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Biomedical subjects

E Ritz

Publications and source records attributed to E Ritz.

At least 703 records · Page 39Linked to original sources
PubMed1986

Dialysis membranes and coagulation system.

Artificial membranes used for hemodialysis differ from endogenous membranes, i.e. endothelial cells, by their variable thrombogenicity. The key step in activation of the coagulation system by dialysis membranes is thrombocyte activation which is preceded by formation of a protein layer of critical thickness. Crucial questions concerning the quality of this protein membrane as a determinant of thrombocyte activation are not well understood. Activation of the contact phase of the intrinsic plasmatic coagulation system by dialysis membranes is well documented. Local action of thrombin in the membrane microenvironment is documented by release of fibrinopeptide A and deposition of fibrin on the membrane. Apart from thrombin, other mechanisms, e.g. PMN elastase, plasma-independent activation of blood cells, facilitatory action of erythrocytes etc., may play a contributory role. With respect to the polycarbonate membrane, some authors find less platelet extraction and unchanged platelet release reaction. In our own studies, polycarbonate membranes were not superior to cuprophane membranes with respect to thrombogenicity.

Animals↗
PubMed1986

Urinary lead excretion in uremic patients.

Urinary excretion of lead (Pb) was measured in the basal state and following the infusion of EDTA (1g of calcium disodium edetate) in healthy German controls and in patients with chronic renal failure with and without gout. When evaluated with Zeeman-compensated atomic absorption spectroscopy using the L'vov platform and urine pretreated with nitric acid and Triton X-100, the control basal Pb excretion (median 28, range 11-19 nmol Pb/24h) and the postinfusion Pb increment (306, range 131-1,587 nmol/4 days/1.73 m2) were considerably lower than most values reported previously in the literature. Elevated Pb body burden was found in 7 of 8 patients who developed gout in the course of renal failure, but only in 2 of 8 patients who had gout prior to development of renal failure; this confirms that appearance of gout in patients with renal failure points to prior Pb exposure. In 7 of 19 nongouty patients with impaired renal function secondary to known renal diseases, urinary Pb excretion was above the 95th percentile of normal. All these patients had occupational Pb exposure. The high prevalence of elevated Pb body burden in patients with renal failure of known cause may not be coincidental and raises the possibility that Pb adversely affects the course of renal disease.

Adult↗
PubMed1986

Different in vitro generation of C3d by cuprammonium and polycarbonate capillary hemodialyzers.

Cellulosic membranes have been shown to activate C3 via the alternative pathway. Generation of the stable product C3d was compared in polycarbonate (PC) and cuprammonium (CU) hollow-fiber minidialyzers with identical geometry, using an in vitro recirculation system with platelet-poor plasma (recirculation rate 20 ml/min; 1,600 fibers; 0.115 m2; 40 ml system priming volume; recirculation time 120 min). After extensive washing, residual protein was removed by reverse transmembrane pressure (1.5 bar) from the air-filled dialysate compartment. Such protein fraction, functionally defined as 'secondary membrane', was similar in quantity for PC and CU fibers. Plasma proteins were present in the membrane without selective adsorption (flat-bed polyacrylamide gel electrophoresis and rocket immunoelectrophoresis using monospecific antibodies). C3d, measured by immunoelectrophoresis, increased with time in the fluid phase compartment of both dialysers, but C3d generation was consistently and significantly (p less than 0.05) less in PC than in CU dialysers. The observation documents an activation of C3 with PC, in contrast to previous reports of no activation. However, C3 activation with PC was less intense than with CU.

Adsorption↗
PubMed1986

No 1,25-dihydroxyvitamin D3 receptors on osteoclasts of calcium-deficient chicken despite demonstrable receptors on circulating monocytes.

1,25-dihydroxyvitamin D3 (1,25(OH)2D3) is known to stimulate osteoclastic bone resorption in vivo and whole organ bone culture systems in vitro. It has not been established whether 1,25(OH)2D3 acts directly on osteoclasts or whether its action on osteoclasts is mediated via other bone cells (e.g., osteoblasts) or recruitment of osteoclast precursor cells. Circulating monocytes have been characterized as osteoclast precursors. In the present study, vitamin D3-replete chicken on a calcium-deficient diet were studied. Circulating monocytes, whole bone cell preparations, and isolated osteoclasts (differential sedimentation) were examined for presence of 1,25(OH)2D3 receptors. Reversible, specific, and saturable binding of [3H]-1,25(OH)2D3 to a 3.5 S macromolecule was demonstrated in nuclear fractions of monocytes (maximal binding capacity, 48 fmol/mg protein; dissociation constant, 1.3 X 10(-10) M) and of whole bone cell preparations. 1,25(OH)2D3 receptors were not demonstrable in osteoclast preparations (70% pure; detection threshold, 2 fmol/mg protein). Data are consistent with indirect action of 1,25(OH)2D3 on osteoclastic bone resorption.

Animals↗
PubMed1986

Vasopressin in hyponatremia: what stimuli?

In hypoosmolar hyponatremia, vasopressin is commonly observed to be less than maximally suppressed. This is attributed to the presence of nonosmolar vasopressin stimuli. However, the exact relationship of nonsuppressed antidiuretic hormone to specific circulatory parameters is controversial. Therefore, in the present study, we examined this question in 100 hypoosmolar hyponatremic patients in the Department of Medicine. Despite plasma hypoosmolality, vasopressin was found to be measurable in 92% of patients. Seventy patients suffered from edematous disorders (congestive heart failure, cirrhosis) or volume contraction per se; in these patients we observed unequivocal, though indirect, evidence of advanced circulatory alterations. These were associated with hyponatremia and nonsuppressed vasopressin. However, the latter could not be related directly to a specific circulatory parameter such as mean arterial blood pressure, creatinine clearance, plasma renin activity (PRA), norepinephrine, or aldosterone. However, patients with nondetectable vasopressin (n = 8) differed significantly from those with high vasopressin concentrations (n = 8: PADH greater than 9 pg/ml); in the latter, pulse rate (104 +/- 3 vs. 82 +/- 5 beats/min), plasma urea concentration (90 +/- 5 vs. 32 +/- 5 mg/dl), plasma urate concentration (7.2 +/- 0.8 vs. 3.6 +/- 0.8 mg/dl), and PRA (36 +/- 7 vs. 9.5 +/- 4.6 ng AI/ml/h) were all significantly higher than in the former. It is concluded that, in hyponatremia, the relationship between circulatory impairment and vasopressin is complex.

Creatinine↗
PubMed1986

Effect of angiotensin I converting enzyme inhibition on circulating atrial natriuretic peptide in humans.

We investigated the effects of inhibition of angiotensin II (ANG II) formation with an ANG I converting enzyme inhibitor, namely Enalapril, on circulating levels of atrial natriuretic peptide (ANP). Seven normal volunteers received a low sodium diet in order to stimulate the renin-angiotensin system (period I). Subsequently, subjects maintained their low dietary sodium intake and received Enalapril perorally (period II). Each study period lasted for 6 days. Results indicated that subjects maintained a low dietary sodium intake with expected changes of the renin system before and during ANG I converting enzyme inhibition. Enalapril elicited a substantial fall in circulating ANP levels in six of the seven subjects studied. The causes of this change will have to be established but may possibly relate to hemodynamic consequences of Enalapril.

Adult↗
PubMed1986

Loss of bone resulting from accumulation of aluminum in bone of patients undergoing dialysis.

The effects of accumulation of aluminum on cancellous bone mass and histomorphometric parameters of bone formation and resorption are evaluated in three separate studies: a cross-sectional study in 120 patients receiving long-term maintenance dialysis, including patients with and without stainable bone aluminum; a longitudinal retrospective study in eight patients receiving hemodialysis, who had progressive accumulation of aluminum in bone. These patients had two bone biopsies 11 to 16 months apart; a longitudinal prospective study in 10 patients receiving long-term hemodialysis, who had histologically proved renal osteodystrophy and stainable bone aluminum. These patients were given deferoxamine for 9 to 12 months. Repeat bone biopsies were done thereafter, and decrease or disappearance of stainable bone aluminum was observed. The results of the independent studies demonstrate that aluminum accumulation in bone is associated not only with disturbed mineralization but also with loss of cancellous bone mass, and that removal of aluminum from bone results in gain in bone volume. The mechanisms of this phenomenon are related to a disproportionately greater effect of aluminum on bone formation than on bone resorption. The negative effect on bone formation is caused by decreased number and activity of osteoblasts, which is reversed by removal of aluminum from bone. In addition, the data show that aluminum induces suppression of bone turnover, with uncoupling between bone formation and resorption whereby the effects on bone formation exceed those on bone resorption. Thus, fractures in patients with renal failure and accumulation of aluminum may result not only from osteomalacia but also from osteopenia.

Adolescent↗
PubMed1986

Endogenous calcitonin does not protect against hyperparathyroid bone disease in renal failure.

The paper challenges the widely held notion that calcitonin antagonizes effects of the parathyroid hormone (PTH) on bone and inhibits the development of hyperparathyroid bone disease in uremic patients. This was done by studying 16 patients on chronic maintenance dialysis with various levels of PTH and endogenous calcitonin. In addition, 2 patients with normal kidney function and high calcitonin levels due to medullary carcinoma of the thyroid were evaluated, one of them with an excessive, the other with a low-normal PTH level. Undecalcified bone histology was done in all patients and quantitative static and dynamic parameters of bone structure, bone formation, mineralization and resorption were correlated with serum calcitonin and PTH levels using Dunn's multiple comparison procedure. Covariables such as bone aluminum accumulation, immobilization or other diseases were taken into consideration or avoided. In contrast to the literature, no correlations were found between calcitonin and PTH or between calcitonin and bone histology, whereas PTH correlated with parameters of bone resorption and formation. One uremic patient with no circulating calcitonin and high PTH did not show excessive signs of PTH activity on bone. In addition, bone histology in the nonuremic patient with high PTH and high calcitonin did reveal signs of a PTH overactivity on bone which were not seen in the other nonuremic patient with high calcitonin only. These findings indicate that endogenous calcitonin is not protective against hyperparathyroid bone disease.

Adult↗
PubMed1985

[Drug treatment of chronic glomerulonephritis: contra].

It is controversial whether the pathomechanisms involved in chronic idiopathic glomerulonephritis are susceptible to therapeutic intervention. Etiological therapy, i.e. elimination of the responsible antigen, is possible only in exceptional cases, e.g. tropical diseases, infected ventriculoatrial shunt etc. Antiinflammatory therapy directed against pathomechanisms initiating or maintaining glomerular inflammation has an uncertain theoretical foundation because of lack of knowledge relating to the exact steps mediating tissue injury. Recent studies suggest keyroles for terminal components of complement system, products of lipoxygenase pathway of arachidonic acid and oxygen radicals-all of which are not readily influenced by available therapeutic modulaties. Finally, progression of glomerular inflammation to renal failure is usually not the cause of cumulative acute inflammatory glomerular lesions but rather the consequence of progressive sclerosis of glomeruli, arterioles and interstitium. As examples of controlled intervention trials, studies on extramembranous and membranoproliferative glomerulonephritis are discussed. The studies show limited and not always statistically significant influence on renal function, however, at the expense of considerable side effects. It is concluded that it is highly questionable whether inflammatory pathomechanisms are influenced by currently available drugs. However, therapeutic nihilism is not appropriate given modalities to influence mechanisms of nonspecific damage, e.g. by antihypertensive medication or dietary intervention.

Azathioprine↗
PubMed1985

The role of surface charge on the accelerating action of heparin on the antithrombin III-inhibited activity of alpha-thrombin.

We have compared surface charge and the surface charge density on the polyanions heparin and potassium polyvinyl sulfate (KPVS), as well as on hydrolyzed heparin and KPVS, with their accelerating effect on the inhibitory action of antithrombin III on thrombin. Polyelectrolyte titration of thrombin with KPVS or heparin at pH 7.4 clearly indicates an electrostatic interaction. In contrast, at the same pH no electrostatic interaction is observed between polyanions and antithrombin III. KPVS accelerates the inhibitory action of antithrombin III to the same extent as heparin on the basis of charge equivalence. Heparin and KPVS with a mean distance between two charged centers of less than 0.75 and 0.95 nm, respectively, accelerate strongly whereas hydrolysates with lower charge densities are far less active. The following observations are indicated. Intramolecular neutralization of oppositely charged residues occurs within thrombin, antithrombin III, and partially hydrolyzed heparin. Heparin acts on the antithrombin III-thrombin reaction through cooperative electrostatic binding to thrombin and nonelectrostatic interaction with antithrombin III. This indicates a quasi-catalytic action of the polyelectrolyte. Hydrolysis of only a few N-sulfate residues within the heparin molecule decreases the linear surface charge density to such an extent that the accelerating action is drastically reduced. The loss of accelerating capacity agrees with the sudden loss of counterion condensation due to the decrease of the linear surface charge density beyond limits postulated by Manning in a theory of polyelectrolytes.

Antithrombin III↗