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Biomedical subjects

E Ritz

Publications and source records attributed to E Ritz.

At least 847 records · Page 47Linked to original sources
PubMed1981

Antibody coating of bacteria in experimental infection of the urinary bladder.

We studied antibody coating of urinary bacteria in experimental cystitis of the rat both in the absence and presence of a foreign body (polyacrylamide sphere). In the absence of a foreign body, inoculation of the bladder urine resulted in generally transient bacteriuria with no significant antibody coating or defects in the bladder uroepithelium, lymphocytic infiltration of bladder mucosa, or plasma cells in the bladder mucosa. Inoculation in the presence of a foreign body resulted in protracted bacteriuria with significant antibody coating of urinary bacteria, defects in the bladder mucosa surface, lymphocytic infiltration of the bladder mucosa, and numerous plasma cells. We conclude that the bladder mucosa is capable of mounting a local immune response against bacterial invasion which leads to antibody coating of urinary bacteria.

Animals↗
PubMed1981

[Hypertension following renal transplantation (author's transl)].

Hypertension is more frequent in transplant recipients than in the general population. The two most frequent causes are reduced function of the transplant and the presence of the recipient's own kidneys. Beyond the immediate postoperative period, administration of glucocorticoids appears to have little influence on blood pressure. The various forms of arterial stenosis of the transplant are infrequent, but clinically important, because they are susceptible to surgical correction or arterial dilatation. The pathogenetic mechanisms and diagnostic problems of the various forms of posttransplant-hypertension are discussed in this review.

Glucocorticoids↗
PubMed1981

Silicone filings in macrophages of viscera: an iatrogenic complication of haemodialysis.

In seven long-term dialysis patients, autopsy material showed varying amount of refractile foreign material in macrophages and giant cells of lung, liver, spleen, bone marrow, skin, thoracic and abdominal lymph nodes, but not in brain, heart, kidney or endocrine organs. Electron microscopy showed its presence within lysosomal membranes of macrophages. Such material was also demonstrable in liver biopsies of patients dialysed for only several months. Possible clinical consequences were hepatosplenomegaly, elevation of transaminases, hypersplenism with pancytopenia and possibly bile duct carcinoma. SEM with X-ray fluorescence showed particles within spleen and liver cells with a characteristic Si K alpha 2.09 kev peak. Identical material was found as fillings on silicone tubing exposed to roller pumps.

Humans↗
PubMed1980

Isotachophoretic determination of urinary citrate in native urine.

The technique of isotachophoresis has been used to develop a specific and sensitive method for the determination of citrate in unprocessed urine. The specificity of the isotachophoretic method was assessed using citrate lyase which caused disappearance of the isotachophoretic citrate signal. The isotachophoretic method compared favourably with the enzymatic method (citrate lyase) for urinary citrate. The normal range for urinary citrate in 25 healthy individuals, as found by isotachophoresis, was 0.33-2.89 mmol/24 h with a mean of 2.1 mmol/24 h.

Citrates↗
PubMed1980

Lack of involvement of sarcoplasmic reticulum in myopathy of acute phosphorous depletion.

Acute and chronic hypophosphatemia are known to cause metabolic myopathy. It has been proposed that impaired Ca transport in subcellular membranes is involved in its genesis. In the present study, calcium transport in the sarcoplasmic reticulum (SR), concentrations of ions or nucleotides and transmembrane potential were investigated in muscles of acutely hypophosphatemic rats, i.e. animals with chronic dietary phosphorous deprivation (PD) and superimposed acute hypophosphatemia resulting from the administration of insulin and glucose. Despite hypophosphatemia and low muscle phosphorous concentration, no significant change of the initial rate of Ca uptake or Ca concentrating ability was observed in the SR of PD rats. Storing capacity was decreased; this may result from altered vesicle geometry. Water content, Na concentration, the concentration of several nucleotides and transmembrane potential of muscle were unchanged in PD rats. The findings document that no intrinsic abnormality of vectorial Ca transport is present in the SR of acutely hypophosphatemic PD animals.

Animals↗
PubMed1980

Interstitial nephritis in a patient with atypical Sjögren's syndrome.

A patient was observed with interstitial nephritis which resulted in renal tubular acidosis (distal type), tubular proteinuria and defective urinary concentrating ability in the absence of edema, elevated arterial blood pressure, glomerular proteinuria or abnormal urinary sediment. The presence of interstitial nephritis was established by renal biopsy which showed dense infiltrates in the interstitium, interstitial fibrosis and thickening and splitting of the pericapillary basal membranes. Immunofluorescence was non contributory. Extrarenal symptoms were discrete (arthralgia of both hands, Raynaud's syndrome upon cold exposure). Mixed connective tissue disease (MCTD) was suspected because of a positive ANF test (speckled pattern), which was completely abolished by ribonuclease pretreatment. However, in hemagglutination tests, no antibodies against ribonuclear protein (ENA) could be demonstrated. The diagnosis of Sjögren's syndrome was established by demonstration of antibodies against SSA and SSB antigens. The observation suggests that in patients with interstitial nephritis the diagnosis of Sjörgren's syndrome must be considered even if extrarenal symptoms of Sjögren's disease are minimal or lacking. The diagnosis can be established with recent serological techniques.

Adult↗
PubMed1980

Urinary sodium excretion in renal stone formers. An epidemiological study.

In the present investigation 238 randomly selected male individuals of the general population (age 19--41 years) and 42 age-matched male patients with recurrent renal stone formation (calcium oxalate and/or calcium phosphate) were studied under outpatient conditions without dietary restrictions. Urinary Na excretion was 207 +/- 82 mmol/24 h (range 55--570) in controls and 208 +/- 100 (range 76--575) in recurrent renal stone formers. Both in controls (r = 0.36; p less than 0.01) and in stone formers (r = 0.4; p less than 0.01) a significant correlation was observed between urinary excretion of sodium and calcium. Urinary sodium excretion was unrelated to systolic or diastolic blood pressure in normotensive or hypertensive individuals. This finding indicates that factors other than sodium are involved in the maintenance of hypertension. Urinary sodium, presumably an index of intake of nutrients, was significantly correlated to several coronary risk factors, e.g. fasting glucose, cholesterol and overweight. There existed a significant inverse relationship between fasting plasma phosphate and urinary sodium, but not between fasting plasma phosphate and serum iPTH or urinary cAMP. This finding points to some function of sodium excretion as one determinant of plasma phosphate.

Adult↗
PubMed1980

Viral hepatitis A and B in hemodialysed patients.

In 113 hemodialysed patients, 167 hospitalized patients, and 143 outpatients the frequency of HAV and HBV markers were studied by testing HBsAg, anti-HBs, anti-HBc, HBeAg, anti-HBe, and anti-HAV. The hemodialysis patients in a dialysis-center had significantly more often HBV markers (85.7%) than those maintained on home-dialysis (46.5%). 29.9% of the hospitalized patients and 32.1% of the outpatients had HBV markers. By the anti-HBc test up to 41% of additional HBV infections could be detected.--The prevalence of anti-HAV was very high in all groups. Significant differences between the hemodialysis patients and the control groups existed only in the age groups up to 39 years.--The frequencies of HAV and HBV markers were related to age, duration of dialysis treatment, transfusional frequency, and transaminases. The HBV appeared as the clinically important hepatitis agent in dialysis.

Adult↗
PubMed1980

Stauffer's syndrome in renal cell carcinoma evidence for intravascular coagulation.

In 40 patients with non-metastasising (n = 31) and metastasising (n = 9) renal cell carcinoma, evidence of Stauffer's syndrome (increase in alkaline serum phosphatase and prolongation of prothrombin time) was found in 18 patients. Prolongation of prothrombin time was not due to depletion of vitamin K-dependent coagulation factors or manifest fibrinolysis, but due to the presence of circulating fibrinogen fibrinmonomer-FDP complexes. Ethanol gelation test was found to be positive in 28/40 subjects and soluble fibrin monomer complexes were increased in 38/40 patients. The resulting disturbance of fibrinogen-fibrin conversion was reflected by an increase in thrombin coagulase time and reptilase time. These findings suggests a state of latent compensated intravascular coagulation (presumably triggered within the vascular tumor). For diagnostic purposes the most sensitive indicator is thrombin coagulase time. Thrombin coagulase time normalised after tumor resection and was positive in patients with recurrent metastases. The increase in alkaline serum phosphatase was due to an increase in the hepatic isoenzyme. Such an increase was much more common than the elevation of total alkaline serum phosphatase. Regan's isoenzyme was only found in 1 subject. In parallel, gamma-GT was elevated in 24 patients. The study shows that Stauffer's syndrome occurs more frequently than commonly assumed when thrombin coagulase time, gamma-GT and the hepatic isoenzyme of alkaline serum phosphatase are determined in patients with renal cell carcinoma. DIC and low grade fibrinolysis may account for the coagulation abnormalities of the syndrome.

Adenocarcinoma↗
PubMed1980

[Phosphate-depletion (author's transl)].

The essential and critical role of inorganic phosphate has been known in veterinary medicine and experimental research on animals for decades. However, only recently has the phosphate depletion syndrome found widespread attention by clinicians. Hypophosphatemia is usually observed in the following clinical situations:chronic alcoholism, recovery phase of diabetic ketoacidosis, administration of phosphate-free solutions in parenteral nutrition, severe respiratory alkalosis, and infusion of fructose. Disturbed organ function in hypophosphatemia is the result of a depletion of inorganic phosphate in the cytoplasm of somatic cells. Such phosphate depletion may be due to either of the following mechanisms or a combination of both. (1) Negative external phosphate balance resulting from phosphate loss in urine or feces or (2) translocation of phosphate from the extracellular into the intracellular space with or without concomitant negative external phosphate balance. In principle, phosphate depletion interferes with the function of all somatic cells. In acute phosphate depletion, the clinically most important disturbances are observed in striated muscle (rhabdomyolysis with myoglobinuric acute renal failure), heart muscle (acute heart failure), and hematological systems (hemolysis, disturbed leukocyte and thrombocyte functions). In contrast, in chronic phosphate depletion skeletal abnormalities (osteomalacia) predominate. Organ disturbances are thought to result from diminished synthesis of ATP and other organic phosphate esters and/or from hypoxia secondary to changes in erythrocyte 2,3-DPG.

Acute Kidney Injury↗
PubMed1980

Phosphate, calcium and lipid metabolism.

Ca and Pi interact with lipid metabolism in several different ways. The enzymes of lipolysis and lipogenesis are sensitive to Ca. Ca and Pi concentrations affect insulin secretion and insulin action. Raising intestinal Ca lowers serum cholesterol and triglycerides presumably by sequestration of cholesterol and bile acids. Administration of vitamin D or increased sensitivity to vitamin D raise serum cholesterol levels. PTH acts primarily by activating adipose tissue lipase. Increased FFA delivery to the liver should increase hepatic lipoprotein synthesis. Experimental data in secondary hyperparathyroidism of renal insufficiency are consistent with this notion. Clinical observations in primary or renal secondary hyperparathyroidism, however, are not explicable by this simple schema.

Adipose Tissue↗
PubMed1980

Function of the sarcoplasmic reticulum (SR) in hypophosphatemic myopathy.

Lipid composition and Ca2+ transport properties were examined in the isolated sarcoplasmic reticulum of non-exercised muscles of markedly phosphorus depleted rats. Phosphorous depletion with a fall of plasma Pi from 8.04 +/- 0.85 to 2.56 +/- 0.48 mg/dl was accompanied by a decrease in muscle Pi and ATP content and by a significant decrease in the phospholipid/protein ratio of sarcoplasmic reticulum. The phosphatidyl -choline/phosphatidyl-ethanolamine ration in sarcoplasmic membranes was increased. Storing capacity for Ca2+ was significantly diminished. In contrast, there was no significant change of kinetic parameters of Ca2+ transport, i.e. of the initial rate of uptake and concentrating ability. These findings do not necessarily exclude changes of cytosolic Ca2+ concentration in phosphate depletion, but they exclude alterations of intrinsic kinetic properties of the sarcoplasmic reticulum as a cause of any such potential changes.

Animals↗
PubMed1980

Abnormalities of glycogen metabolism in cardiomyopathy of phosphorous depletion.

In severely phosphorous depleted rats, no change of glycogen content or activities of enzymes catalysing glycogen synthesis or breakdown was observed. In contrast in heart muscle, a decrease of myocardial glycogen content was observed which was accompanied by increased activity of phosphorylase and decreased activity of synthetase. It is assumed that these changes result from increased catecholamine action secondary to an activation of the sympathetic nerve system resulting from impaired contractile state of the myocardium. The changes observed are analogous to those found in heart failure.

Animals↗
PubMed1980

Acquired cystic transformation of the kidneys of haemodialysed patients.

In the present study, the kidneys of patients who had been on maintenance haemodialysis for variable periods of time were examined at autopsy. In 21 of the 22 patients, multiple pinhead-size to pea-size, non-loculated cysts were observed both in the cortex and the medulla. In some of the cysts (4/20 patients), papillary adenomata were observed which were visible by light microscopy in 3 cases and macroscopically in 1 case. Clinical complications resulting from haemorrhage or neoplastic transformation were not observed in any of the patients of this series. Similar cysts, smaller in size and fewer in number, were also observed in kidneys of uraemic patients who had not been dialysed. Thus, the lesion does not appear to be a specific consequence of maintenance haemodialysis. It appears more likely that extensive cystic transformation of the kidneys of patients in terminal renal failure is made possible by prolonged survival on maintenance haemodialysis. The possibility of malignant transformation of the papillomata cannot be refuted, but epidemiological surveys fail to document more frequent occurrence of renal carcinoma in dialysed patients.

Adult↗
PubMed1980

Chromosomes in tumors derived from mouse tumor x diploid cell hybrids obtained in vitro.

Hybrids formed in vivo between Cl.1D tumor cells and host cells have been shown to carry a copy of each chromosome pair contributed by the host cell parent (1). However, in these hybrids, the tissue type of the host cell parents remained unknown. In the present study, hybrids between the malignant Cl.1D fibroblasts and either normal diploid fibroblasts (CF hybrids) or normal thymocytes (CT hybrids) were examined. These hybrids produced tumors when injected into host mice. Metaphases of growing hybrid cell tumors were analyzed. Neither CF nor CT malignant hybrids showed loss of any specific chromosome pair contributed by the normal cell parent. Since elimination of any chromosome pair contributed by the diploid fibroblast parent is not a prerequisite for CF hybrid tumoral growth, it seems unlikely that malignancy of hybrids results from nonexpression of normal alleles of those genes putatively implied in malignancy of Cl.1D cells.

Aneuploidy↗