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Biomedical subjects

M Haag-Weber

Publications and source records attributed to M Haag-Weber.

43 records · Page 3Linked to original sources
PubMed1989

Endocrine and metabolic abnormalities following kidney transplantation.

Various endocrine and metabolic disturbances associated with long standing uremia persist after kidney transplantation or arise from the use of immunosuppressive drugs. Hyperlipidemia for long time being implicated as the cause of corticosteroids is also observed in renal transplant recipients treated with cyclosporin A monotherapy. After conversion from cyclosporin to azathioprine serum cholesterol and triglyceride concentration fall, and elevation of LDL-cholesterol may also be reversed. There is a tendency for higher HDL-cholesterol in azathioprine and prednisolone treated transplant patients. Those patients who are at risk for clinically significant cholesterol elevations can be predicted by their pretransplant lipid levels, specifically the LDL-fraction. Risk-benefit ratio of conversion and of treatment with lipid-lowering drugs, especially with lovastatin, should be carefully examined, also in view of glucose intolerance. Higher incidence of diabetes mellitus requiring insulin therapy in cyclosporin treated transplant recipients has been reported. Cyclosporin may cause toxic effects on pancreatic beta-cells resulting in inhibition of insulin secretion. High doses of cyclosporin induce inhibition of glycogen synthesis in rat liver. Glucose intolerance is reversible after reduction of cyclosporin dose or conversion to azathioprine. Therefore glucose metabolism in kidney transplant recipients treated with cyclosporin should be carefully followed. Immunosuppressive therapy may affect reproductive function, arachidonate metabolism and renin-angiotensin-aldosterone system as well as posttransplant calcium and phosphate metabolism. Endocrine and metabolic abnormalities are associated with long standing uremia. After successful kidney transplantation several observations are normalized but further complications arise from the use of immunosuppressive drugs. The present paper reviews various endocrine and metabolic disturbances described following renal transplantation.

Animals↗
PubMed1989

Neutrophil activation during hemodialysis.

Oxidative metabolism of PMNs of uremic patients is enhanced due to unknown serum (plasma) factors which are removed during hemodialysis. Respiratory burst activity is diminished in both PMA-stimulated and unstimulated states compared to healthy controls. Hemodialysis normalizes stimulated and decreases unstimulated hydrogen peroxide production. Several authors found that resting and stimulated chemiluminescence (CL) during hemodialysis correlates with complement activation, whereas other authors describe CL using dialyzer membranes with only mild anaphylatoxin formation. Alterations of PMN carbohydrate metabolism in uremic patients improves during HD with polysulfone. HD with PMMA, however, activates glycogenolysis. These alterations may be responsible for disturbance in phagocytosis. Degranulation during HD also occurs in absence of complement activation. Calcium channel blockers decrease activation of PMNs using dialyzers with only little anaphylatoxin formation.

Carbohydrate Metabolism↗
PubMed1989

Beta-2-microglobulin and main granulocyte components in hemodialysis patients.

Plasma levels of granulocyte elastase in complex with alpha 1-proteinase inhibitor (E-alpha 1-PI) increased during hemodialysis from 110 +/- 10 to 506 +/- 66 micrograms/L using dialyzers made of polyamide, from 95 +/- 2.2 to 211 +/- 54 micrograms/ml with hemophane and from 114 +/- 10 to 203 +/- 25 using dialyzers made of polysulfone. Plasma lactoferrin values were also significantly higher during hemodialysis with polyamide (772 +/- 110 micrograms/L) compared with hemophane (268 +/- 2.2) and the polysulfone (278 +/- 31 micrograms/L) dialyzer. After dialysis each dialyzer was rinsed. We found the lowest concentration of lactoferrin (902 +/- 254 micrograms/L) and E-alpha 1-PI (739 +/- 162 micrograms/L) after rinsing polysulfone dialyzers, whereas the highest concentrations were observed after rinsing the polyamide dialyzer (lactoferrin: 2,426 +/- 314; E-alpha 1-PI: 1,134 +/- 144 micrograms/L). Hemodialysis with polysulfone dialyzers caused significantly lower plasma levels of beta-2-microglobulin compared with polyamide or hemophane membranes despite significantly lower levels in the rinsing solutions. Our data indicate that low plasma levels of main granulocyte component observed with polysulfone and hemophane dialyzers are not the result of higher membrane adsorption of E-alpha 1-PI and lactoferrin. These main granulocyte components are not related to beta-2-microglobulin levels of both plasma and rinsing solutions.

Aged↗
PubMed1989

Metabolic response of neutrophils to uremia and dialysis.

Oxidative metabolism of polymorphonuclear leukocytes (PMNs) in uremic patients is enhanced due to unknown serum or plasma factor(s) which are removed during hemodialysis. Respiratory burst activity is diminished in both PMA-stimulated and unstimulated states compared to healthy controls. Hemodialysis treatment normalizes stimulated hydrogen peroxide production and decreases unstimulated hydrogen peroxide production. Several authors found that resting and stimulated chemiluminescence (CL) during hemodialysis correlate with complement activation, whereas other authors describe the development of CL using dialyzer membranes with only mild anaphylatoxin formation. Alterations in PMN carbohydrate metabolism in uremic patients improve during HD. These alterations may be responsible for disturbances in phagocytosis. Degranulation during HD also occurs in the absence of complement activation. Calcium channel blockers decrease activation of PMNs when dialyzers with only little anaphylatoxin formation are used. Acute renal failure and sepsis induce activation of PMNs. Hemodialysis with membranes made of cuprophan leads to further activation of these PMNs and may contribute to granulocyte dysfunction.

Acute Kidney Injury↗
PubMed1988

Granulocyte activation during haemodialysis in the absence of complement activation: inhibition by calcium channel blockers.

The effect of the calcium channel blockers nifedipine (9 and 18 micrograms kg-1 h-1), diltiazem (100 and 200 micrograms kg-1 h-1) and verapamil (19 micrograms kg-1 h-1) continuously infused during haemodialysis on granulocyte and complement activation was investigated. Plasma levels of lactoferrin, elastase in complex with alpha 1-proteinase inhibitor (E-alpha 1PI) and C3a were measured in patients dialysed with dialysers made of cuprophane, polymethylmethacrylate (PMMA) and polyacrylonitrile (PAN). Calcium channel blockers caused no change of blood pressure during haemodialysis in all patients. There was no effect of nifedipine, diltiazem or verapamil on plasma lactoferrin, E-alpha 1PI or C3a levels in patients dialysed with cuprophane. However, plasma lactoferrin and E-alpha 1PI values were significantly reduced by all calcium channel blockers in patients dialysed with PMMA, and also by nifedipine and verapamil in patients dialysed with PAN. Our data indicate that calcium channel blockers inhibit granulocyte activation occurring in dialysers with very little anaphylatoxin formation. These drugs, however, are ineffective in patients dialysed with cuprophane where complement activation takes place. Therefore, granulocyte activation during haemodialysis in the absence of complement activation seems to be mediated by calcium ions.

Aged↗
PubMedDate not supplied

Is absorption of high-dose oral iron sufficient in peritoneal dialysis patients?

OBJECTIVE: Iron supplementation plays a major role in erythropoietin-treated end-stage renal disease patients. For peritoneal dialysis (PD) patients, oral iron substitution is more convenient than intravenous therapy. However, disturbed iron absorption and adverse effects may be limiting factors for oral treatment. Nevertheless, we compared the response to a high-dose and low-dose oral iron absorption test between PD patients and healthy control subjects. PATIENTS AND INTERVENTIONS: In 34 PD patients and 15 healthy control subjects, blood samples were taken at baseline as well as 2, 4, and 8 hours after oral intake of 4 tablets iron sulfate (105 mg elemental iron per tablet). In a subgroup of 6 PD patients and 6 control subjects, the oral iron absorption test was repeated using 1 tablet iron sulfate. RESULTS: There was no significant difference in the increase in serum iron during the test between the two groups. As known for healthy subjects, iron absorption was significantly better in PD patients with absolute iron deficiency compared to those with functional iron deficiency. Iron-repleted PD patients showed the lowest iron absorption, indicating that a high dose of oral iron did not overwhelm the ability of the bowel tract to reject unneeded iron. Increasing the oral iron dose from 1 to 4 tablets was followed by a better response in a small subgroup of PD patients compared to control subjects. Side effects such as nausea and vomiting occurred more frequently during high-dose oral iron in control subjects than in PD patients (20% vs 8.8%). CONCLUSION: High-dose oral iron is well absorbed in iron-depleted PD patients. This kind of oral iron therapy should be considered in some subgroups of PD patients with iron deficiency, particularly in those patients with poor vascularization of arm veins or intolerance to intravenous iron preparations.

Absorption↗