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Biomedical subjects

K D Bock

Publications and source records attributed to K D Bock.

At least 73 records · Page 4Linked to original sources
PubMed1977

Symptoms and course of chronic hypokalemic nephropathy in man.

The symptoms and clinical course of chronic hypokalemic nephropathy are described in 21 patients with longstanding potassium deficiency. In 14 patients (group A) the potassium depletion was caused by malnutrition and/or abuse of laxatives and/or diuretics. 7 patients (group B) suffered from primary (6 cases) or secondary (1 case) aldosteronism. The average duration of potassium depletion was 8.8 years in group A and 3.4 years in group B. Depending on the duration of potassium depletion, chronic renal disease develops which may end in terminal renal failure. Urinalysis is non-specific or negative. The clearance of creatinine slowly decreases. Metabolic alkalosis is a constant finding and in group A occurs with a tendency to hyponatremia and hypochloremia, with the development of metabolic acidosis only in advanced renal insufficiency. In contrast to patients of group B, patients of group A have normal or low blood pressures converting to hypertension, if at all only in the late phase. The cases of group A had secondary aldosteronism (and, correspondingly, a hyperplastic juxtaglomerular apparatus). Although urinary tract infection is a regular finding in advanced stages, the clinical, radiological and histological evidence suggests that bacterial pyelonephritis, if occurring at all, is rather a complication than the cause of the disease. In 5 patients 7 instances of acute renal failure of unknown origin were observed which was lethal in one case. Another patient died from terminal renal failure, a third from an intercurrent pneumonia. Renal histology obtained from 13 patients showed the picture of diffuse chronic abacterial interstitial nephritis.

Adult↗
PubMed1976

[Oral contraceptives in prophylaxis of acute exacerbations of intermittent porphyria (author's transl)].

Out of 14 women with acute intermittent porphyria seven were treated for an average of five years with ovulation inhibitors. In another two cases a bilateral surgical oophorectomy and a radiotherapeutic castration were performed. Five untreated women formed the control group. In contrast to the control group there were no further acute exacerbations in the group treated with oral contraceptives. The two patients with oophorectomy and irradiation castration died following multiple acute exacerbations. In four of the women treated with oral contraceptives the development of persistent, and in some cases severe, arterial hypertension was observed. The pathogenesis cannot be explained.

Acute Disease↗
PubMed1976

[Acute intermittent porphyria: report on 17 patients with 49 attacks (author's transl)].

In 17 patients (15 women, 2 men) with acute intermittent porphyria in the incidence of 23 clinical symptoms during 49 attacks was calculated. The most frequent symptoms in percentage of attacks were: Red colour of the urine 100%, abdominal pain 92%, tachycardia 88%, hypertension 75%, vomiting 54%, peripheral neuropathy 50%. In 35% of acute attacks a transient normochromic, normocytic anemia developed which is probably due to a disturbance of heme synthesis. Oliguria was found in 25%, azotemia in 12.5% of attacks. 4 patients with an average of 5 preceding acute attacks showed a persistent reduction of renal function during the symptom-free interval, in contrast to 12 patients with an average of 1.7 previous attacks and normal renal function. During the observation period from 1960-1974 3 (= 18%) of the 17 patients died.

Acute Disease↗
PubMed1976

[Laxative abuse, plasma potassium levels and chronic interstitial nephritis due to phenacetin abuse (author's transl)].

In 154 patients with phenacetin nephropathy and in 26 patients with phenacetin abuse but without nephropathy a laxative abuse was observed in 3.2% and 15.4%, hypokalemia (3.5 maequ/l or less) in 9.1% and 3.9, respectively. The mean plasma potassium concentration was normal in both groups (4.45 and 4.22 maequ/l, respectively). These data do not support the recently proposed hypothesis that the simultaneous abuse of laxatives contributes to the development of analgesic nephropathy, and that the absence of laxative intake might explain the lack of renal damage in some phenacetin abusers. Although it cannot be excluded that long-standing potassium deficiency in consequence of an abuse of laxatives or diuretics exerts an additional nephrotoxic effect in some cases, this mechanism seems not to be involved in the majority of patients with phenacetin nephropathy.

Cathartics↗
PubMed1976

Normal limits of urinary excretion of eleven enzymes.

Urinary excretion of lactate dehydrogenase, hydroxybutyrate dehydrogenase, gamma-glutamyltransferase, alkaline phosphatase, arylsulphatase A, alpha-glucosidase, beta-galactosidase, trehalase, N-acetyl-beta-glucosaminidase, beta-glucuronidase, and leucinearylamidase was studies in a carefully selected group of 100 healthy subjects, 50 women and 50 men. Enzyme activities were assayed in 3-h morning samples after gel filtration of the urine. Activities were related to time volume, and to urinary creatinine concentration. Several transforming functions had to be applied to enzyme output data to obtain an approximation to gaussian frequency distribution. Men showed a significantly higher excretion of gamma-glutamyltransferase, alpha-glucosidase, trehalase, N-acetyl-beta-glucosaminidase,beta-glucuronidase, and leucine arylamidase activity than did women if enzyme activity was related to urinary time volume. Women excreted more lactate dehydrogenase, hydroxybutyrate dehydrogenase, gamma-glutamyltransferase, alkaline phosphatase, alpha-glucosidase, trehalase, and N-acetyl-beta-glucosaminidase activity than did men, if urinary creatinine was used as the basis of reference. Reference intervals were calculated as 2.5 and 97.5 percentiles for both sexes.

Acetylglucosaminidase↗
PubMed1975

[Clinical experimental studies in patients with asympathicotonic hypotension].

Three patients with postural hypotension (two of the idiopathic type, one possibly due to familial dysautonomia) were found to have not only the pathognomonic postural hypotension, without rise in heart rate, cardiac output and peripheral vascular resistance, but also a similarly abnormal regulatory mechanism on ergometric stress when recumbent. There was a delayed-response to the bloodpressure fall on Valsalva a manoeuvre, and the blood volume was reduced. A combined effect of these factors explains that these patients have a more marked impairment of physical capcity than might be expected merely from the orthostatic hypotension. The actions of noradrenaline, adrenaline, phenylephrine, isoproterenol, angiotensin and tyramine on blood pressure and heart rate were different from normal. Plasma-renin activity was reduced in all three patients and could not be raised. Urinary excretion of adrenaline and noradrenaline was markedly diminished. Reactions to noradrenaline and tyramine, as well as the excretion pattern of the catecholamine metabolites suggest a disorder of active adrenaline liberation. Furthermore, different disorders of catecholamine metabolism underlie idiopathic orthostatic hypotension and familial autonomia. Therapeutic trials with fludrocortisone, beta-receptor blockers and levodopa brought improvement, but long-term results are not yet available.

Achievement↗