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Jochen H H Ehrich

Publications and source records attributed to Jochen H H Ehrich.

At least 19 recordsLinked to original sources
PubMed2007

Malaria-induced renal damage: facts and myths.

Malaria infections repeatedly have been reported to induce nephrotic syndrome and acute renal failure. Questions have been raised whether the association of a nephrotic syndrome with quartan malaria was only coincidental, and whether the acute renal failure was a specific or unspecific consequence of Plasmodium falciparum infection. This review attempts to answer questions about "chronic quartan malaria nephropathy" and "acute falciparum malaria nephropathy". The literature review was performed on all publications on kidney involvement in human and experimental malarial infections accessible in PubMed or available at the library of the London School of Hygiene and Tropical Medicine. The association of a nephrotic syndrome with quartan malaria was mostly described before 1975 in children and rarely in adult patients living in areas endemic for Plasmodium malariae. The pooled data on malaria-induced acute renal failure included children and adults acquiring falciparum malaria in endemic areas either as natives or as travellers from non-tropical countries. Non-immunes (not living in endemic areas) had a higher risk of developing acute renal failure than semi-immunes (living in endemic areas). Children with cerebral malaria had a higher rate and more severe course of acute renal failure than children with mild malaria. Today, there is no evidence of a dominant role of steroid-resistant and chronic "malarial glomerulopathies" in children with a nephrotic syndrome in Africa. Acute renal failure was a frequent and serious complication of falciparum malaria in non-immune adults. However, recently it has been reported more often in semi-immune African children with associated morbidity and mortality.

Africa↗
PubMed2007

Schimke immunoosseous dysplasia: suggestions of genetic diversity.

Schimke immunoosseous dysplasia (SIOD), which is characterized by prominent spondyloepiphyseal dysplasia, T-cell deficiency, and focal segmental glomerulosclerosis, is a panethnic autosomal recessive multisystem disorder with variable expressivity. Biallelic mutations in switch/sucrose nonfermenting (swi/snf) related, matrix-associated, actin-dependent regulator of chromatin, subfamily a-like 1 (SMARCAL1) are the only identified cause of SIOD. However, among 72 patients from different families, we identified only 38 patients with biallelic mutations in the coding exons and splice junctions of the SMARCAL1 gene. This observation, the variable expressivity, and poor genotype-phenotype correlation led us to test several hypotheses including modifying haplotypes, oligogenic inheritance, or locus heterogeneity in SIOD. Haplotypes associated with the two more common mutations, R820H and E848X, did not correlate with phenotype. Also, contrary to monoallelic SMARCAL1 coding mutations indicating oligogenic inheritance, we found that all these patients did not express RNA and/or protein from the other allele and thus have biallelic SMARCAL1 mutations. We hypothesize therefore that the variable expressivity among patients with biallelic SMARCAL1 mutations arises from environmental, genetic, or epigenetic modifiers. Among patients without detectable SMARCAL1 coding mutations, our analyses of cell lines from four of these patients showed that they expressed normal levels of SMARCAL1 mRNA and protein. This is the first evidence for nonallelic heterogeneity in SIOD. From analysis of the postmortem histopathology from two patients and the clinical data from most patients, we propose the existence of endophenotypes of SIOD.

Algorithms↗
PubMed2006

Young for young! Mandatory age-matched exchange of paediatric kidneys.

Some allocation systems include a mandatory donation of paediatric kidneys to children, others do not. Both approaches have medical and organisational advantages and disadvantages for adults and children. This article discusses why "young for young" is the best allocation system for children. Primary age-matched kidney allocation to children is one important factor leading to: (1) higher long-term glomerular filtration rates (GFRs) and graft survival and, thereby, to lesser need for dialysis; (2) better psychosocial rehabilitation, growth and development of children and, last but not least, (3) likely increase of the donor pool. As a consequence, health care costs will be reduced for children with end-stage renal failure. The chance of adults receiving an adequate kidney would be only minimally reduced by this policy. Therefore, we recommend an age-matched allocation programme giving children with end- stage kidney diseases a better prognosis.

Adult↗
PubMed2006

Growth impairment shows an age-dependent pattern in boys with chronic kidney disease.

The impact of chronological age on longitudinal body growth from early childhood through adolescence using detailed anthropometric methods has not yet been studied in children with chronic kidney disease (CKD). We have evaluated growth failure by measuring four components of linear growth: body height (HT), sitting height (SHT), arm length (AL) and leg length (LL). Data were prospectively collected for up to 7 years on 190 boys (3-21 years old) with congenital or hereditary CKD (all had developed at least stage 2 CKD by the age of 10 years). Patients showed the most severe growth failure in early childhood, followed by an acceleration in growth in pre-puberty, a slowing-down of growth at puberty, as expected, and thereafter a late speeding-up of growth until early adulthood. This pattern was observed irrespective of the degree of CKD and different treatment modalities, such as conservative treatment, recombinant human growth hormone (rhGH) therapy or transplantation. LL showed the most dynamic growth changes of all the parameters evaluated and emerged as the best indicator of statural growth in children with CKD. A specific age-dependent pattern of physical growth was identified in pediatric male CKD patients. This growth pattern should be considered in the evaluation of individual growth and the assessment of treatment efficacy such as rhGH therapy.

Adolescent↗
PubMed2006

Thirty years of the Union of National European Paediatric Societies and Associations (UNEPSA).

BACKGROUND: The Union of National European Paediatric Societies and Associations was founded in 1976 in Rotterdam. Thirty years later, the authors--former presidents and secretaries general--present a retrospective on the activities and achievements of UNEPSA. In 2006, 36 of 46 (78%) European countries, including some countries of the former Soviet Union, were members of UNEPSA. UNEPSA has created a forum for the mutual discussion of matters concerning paediatrics. UNEPSA is closely linked with the International Pediatric Association (IPA). It was never UNEPSA's ambition to promote a uniform European paediatrics. In the 30 years of its existence, it became clear that the diversity of paediatric care in different countries in Europe is extreme. During the "cold war", UNEPSA was able to cross boundaries between socialist and capitalist countries in Europe, and it was due to the activity of individual members of the UNEPSA council that clinical co-operation and research activities were initiated crossing many political borders. Annual meetings of national paediatric presidents focus on the most urgent problems of paediatric health care. "Europaediatrics" became the tri-annual congress for all general paediatricians and paediatric sub-specialists in Europe. The main research activities of UNEPSA concentrated on identifying the demography of primary, secondary and tertiary care paediatrics in Europe. CONCLUSION: UNEPSA is an active paediatric association representing more than three quarters of all European countries. After 30 years, it is still an expanding and vital instrument in improving the medical care of all children and the co-operation of their carers in Europe.

Europe↗
PubMed2006

Schimke versus non-Schimke chronic kidney disease: an anthropometric approach.

Schimke-immuno-osseous dysplasia is a rare autosomal-recessive multisystem disorder with the main clinical features of disproportionate growth deficiency, defective cellular immunity, and progressive renal disease. It is caused by mutations of SMARCAL1, a gene encoding a putative chromatin remodeling protein of unknown function. Because a detailed description of the clinical features is an essential first step in elucidating the function of SMARCAL1, we present the first detailed anthropometric data for Schimke-immuno-osseous dysplasia patients. By comprehensive anthropometric examination (28 parameters) of 8 patients (3 females) with the typical findings of Schimke-immuno-osseous dysplasia (mean age: 14.8 years; range: 4.9-30.5 years) and 304 patients (117 females) with congenital and hereditary chronic kidney disease (mean age: 10.7 +/- 4.8 years; range: 3-21.8 years), we show that Schimke-immuno-osseous dysplasia patients differ significantly from those with other forms of chronic kidney disease. z scores were calculated with reference limits derived from 5155 healthy children (2591 females) aged 3 to 18 years. The key finding was that, in the latter group, median leg length was significantly more reduced than sitting height, whereas in Schimke-immuno-osseous dysplasia patients, the reduction of sitting height was significantly more pronounced than for leg length. Therefore, the ratio of sitting height/leg length might be a simple tool for the clinician to distinguish Schimke-immuno-osseous dysplasia from other chronic kidney disease patients. Schimke-immuno-osseous dysplasia is very likely if this ratio is < 0.83. However, other forms of chronic kidney disease have to be discussed in case of a ratio > 1.01.

Adolescent↗
PubMed2006

[Schimke immuno-osseous dysplasia. A pediatric disease reaches adulthood].

BACKGROUND: Schimke immuno-osseous dysplasia (SIOD) is a rare autosomal recessive multisystemic disorder caused by mutations of the SMARCAL 1 gene (SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily a-like 1). CLINICAL FEATURES: Main clinical features are: disproportional growth deficiency due to spondyloepiphyseal dysplasia, nephrotic syndrome with focal and segmental glomerulosclerosis, and defective cellular immunity. Patients with severe SIOD have life-limiting complications like cerebral ischemia due to vaso-occlusive processes. Only a few patients reached adulthood. CASE REPORTS: The clinical course of four adult SIOD patients is presented. CONCLUSION: Even patients with severe SIOD can reach adulthood. Therefore, doctors working in the field of internal medicine and family doctors should be familiar with the clinical picture of SIOD.

Adolescent↗
PubMed2006

ABO-incompatible kidney transplantation of an 8-yr-old girl with donor/recipient-constellation A1B/B.

BACKGROUND: Antigen-specific immunoadsorption combined with rituximab offers the possibility for ABO-incompatible kidney transplantation without splenectomy. PATIENT AND METHOD: An 8-year-old mentally retarded girl with steroid-resistant nephrotic syndrome and focal segmental glomerulosclerosis due to mitochondriopathy poorly tolerated hemodialysis. Paternal blood group A1B was incompatible with blood group B of the child. Therefore, we decided to perform the first ABO-incompatible renal transplantation in a child in Germany using antigen-specific immunoadsorption. Rituximab (1 x 375 mg/m2) was administered 2 weeks before the first immunoadsorption (Glycosorb) ABO A-column). Triple-drug immunosuppression (tacrolimus, mycophenolate mofetil and prednisolone) was simultaneously started with immunoadsorption. Initial tacrolimus levels were targeted between 15 and 20 ng/ml. Before transplantation, six immunoadsorptions were applied on days -9, -7, -4, -3, -2 and -1. Intravenous immunoglobulin (0.5 g/kg) was administered preoperatively. After transplantation, three immunoadsorptions were performed on days +4, +6 and +8. RESULTS: Before transplantation, antibody (Ab) titers against paternal erythrocytes (20 degrees C) were reduced from 1 : 64 to 1 : 4 by six antigen-specific immunoadsorptions. After transplantation, we performed three more immunoadsorptions and the Ab titers were stable between 1 : 1 and 1 : 8. One, 2 and 8 months later we observed increases in the Ab titer up to 1 : 32 requiring no change in immunosuppressive therapy. No side effects of immunoadsorption were observed. The girl had excellent initial graft function with a serum creatinine of 55 to 70 micromol/l. Two weeks after transplantation, graft biopsy showed no signs of rejection; there was focal positivity for C4d only. Twelve months after transplantation, renal function was stable, with a serum creatinine of 117 micromol/l. Episodes of rejection or severe infections were absent. CONCLUSION: ABO-incompatible transplantation using antigen-specific immunoadsorption and rituximab may serve as a suitable alternative for children urgently needing renal transplantation and missing a blood group-compatible donor.

ABO Blood-Group System↗
PubMed2005

Nephrotic syndrome in African children: lack of evidence for 'tropical nephrotic syndrome'?

BACKGROUND: Infections such as malaria, schistosomiasis, hepatitis B and HIV have been suggested as major causes of the nephrotic syndrome (NS) in African children. We retrospectively analysed the course of the NS in 32 children from Ghana and reviewed the literature on NS from 18 different African countries for the presence of 'the tropical nephrotic syndrome'. METHODS: Thirty-two children (22 boys, 10 girls, median age 12 years, range 1-18 years) with NS were treated from 2000-2003 at Battor Hospital, Ghana. Thirteen out of 32 children underwent a renal biopsy which was investigated by light, immune and electron microscopy. All 32 patients were initially treated with oral prednisone (PRED) therapy (29 with standard therapy for 8 weeks and three individually tailored), and steroid-resistant children received also intravenous methylprednisolone pulses (three children) or oral cyclophosphamide (two children). RESULTS: All patients fulfilled the clinical and laboratory criteria of a NS. The initial median serum creatinine was 65 micromol/l (range 44-133 micromol/l). Renal biopsy was performed in 13/32 children and revealed focal and segmental glomerulosclerosis (FSGS) in 10 patients, minimal change disease (MCNs) in two and no conclusive result in one patient. Glomerular immune complex deposition was absent in all biopsies. After treatment with PRED, oedema disappeared in 24/32 patients; however, proteinuria normalized in 16/32 patients only. The NS relapsed in 9/16 steroid-sensitive patients after cessation of PRED therapy, and two children were frequent relapsers. The steroid-resistant NS did not respond to an intensified immunosuppression in 5/16 children receiving methylprednisolone or cyclophosphamide. Five out of 32 children died, all were steroid resistant. CONCLUSIONS: There was no evidence for a dominating role of steroid-resistant 'tropical glomerulopathies' in children with a NS in Ghana. Similar to South Africa, focal and segmental glomerulosclerosis (FSGS) and minimal change disease were the most frequent findings on histology. Contrary to Nigeria, membrano-proliferative glomerulonephritis was not found in these patients. We conclude from this data and from the literature that the histological pattern of NS may vary between different African countries. Concerning therapy of NS under tropical conditions, we emphasize that despite the limited therapeutic facilities half of these patients may benefit from corticosteroids; however, steroid resistance and FSGS resulted in a high mortality.

Adolescent↗
PubMed2005

Schimke-immuno-osseous dysplasia: new mutation with weak genotype-phenotype correlation in siblings.

Schimke-immuno-osseous dysplasia (SIOD) is a multisystem disorder with the following consistent clinical features: spondyloepiphyseal dysplasia with disproportional growth deficiency, nephrotic syndrome with focal and segmental glomerulosclerosis, and defective cellular immunity. Transitory ischemic attacks due to vaso-occlusive processes are complications in some patients with severe SIOD. Recently, mutations of SMARCAL1, which encodes a putative chromatin remodelling protein, have been associated with SIOD. Patients with milder disease were observed to harbor a missense mutation on each allele, whereas patients with a severe form of the disease were predicted to have at least one allele with a nonsense, frameshift or splicing mutation. We report two brothers who are both compound heterozygous for the mutations 836 T>C and 2542 G>T detected in exons 4 and 17, respectively. We demonstrate the lack of genotype-phenotype correlation in these patients as one brother shows some features of the severe form while the other does not. Neither clinical nor molecular findings can fully predict the clinical course of SIOD.

Adult↗
PubMed2005

Mitochondrial function in schimke-immunoosseous dysplasia.

Schimke-immunoosseous dysplasia (SIOD) is a multisystemic disorder caused by a mutation of a putative chromatin remodelling protein. Spondyloepiphyseal dysplasia with disproportionate growth deficiency, nephrotic syndrome with focal and segmental glomerulosclerosis, defective cellular immunity, and transient ischemic attacks are major clinical features in the severe form of SIOD. In the present study we tested the hypothesis that mitochondrial dysfunction may be an underlying pathophysiologic mechanism in this multisystemic disease. Mitochondrial parameters were studied in blood (lactate, pyruvate, ketone bodies, alanine) and in urine (organic acids) of four patients with the severe form of SIOD. Activities of respiratory chain enzymes were measured spectrophotometrically in fibroblasts of two of these patients. In patients with the severe form of SIOD normal concentrations of lactate as well as normal lactate/pyruvate- and ketone-body ratios were found in plasma. Alanine, the long-term parameter for lactate, was normal as well; metabolites of the citrate cycle were not found in the urine. Activities of respiratory chain enzymes I-V were not significantly reduced in fibroblasts from two patients with the severe form of SIOD. There was no evidence for mitochondrial dysfunction in SIOD. The underlying pathophysiology of SIOD remains unclear.

Arteriosclerosis↗
PubMed2005

The Cockcroft-Gault formula should not be used in children.

BACKGROUND: Although designed for adults, the Cockcroft-Gault formula was recently proposed for use in children > or =13 years of age. METHODS: We compared the feasibility of the Cockcroft-Gault formula against the standard pediatric Schwartz formula and a novel cystatin C-based formula. Our patient cohort included 262 children aged 1 to 18 years with various renal pathologies, who underwent a 99-technetium diethylenetriaminepentaacetate ((99)Tc DTPA) glomerular filtration rate (GFR) renal scan. Calculations were performed in Systeme International (SI) units using published constants and recalculated constants from our patient population. Agreement was assessed using Bland and Altman analysis. RESULTS: Published and recalculated constants for the Cockcroft-Gault formula were 1.23 and 0.96, respectively, for boys, and 1.05 and 0.90, respectively, for girls. The published and recalculated constants for the Schwartz formula were 48 and 49.9, respectively, for boys > or =13 years old, and 38 and 46.2, respectively, for all girls and for boys <13 years old. Using published constants, there was agreement between GFR and Cockcroft-Gault formula in boys > or =13 years old (average bias 5.0 +/- 23.5%) while there was an average error of -19.0%+/- 36.4% for all ages. Similarly, the average bias with Schwartz for boys > or =13 years old was -6.8 +/- 24.0% and for all patients was -12.8 +/- 24.2%. Using recalculated constants, the average bias with Cockcroft-Gault in boys > or =13 years old was -19.8 +/- 23.5% and for all patients was -38.5 +/- 35.2%. Similarly, the average bias with Schwartz for boys < or =13 years old was -1.1 +/- 24.3% and for all patients was 3.0 +/- 24.0%. The novel cystatin C-based GFR calculations showed an average error of -4.9 +/- 20.3% in the adolescent boys and 2.4 +/- 20.4% for all ages. CONCLUSION: Cockcroft-Gault formula showed the worst agreement with GFR, regardless of using published or recalculated constants. The cystatin C-based approach resulted in the least error, and should be used for estimation of GFR.

Adolescent↗
PubMed2004

Advantages of cyclosporin A using 2-h levels in pediatric kidney transplantation.

Clinical trials in adult liver and heart recipients have shown that management of cyclosporine (CsA) dose with 2-h levels (C2) leads to lower rejection rates and serum creatinine levels compared with C0 monitoring. Therefore, we investigated whether C2 monitoring might also improve late graft survival after kidney transplantation in children. To date, no results in adult renal transplantation and in pediatric transplantation have been published. Forty-nine stable pediatric kidney recipients with a minimum time of 1 year after transplantation (mean=7+/-5 years) entered the study. None of the patients had experienced an acute rejection up to 6 months before entering the study. CsA dosing was based on C0 monitoring for the first 6 months and then based on C2 monitoring for the following 6 months. C0 and C2 levels were measured at 4-weekly intervals. Percentage decline in glomerular filtration rate (GFR) and mean coefficients of variation of CsA levels (C(var)) were calculated and compared during the 6-months periods. At the beginning of the study, the mean calculated GFR was 53+/-15 ml/min per 1.73 m(2). During the 6 months of C0 monitoring, the mean GFR decreased to 49+/-12 m/min per 1.73 m(2 )( P=0.001, paired t-test). Six months after switching to C2 monitoring, the mean GFR remained stable, at 49+/-15 ml/min per 1.73 m(2 )( P=0.3 paired t-test). The largest increase in GFR (3.9+/-7.9%) was found in patients with a decrease of their CsA dose of more than 5% under C2 monitoring. C(var) was significantly lower under C2 than under C0 monitoring (0.24+/-0.10 vs. 0.30+/-0.15, P=0.02, unpaired t-test). We conclude that the switch to C2 monitoring helped to identify patients with CsA overdosing as well as to reduce variation in CsA level, which resulted in a halt in GFR decline.

Child↗
PubMed2004

Demography of paediatric renal care in Europe: organization and delivery.

BACKGROUND: Members of the European Society of Paediatric Nephrology (ESPN) initiated a study of the demography and policy of paediatric renal care among European countries at the end of the 20th century. METHODS: A questionnaire was mailed to the presidents of each of 43 national renal paediatric societies or working groups in Europe. Data on each country's population, income as reflected by its gross national product and infant mortality rate, were obtained from the United Nations. The paediatric health care systems were previously divided into three types: general practitioner care system, paediatric care system and combined care system (CCS). RESULTS: In 1998, 842 specialized paediatric nephrologists worked in hospitals in 42 European countries. The median number of paediatric nephrologists per million child population (pmcp) was 4.9 (range 0-15). The median number of children served per paediatric nephrologist was significantly higher in countries with the general practitioner care system than in those with the paediatric or combined care system (CCS), namely 370 747 vs 169 456 and 191 788, respectively. In addition to specially trained paediatric nephrologists, there were 1087 paediatricians with a part-time interest/activity in paediatric nephrology in hospitals in 34 European countries. Eastern European countries had significantly more general paediatricians with part-time nephrological activities than countries belonging to the European Union (EU), 16.7 vs 6.6 pmcp. In 1998, 92% of 42 European countries offered paediatric dialysis facilities for acute renal failure and 90% for chronic renal failure and 55% offered paediatric renal transplantation (RTx). Only 30% of Eastern European countries (central omitted) offered paediatric RTx vs 87% of EU countries. The availability of paediatric RTx was associated significantly with the countries' gross national product (r = 0.53, P<0.001). The median number of paediatric hospitals offering dialysis for childhood chronic renal failure was 1.5 pmcp (range 0-5.0) and the median number of paediatric hospitals offering paediatric RTx was 0.4 pmcp (range 0-3.5). Fewer children were on dialysis or were transplanted in Eastern European countries than in the EU. CONCLUSIONS: At the end of the 20th century, there was a marked variation in delivery of paediatric renal care within Europe. This was related to factors such as size of the population, geographical and political situation, the type of primary paediatric care system and economic situation. European countries were far from equal with regard to access of renal replacement therapy for children. Improvement of the economic situation is beyond the capabilities of paediatric nephrologists. However, in these days of world-wide globalization paediatricians in greater Europe should be able to achieve better cooperation and exchange of ideas and information which would be the first step towards equality of renal care for children.

Adolescent↗
PubMed2004

Renal allograft function in matched pediatric and adult recipient pairs of the same donor.

BACKGROUND: To study the effect of donor age on kidney function, the authors investigated matched pairs from the same kidney donor given to a pediatric or an adult recipient. METHODS: Fifteen matched pairs of an adult and a pediatric patient, selected from the Eurotransplant registry, receiving the renal graft from the same cadaveric donor were selected for analysis of graft function over 7 years. Nine matched pairs were from adult donors (mean age, 40 years; range, 23-60 years) and six from pediatric donors (mean age, 11 years; range, 4-15 years). All recipients had comparable immunosuppression with cyclosporine A, prednisolone, and azathioprine and comparable numbers of acute rejection, cytomegalovirus reactivation, and antihypertensive therapy. Mean age of pediatric and adult recipients at transplantation was 5 years (range, 1-9 years) and 38 years (range, 25-60 years), respectively. RESULTS: The calculated glomerular filtration rate (GFR) corrected to body surface area was not different in adult and pediatric recipients. Initial absolute GFR was significantly lower in pediatric recipients (27 mL/ min; range, 17-38 mL/min) than in adult recipients (54 mL/min; range, 25-74 mL/min) (P <0.05) and remained lower in the following years. Initially, pediatric donor kidneys transplanted into pediatric recipients showed a lower absolute GFR than those transplanted into adults, however, approaching the GFR in adult recipients later. Adult donor kidneys transplanted into pediatric recipients showed a persistently lower absolute GFR in children compared with those transplanted into adult recipients. CONCLUSIONS: The authors conclude that adult donor kidneys in pediatric recipients decrease GFR in the early stages and lack an increase in GFR with growth of the child.

Adolescent↗
PubMed2004

Generalized atherosclerosis sparing the transplanted kidney in Schimke disease.

Schimke-immuno-osseous dysplasia (SIOD) is a multisystem disorder caused by a mutation of the chromatin remodeling protein. The main clinical findings are spondyloepiphyseal dysplasia with disproportional growth deficiency, nephrotic syndrome with focal and segmental glomerulosclerosis, and defective cellular immunity. Transitory ischemic attacks due to vaso-occlusive processes are still an untreatable and life-limiting complication in patients with SIOD. The underlying pathophysiology of vaso-occlusive processes in SIOD is unclear. We report the clinical and pathological findings of the eldest published patient with the severe form of SIOD, who died at the age of 23 years due to pulmonary hypertension with subsequent right heart failure. The autopsy revealed a severe generalized atherosclerosis including the brain, heart, and pulmonary arteries. However, the kidney that was transplanted at the age of 5 years showed a good graft function without glomerular sclerosis and with only minimal nephrosclerosis on histology. Thus, the absence of severe vaso-occlusive processes in the transplanted organ and in the severely atherosclerotic host may indicate that the vaso-occlusive processes in SIOD are not caused by post-transplant cardiovascular morbidity such as arterial hypertension and hyperlipidemia. Instead, vascular factors of the host such as endothelial dysfunction may explain the pathophysiology of atherosclerosis in SIOD.

Adolescent↗