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L Fricke

Publications and source records attributed to L Fricke.

49 records · Page 3Linked to original sources
PubMed1992

Beta2-microglobulinuria as an early sign of cytomegalovirus infection following renal transplantation.

The frequency of cytomegalovirus infection was studied in a prospective study of 106 kidney recipients. The detection of cytomegalovirus-immediate-early-antigen and cytomegalovirus-immunoglobulin (IgM) antibodies in serum was used as the reference method and showed that 23.6% (25/106) of all patients were infected. In addition, four urinary proteins (IgG and transferrin as glomerular markers and alpha1-microglobulin and beta2-microglobulin as tubular markers) were quantitatively measured in 24-h urine samples from all of the patients using an immunoluminometric assay (ILMA). In all cytomegalovirus infection cases a pronounced but isolated increase of urinary beta2-microglobulin excretion was observed. In 20 of 25 infected patients, the beta2-microglobulinuria occurred 1-21 days (median 5.0) earlier than the appearance of the cytomegalovirus-immediate-early-antigen in blood. Thus, it can be seen that the quantitative measurement of beta2-microglobulin in urine is useful for the early detection of cytomegalovirus infection following renal transplantation.

Biomarkers↗
PubMed1991

[Beta 2-microglobulinuria in cytomegalovirus infections following kidney transplantation].

In a prospective study the occurrence of cytomegalovirus (CMV) infection was diagnosed by demonstrating CMV-immediate early antigen (IEA) in the blood in 13 out of 68 (19%) patients who had undergone renal transplantation (27 women, 41 men, mean age 46.3 [21-64] years). Twenty-four hour urine samples were collected at the same time for quantitative determination of selected marker proteins by immunoluminometric assays (IgG and transferrin as glomerular markers, alpha 1-microglobulin and beta 2-microglobulin as tubular markers). In all 13 confirmed cases of CMV infection there was an isolated rise in urinary beta 2-microglobulin excretion amounting to more than three times the normal. In 11 of the 13 cases the beta 2-microglobulinuria was noted before the CMV-IEA test became positive. This suggests that quantitative assay of beta 2-microglobulin in the urine may be of value in the early diagnosis of CMV infection--a matter of some prognostic importance--and may hence offer additional support for therapeutic decisions.

Adult↗
PubMed1988

[Therapy of amyloid nephrosis in Crohn disease: plasmapheresis plus azathioprine?].

A 38-year old woman with serious nephrotic syndrome due to kidney amyloidosis in consequence of Crohn's disease was observed. The long-term prognosis of this illness is serious, but since in the literature several good results have been mentioned under treatment with immunosuppressives, in the present case an aggressive immunosuppression was carried out, which was started under the conception that, in consequence of elimination of preamyloid substances from the serum by plasmapheresis in combination with an additional inhibition of the reproduction of these substances by azathioprine, the clinical picture could be favourably influenced. During therapy with long-term intermittent plasmapheresis in combination with azathioprine a complete remission of the nephrotic syndrome was achieved.

Adult↗
PubMed1986

[Initial experiences with PTA of hemodialysis shunts].

Our experience of using PTA for stenoses of haemodialysis fistulae in 11 cases is described. PTA is the procedure of choice for re-establishing adequate shunt function. Intraluminal pressure measurements on the venous limb of well functioning Cimino shunts produced values of 7.5 to 44.5 mmHg, average 24.5 mmHg. These values are the basis for judging the success of a dilatation. Shunt angiography with DSA with a highly diluted non-ionic contrast medium injected via a remaining dialysis needle is an effective procedure with minimal discomfort to the patient.

Angioplasty, Balloon↗
PubMed1978

Increased histidine and histamine content in the brain of chronic uremic rats. Cause of enhanced cerebral cyclic adenosine monophosphate in uremia?

In rats with experimental chronic renal insufficiency (90% nephrectomy) the histidine content in brain was increased (+ 35%) in spite of normal plasma values and decreased concentrations in the striated muscle (-23%). The finding of a raised histidine level in the brain seems to be a uremia specific disorder, probably cuased by a local disturbance in histidine metabolism. In addition an increase of the histidine decarboxylation product histamine could be observed in the brain of rats with chronic renal insufficiency, as compared to pair-fed controls. This increase was directly related to the severity of azotemia. In the pathogenesis of the histamine alteration the increased histidine content in the brain of uremic rats must be considered, since the specific histidine decarboxylase is not saturated by the normal endogenous level of the amino acid precursor. Probably the increased histamine contributes to the raised cerebral cyclic AMP in the brain of uremic rats.

Animals↗
PubMed1977

Intracellular histidine content of various tissues (brain, striated muscle and liver) in experimental chronic renal failure.

Intracellular histidine levels were determined in brain, striated muscle and liver of rats with chronic renal insufficiency (5/6-nephrectomy) and compared both with normal rats and food-restricted (pair-fed) animals. There was no difference in plasma histidine concentration of the three groups whereas in the brain of the uremic rats histidine was significantly increased. Since there existed no alteration of the cerebral histidine in the corresponding pair-fed group, the finding of a raised histidine level in the renal insufficient rats seems to be due to a specific uremic disorder caused by a cerebral disturbance in histidine metabolism.

Animals↗
PubMed1975

[Raised cAMP content of striated muscle in experimental chronic renal failure (author's transl)].

3', 5'-Adenosine monophosphate (cAMP) levels were determined in skeletal and heart muscle tissue of rats in chronic renal failure. Compared to normal animals no alteration in cAMP concentration was observed in heart muscle, whereas the cAMP levels in skeletal muscle were increased by 34%. This cAMP rise may be caused by the elevated plasma catecholamines, glucagon or parathyroid hormone levels in uraemia. The results suggest that the increased cAMP levels in skeletal muscle of rats in chronic renal failure contribute to the raised cAMP levels in the plasma.

Animals↗
PubMed1975

[Increased cAMP concentration in parotid secretion in arterial hypertension: relationship to plasma-renin activity (author's transl)].

Hypertensives with normal and increased plasma-renin activity have an increased salivary excretion of cyclic adenosine monophosphate (cAMP) such as can be obtained in normal persons by stimulation of beta-adrenergic fibres. Propanolol, as a beta-receptor blocker, reduces such increased cAMP levels in hypertensives to minimal levels. The results suggest that beta-receptors are stimulated in hypertensives with normal or increased renin activity.

Cyclic AMP↗