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Biomedical subjects

K Kisters

Publications and source records attributed to K Kisters.

At least 37 records · Page 2Linked to original sources
PubMed2001

Antihypertensive treatment in renal transplant patients--is there a role for ACE inhibitors?

During the past two decades great progress was achieved with regards to short-term kidney graft survival. However, long-term graft survival did not improve similarly. Many factors contribute to chronic graft nephropathy eventually resulting in late graft loss, among these arterial hypertension is of major importance. In patients with chronic renal disease of diabetic and non-diabetic origin, angiotensin converting enzyme inhibitors have been convincingly shown to slow the progression of renal failure. The achieved nephroprotection correlates with the reduction of proteinuria by ACE inhibitor treatment. Also in renal transplant patients, ACE inhibitors have been shown unequivocally to reduce urinary protein excretion. The prevention of hyperfiltration, particular in the context of a reduced number of functional nephrons in patients with chronic graft nephropathy, could be important to prolong graft survival after renal transplantation. Moreover, ACE inhibitors may exert beneficial effects on immunologic processes contributing to chronic graft nephropathy. Many studies published in the last decade show convincingly that ACE inhibitors are safe and effective for the treatment of hypertension in renal allograft recipients. However, no data exist so far showing that ACE inhibitors are superior to other antihypertensive drugs in renal transplant patients and that they prolong graft survival. Studies investigating this issue are warranted. Apart from effects on the graft, ACE inhibitors may improve alterations of the cardiovascular system generally observed in renal transplant patients, such as structural alterations of large arteries, left ventricular hypertrophy, disturbed mechanical vessel wall properties and endothelial dysfunction. Therefore, angiotensin converting enzyme inhibitors could reduce cardiovascular morbidity and mortality in kidney transplant patients.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

[Classic case of benign recurrent intrahepatic cholestasis (Summerskill-Halshe-Tygstrup syndrome)].

BACKGROUND: The benign recurrent intrahepatic cholestasis is an autosomal recessively inherited liver disease. The gene was mapped to a region on chromosome 18q21-22. Because of its rareness this disease is first considered in the differential diagnosis of cholestasis after many years of extensive investigations. CASE REPORT: We report about a 17-year-old patient, who suffered from intermittent attacks of cholestatic jaundice and pruritus. Clinical course, laboratory data and invasive investigations led to the diagnosis of a typical case of benign recurrent intrahepatic cholestasis (Summerskill-Walshe-Tygstrup syndrome). CONCLUSION: This disease is remarkable for a discrepancy between a rise of serum bile acids at the onset of each attack and a later rise of bilirubin. Typically high bilirubin levels are noted, and bilirubin can even reach more than 50 mg/dl. The serum alkaline phosphatase is increased, too, whereas the values for the transaminases and gamma GT are normal or only slightly elevated. Histological studies reveal a cholestasis, bile plugs in the bile canaliculi, a perilobular fibrosis and inflammatory infiltrations of the periportal zones. Differential diagnosis includes an abundance of diseases with cholestasis. Treatment is difficult, purely symptomatic and often without marked effect. Nevertheless prognosis is good, histories of about 50 years were without evidence of progression to cirrhosis.

Adolescent↗
PubMed2000

[Alterations of arterial vessel wall properties in hyperparathyroidism].

Alterations of arterial vessel wall function are associated with increased cardiovascular morbidity and can be measured by noninvasive ultrasound techniques. There is increasing evidence that hyperparathyroidism contributes not only to structural changes of the cardiovascular system but to disturbances in functional arterial vessel wall properties. It has been shown that elevated concentrations of parathyroid hormone are associated with decreased arterial distensibility and increased intima-media thickness in patients with renal insufficiency. A permissive role of parathyroid hormone in the pathogenesis of uremic vessel wall changes has been discussed. The endothelium is a newly recognized target organ of parathyroid hormone. In patients with primary hyperparathyroidism endothelial dysfunction has been demonstrated, that seems to be reversible after parathyroidectomy. Effects on arterial vessel wall function may contribute to increased blood pressure observed in hyperparathyroidism. The complex cardiovascular effects of parathyroid hormone and changes in vascular tone, arterial distensibility and endothelial function in hyperparathyroidism are discussed.

Arteriosclerosis↗
PubMed2000

[Alterations of the arterial vessel wall in renal failure].

Cardiovascular events are the main cause of death in patients with end-stage renal disease. Functional and structural alterations of the arterial system substantially contribute to the high cardiovascular mortality in these patients. Structural alterations of the arterial wall comprise intima-media thickening and atherosclerotic plaque formation. Moreover, mechanical vessel wall properties of large arteries are significantly disturbed. This is already observed in young patients. Reduced arterial distensibility impairs large artery cushioning function. This results in increased ventricular afterload promoting left ventricular hypertrophy and in reduced coronary perfusion. After renal transplantation, structural alterations of the arterial wall and disturbed mechanical vessel wall properties persist. Moreover, renal failure is characterized by a severe impairment of endothelial function. Disturbed endothelial function results from reduced production of endothelium-dependent endogenous vasodilators and/or blunted vascular effects of these substances. Uremia is associated with the accumulation of an endogenous inhibitor of the endothelial nitric oxide synthase. Impaired endothelial function in renal failure promotes the progression of structural lesions of the arterial wall. Also in renal transplant recipients, substantially impaired endothelial function is observed despite correction of uremia. Hyperparathyroidism commonly observed in renal failure contributes to the disturbed functional vessel wall properties of large arteries. In patients with end-stage renal disease, decreased large artery distensibility is an independent risk factor for increased cardiovascular mortality. This may apply also to intima-media thickening and to impaired endothelial function.

Arteriosclerosis↗
PubMed2000

[Diagnosis and therapy of renovascular hypertension].

BACKGROUND: Renovascular hypertension as a secondary form of hypertension can be improved or cured in many cases by interventional radiology or vascular surgery. BASIS: The renin-angiotensin-aldosterone system and the development of hypertension are linked in renovascular hypertension. CLINICAL APPEARANCE: Early clinical symptoms are of special interest in diagnosing renovascular hypertension. DIAGNOSIS AND THERAPY: Nowadays, angioplasty or stenting have mostly replaced surgery in view of treatment of renovascular hypertension. CONCLUSION: Renovascular hypertension, if diagnosed early, can be improved or cured in many cases regarding hypertension and/or renal insufficiency.

Angioplasty, Balloon↗
PubMed2000

Impaired flow-mediated vasodilation of the brachial artery in patients with primary hyperparathyroidism improves after parathyroidectomy.

OBJECTIVE: The endothelium is a newly recognised target tissue of parathyroid hormone (PTH). It is not clear whether hyperparathyroidism affects endothelial function and whether parathyroidectomy (Ptx) has an influence on arterial vessel wall properties. We studied brachial flow-mediated vasodilation (FMD) and brachial and carotid intima-media thickness (IMT) in patients with primary hyperparathyroidism (pHPT) before and after Ptx and in healthy controls. METHODS: 19 patients with pHPT (mean+SEM, age 45+/-4.7 years, PTH 238+/-52 ng/l) were studied. Diabetes, hypertension and vascular disease were excluded. Twenty healthy volunteers matched for age, sex and blood pressure served as controls. Enddiastolic diameter, FMD and nitroglycerine-induced (NMD) dilation of the brachial artery were measured by a multigate pulsed doppler system (echo-tracking), IMT was determined using automatic analysis of the M-line signal. Healthy volunteers where studied on one occasion, patients were studied at baseline and 6 months after Ptx. RESULTS: Six months after Ptx PTH had decreased to normal, blood pressure levels remained unchanged. Endothelium dependent FMD at baseline was impaired in patients compared to controls (4.7+/-1.2 vs. 18.2+/-3.7%, P<0.01), however, FMD improved significantly after Ptx (16.7+/-3.0%, P<0.01). Nitroglycerine-induced dilation, IMT and artery diameter were not different between groups and did not change after Ptx. CONCLUSIONS: Impaired endothelium dependent vasodilation in patients with primary hyperparathyroidism improves after successful parathyroidectomy. Endothelial dysfunction associated with primary hyperparathyroidism occurs without detectable structural wall alterations of the brachial artery and appears therefore to be an early and reversible arterial alteration.

Adult↗
PubMed2000

Membrane, intracellular, and plasma magnesium and calcium concentrations in preeclampsia.

Changes in intracellular calcium and magnesium concentrations seem to be involved in the pathogenesis of preeclampsia, whereas the role of cell membranes has not been studied in detail yet. To investigate the changes in calcium and magnesium metabolism in normal pregnancy and preeclampsia, plasma, intracellular, and membrane calcium and magnesium concentrations were determined in a clinical study. Twenty-five control, 18 untreated healthy pregnant, and 16 nulliparas preeclamptic women were investigated. Plasma, cellular, and membrane (erythrocytes) calcium and magnesium contents were measured by atomic absorption spectroscopy. Plasma and intracellular magnesium concentrations were significantly lower in the healthy pregnant group and the preeclamptic group as compared to controls (P < .01). In erythrocyte membranes magnesium content was found significantly decreased in the preeclamptic women as compared to healthy subjects (P < .001). There was a significant decrease in the plasma calcium concentration in the preeclamptic group compared to controls or healthy pregnant women (P < .05). Membranous calcium content was significantly increased in the preeclamptic group versus controls or healthy pregnant women (P < .001) and an inverse correlation with membranous magnesium content was found (r = -0.79,P < .01). Lowered plasma, intracellular, and membrane magnesium concentrations in preeclampsia may contribute to the development in hypertension in pregnancy. In addition, a disturbed calcium homeostasis is observed in preeclampsia.

Adult↗
PubMed2000

Studies on flow-mediated vasodilation and intima-media thickness of the brachial artery in patients with primary hyperparathyroidism.

The endothelium is a newly recognized target organ of parathyroid hormone (PTH) and may contribute to its effects on vascular tone and blood pressure regulation. Flow-mediated vasodilation (FMD), brachial and carotid intima-media thickness (IMT) were studied in patients with primary hyperparathyroidism (pHPT) and controls to evaluate endothelial function and structural arterial vessel wall alterations. Sixteen patients with pHPT (mean +/- SEM, age 44 +/- 5 years; PTH 229 +/- 72 ng/L; serum calcium 3.0 +/- 0.06 mmol/L; serum phosphate 2.0 +/- 0.2 mg/L) and 16 normocalcemic control subjects matched for age, sex, and blood pressure were included. Diabetes, hypertension, and vascular disease were excluded in both groups. End-diastolic diameter, flow-mediated (FMD) and nitroglycerin-mediated (NMD) dilation of the brachial artery were measured by a multigate pulsed Doppler system (echo-tracking). IMT was determined using automatic analysis of the M-line signal. Endothelium-dependent FMD was impaired in patients compared to controls (4.6 +/- 1.6% v 19.2 +/- 3.9%, P < .001). NMD (23.8 +/- 3.1% v. 22.4 +/- 2.8%, P = NS), carotid and brachial IMT (0.60 +/- 0.04 mm v 0.64 +/- 0.06 mm, P = NS, and 0.46 +/- 0.04 mm v 0.47 +/- 0.08 mm, P = NS, respectively) and artery diameters were not different. Endothelium-dependent vasodilation is impaired in patients with primary hyperparathyroidism despite normal IMT. Endothelial dysfunction may contribute to increased cardiovascular morbidity and mortality in pHPT.

Adult↗
PubMed2000

Intracellular Mg++ concentrations in smooth and striated muscle cells in spontaneously hypertensive rats.

Decreased intracellular Mg++ concentrations seem to be involved in the pathogenesis of primary hypertension. Of special interest is the smooth muscle cell with its electrolyte metabolism in primary hypertension, but also heart muscle cells and their Mg++ concentrations are of growing interest. Therefore, in aortic smooth muscle cells and striated heart muscle cells (left ventricle) from 20 spontaneously hypertensive rats (SHR) of the Münster strain and 20 normotensive Wistar-Kyoto rats (WKY), the intracellular Mg++ content was measured. The electron probe x-ray microanalysis technique was used to determine intracellular Mg++ concentrations under nearly in vivo conditions in aortic cryosections 3 microm thick and striated heart muscle cells 4 microm thick (Camscan CS 24 apparatus). Vascular smooth muscle Mg++ content was 36.4 +/- 3.1 mmol/kg dry weight in SHR versus 48.6 +/- 3.7 mmol/kg dry weight in WKY (P < .001). In striated heart muscle cell Mg++ concentrations, there was no significant difference in SHR and WKY (79.9 +/- 5.6 versus 80.3 +/- 5.9 mmol/ kg dry weight). In conclusion, the present study revealed that genetic hypertension in the spontaneously hypertensive rat is accompanied by significantly decreased intracellular Mg++ concentrations in vascular smooth muscle cells. In striated heart muscle cells, Mg++ content was not significantly different in SHR and WKY. Mg++ handling is different in vascular smooth muscle and striated heart muscle cells in WKY and SHR (P < .01).

Animals↗
PubMed2000

Alterations of plasma calcium and intracellular and membrane calcium in erythrocytes of patients with pre-eclampsia.

BACKGROUND: Changes in plasma and intracellular calcium levels have been suggested in the pathogenesis of pre-eclampsia, however, membrane calcium content has not been studied so far. We compared intracellular and membrane calcium concentrations in erythrocytes of women with pre-eclampsia, healthy pregnant woman and controls to determine a possible alteration of membrane calcium in pre-eclampsia. SUBJECTS AND METHODS: Eighteen untreated, healthy pregnant woman and 16 pregnant nulliparous women with manifest pre-eclampsia were included, 25 healthy, age-matched woman served as controls. Atomic absorption spectroscopy was used for measurement of intracellular and membrane calcium content in erythrocytes and plasmalemmal preparations. RESULTS: Plasma Ca++ concentrations were significantly lower in pre-eclamptic women (1.96 +/- 0.15 mmol/l, P < 0.01, mean +/- s.e.m.) compared to healthy controls (2.43 +/- 0.14 mmol/l) or women with uncomplicated pregnancies (2.20 +/- 0.10 mmol/l). Intracellular Ca++ concentrations were not different between groups, however, membrane Ca++ content was significantly increased in the pre-eclamptic patients (1.23 +/- 0.36 micromol/g membrane protein, P < 0.01) compared to control subjects (0.83 +/- 0.16 micromol/g) and healthy pregnant women (0.77 +/- 0.13 micromol/g). CONCLUSION: Membrane calcium content is significantly increased in pre-eclamptic women despite low plasma Ca++ concentrations. This finding suggests an altered membrane ion transport and may be of importance for the pathogenesis of pre-eclampsia.

Adult↗
PubMed2000

Reduced iopromide elimination in hemodialysis with cuprophan membranes.

PURPOSE: To evaluate the influence of different membrane materials on the efficiency of iopromide elimination. MATERIAL AND METHODS: Twenty stable patients with chronic renal failure after coronary angiography were investigated for contrast medium elimination during hemodialysis directly after contrast medium application. RESULTS: Clearance during hemodialysis with cuprophan membranes was 102 +/- 7 mg/ml in contrast to 153 +/- 4 mg/ml in polysulfone membranes. Elimination half-time was 94 +/- 5 min in cuprophan and 79 +/- 3 min in polysulfone membranes, and the elimination rate after 120 min was 59 +/- 2% and 66 +/- 1.5% respectively. Plasma clearance of iopromide was elevated in polysulfone membranes (188 +/-17 ml/min); however, not significantly different to cuprophane membranes (153 +/-11 ml/min). Accordingly, 24-h urinary iopromide excretion was reduced to 26 +/- 4 g/24 h vs. 32 +/- 7 g/24 h. CONCLUSION: Hemodialysis for iopromide elimination with polysulfone membranes is more effective than with cuprophan membranes.

Cellulose↗