Contribution of Proteases to Hypercatabolism in Acute Renal Failure

Heidland, A.; Hörl, Walter H.

doi:10.1007/978-1-4612-5284-9_67

Cited by 5 publications

(5 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Potential sources are the striated mus cle in rhabdomyolysis and following multiple traumatic injuries [3][4][5], the kidney [particularly the cortex, see ref. 24], the lung [25], the pancreas [26], white blood cells [8][9][10][11] and a variety of bacterial strains [27][28][29][30][31] in pa tients with septicemia. Different strains of Pseudomonas aeruginosa were identified in blood cultures obtained from patients with septicemia showing proteolytic diges tion of elastin by pseudomonas elastase [32].…”

Section: Discussionmentioning

confidence: 99%

Detection of a Metalloproteinase in Patients with Acute and Chronic Renal Failure

Hörl¹,

Wanner²,

Thaiss³

et al. 1986

Am J Nephrol

View full text Add to dashboard Cite

The effect of different dialyzer membrane materials (cuprophan, cellulose hydrate, polyacrylonitrile, polymethylmethacrylate, ethylene-vinyl alcohol copolymer) on the ultrafiltrate proteinase activity was investigated in 26 patients with acute renal failure (ARF) and 40 patients undergoing regular hemodialysis treatment (RDT). Furthermore, the proteinase activity was characterized in vitro using azocasein and phosphorylase kinase as substrates in the absence and presence of different proteinase inhibitors. Proteinase activity of ultrafiltrates obtained from ARF patients was significantly enhanced with the dialyzer KF 101 (ethylene-vinyl alcohol copolymer). The digestion pattern of phosphorylase kinase revealed an identical type of proteinases in ultrafiltrates of ARF and RDT patients. The pH optimum of this proteinase was at alkaline pH. The proteinase activity could be inhibited in the presence of EDTA, whereas serine proteinase inhibitors were ineffective. Furthermore, the inactivated proteinase after Sephadex G-10 chromatography (in order to separate ultrafiltrate electrolytes and trace elements from protein) could be reactivated after the addition of Mg⁺⁺ and/or Ca⁺⁺. We conclude that a metalloproteinase can be found in ARF and RDT patients, and that KF 101 is more effectively eliminating the proteinase activity in ARF patients than other dialyzer membranes.

show abstract

Section: Discussionmentioning

confidence: 99%

Detection of a Metalloproteinase in Patients with Acute and Chronic Renal Failure

Hörl¹,

Wanner²,

Thaiss³

et al. 1986

Am J Nephrol

View full text Add to dashboard Cite

show abstract

“…Also in ARF activated PMNs are documented together with enhanced striated muscle breakdown [5,7, 1@ Therefore, one may assume that muscle degradation in ARF can be, at least partly, mediated by PGs. To proof this hypothesis, we examined whether the application of indomethacin takes beneficial effects on the hypercatabolism in acutely uremic rats.…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin synthetase inhibitors are not beneficial in the hypercatabolic state of acute uremia in rats

1988

View full text Add to dashboard Cite

In rats the effect of prostaglandin synthetase inhibition on the enhanced protein degradation in acute uremia was investigated. After 48 h of bilateral nephrectomy the urea nitrogen appearance, an indicator of net protein degradation, was calculated, and N tau-methylhistidine (N tau-MH) serum concentration was measured for judging myofibrillar breakdown. Also serum urea nitrogen, creatinine, and potassium serum concentrations were followed up. All bilateral nephrectomized rats showed severe uremic disturbances with increased (P less than 0.01) concentrations of serum urea nitrogen, creatinine, and potassium. Moreover, the urea nitrogen appearance and N tau-MH serum concentration increased (P less than 0.05) significantly. Administration of indomethacin (4 mg.kg-1b.wt./12 hi.p.) in bilateral nephrectomized rats did not influence the analyzed parameters significantly. Thus, we could not demonstrate a positive influence on the increased skeletal muscle degradation in acutely uremic rats by prostaglandin synthetase inhibition. These data suggest that in our model of acute uremia prostaglandins do not play a major role in the degradation of striated muscle.

show abstract

“…//¿»Wet al [30] described increased proteolytic activity in vitro in ultrafiltrates of plasma from hypercatabolic patients with acute renal fail ure. Heidland and Horl [31] suggested that the enhanced proteolytic activity may be caused by a reduction in con centration or function of proteinase inhibitors. Baracosex al.…”

Section: Trauma or Surgerymentioning

confidence: 99%