Scandiatransplant report 2009.

Scandiatransplant is the Nordic organ exchange organization that has existed for 41 years by a close collaboration between transplant centers. It has been valuable to ensure the optimal usage of available organs for transplantation. Analyzing the database for the past 15 years (1995-2009) revealed that the fraction of organ donors in the age category 60 to 90 years has increased considerably. The number of retrieved organs from deceased donors increased for kidney, liver, and lungs but only slightly for hearts. In the last time period, the mean number of organs retrieved per deceased donor counting only those having a recipient increased to 3.7 for younger donors and to 2.6 from the older group. In 2009, the STAMP (Scandiatransplant acceptable mismatch program) was launched to help highly immunized kidney patients. In 2009, kidney transplantations exhibited for Norway, 60 per million people (pmp); more than 40 pmp for Sweden and for Denmark; approximately 35 pmp for Finland; and more than 20 pmp for the living donor kidney transplantations in Iceland. The best year ever within Scandiatransplant with respect to total number of organ transplantations from deceased and living donors was 2009.

Aspects of present and future data presentation in Scandiatransplant.

Scandiatransplant is the Nordic organ exchange organization having existed for almost 40 years. With close collaboration between transplant centers in the Nordic countries, it has been valuable to ensure the optimal usage of available organs. The heart is the most often exchanged organ within the collaboration. It has been decided to create a priority for hyperimmunized kidney patients for compulsory exchange of organs from deceased donors. The age of the deceased organ donors has changed from younger to older donors. The evaluation of deceased kidney transplantations and deceased liver transplantations from 1995 to 2007 is shown for 4 countries. Iceland by itself is performing living donor kidney transplantations with great intensity. Scandiatransplant will make efforts to present more data than just transplantation to yield a more complete picture of organ transplantation.

Cutaneous infection caused by Paecilomyces lilacinus in a renal transplant patient: treatment with voriconazole.

Moulds belonging to the genus Paecilomyces are rare opportunistic pathogens. About 100 cases have been reported in immunocompromised hosts or in relation to surgical procedures. We describe here a cutaneous infection due to P. lilacinus in a renal transplant patient, which responded to voriconazole treatment.

[Autosomal dominant polycystic kidney disease in Iceland - genetic study.].

OBJECTIVE: Autosomal dominand polycystic kidney disease (ADPKD) is one of the most common genetic diseases in humans and accounts for 8-10% of end-stage renal failure. The disease is caused by mutations in at least three different genes. About 85% of families with ADPKS have a mutation in a gene (PKD1) on chromosome 16p, whereas 10-15% have a mutation in a gene (PKD2) on chromosom 4q. In a few families, a third gene (PKD3) of unkonown location appears to be involved. The purpose of this study was to determine the genotype of Icelandic families with ADPKD. MATERIAL AND METHODS: We isloated DNA from 229 family members and generated genotypes for polymorphic markers with conventional methods. Linkage analysis and haplotype analysis weere performed in 14 ADPKD families, employing merkers from the PKD1 and PKD2 regions. RESULTS: The abnormal gene could be located in 13 families. Eleven families demonstrated linkage to the PKD2 locus. Comparison of the haplotypes of the PKD1 families indicates that nine different mutations cause ADPKD1 in Iceland, including one de novo mutation. The two ADPKD2 families each have a distinct haplotype. Thererfor, at least 11 different mutations cause ADPKD in Icelnad. In cooperation with Dutch scientists, one mutation in the PKD2 gene was defined, a 16 bp deletion of a spice site between intron 1 and exon 2. CONCLUSIONS: Our results demonstrate marked genetic heterogeneity of ADPKD in the Icelandic population. As expected, most of the families have evidence for mutation in the PKD1 gene. The stage has been set for future work, which will focus on detecting mutations in the PKD genes and defining the correlation between mutations and phenotype of the disease.

[Peritonitis associated with peritoneal dialysis.].

Continuous ambulatory peritoneal dialysis (CAPD) is now a recognised treatment for end stage renal disease. An estimated number of 27.000 patients was being treated by CAPD world-wide in the year 1985. The most important complication is infection, peritonitis. The CAPD program started in Iceland in April 1985 at the dialysis department of the National University Hospital. The aim of this study was to estimate the incidence of infection associated with peritoneal dialysis during the first five years. All positive cultures of peritoneal dialysates from the Department of Bacteriology, and the hospital records of patients on CAPD, during the time period 12.04.1985 to 12.04.1990, were studied retrospectively. CAPD was considered started as soon as the peritoneal catheter had been inserted. Peritonitis was considered to be present when the white blood cell count was > 100/ul or there were clinical signs of infection together with a positive culture from the dialysate. During the study period 27 patients were treated by CAPD for 609.6 treatment months. Peritonitis was diagnosed 83 times in 18 of these patients, giving an incidence of 1.63/treatment year. The most common cause was Staphylococcus aureus, which was isolated 35 times (42%). Other causative organisms were: 17 coagulase negative staphylococci (21%), three Gram negative rods (4%), one yeasts and three mixed cultures. In 12 (14%) of the peritonitis episodes, no organisms were isolated. Admission to hospital was considered necessary in 74% of the episodes. One patient died of peritonitis. Studies have demonstrated various infection rates (0.23-6.3 infections/year), but has usually been between 0.8 and 1.2 infections/year. It is of interest to note that the most common causative organism in this study was S. aureus, as opposed to coagulase negative staphylococci, that have normally been the most prevalent. S. aureus usually causes tunnel infections, that are difficult to clear, without removing the catheter. This study demonstrates an above average prevalence of infection, which should prompt a reevaluation of the current management protocols.

Effect of chronic respiratory acidosis on urinary calcium excretion in the dog.

It is currently believed that the two chronic acidemic disorders exert disparate effects on urinary calcium excretion: chronic metabolic acidosis induces consistent hypercalciuria, but no appreciable change or even a decrease in calcium excretion is reported to attend chronic respiratory acidosis. Whereas the effect of metabolic acidosis is well documented, little work has been carried out in chronic hypercapnia. In fact, most of the studies on chronic respiratory acidosis were short in duration, had employed only mild hypercapnia, or had failed to control carefully the prevailing metabolic conditions. We have carried out balance observations in nine dogs exposed to a 10% CO2 atmosphere in an environmental chamber for a period of two weeks. Chronic respiratory acidosis led to a significant increase in urinary calcium excretion from a mean control value of 0.4 +/- 0.1 mmol/day to 0.6 +/- 0.1 mmol/day during both week 1 and 2 of hypercapnia (P less than 0.05). Hypercalciuria occurred even though filtered load of calcium fell. Mean fractional excretion of calcium increased significantly during each week of hypercapnia averaging 0.60 +/- 0.12% during control, 1.05 +/- 0.13% during week 1, and 1.26 +/- 0.17% during week 2 of hypercapnic exposure (P less than 0.05). There were no changes in plasma levels of immunoreactive parathyroid hormone or 1,25-dihydroxyvitamin D3. These findings suggest that chronic respiratory acidosis, just like chronic metabolic acidosis, augments urinary calcium excretion by a direct depressive effect on the tubular reabsorption of calcium.

The effect of potassium ion depletion on postinfarction canine cardiac arrhythmias.

The effect of potassium ion (K+) depletion on postmyocardial infarction ventricular arrhythmias was investigated in 32 dogs: 12 control animals, 10 animals that ate a diet extremely low in K+ for 15 days, and 10 others that, in addition to dietary K+ deprivation, received 50 mg of hydrochlorothiazide four times. The experimental myocardial infarction was created by proximal left anterior descending coronary artery ligation. In a subgroup of 24 animals selected for relatively uniform size of myocardial infarction (14% to 22% of left ventricular mass), eight animals with mean cumulative K+ balance of -4.01 +/- 2.19 meq/kg developed spontaneous ventricular fibrillation within 4 to 17 min of coronary ligation, whereas 16 animals with a mean cumulative K+ balance of -0.11 +/- 1.82 meq/kg didn't. By univariate analysis cumulative K+ deficit (p = .001) and plasma K+ concentration (p = .039) correlated significantly with spontaneous ventricular fibrillation. Multivariate analysis of the entire population of 32 animals identified cumulative K+ deficit and size of myocardial infarction as the only independent predictors of ventricular fibrillation. Cumulative K+ deficit was also an independent predictor of ventricular fibrillation induced by programmed cardiac stimulation in the conscious state 1 day after myocardial infarction.

Use of magnesium hydroxide and low magnesium dialysate does not permit reduction of aluminum hydroxide during continuous ambulatory peritoneal dialysis.

In an effort to reduce the ingestion of aluminum in phosphate-binding antacids, we treated seven patients on continuous ambulatory peritoneal dialysis (CAPD) with low magnesium dialysate and phosphate binders containing both aluminum and magnesium hydroxide. The total amount of phosphate binders prescribed was adjusted to maintain the serum phosphorus at normal levels. The dose of magnesium hydroxide was limited by intolerable gastrointestinal side effects in six of the seven patients. One patient also developed symptomatic hypermagnesemia. When magnesium hydroxide was prescribed in tolerable doses, the mean aluminum dose was not significantly decreased compared with the dose when taking aluminum hydroxide alone. We conclude that substitution of magnesium hydroxide for aluminum hydroxide as a phosphate binder fails to reduce the dose of aluminum in most patients on CAPD.