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Biomedical subjects

K Kisters

Publications and source records attributed to K Kisters.

At least 55 records · Page 3Linked to original sources
PubMed2000

Measurement of skeletal status after renal transplantation by quantitative ultrasound.

BACKGROUND: Osteoporosis remains a major problem following kidney transplantation. Radiographic measures of bone mass are of limited predictive value after transplantation and are complicated by preexisting renal osteopathy. Quantitative ultrasound (QUS) is a new and non-invasive method to assess skeletal status, however, no data exist on ultrasonic bone parameter after kidney transplantation. We evaluated the potential use of this novel method in renal allograft recipients and studied the accuracy compared to normal controls. METHOD: Thirty patients (NTP, age 47.5 +/- 13.0 years) were studied 4.8 +/- 3.2 years after transplantation. Twenty-five healthy control persons (CON) were matched for age and sex. The left and right os calcis were studied by QUS and speed of sound (SOS) and broadband ultrasound attenuation (BUA) were measured. Bone stiffness (BS) was calculated from these parameters and corrected for age (CBS). Differences between right and left os calcis were compared to CON to assess the side variability. RESULTS: Mean +/- SD BS was 75 +/- 22% compared to young adults, age-corrected CBS was decreased in NTP with 86 +/- 25% of normal, indicating a two-fold increased risk of fracture. SOS was 1525 +/- 47.7 m/s, BUA 105 +/- 22 dB/MHz. Mean difference between right and left os calcis was significantly higher in NTP than in CON (7.2 +/- 7.1% vs. 2.1 +/- 2.1%, p < 0.01). Limits of agreement of the measurements (MW of differences +/- 2 SD) according to a Bland-Altmann-type statistic were -16.9% and 20.7%. There was no correlation between CBS and age, cumulative steroid dose, parathyroid hormone concentrations or time after transplantation. CONCLUSION: Our data show altered bone structure expressed by low bone stiffness values measured by quantitative ultrasound in kidney transplant patients. However, because of relatively high inter-feet variance of QUS results we suggest measurement of both ossa calcis to minimize measurement error after transplantation.

Biomechanical Phenomena↗
PubMed2000

Importance of decreased intracellular phosphate and magnesium concentrations and reduced ATPase activities in spontaneously hypertensive rats.

A decrease in total magnesium content is not a direct proof of a decreased magnesium ion concentration. It could reflect a phosphate alteration or an ATP metabolism disorder. Plasma phosphate levels are lower in spontaneously hypertensive rats (SHRs) than in Wistar-Kyoto (WKY) rats, and defects in membrane regulation or mitochondrial ATP synthase occur. Only sparse data exist concerning cellular magnesium and phosphate concentrations in hypertensive cells. In aortic smooth muscle cells from 10 SHRs of the Münster strain and 10 age-matched normotensive WKY rats, the intracellular phosphate and magnesium content was measured by electron probe X-ray microanalysis (Camscan CS 24 apparatus, Cambridge, U.K.). The Mg++ content was 0.90+/-0.15 g/kg dry weight in SHRs versus 1.15+/-0.10 g/kg dry weight in WKY rats (p<0.05). Vascular smooth muscle phosphate content was 23.6+/-0.79 g/kg dry weight in WKY rats versus 15.81+/-1.22 g/kg dryweight in SHRs (p<0.01). In seven animals, erythrocytic ATP content was 180.2+/-102 in SHRs vs. 432+/-72 micromol/L cells in WKY rats (p< 0.01). The Na+/K+-ATPase activity was significantly decreased in hypertensive animals as compared to controls (6.49+/-2.3 vs. 12.64+/-2.9 nmol inorganic phosphate/mg protein/min (p< 0.01)). Aortic smooth muscle cells from SHRs are characterized by markedly lowered cellular phosphate and magnesium concentrations and an altered ATP metabolism, possibly due to a membrane defect or a magnesium deficit in hypertensive cells.

Adenosine Triphosphate↗
PubMed1999

[Kikuchi-Fusimoto disease: the differential diagnosis of cervical lymphadenitis with recurrent attacks of fever].

HISTORY AND CLINICAL FINDINGS: A 49-year-old, otherwise healthy woman had recurrent fever and lymphadenopathy with leukopenia for nineteen years. Her symptoms prompted successless antibiotic therapy and extensive evaluations of fever of unknown origin. At admission there were several enlarged cervical lymph nodes and subfebrile temperatures. INVESTIGATIONS: Neither laboratory findings nor imaging did show an infectious, rheumatologic or hematologic cause of her symptoms. Histopathological examination of an lymph node biopsy revealed histiocytic, necrotizing lymphadenitis (Kikuchi-Fusimoto disease) as the underlying disease. TREATMENT AND COURSE: After spontaneous resolution without specific therapy the patient is now symptomless and well 9 months after diagnosis. CONCLUSION: Kikuchi-Fusimoto disease is a cause of benign and usually self-limiting lymphadenopathy. Clinicians and pathologists should be aware of this uncommon differential diagnosis since early histologic recognition will minimize potentially and unnecessary evaluations and treatments.

Biopsy↗
PubMed1999

Lowered Total Intracellular Magnesium Status in a Subgroup of Hypertensives.

A new method to determine total Mg++ content in lymphocytes was developed, offering advantages for routine measurements as compared to fluorescence methods. Intracellular total Mg++ measurements were performed in lymphocytes of 18 healthy subjects and 19 untreated essential hypertensive patients. Mg++ content was referred to lymphocytic and membrane protein, which was determined according to Bradford's method. Mg++ measurements were performed by atomic absorption spectroscopy using a Video 12 apparatus of Thermo Electron Instrumentation Laboratory, Andover, USA. The results show that in patients with essential hypertension total intralymphocytic Mg++ content is significantly lower (0.07 +/- 0.05 mmol/g lymphocytic protein, mean +/- s.d.) as compared to controls (0.11 +/- 0.04 mmol/g lymphocytic protein, mean +/- s.d., p < 0.05). Free intracellular Mg++ content was measured in lymphocytes by the fluorescent indicator mag-fura-II, showing no significant differences in normotensives and hypertensives (0.30 +/- 0.16 versus 0.38 +/- 0.17 mmol/l). Additionally, in platelets free intracellular Mg++ concentrations were not found of significant difference in normotensives and hypertensives (0.52 +/- 0.23 versus 0.47 +/- 0.27 mmol/l) using mag-fura-II. In plasma Mg++ concentrations there was no significant difference in the normotensive and hypertensive group (0.92 +/- 0.07 versus 0.88 +/- 0.07 mmol/l). There was no correlation between plasma or free or total cellular magnesium concentrations in both groups. Furthermore this method seems also suitable for routine measurements of total intracellular Mg++ concentrations in even larger measurements like mag-fur-II. Lowered total intracellular Mg++ concentrations in a subgroup of primary hypertensives may contribute to the development of this disorder, perhaps due to different buffering systems.http://link.springer-ny.com/link/service/journals/00547/bibs/8n3p154.html

Journal Article↗
PubMed1999

Electron-probe X-ray Microanalysis of Magnesium and Sodium Ion Content in Vascular Smooth Muscle Cells from Spontaneously Hypertensive and Normotensive Rats.

Whereas in blood cells decreased magnesium concentrations and increased sodium concentrations in essential hypertension have often been described, only sparse data exist on cellular magnesium or sodium content in vascular smooth muscle cells. Therefore, in aortic smooth muscle cells from seven spontaneously hypertensive rats (SHR) of the Münster strain and seven normotensive Wistar-Kyoto rats (WKY), the intracellular magnesium and sodium content were measured by electron-probe X-ray microanalysis. Measurements were performed in aortic cryosections 3 µm thick. The magnesium ion content was 0.93 +/- 0.17 g/kg dry weight in SHR vs 1.14 +/- 0.12 g/kg dry weight in WKY (p < 0.05). Vascular smooth muscle sodium ion content was measured at 6.85 +/- 0.59 g/kg dry weight in WKY and 12.47 +/- 1.62 g/kg dry weight in SHR (p < 0.05). In conclusion, aortic smooth muscle cells from SHR are characterized by a markedly lowered intracellular magnesium ion content and increased sodium ion concentrations compared with normotensive cells. The results may be due to genetically determined disturbances in transmembrane magnesium and sodium ion transport. Cellular magnesium and sodium handling may be disturbed in SHR aortic smooth muscle as it is in hypertensive blood cells.

Journal Article↗
PubMed1999

Na+ and Mg2+ contents in smooth muscle cells in spontaneously hypertensive rats.

Whereas in blood cells decreased magnesium concentrations and increased sodium concentrations in essential hypertension have often been described, only sparse data exist on cellular magnesium or sodium content and exchange in vascular smooth muscle cells. Therefore in aortic smooth muscle cells from 10 spontaneously hypertensive rats (SHR) of the Münster strain and 10 normotensive Wistar-Kyoto rats (WKY) aged 8 to 10 months, the intracellular magnesium and sodium content was measured. Electron-probe X-ray microanalysis was used to determine intracellular Mg2+ and Na+ concentrations in aortic cryosections 3 microm thick. The magnesium ion content was 0.90 +/- 0.15 g/kg dry weight in SHR versus 1.15 +/- 0.10 g/kg dry weight in WKY (means +/- SD, P < .05). Vascular smooth muscle sodium ion content was 6.66 +/- 0.39 g/kg dry weight in WKY and 12.61 +/- 0.91 g/kg dry weight in SHR (P < .01). Aortic smooth muscle cells from SHR are characterized by markedly lowered intracellular magnesium ion content and increased sodium ion concentrations in animals 8 to 10 months old, compared with normotensive cells. The results may be due to genetically determined disturbances in transmembrane magnesium and sodium ion transport.

Animals↗
PubMed1999

Flow-mediated vasodilation and distensibility in relation to intima-media thickness of large arteries in mild essential hypertension.

Whether endothelial dysfunction in essential hypertension is a cause or a consequence of structural vessel wall alterations is not known. The purpose of the present study was to compare flow-mediated vasodilation and mechanical vessel wall properties of large arteries between never treated mild essential hypertensive patients with normal intima-media thickness (IMT) and those exhibiting intima-media thickening. We measured brachial and carotid artery diameter and distension by Doppler frequency analysis of vessel wall movements in M-mode in ten essential hypertensive patients with normal carotid artery IMT (HYP1), in ten patients with increased IMT (HYP2), and in 13 normotensive control subjects (CON). Thereafter, we measured changes in brachial artery (BA) diameters during distal reactive hyperemia after 4 min of forearm occlusion. Nitroglycerin-mediated vasodilation was measured to assess endothelium-independent vasodilation, and BA blood flow was estimated using a pulsed Doppler system. Intima-media thickness of the carotid arteries was examined by high resolution B-mode ultrasound. IMT was 0.66 +/- 0.02 mm in the HYP1 group, 0.84 +/- 0.03 mm in the HYP2 group (P < .01 v HYP1, P < .01 v CON), and 0.71 +/- 0.04 mm in the CON group. Forearm occlusion was reduced in both the HYP1 group (3.4% +/- 3.6%, P < .01 v CON) and the HYP2 group (6.4% +/- 1.5%, P < .05 v CON) when compared with the CON group (16.5% +/- 2.8%). Nitroglycerin-mediated vasodilation and BA blood flow were not different between study groups. BA distension (as well as carotid artery distension) was significantly lower in the HYP1 group (52 +/- 6 microm, P < .05 v CON), but not in the HYP2 group (72 +/- 10 microm) when compared with the CON group (88 +/- 13 microm). The data suggest that endothelial dysfunction and reduced distensibility of large arteries in patients with essential hypertension occur in the absence of structural vessel wall alterations.

Adult↗
PubMed1999

Studies on diurnal blood pressure variation in kidney diseases associated with excessive salt and water retention.

Salt and water retention, a cardinal feature of nephrotic syndrome, was suggested to be an important factor leading to reduced diurnal blood pressure (BP) variation in renoparenchymal disease. Twenty-four hour BP (SpaceLabs SL 90207), 24-h urine excretion of catecholamines, plasma renin activity and plasma aldosterone concentration were therefore determined in 10 nephrotic patients with normal serum creatinine levels (group A, serum creatinine 1.0+/-0.2 mg/dl), in 10 nephrotic patients with increased serum creatinine levels (group B, serum creatinine 2.4+/-0.9 mg/dl) and in 20 controls matched in respect of age and BP. To study the direct influence of fluid volume overload, diurnal BP variation was determined before and after volume depletion by ultrafiltration in 10 patients with end-stage renal failure. Diurnal BP variation was characterised by the difference of mean BP during daytime (10 pm to 8 am) and night-time (8 am to 10 pm). In group A, the systolic and diastolic day-night difference was not changed when compared with the controls (NS). In contrast, in group B the day-night difference was significantly lower than in the controls (P < 0.01). Twenty-four hour urine catecholamine excretion and plasma aldosterone were comparable between the study groups. Plasma renin activity, however, was significantly increased in group A (P < 0.05). Nocturnal BP drop was not related to plasma renin activity in the nephrotic patients. The blunted diurnal blood pressure variation in end-stage renal failure was not influenced by ultrafiltration. The study demonstrates that the blunted diurnal BP variation in kidney disease is unaffected by marked changes in total exchangeable sodium and fluid volume, but is sensitive to changes in glomerular filtration rate.

Adult↗
PubMed1999

Studies on cardiac sympathovagal balance and large artery distensibility in patients with untreated essential hypertension.

BACKGROUND: Power spectral analysis of heart rate variability and arterial distensibility are non-invasive measures of cardiac autonomic modulation and mechanical vessel wall properties, respectively. The aim of the present study was to assess cardiac sympathovagal balance, carotid and brachial artery distensibility and a possible relation between these parameters in mildly hypertensive patients as compared to normotensive controls. METHODS: Total power (TP, 0.01 to 0.5 Hz) and spectral components (low frequency 0.04-0.15 Hz, mainly sympathetic cardiac modulation; high frequency 0.15-0.4 Hz, mainly vagal cardiac modulation) and cardiac sympathovagal balance (LF/LH ratio) of short term heart rate variability (ECG-recording) were calculated in 15 untreated essential hypertensive patients (HYP) and 15 age- and sex-matched healthy controls (CON). Brachial and carotid artery distensibility coefficient (DC) was measured with a multigate doppler system (echo-tracking). RESULTS: TP (ms2 x 10(-3)) (11.2 +/- 0.8 vs 13.6 +/- 0.9, P < 0.03), LF/HF ratio (1.07 +/- 0.08 vs 0.75 +/- 0.07, P < 0.01) and HF (ms2 x 10(-3)/%) (0.7 +/- 0.1/49 +/- 2 vs 1.3 +/- 0.2/58 +/- 2, P < 0.01/P < 0.01) were significantly reduced in HYP compared to CON subjects. LF (ms2 x 10(-3)/%) was 0.7 +/- 0.1/50 +/- 2 vs 0.9 +/- 0.1/41 +/- 2, P = 0.16/P < 0.01. Carotid artery DC (15 +/- 2 vs 26 +/- 2, P < 0.001) and brachial artery DC (4.7 +/- 0.6 vs 9 +/- 1.0, P < 0.001) were significantly reduced in HYP. There was a significant correlation between carotid DC and LF/HF (rho = -0.41, P < 0.03). CONCLUSION: The data shows reduced heart rate variability and altered cardiac sympathovagal balance as well as impaired arterial distensibility in untreated mildly hypertensive patients. The relative increase in sympathetic modulation and decreased carotid distensibility appear to be related.

Adult↗
PubMed1999

Chronic intoxication by doxycycline use for more than 12 years.

We report the clinical case of a 12-years' intoxication by doxycycline. A patient with a depersonalization and derealization syndrome took 1 g doxycycline per day. In addition to hepatocellular necrosis with cholestasis, nephrotoxicity, leukopenia, anaemia and skin hyperpigmentation he suffered from hitherto unreported adverse cardiac events as intermittent supraventricular tachycardia and sporadic Wenckebach heart block. Despite a long period of self-medication these side-effects were reversible.

Adult↗
PubMed1999

Flow-mediated vasodilation and distensibility of the brachial artery in renal allograft recipients.

BACKGROUND: Alterations of large artery function and structure are frequently observed in renal allograft recipients. However, endothelial function has not yet been assessed in this population. METHODS: Flow-mediated vasodilation is a useful index of endothelial function. We measured the diameter and distensibility of the brachial artery at rest using high-resolution ultrasound and Doppler frequency analysis of vessel wall movements in the M mode. Thereafter, changes in brachial artery diameter were measured during reactive hyperemia (after 4 min of forearm occlusion) in 16 cyclosporine-treated renal allograft recipients and 16 normal controls of similar age and sex ratio. Nitroglycerin-mediated vasodilation was measured to assess endothelium-independent vasodilation. Brachial artery blood pressure was measured using an automatic sphygmomanometer, and brachial artery flow was estimated using pulsed Doppler. RESULTS: Distensibility was reduced in renal allograft recipients (5.31 +/- 0. 74 vs. 9.10 +/- 0.94 x 10-3/kPa, P = 0.003, mean +/- sem), while the brachial artery diameter at rest was higher (4.13 +/- 0.14 vs. 3.25 +/- 0.14 mm, P < 0.001). Flow-mediated vasodilation was significantly reduced in renal allograft recipients (0.13 +/- 0.08 vs. 0.60 +/- 0.08 mm or 3 +/- 2 vs. 19 +/- 3%, both P < 0.001). However, nitroglycerin-mediated vasodilation was similar in renal allograft recipients and controls (0.76 +/- 0.10 vs. 0.77 +/- 0.09 mm, NS, or 19 +/- 3 vs. 22 +/- 2%, NS). There were no significant differences in brachial artery flow at rest and during reactive hyperemia between both groups. The impairments of flow-mediated vasodilation and distensibility in renal allograft recipients remained significant after correction for serum cholesterol, creatinine, parathyroid hormone concentrations, end-diastolic diameter, as well as blood pressure levels, and were also present in eight renal allograft recipients not treated with cyclosporine. Flow-mediated vasodilation was not related to distensibility in either group. CONCLUSIONS: The results show impaired endothelial function and reduced brachial artery distensibility in renal allograft recipients. The impairments of flow-mediated vasodilation and distensibility are not attributable to a diminished brachial artery vasodilator capacity, because endothelium-independent vasodilation was preserved in renal allograft recipients.

Adult↗
PubMed1999

Clearance of iopromide during haemodialysis with high- and low-flux membranes.

PURPOSE: The present clinical trial addressed the clearance of the contrast medium iopromide, a middle-sized molecule, during dialysis with high- and low-flux membranes. MATERIAL AND METHODS: Twenty chronic haemodialysis patients without residual renal function were dialysed either with low-flux haemophan or high-flux polyamide directly after application of the contrast medium. Iodine concentrations were determined by radiofluorescence methods. RESULTS: Plasma concentrations of iodine before dialysis ranged between 1.1 and 3.9 mg/ml. The mean clearance rates for both membranes were comparable (110+/-1.4 ml/min high-flux and 108+/-1.9 ml/min low-flux), the sieving-coefficient was 0.83 for both membranes. After three hours of dialysis, 58% (high-flux) and 62% (low-flux) of iopromide was removed, half time of elimination was reached after 140+/-16 min (high-flux) and 122+/-11 min (low-flux). CONCLUSION: Our results demonstrated that elimination of iopromide is not dependent on the pore size of the membrane during dialysis. Due to higher blood flow rate, we found a higher elimination rate and a reduced half-time of elimination than prior investigations.

Contrast Media↗