Biomedical subjects

E Kühler

Publications and source records attributed to E Kühler.

3 recordsLinked to original sources

PubMed2001

Modulation of calcium oxalate monohydrate crystallization kinetics by urine of preterm neonates.

Preterm neonates frequently develop nephrocalcinosis (NC). However, the cause has not yet been elucidated. This study focuses on the effects of urine from preterm neonates on crystallization kinetics. Urine samples were collected and renal ultrasound examinations of preterm neonates (gestational age < 32 weeks) were performed during the first weeks of life, at term, and ages 6, 12, and 24 months. The effect of urine on crystallization was determined using a seeded crystal growth system, which measures the square root of solubility product ( radicalLc), percentage of growth inhibition (GI), and agglomeration inhibition ([tm]) of calcium oxalate crystals. Data for preterm neonates in the first weeks of life (n = 19) were compared with those for full-term neonates (n = 17) and healthy adults. Moreover, the correlation between [tm] and urinary (U)citrate level was studied. Mean radicalLc (0.27 +/- 0.1 versus 0.36 +/- 0.08 mmol/L) and mean [tm] (81 +/- 32 versus 143 +/- 97 minutes) were lower and mean Ucalcium-creatinine (2.20 +/- 1.74 versus 0.46 +/- 0.73 mol/mol) and Uoxalate-creatinine ratios (0.39 +/- 0.21 versus 0.16 +/- 0.09 mol/mol) were greater in preterm neonates in the first weeks of life compared with full-term neonates (p < 0.05). Furthermore, [tm] was less than the lower limit for healthy adults for all but one preterm neonate; [tm] increased and Ucalcium-creatinine and Uoxalate-creatinine ratios decreased with age (p < 0.005). There was a correlation between [tm] and citrate excretion (coefficient of 38; P < 0.001). Patients with and without NC at term did not differ statistically in mean radicalLc, percentage of GI, or [tm]. In conclusion, urine from preterm neonates in the first weeks of life is highly supersaturated and has a defective ability to inhibit calcium oxalate crystal agglomeration. This ability improves with age and is citrate mediated. We suggest that both the high level of supersaturation and defective ability to inhibit calcium oxalate crystal agglomeration contribute to the high incidence of NC.

Adult↗

PubMed1994

[The clinical value of plasma fibronectin in pregnancy].

We have measured plasmatic fibronectin in 23 normotensive pregnant women during pregnancy (overall 161 values). On the average 6 samples from every woman have been taken. Plasmatic fibronectin rose continuously from 313 +/- 76 mg/l in the first trimester to 416 +/- 194 mg/l in the third trimester. Normal pregnant women (n = 173, 358 +/- 140 mg/l) were compared with pregnant patients with preeclampsia (n = 37), woman with chronic hypertension in pregnancy (n = 25) and normotensive pregnant patients with intrauterine growth retardation (IUGR, n = 5). In the group with chronic hypertension (466 +/- 119 mg/l) there was no significant difference to the normal group, but we found a significant (p < 0.01) different value of fibronectin (748 +/- 195 mg/l) in the group of patients with preeclampsia. A tendency to higher fibronectin values was also noticed in the group with IUGR (739 +/- 212 mg/l). Because of the low number of patients this difference was not statistically significant. We conclude, that plasmatic fibronectin is an important, but not absolutely specific screening parameter for estimation of the endothelial injury in hypertensive disorders of pregnancy. We believe, that fibronectin is one the best parameters to forecast a preeclampsia.

Adult↗

PubMed1986

[Gallbladder perforation in an autopsy sample].

Evaluation of 135 post-mortem reports over a period from 1953 to 1985 showed that 107 patients without adequate therapy for peritonitis had died of gallbladder perforation within 32 hours from surgery. Another 28 had died of gallbladder perforation following cholecystectomy. Forty patients had been hospitalised in moribund condition and died within 24 hours from admission. Three patients died of the consequences of undetected postoperative or posttraumatic cholecystitis, while another five died following appendectomy or herniotomy, after destructive cholecystitis in them had escaped detection. Cholecystectomy was performed on 28 patients for perforated destructive cholecystitis, and 25 of these died of peritonitis within 32 hours. Bronchopneumonia was the major cause of death of two patients and purulent cholangitis in a third case. Once early operation for acute cholecystitis had been introduced in 1965, no single patient was recordable from the post-mortem documentation who had died of the sequels of untreated gallbladder perforation below the age of 60.

Aged↗