 %) as compared to lean control animals. This decline in glomerular gelatinolytic activity was due to a reduction in gelatinase B [matrix metalloproteinase (MMP)-9]. Glomerular MMP-9 mRNA was reduced 4.6 ± 0.6-fold (n = 3; p < 0.05), MMP-9 protein was not detectable by Western blotting and MMP-9 activity was considerably suppressed in gelatin zymograms. MMP-2, in terms of mRNA expression and activity, was unchanged. Tissue inhibitor of metalloproteinases (TIMP)-1 mRNA expression, TIMP-1 protein (immunohistochemistry) and TIMP-1 activity (reverse zymography) were enhanced in glomeruli from obese rats, while TIMP-2 mRNA remained unchanged. Moreover, mRNA for the a 1 IV collagen chain was 2.1 ± 0.8-fold higher in glomeruli isolated from obese animals (n = 3; p < 0.05). These findings indicate that matrix expansion in glomeruli from obese Zucker rats is due to both enhanced synthesis of matrix components as well as reduced degradation by matrix metalloproteinases. Apparently the latter effect is based on a reduction in MMP-9 and up-regulation of its inhibitor TIMP-1. [Diabetologia (1997[Diabetologia ( ) 40: 1035[Diabetologia ( -1043 Keywords Glomerulosclerosis, matrix metalloproteinase, tissue inhibitor of metalloproteinases, obese Zucker rat.Received: 16 January 1997 and in final revised form: 28 April, 1997Corresponding author: Dr. L. Schaefer, Med. Univ-Poliklinik, Albert-Schweitzer-Str. 33, 48129 Muenster, Germany Abbreviations: MMP, Matrix metalloproteinase; TIMP-1, -2: tissue inhibitor of metalloproteinases-1, -2; TPA, 12-O...

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