Center for Nephrology and Dialysis

Kragujevac, Serbia

Center for Nephrology and Dialysis

Kragujevac, Serbia
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Cardiovascular diseases represent a considerable cause of death among patients with transplanted kidney. The study was aimed at defining risk factors, pathogenic progression mechanisms for cardiovascular diseases and pointing at clinical importance for early detection and timely treatment of cardiovascular diseases in patients with transplanted kidney. Expert papers and clinical studies dealing with etiopathogenesis, diagnosis and treatment of cardiovascular diseases in patients with transplanted kidney were analyzed. Increased incidence of cardiovascular diseases in patients with transplanted kidney is the consequence of high prevalence of traditional risk factors (obesity, cigarette smoking, hypertension, hyperlipidemia, diabetes mellitus), risk factors due to status of transplantation and its treatment (immunosuppressive agents, graft rejection, viral infections (cytomegalovirus) and risk factors due to chronic reduction of allograft (anemia, volume strain stress, hyperhomocysteinemia, oxidative stress, secondary hyperparathyroidism, microinflammation). Left ventricular hypertrophy, ischemic heart disease and heart weakness bear the highest prevalence among cardiovascular diseases. Early detection of disease in patients with increased risk for progression of cardiovascular diseases enables optimization and individualization of immunosu-ppressive therapy, reaching aimed values for cardiovascular risk factors, all with the view to reduce cardiovascular morbidity and mortality, increase of allograft survival and better life quality of patients with transplanted kidney.


Neumann H.P.H.,Albert Ludwigs University of Freiburg | Bacher J.,Albert Ludwigs University of Freiburg | Nabulsi Z.,Albert Ludwigs University of Freiburg | Ortiz Bruchle N.,RWTH Aachen | And 12 more authors.
International Urology and Nephrology | Year: 2012

Background: ADPKD is one of the most common inherited disorders, with high risk for end-stage renal disease. Numerous patients, however, have no relatives in whom this disorder is known and are unsure whether they may transmit the disease to their offsprings. The aim of this study was to evaluate whether germline mutation analysis adds substantial information to clinical symptoms for diagnosis of ADPKD in these patients. Methods: Clinical data included renal function and presence of liver or pancreas cysts, heart valve insufficiency, intracranial aneurysms, colonic diverticles, and abdominal hernias. Family history was evaluated regarding ADPKD. Germline mutation screening of the PKD1 and PKD2 genes was performed for intragenic mutations and for large deletions. Results: A total of 324 adult patients with ADPKD including 30 patients without a family history of ADPKD (sporadic cases) were included. PKD1 mutations were found in 24/30 and PKD2 mutations in 6 patients. Liver cysts were present in 14 patients and intracranial aneurysms in 2 patients. Fourteen patients (45%) had no extrarenal involvement. Compared to the 294 patients with familial ADPKD, the clinical characteristics and the age at the start of dialysis were similar in those with sporadic ADPKD. Conclusion: The clinical characteristics of patients with sporadic and familial ADPKD are similar, but sporadic ADPKD is often overlooked because of the absence of a family history. Molecular genetic screening for germline mutations in both PKD1 and PKD2 genes is essential for the definitive diagnosis of ADPKD. © 2012 Springer Science+Business Media, B.V.


Petrovic D.,Center for Nephrology and Dialysis | Obrenovic R.,University of Belgrade | Trbojevic-Stankovic J.,Clinical Center Dr Dragisa Misovic | Majkic-Singh N.,University of Belgrade | Stojimirovic B.,Institute of Urology and Nephrology
Journal of Medical Biochemistry | Year: 2011

Cardiovascular diseases are the leading cause of death in hemodialysis (HD) patients. The annual cardiovascular mortality rate in these patients is 9%, with left ventricular (LV) hypertrophy, ischemic heart disease and heart failure being the most prevalent causes of death. The aim of this study was to determine the cardiovascular mortality rate and estimate the influence of risk factors on cardiovascular mortality in HD patients. A total of 115 patients undergoing HD for at least 6 months were investigated. Initially a cross-sectional study was performed, followed by a two-year follow-up study. Beside the standard biochemical parameters, C-reactive protein (CRP), homocysteine, cardiac troponins (cTn) and the echocardiographic parameters of LV morphology and function (LV mass index, LV fractional shortening, LV ejection fraction) were determined. Results were analyzed using Cox regression analysis, Kaplan-Meier and Log-Rank tests. The average one-year cardiovascular mortality rate was 8.51%. Multivariate Cox regression analysis identified increased CRP, cTn T and I, and LV mass index as independent risk factors for cardiovascular mortality. Patients with cTnT > 0.10 ng/mL and CRP > 10 mg/L had significantly higher cardiovascular mortality risk (p < 0.01) than patients with cTnT > 0.10 ng/mL and CRP ≤ 10 mg/L and those with cTnT ≤ 0.10 ng/mL and CRP ≤ 10 mg/L (p < 0.01). HD patients with high cTnT and CRP have a higher cardiovascular mortality risk.


Petrovic D.,Center for Nephrology and Dialysis | Obrenovic R.,University of Belgrade | Trbojevic-Stankovic J.,Clinical Hospital Center Dragisa Misovic | Majkic-Singh N.,University of Belgrade | Stojimirovic B.,Institute for Urology and Nephrology
Journal of Medical Biochemistry | Year: 2012

Hyperphosphatemia is a potent stimulator of vascular and valvular calcifications in hemodialysis patients. To determine the prevalence of hyperphosphatemia and assess its effect on the outcome of hemodialysis patients, a total of 115 chronic hemodialysis patients were studied. Laboratory parameters were determined at baseline, and after 12 and 24 months of follow-up. Valvular calcification was assessed with echocardiography. Laboratory parameters were statistically analyzed with ANOVA. Survival analysis was performed with the Kaplan-Meier test and Log-Rank test. Hyperphosphatemia was present in 31.30% of the patients, high calcium-phosphate (Ca × P) product in 36.52% and valvular calcifications in 48.70%. Patients with serum phosphate >2.10 mmol/L and Ca × P product >5.65 mmol2/L2 at baseline were at high risk for all-cause and cardiovascular mortality. Hyperphosphatemia is a risk factor for adverse outcome in patients on regular hemodialysis.


Neumann H.P.H.,Albert Ludwigs University of Freiburg | Jilg C.,Albert Ludwigs University of Freiburg | Bacher J.,Albert Ludwigs University of Freiburg | Nabulsi Z.,Albert Ludwigs University of Freiburg | And 20 more authors.
Nephrology Dialysis Transplantation | Year: 2013

BackgroundAs we emerge into the genomic medicine era, the epidemiology of diseases is taken for granted. Accurate prevalence figures, especially of rare diseases (RDs, ≤50/100 000), will become even more important for purposes of health care and societal planning. We noticed that the numbers of affected individuals in regionally established registries for mainly hereditary RDs do not align with published estimated and expected prevalence figures. We therefore hypothesized that such non-population-based means overestimate RDs and sought to address this by recalculating prevalence for an important 'common' hereditary disease, autosomal-dominant polycystic kidney disease (ADPKD) whereby presumed-prevalence is 100-250/100 000MethodsThe Else-Kroener-Fresenius-ADPKD- Study in south-west Germany with a population of 2 727 351 inhabitants was established with the cooperation of all nephrology centres. Furthermore, general practitioners, internists, urologists, human geneticists and neurosurgery centres were contacted with questionnaires for demographic, family and kidney function data. Germline-mutation screening of susceptibility genes PKD1 and PKD2 was offered. Official population data for 2010 were used for overall and kidney function-adjusted prevalence estimations.ResultsA total of 891 subjects, 658 index-cases and 233 relatives, aged 10-89 (mean 52), were registered, with >90% response rate, 398 by nephrologists and 493 by non-nephrologists. Molecular-genetic analyses contributed to confirmation of the diagnosis in 57%. The overall prevalence of ADPKD was 32.7/100 000 reaching a maximum of 57.3/100 000 in the 6th decade of life.ConclusionsPrevalence of ADPKD is overestimated by 2- to 5-fold and close to the limit of RDs which may be of broad clinical, logistic and policy implications. © 2013 The Authors.


Reinke P.,University Hospital Charite | Budde K.,University Hospital Charite | Hugo C.,TU Dresden | Petersen P.,University Hospital of Tuebingen | And 8 more authors.
Transplantation Proceedings | Year: 2011

Gastrointestinal (GI) complications such as diarrhea or indigestion frequently occur in renal graft recipients treated with mycophenolate mofetil (MMF), requiring dose reductions to reduce side effects, thereby increasing the risk of rejection episodes and graft loss. In a prospective clinical trial, the immunosuppressive therapy of renal graft recipients was converted from MMF to enteric-coated mycophenolate sodium (EC-MPS) to identify a strategy to reduce GI symptoms without dose reduction. At baseline and 68 weeks later patients filled in 4 questionnaires related to GI symptoms and general and health-related quality of life. In 15 German study centers, 196 renal graft recipients (mean age 49.5 ± 13.5 years; male/female, 120/76) were included; 51.0% of patients suffered from GI complications at baseline. The Gastrointestinal Symptom Rating Scale score decreased significantly (P < .001) in patients with GI complications from 2.61 ± 0.86 at baseline to 2.14 ± 0.86 at visit 2. Health-related and general quality of life improved significantly. Fifty percent of patients with GI symptoms and 34% of the total per protocol population reported an improvement of their physical condition after converting the medication. In conclusion, conversion from MMF to EC-MPS reduces GI complications in renal graft recipients, reduces the patients' physical discomfort, and maintains their quality of life. (ClinicalTrials.gov number NCT00149968.) © 2011 Elsevier Inc.


Nowack R.,Center for Nephrology and Dialysis | Balle C.,Center for Nephrology and Dialysis | Birnkammer F.,Center for Nephrology and Dialysis | Koch W.,Center for Nephrology and Dialysis | And 2 more authors.
Journal of Medicinal Food | Year: 2011

The incidence and severity of interactions of herbal products with calcineurin inhibitor (CNI) metabolism in renal transplant recipients have not been systematically investigated. These patients have a high rate of herbal product consumption, including products interfering with CNI metabolism. The study aimed at identifying an impact of herbs and foods on CNI metabolism in a cohort of renal transplant recipients by conducting dietary interviews (1) in patients with very low and high CNI maintenance dose requirements and (2) by retrospective analysis of unexplained marked deviations from CNI baseline trough levels. Of 73 renal transplant recipients, 59 were treated with a CNI-based immunosuppressive regimen. Seven patients with an exceptionally high or low CNI dose were interviewed. Five of these seven patients had not consumed any plant product with known influence on CNI metabolism. In one patient chicory-coffee and bitter chocolate had been suspected as contributing to high CNI dose requirement, but the dose could not be lowered after discontinuation of these foods. Participating nephrologists reported three as yet unexplained temporary deviations from baseline CNI trough levels, of which two could be linked to newly started consumption of high volumes of herbal teas and the other to St. John's wort. Consumption of herbal products within the study cohort had no detectable impact on maintenance doses of CNI. However, herbal products, and specifically teas when consumed by the liter, could be linked to temporary strong deviations from CNI trough levels. The study demonstrates that as yet unnoticed herbal interactions with CNI can be detected by detailed dietary analysis, but that the overall impact on maintenance doses of CNI appears to be low. © 2011, Mary Ann Liebert, Inc.


Petrovic D.,Center for Nephrology and Dialysis | Canovic P.,University of Kragujevac | Mijailovic Z.,Clinical Center Kragujevac | Jovicic B.P.,Clinical Center Kragujevac | Jacovic S.,Agency for Medicines and Medical Devices of the Republic of Serbia
Medicinski Casopis | Year: 2015

Hemolytic uremic syndrome (HUS) is a clinical syndrome that is manifested by thrombocytopenia, hemolytic anemia and acute renal failure. A typical HUS is caused by the action of verotoxin on endothelial cells of small blood vessels of the kidneys and the brain. The disorder of regulation of the alternative pathway of the complement system (mutations of genes for proteins that regulate the activity of the alternative complement system, antibodies to the complement factor H) plays the main role in the pathogenesis of atypical HUS. The disease is clinically manifested by symptoms and signs of damage to the kidneys and brain. The diagnosis of HUS is set on the basis of the reduced number of platelets, microangiopathic hemolytic anemia (negative Coombs test, decreased haptoglobin concentration, increased serum total bilirubin and lactate dehydrogenase, the number of schizonts in peripheral blood smear) and increased creatinine concentration in serum. To distinguish the typical from the atypical HUS it is necessary to perform microbiological examination chairs, measured titer anti-verotoxin antibodies and anti-lipopolysaccharide-antibodies and determine the activity of the enzyme ADAMTS13 (mutations in ADAMTS13, anti-ADAMTS13 antibody) and examine the activity of the alternative pathway of the complement system (C3 component of complement, the complement factor H. I, B, expression of MCP on mononuclear cells from peripheral blood. anti-CFH-antibodies). Patients with typical HUS infection are treated with solutions for infusion, antibiotics that do not increase the release of verotoxin dialysis and supportive therapy. In patients with atypical HUS, a therapeutic plasmapheresis is a first-line process, while in patients where there is resistance or dependence of applied plasmapheresis the blocker of the C5 component of complement (eculizumab) is used. © 2015, Serbian Medical Society. All Rights Reserved.


Petrovic D.,Center for Nephrology and Dialysis | Jagic N.,Center for Radiology Diagnostics | Miloradovic V.,Clinical Center Kragujevac | Nikolic A.,Clinical Center Kragujevac | Stojimirovic B.,Institute for Urology and Nephrology
Serbian Journal of Experimental and Clinical Research | Year: 2011

Cardiovascular diseases present a leading cause of death in patients treated with haemodialysis. The rate of cardiovascular mortality in this population is approximately 9% on an annual basis, with left ventricular hypertrophy, ischemic heart diseases and heart failure having the highest rates of mortality. Left ventricular hypertrophy is present in 75-80% of haemodialysis- treated patients. The most important risk factors for the progression of left ventricular hypertrophy are: hypertension, arteriosclerosis, secondary aortic stenosis, anaemia, increased volume of extracellular fluid and increased blood flow through the vascular access for haemodialysis. Left ventricular hypertrophy is present when the left ventricular mass index on echocardiography exceeds 131 g/m2 in males and 100 g/m2 in females. Left ventricular hypertrophy is a risk factor of unfavourable outcome in patients treated with haemodialysis. The identification of patients with increased risk of progression of left ventricular hypertrophy, the timely implementation of adequate treatment, and the realisation and maintenance of targeted values of risk factors decelerates the progression of the hypertrophy and leads to the regression of existing left ventricular hypertrophy, the reduction of cardiovascular morbidity and mortality rates and the improvement of the quality of life of patients treated with haemodialysis.


Petrovic D.,Center for Nephrology and Dialysis | Jagic N.,Center for Radiology Diagnostics | Miloradovic V.,Clinical Center Kragujevac | Nikolic A.,Clinical Center Kragujevac | Stojimirovic B.,Institute for Urology and Nephrology
Serbian Journal of Experimental and Clinical Research | Year: 2010

Cardio-Renal Syndrome is defined as pathophysiological dysfunction of the heart and kidneys in which an acute or chronic abnormality of one organ favours either the acute or chronic disorder of the other one. Due to complex interactions between the heart and kidneys, Cardio-Renal Syndrome is divided into five types: Cardio-Renal Syndrome type 1 (Acute Cardio-Renal Syndrome) is defined as acute kidney dysfunction as a result of acute heart failure. Cardio-Renal Syndrome type 2 (Chronic Cardio-Renal Syndrome) is a progressive chronic kidney disorder as a result of chronic heart failure. Cardio-Renal Syndrome type 3 (Acute Reno-Cardial Syndrome) is defined as an acute heart abnormality due to acute kidney dysfunction. Cardio-Renal Syndrome type 4 (Chronic Reno-Cardial Syndrome) is defined as a chronic heart function disorder as a result of a chronic kidney disorder. Cardio-Renal Syndrome type 5 (Secondary Cardio-Renal Syndrome) is defined as either a permanent or temporary abnormality of both organs due to systemic disease. Early detection of kidney and heart disease and timely and adequate therapy can prevent the development of Cardio-Renal syndrome and reduce the overall expense of therapy.

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