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Biomedical subjects

R Heintz

Publications and source records attributed to R Heintz.

At least 55 records · Page 3Linked to original sources
PubMed1976

[Amyloidosis in familial mediterranean fever: clinical and renal-biopsy features (author's transl)].

In two Turkish female patients, aged 14 and 29 years, with familial mediterranean fever amyloidosis of the perireticular type was found. The disease was characterized by feverish bouts, abdominal colics, and joint involvements. The younger patient had the diagnosis confirmed at an early stage by renal biopsy, and under heparin and azathioprine the clinical signs, especially the nephrotic syndrome, regressed over a period of seven months. The second patient died of treatment-resistant shock in acute renal failure, due to rapidly progressing renal amyloidosis.

Acute Kidney Injury↗
PubMed1976

[Number and kinds of drug side-effects in a medical clinic (author's transl)].

All drug side-effects - definite, probable and suspected - were noted during one year in 1592 patients. The severity of the side-effects was classified into mild (15%), moderate (6.5%), and severe (1%) forms. Fatal side-effects occurred without exception only in those patients who were severely ill so that any risk of treatment had been fully justified. Among patients with renal failure, malignant haematological diseases or Hodgkin's disease there was a particularly high incidence of side-effects. Although the proportion of the latter patients was only 15% of all in-patients, they accounted for 35% of patients with side-effects.

Adrenal Cortex Hormones↗
PubMed1976

Plasma renin activity (PRA) and aldosterone (PA) in patients with chronic glomerulonephritis (GN) and hypertension.

Patients with chronic glomerulonephritis and mild hypertension show a consistent behaviour in their renin-aldosterone-system. There is a close correlation between the elevation of mean blood pressure and destruction of glomeruli. No correlation has been found between renin values and the degree of hypertension. Thus the cuase of mild hypertension occurring in the early stages of chronic GN remains to be elucidated. Normal PRA values in spite of hypertension and expansion of ECFV accompaning progression of chronic glomerulonephritis could be a sign of "relative hyperreninemia". Apparently various mechanisms are involved in the pathogenesis of renal hypertension. These include sodium retention, increased cardiac output. anemia, renin, aldosterone, prostaglandins, expanded plasma volume and peripheral vasoconstriction. These factors are more or less active in the different stages of hypertension and renal failure.

Adult↗
PubMed1976

Effect of urine metabolites from healthy and uremic subjects on gluconeogenesis in slices of rat kidney cortex and liver.

A high molecular weight fraction was obtained by extended dialysis of urine of healthy and uremic subjects. After addition to the incubation medium, this fraction inhibited gluconeogenesis by rat kidney cortex slices. From the six subfractions extracted by gel chromatography (Sephadex G 100) fraction IV caused a decrease of glucose formation. The activity of PEP-carboxykinase but not of pyruvate carboxylase was reduced, indicating a decreased formation of phosphoenol pyruvate. The total high molecular weight fraction stimulated glucose release by liver slices from fed but not from starved rats. In the absence of amino acids, urea formation was not stimulated. The activity of pyruvate carboxylase was reduced in both groups, PEP-carboxykinase activity was, however, only reduced in the starved group. The addition of uremic serum caused increased glucose release. Inhibition of PEP-carboxykinase activity by quinolinic acid (15 mM) resulted in inhibition of glucose formation by 35% in the uremic group and 54% in the control group in livers of 24 hr starved rats. Thus in uremia there may be incorporation of serine carbon skeletons into glucose via hydroxypyruvate, not via pyruvate. Chromatography on calibrated columns indicated that about 40% of the urinary fractions had molecular weights in the upper range of the "middle molecules" category. The positive correlation between toxicity and the total amount of high molecular weight substances excreted do not confirm the hypothesis of augmented retention of "toxins" in uremic patients. It must be appreciated that these results refer only to the undialyzable fraction of urine which contains only 0.5% by weight of the total urine solids.

Animals↗
PubMed1975

[Stimulation of renin secretion in vitro by a factor in serum of rats (author's transl)].

The stimulating effect of rat serum on renin release from kidney slices of this species was demonstrated. This "renin-releasing-factor" is not dialysable. It can be activated at 56 degree C. The factor is found in the gamma-Globulin and the albumin fraction of serum. Its role is discussed in a possible system of humoral regulation of RAS in the manner of a feed back mechanism including a releasing system.

Animals↗
PubMed1975

[The effect of acute diuresis augmentation on urea and creatinine clearance in healthy people and in patients with chronic renal insufficiency (author's transl)].

According to earlier observations no further augmentation of urea clearance should be possible above a urine flow of 2 ml/min (so-called augmentation limit). In normal people and in patients with renal insufficiency no augmentation limit of urea and creatinine clearance could be ascertained: increasing urine flow was correlated with augmentation of urea and creatinine clearance. Calculating the protein equivalent the augmentation of urea excretion by increased diuresis seems to be of clinical importance only in the treatment of renal insufficiency with small basic diuresis.

Creatinine↗
PubMed1975

The clinical picture of renal hypertension.

Renal hypertension can usually be recognized only by examining all the features of the hypertensive illness. On the other hand, the investigation of a case of hypertension whose genesis was previously unclear can lead to the diagnosis of a hitherto unrecognized renal disease. The blood pressure values found in patients with renal hypertension are of widely differing degrees of severity. Slight rises in blood pressure (e.g. 140/90 mm Hg), can be a sign of renal disease in adolescent patients. 10-15% of the cases of chronic renal hypertension develop into malignant hypertension. High diastolic values above 120 mm Hg without renal symptomatology and without reduced renal function speak against a primary renal cause of the rise in blood pressure. The finding of hypertension developing during the course of renal disease is, with respect to the hypertensive cardiovascular complications, just as important as in the case of essential hypertension. Complications which can occur during renal hypertension include cardiac insufficiency, hypertensive encephalopathy, retinopathy, hypertensive crises and acceleration of the renal disease.

Acute Disease↗