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Biomedical subjects

E Ritz

Publications and source records attributed to E Ritz.

At least 685 records · Page 38Linked to original sources
PubMed1987

The charted and the uncharted waters of hyponatremia.

It was observed that hyponatremia has been evaluated by many studies of patients and laboratory animals. In virtually all of these the presence of nonosmotic ADH has been shown, but several details of this relationship remain controversial at this time. The role of specific receptor areas for ADH stimulation requires further study, particularly in the hyponatremia of a decreased effective arterial blood volume. In addition, it will be important to define the suspected vascular effects of nonosmotic ADH more specifically. Other areas of uncertainty include: the degree to which the tubular effect of ADH in hyponatremia may be modified by a decreased delivery of fluid to the loops of Henle; the potential stimulation of ADH by stress in clinical hyponatremia; and the meaning of very low or non-measurable concentrations of ADH in hyponatremia. New experimental tools such as vasopressin antagonists and agonists, measurements of baroreceptor input, and tests of proximal fluid reabsorption can be expected to clarify some of these questions in the near future.

Animals↗
PubMed1987

Determinants of plasma beta 2 microglobulin concentration: possible relation to membrane biocompatibility.

Beta 2 microglobulin (beta 2m) concentrations were measured by radioimmunoassay in the serum of haemodialysed patients. beta 2m was higher in males (n = 48) than in females (n = 26), i.e. 40.3 +/- 10.1 mg/l (SD) vs 31.2 +/- 8.0, P less than 0.01). beta 2m was not significantly higher in patients with bone cysts (37.7 +/- 11.4 mg/l vs 37.0 +/- 10.0), but median duration of dialysis was significantly (P less than 0.01) longer in patients with bone cysts (90 vs 57 months). beta 2m was lower in patients maintained on dialysis for less than 1 year and whose residual urine volume was greater than 0.1 litre per day. During one single session of dialysis, using cuprophane membranes, beta 2m increased acutely at 15 min and had risen by 32.4% at the end of the dialysis session, more than could be explained by haemoconcentration. In contrast, beta 2m acutely decreased by 38.7% during a single session using polysulphone membranes and the steady state predialysis values were lower by 37.1% after two weeks intermittent haemodialysis with polysulphone membranes. After re-exposure to cuprophane serum beta 2m increased to the original value. It is concluded that beta 2m concentrations on dialysis are a function of residual urinary volume, sex, and type of membrane used. Data are consistent with effective removal of beta 2m by membranes with high cut-off.

Biocompatible Materials↗
PubMed1987

Genetic polymorphism of C3 and Bf in IgA nephropathy.

C3 and Bf alleles were examined in the general population, in 67 patients with biopsy-confirmed mesangial IgA nephropathy and 81 patients with other types of glomerulonephritis, from the Heidelberg and Leiden renal programmes respectively. In both populations, a significant excess of homozygous phenotype C3FF (3.4% in controls; 10.4% in IgA nephropathy) and a deficit of C3FS heterozygous phenotype (35.8% in controls; 19.4% in IgA nephropathy) were observed in patients with IgA nephropathy, but not in other types of glomerulonephritis. No difference of C3 gene frequencies was found. C3FF was associated with an adverse clinical outcome (a higher prevalence of renal failure and hypertension). A significant excess of Bf-F gene frequency was noted (0.20 in controls; 0.33 in IgA nephropathy). In addition, an excess of phenotype BfFF was found (none in controls; 10.4% in IgA nephropathy). BfFF homozygotes also carried a higher risk of an adverse outcome (renal failure and hypertension). The data suggest a role for genetically coded (presumably) immunological factors in the genesis and course of IgA nephropathy.

Adult↗
PubMed1987

Recombinant human erythropoietin therapy in haemodialysis patients--dose determination and clinical experience.

Recombinant human erythropoietin (R-Hu-EPO) was given to stable, long-term haemodialysis patients with haematocrit less than or equal to 25% who required no blood transfusions. Thirteen patients were initially given R-Hu-EPO at 24 U/kg i.v. at the end of each dialysis session, with a doubling of the dose every second week until a dose of 96 U/kg (n = 6) or 192 U/kg (n = 7) was reached after 8 weeks. In addition, three patients were given 24 U/kg for 2 weeks and subsequently 48 U/kg for 14 weeks. Median haematocrit increased from 19.4% (14.8-24.3) to 30.0% and 32.5% with 96 or 192 U/kg respectively. Starting 7 days after R-Hu-EPO a log dose-dependent increase in reticulocyte counts was noted. A consistent decrease in ferritin concentrations was observed despite oral supplementation of iron. A continuous rise in platelet counts was noted. Irrespective of blood-pressure status, predialysis blood pressure increased in six of nine patients who were not on antihypertensive medication; increased antihypertensive therapy was required in the others. A rise in bilirubin within the normal range was seen at the end of the study. No severe clinical side-effects occurred; specifically, there were no thrombotic episodes with the exception of clotting of two fistulae with known stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

No evidence for endotoxin transfer across high flux polysulfone membranes.

Recently, there has been some concern that high-flux membranes may expose dialysis patients to the risk of endotoxin transfer secondary to backfiltration within the dialyzer. To evaluate the safety of high-flux polysulfone dialyzers, we examined in an in vitro recirculation system whether lipopolysaccharides (LPS) and lipid A respectively penetrate from the dialysate to the blood compartment and vice versa using a F-60 hemofilter (Fresenius AG). For the detection of endotoxin, a sensitive, kinetic limulus amebocyte lysate (LAL) microtiter test was used. It can be concluded that LPS and lipid A do not pass from either side through the filter system used when saline was recirculated for more than 10 h on both sides of the membrane.

Blood↗
PubMed1986

[Kidney function in lead burden].

Renal failure as a consequence of manifest lead intoxication (nephropathia saturnina) has almost completely disappeared in the FRG. However, there has been rising concern that increased lead burden, primarily as a result of environmental pollution, may adversely affect blood pressure and renal function even in the absence of extrarenal signs of lead intoxication. Such concern is based on epidemiological studies which demonstrated a relation between blood lead level and blood pressure and on experimental studies which showed that lead activates several pressor mechanisms. Furthermore, increased body lead burden is found in a substantial proportion of patients with renal failure, particularly when concomitant gout is present. Unfortunately, none of the above findings constitute irrefutable evidence and further studies are clearly necessary.

Calcium↗
PubMed1986

Amyloid kidney stones of uremic patients consist of beta 2-microglobulin fragments.

Urinary stones with amyloid structure, obtained from uremic patients, were analyzed according to molecular weight, amino acid sequence, and antigenic content. A major protein of approximately 7 kD, designated AB protein, was isolated by size exclusion using HPLC in 60% formic acid. AB protein reacted in immunodiffusion only with an antiserum to beta 2-microglobulin, with beta 2m spurring over AB protein. N-terminal amino acid sequence analysis defined two fragments homologous to beta 2m. One fragment commenced with Ile at position 7 and the other with Ser at position 20, with a cleavage point subsequent to a lysyl residue in both. It is concluded that beta 2m is a precursor of urinary amyloid stones and intratubular concretions of patients with preterminal and terminal renal failure; limited proteolysis is involved in AB amyloid generation.

Amino Acid Sequence↗
PubMed1986

[Acute kidney failure caused by Hantaan virus. Case report from the West Germany].

A man aged 41 years who spent his leisure time in a marshy region infested with brown rats developed an infectious disease with high fever associated with diarrhoea, arthralgia and lumbago. In the course of the disease an acute renal failure occurred not requiring dialysis which spontaneously receded. Histology revealed signs of an acute renal failure with sparse interstitial round-cell infiltrations. Serological investigations showed a rising titre against Hantaan virus, Strain CG 1820 (1:1024). According to experience in neighbouring countries, it may be assumed that quite a number of cases of spontaneous acute renal failure occurring in the Federal Republic of Germany is caused by Hantaan virus.

Acute Kidney Injury↗
PubMed1986

Urinary sIgA in children with urinary tract infection.

Urinary secretory IgA (sIgA) was measured using a specific ELISA with insolubilized anti-IgA and enzyme-linked antisecretory component. This test was applied to unprocessed urine from healthy children and from children with urinary tract infection. Normal range was a function of age. In 175 healthy children the excretion rate of sIgA was low in infants younger than 6 months but was constant between ages 6 months to 15 years (median 0.69 mg/gm creatinine, range 0.15 to 3.4 mg/gm creatinine), whereas sIgA concentration (milligrams per liter of urine) increased continuously with age. No sex difference was noted. There were no significant circadian changes or day-to-day variability. Thirty girls, age 1 to 16 years, were examined; they had a history of recurrent symptomatic episodes of urinary tract infection but had anatomically normal tracts and no symptoms, and no bacteriuria at the time of study. sIgA excretion rate was significantly lower (0.45 mg/gm, creatinine, 0.08 to 0.75 mg/gm creatinine) than in controls. In contrast, 11 girls examined at the time of symptomatic urinary tract infections, and who had normal urinary tracts, had significantly (P less than 0.01) higher sIgA excretion rates (1.4 mg/gm creatinine, 0.8 to 3.4 mg/gm creatinine) than those in either control subjects or girls without symptoms at the time of study. Urinary sIgA excretion rates were highest (2.0 mg/gm creatinine, 0.44 to 3.69 mg/gm creatinine) in children with symptomatic urinary tract infections who had an abnormal urinary tract. We conclude that low urinary sIgA values may be a marker for recurrent symptomatic bacteriuria in girls with normal urinary tracts.

Adolescent↗
PubMed1986

Reduced chronotropic responsiveness of the heart in experimental uremia.

Cardiac beta-adrenoceptor responsiveness was evaluated in experimental uremia by in vivo and in vitro techniques. Uremia was induced in rats by bilateral nephrectomy for 48 h. In rats with chronic intra-arterial and intravenous catheters, cardiovascular reflexes and the renin-angiotensin system were blocked with atropine, pentolinium, and a converting-enzyme inhibitor, respectively. Blood pressure (BP) and heart rate (HR) were continuously recorded. Cumulative doses of isoproterenol were injected intravenously. In uremic rats, the dose-response curve for the HR response showed a lower maximal response (P less than 0.01) and no significant difference in 50% effective dose values compared with controls, whereas the BP decrease caused by isoproterenol was similar in control and uremic rats. When forskolin was injected intravenously to stimulate adenylate cyclase in a receptor-independent manner, the maximal HR increase was lower in uremic rats (P less than 0.01). beta-Adrenoceptor density and affinity, measured by 125I-cyanopindolol binding to sarcolemmal membranes, was not different between control and uremic rats. Also binding affinities for the agonist isoproterenol were not different between groups. Basal adenylate cyclase activity, as well as activity after maximal stimulation by isoproterenol and by forskolin were lower in uremic than in control rats (P less than 0.01). The results show that the chronotropic response of the heart is reduced in uremia. Such hyporesponsiveness may be due, at least in part, to a reduced activity of cardiac adenylate cyclase.

Adenylyl Cyclases↗