Biomedical subjects

F Schabel

Publications and source records attributed to F Schabel.

31 records · Page 2Linked to original sources

PubMed1978

[Thrombosis of the renal artery in a newborn (author's transl)].

Very rare informations about thrombosis of the renal artery in newborns in the literature could be found. In a six years old girl in the course of a perinatal asphyxia complicated by shock a renal artery thrombosis was observed. Profuse bleeding, anemia, thrombopenia, prolonged bleeding time and coagulation time and a low percentage of the thrombotest suggested an intravascular coagulation as a possible factor of this disease. The treatment of the coagulopathia was effective. The physical and psychical development of the girl is normal. The inhibition of the renal function, however, is in a compensated state.

Child Development↗

PubMed1978

[Renal glycosuria with loss of phosphate (author's transl)].

Three of six members of one family have a renal glycosuria of variable degree. In addition to this they have a mild loss of phosphate under normal conditions. In one patient the phosphate-loss becomes very high after a loading dose. After describing the different data the mechanism of renal glucose transport and its relationship to phosphate transport as well as the genetic of renal glucosuria are discussed. The combination of renal glycosuria and renal loss of phosphate is very rare. The difference in regard to gluco-phosphaturia is mentioned.

Adult↗

PubMed1978

[Tubular secretion of phosphate in the human kidney (author's transl)].

There are a few scattered publications on primary tubulopathies, where a net secretion of phosphorus by renal tubules, a mechanism usually not existing in man, is shown. By means of a further case, we are able to demonstrate a 30% increase of phosphate excretion over filtration after a phosphate load. The mechanism of action will be discussed. Under certain conditions like a rapid increase in serum phosphorus or after volume expansion a tubular secretory mechanism of phosphate can be unmasked. As this secretory mechanism goes into action only beyond a certain serum threshold of phosphorus and a transport maximum cannot be shown it is most likely that passive transport by means of an increased diffusion cell to lumen is the proposed mechanism involved.

Adolescent↗

PubMed1978

[Anaphylactoid purpura in infancy and childhood (author's transl)].

The clinical picture and the laboratory data of 40 patients with anaphylactoid purpura as well as its etiology and pathogenesis are discussed. The clinical expression and the rate of complications does not differ from that described in the literature. 45% of the patients showed renal involvement, three patients had severe glomerulonephritis. Up to now there is a lack of typical laboratory tests to confirm the diagnosis of anaphylactoid purpura. This study suggests neutrophilia and initial creased fibrin/fibrinogen split products in serum and decreased C3 levels are poor prognostic criteria correlating with appearence and severity of a complicating glomerulonephritis.

Adolescent↗

PubMed1977

[Tubular and intestinal phosphate transport in vitamin D-resistant (hypophosphatemic) rickets (author's transl)].

Renal clearance and intestinal absorption studies were performed to investigate the renal and intestinal handling of phosphate under various conditions in two female patients with VDRR. The two types of transepithelial phosphate transport in the renal proximal tubule and intestinal mucosa are discussed. The defective parathormone sensible transport mechanism is slightly depressed under the influence of parathormone and activated after treatment of vitamin D in one patient, in the other no further inhibition by PTH could be observed. Electrolyte excretion in urine remains stable during treatment with vitamin D 3. Therapy consists of administration of oral phosphate and of pharmacologic doses of vitamin D.

Child↗

PubMed1977

[Acid-base balance during exchange transfusion (author's transl)].

During exchange transfusion with ACD blood severe metabolic acidosis may occur. ACD blood contains increasing amounts of acid which depends on the age of the blood. The mature newborn infant has different ways to compensate metabolic acidosis: the lungs, the immature kidneys and the conversion of citrate to bicarbonate. In preterm infants as well as in newborns with respiratory distress syndrome and mechanical ventilation the compensatory mechanisms may be reduced or even absent. Therefore ACD blood may lead to severe complications. To prevent acidosis adequate buffering with TRIS is recommended.

Acidosis, Respiratory↗

PubMed1977

[Polycythemia in the newborn infant (author's transl)].

Respiratory distress syndrome and cyanonis in newborns (first neonatal week) may be caused by polycythemia. During 14 months twentyone newborns with symptoms of cardiorespiratory or neurological distress caused by polycythemia on the neonatological division of our hospital were observed. The values of hemoglobin ranged between 22.7 and 28.6 g% (mean 25.65 g%), the values of hematocrit ranged between 72 and 90% (mean 81%). The central venous hematocrit measured on 14 patients ranged between 65 and 77% (mean 71%). On 20 newborns isovolemic haemodilution by 5% plasma was performed. The volume of exchange was calculated according to the formula: Sign and symptoms seemed to improve rapidly following treatment, clinically reflecting the fall in hemoglobin and hematocrit.

Exchange Transfusion, Whole Blood↗

PubMed1976

[Burkitt's lymphoma (author's transl)].

Burkitt's lymphoma occurs endemically in Central Africa, but is also found sporadically in areas with temperate climate. A case of Burkitt's lymphoma found in our area is described. The literature in regard to the clinical symptoms, etiology and treatment of Burkitt's lymphoma is reviewed. At the present time cyclophosphamide is considered to be the drug of choice; it leads to a remission rate of about 90%.

Antibodies, Viral↗

PubMed1976

[Medullary sponge kidney: a short review and a report of two cases (author's transl)].

Radiologically the collecting tubules in the medulla are dilated up to cystic proportions. There may be no clinical symptoms, but frequently the dilated tubules predispose to infection and lithiasis. Such cysts do not interfere with renal function. X-ray diagnosis, frequency, therapy and etiology are discussed. Two further cases of MSK in childhood are described.

Adolescent↗

PubMed1975