A systematic review and meta-analysis of mortality and kidney function in uranium-exposed individuals.

BACKGROUND: Humans are exposed to uranium (U) in a variety of applications. Both animal and observational human studies support an associated U nephrotoxicity. Few statistical syntheses of the human data have been performed and these analyses are limited in the types of exposures considered. OBJECTIVES: This study aims to evaluate the state of current evidence and to expand on existing meta-analyses by systematically evaluating kidney-associated causes of mortality in multiple U-exposed populations. This study also aims to evaluate the effect of U exposure on kidney function and biomarkers of kidney injury. METHODS: The published and grey literature were systematically reviewed for studies that reported Standardized Mortality Ratios (SMR) for kidney cancer, chronic nephritis/nephrosis, all-cause mortality, diabetes, all circulatory/heart disease, and/or ischemic heart disease in U-exposed humans. Studies that reported kidney biomarker measures for U-exposed versus control subjects were identified separately. RESULTS: 36 studies were included. The studies were parsed into subgroups based on setting of exposure. Analysis of kidney cancer and chronic nephritis/nephrosis mortality demonstrated an SMR of 0.93 (95CI: 0.82-1.05) and 0.82 (95CI: 0.70-0.96), respectively. The other clinical outcomes evaluated also demonstrated mortality deficits in exposed relative to unexposed individuals. Subgroup analyses demonstrated similar mortality deficits. Conversely, biomarker analyses suggested better kidney function in the controls, but none of these differences reached significance. DISCUSSION: Given that most of the included mortality studies were conducted in occupational populations, the mortality deficits observed in our analyses were likely due to the healthy-worker effect. Additionally, our analyses of kidney biomarkers were severely limited by low precision due to a low number of available studies and small study-size. Future work needs to evaluate the progression of chronic and to end-stage kidney disease in community-based populations to better assess the full impact of prolonged chronic U exposure on kidney outcomes.

[Laparoscopic pyeloplasty combined with ultrasonic lithotripsy via nephroscope for treatment of ureteropelvic junction obstruction with renal calculi].

OBJECTIVE: To investigate the efficacy and safety of laparoscopic pyeloplasty combined with ultrasonic lithotripsy via nephroscope in the treatment of ureteropelvic junction obstruction (UPJO) with renal calculi. METHODS: From June 2016 to January 2022, eight patients including five males and three females underwent laparoscopic pyeloplasty combined with ultrasonic lithotripsy via 19.5F(1F≈0.33 mm) nephroscope in Peking University People' s Hospital. The age ranged from 23-51 years (mean: 40.5 years) and the body mass index (BMI) ranged from 18.8-32.4 kg/m2 (mean 27.0 kg/m2). The lesion located on the left side in all of the eight patients. Two patients had solitary kidney and one patient had horseshoe kidney. Solitary stone was seen in one patient and the other seven patients suffered multiple stones, with two patients had staghorn stones. The largest diameter of stones ranged from 0.6-2.5 cm (mean: 1.5 cm). CT or ultrasound showed that moderate nephrosis was seen in five patients and severe nephrosis was seen in three patients. During surgery, after exposure of renal pelvis and proximal ureter, a small incision of 1.5 cm was performed in the anterior wall of the renal pelvis, and a 19.5F nephroscope was introduced into renal pelvis through laparoscopic trocar and renal pelvis incision. Stones were fragmented and sucked out by 3.3 mm ultrasonic probe placed through nephroscope. After stones were removed, modified laparoscopic pyeloplasty was performed. RESULTS: Surgery was successfully completed in all of the eight patients without conversion to open surgery. The operation time ranged from 160-254 min (mean 213 min) and the time of nephroscopic management time was 25-40 min (mean: 33 min). The hemoglobin was decreased by 3-21 g/L (mean: 10.3 g/L). The stone-free rate was 75% (6/8 cases), stones were incompletely removed in two patients due to abnormal intrarenal structure. The modified Clavien classification system (MCCS) grade ⅢA complication occurred in one patient postoperatively, which was nephrosis due to intrarenal bleeding, and nephrostomy was performed. With the mean follow-up of 30 months (ranged from 2-68 months), there was no evidence of obstruction in all the patients, and one patient underwent percutaneous nephrolithotomy to treat residual calculi. CONCLUSION: Laparoscopic pyeloplasty combined with ultrasonic lithotripsy via 19.5F nephroscope is feasible and safe, and could be a complementary method to treat UPJO and renal calculi.

Analysis of chronic kidney disease among national hospitalization data with 14 million children.

BACKGROUND: The main purpose was to determine basic epidemiological data on CKD among hospitalized pediatric patients in China. METHODS: Data from pediatric inpatients with CKD hospitalized from June 1, 2013 to May 31, 2017 were extracted from the electronic records of HQMS database, which includes over 14 million inpatients. Codes from the 10th revision of the International Classification of Diseases (ICD-10) were used to search the database. RESULTS: A total of 524 primary diseases of CKD were included in this study. In all, there were 278 231 pediatric inpatients with CKD, which accounted for 1.95 % of the 14 250 594 pediatric inpatients registered in the HQMS database. The number of pediatric inpatients with CKD was 67 498 in 2013, 76 810 in 2014, 81 665 in 2015 and 82 649 in 2016, which accounted for 1.93 %, 1.93 %, 1.99 and 2.09 %, respectively, of the total population of pediatric inpatients. The etiology of CKD was secondary nephrosis in 37.95 % of cases, which ranked first and followed by CAKUT with a percentage of 24.61 %. Glomerular diseases and cystic kidney disease accounted for 21.18 and 5.07 %, respectively. Among all 278 231 patients, 6 581 (2.37 %) had a primary discharge diagnosis of CKD. The renal pathology findings of CKD showed that IgA accounted for 51.17 %. CONCLUSIONS: This study provides a descriptive analysis of the hospitalized population of pediatric CKD patients. Our study provides important, fundamental data for policy making and legislation, registry implementation and the diagnosis, treatment and prevention of CKD in China.

Novel homozygous OSGEP gene pathogenic variants in two unrelated patients with Galloway-Mowat syndrome: case report and review of the literature.

BACKGROUND: Galloway-Mowat syndrome (GAMOS) is a rare autosomal recessive disorder characterized by early-onset nephrotic syndrome and microcephaly with brain anomalies. WDR73 pathogenic variants were described as the first genetic cause of GAMOS and, very recently, four novel causative genes, OSGEP, LAGE3, TP53RK, and TPRKB, have been identified. CASE PRESENTATION: We present the clinical and genetic characteristics of two unrelated infants with clinical suspicion of GAMOS who were born from consanguineous parents. Both patients showed a similar clinical presentation, with early-onset nephrotic syndrome, microcephaly, brain atrophy, developmental delay, axial hypotonia, and early fatality. We identified two novel likely disease-causing variants in the OSGEP gene. These two cases, in conjunction with the findings of a literature review, indicate that OSGEP pathogenic variants are associated with an earlier onset of nephrotic syndrome and shorter life expectancy than WDR73 pathogenic variants. CONCLUSIONS: Our findings expand the spectrum of pathogenic variants in the OSGEP gene and, taken in conjunction with the results of the literature review, suggest that the OSGEP gene should be considered the main known monogenic cause of GAMOS. Early genetic diagnosis of GAMOS is of paramount importance for genetic counseling and family planning.

Familial congenital choanal atresia with GATA3 associated hypoparathyroidism-deafness-renal dysplasia syndrome unidentified on auditory brainstem response.

Hypoparathyroidism-deafness-renal dysplasia (HDR) syndrome is a rare autosomal dominant disorder primarily caused by GATA3 haploinsufficiency and is challenging to diagnose in early childhood. We report a Japanese family with HDR syndrome and congenital choanal atresia. The 6-year-old female proband was diagnosed with epilepsy at the age of three. Under carbamazepine monotherapy, the patient presented hypoparathyroidism accompanied by severe hypocalcemia. Subsequently, renal ultrasound analysis revealed bilateral multicystic dysplastic kidneys. Because she had difficulty hearing, we sequenced GATA3 and determined that she had a c.708_709insC (p.Ser237Glnfs*66) allelic variant in exon 3. As a result, we found a family of this disease. Each family member, including her grandfather, mother, and two siblings, had HDR syndrome of varying clinical penetrance. We found a craniofacial anomaly, congenital choanal atresia, which was inherited as an autosomal dominant trait. Hypocalcemia coupled with vitamin D deficiency, triggered by carbamazepine treatment, ultimately revealed the proband's childhood- onset HDR syndrome. Pure-tone audiometry revealed different severities of deafness as well as the progression of sensory hearing loss. However, auditory brainstem response for hearing screening is probably insufficient for ascertaining HDR syndrome in the early stages of life. We presented new clinical clues to diagnose the HDR syndrome.

Nephrological and urological complications of homozygous c.974G>A (p.Arg325Gln) OSGEP mutations.

BACKGROUND: Galloway-Mowat syndrome (GAMOS) (OMIM #251300) is a severe autosomal recessive disease characterized by the combination of early-onset steroid-resistant nephrotic syndrome (SRNS) and microcephaly with brain anomalies caused by WDR73 as well as OSGEP, TP53RK, TPRKB, or LAGE3 mutations. OBJECTIVE: We report on the hitherto undescribed urological and nephrological complications of the homozygous c.974G>A (p.Arg325Gln) OSGEP mutations in a 7-year-old Caucasian girl. CASE DIAGNOSIS: The patient came to the attention of pediatric nephrology at the age of 3 years and 11 months, when she presented with status epilepticus due to profound hypomagnesemia (0.31 mmol/L, normal 0.65-1.05). A 24-h urine demonstrated a magnesium loss of 0.6 mmol/kg/day with associated proteinuria suggesting renal tubulopathy. Subsequently, she developed recurrent urinary tract infections (UTIs) and was diagnosed with neurogenic bladder dysfunction. The patient continued to have UTIs associated with seizures and sequential cultures growing multi-drug-resistant organisms despite of antibiotic prophylaxis. In addition, the proteinuria (median microalbumin/creatinine ratio 647 mg/mmol) increased, and she developed partial Fanconi syndrome. At age 7, she developed a large bladder calculus (3.3 × 3.2 cm) and three left non-obstructing renal calculi associated with elevated urinary cystine, hypercalciuria, and ongoing hypomagnesemia and required surgical intervention. Glomerular filtration rate (GFR) remained normal and she never developed frank nephrotic syndrome (average albumin 31 g/L). CONCLUSIONS: It is unclear if patients with OSGEP mutations with tubular symptoms rather than nephrotic syndrome should be considered a different entity. Nephrological and urological complications of OSGEP mutations can be challenging and require a multidisciplinary approach.

Extending the ophthalmological phenotype of Galloway-Mowat syndrome with distinct retinal dysfunction: a report and review of ocular findings.

BACKGROUND: Galloway-Mowat syndrome (GMS) is a rare autosomal recessive condition first described in 1968 and characterized by microcephaly and infantile onset of central nervous system (CNS) abnormalities resulting in severely delayed psychomotor development, cerebellar atrophy, epilepsy, and ataxia, as well as renal abnormalities such as nephrotic syndrome, proteinuria, end-stage renal disease (ESRD), and hiatal hernia. CASE PRESENTATION: We describe a GMS case diagnosed with homozygous missense mutation in the WDR73 gene, with absence of renal abnormalities. We expanded the clinical phenotype of GMS with WDR73 gene defect to include retinal dysfunction with missense mutation and developmental dysplasia of the hip. We compared eye findings of our case to previously reported cases, and we present an electroretinogram (ERG) picture for the first time in the literature. CONCLUSION: We recommend that clinicians screen patients with GM syndrome for retinal dysfunction and that a skeletal survey should be done to detect developmental dysplasia of the hip (DDH) so as to provide for early intervention.

Unusual Proliferative Glomerulonephritis in a Patient Diagnosed to Have Hypoparathyroidism, Sensorineural Deafness, and Renal Dysplasia (HDR) Syndrome with a Novel Mutation in the GATA3 Gene.

Hypoparathyroidism, sensorineural deafness, and renal dysplasia (HDR) syndrome is a rare autosomal dominant disease caused by GATA3 mutations. Although several cases with variable renal features have been reported, the presence of histological changes within the glomeruli in adult patients is unclear. We herein report an adult case of HDR syndrome with a novel p.C288W (TGC>TGG) missense mutation in GATA3. His renal histology showed a membranoproliferative glomerulonephritis-like glomerular lesion. Additional renal histological analyses of HDR syndrome patients will be needed to clarify the role of GATA3 in both the developing and adult kidney.

Vitamin D deficiency in a patient with HDR syndrome.

The case of a patient with clinical symptoms, laboratory and imaging findings of hypoparathyroidism, sensorineural deafness, renal dysplasia HDR, or Barakat syndrome (hypoparathyroidism, deafness, renal dysplasia), and vitamin D deficiency, is presented. A Caucasian man aged 51 years with a history of chronic hypocalcaemia since childhood, was admitted with hypertonia of the body and extremities, and loss of consciousness. On admission, he was found to have severe hypocalcaemia, hyperphosphataemia, severe hypoparathyroidism, low serum magnesium and mild renal insufficiency. Calcium gluconate was administered intravenously supplemented with magnesium, and the patient recovered consciousness while clinical and laboratory findings improved. Evaluation revealed left renal aplasia and sensorineural deafness affecting both ears. Vitamin D deficiency was also present. He was given calcium and vitamin D supplements orally, and the hypocalcaemia was corrected. This case is described as it is an extremely rare case of HDR syndrome with concurrent vitamin D deficiency.

[Merkel cell carcinoma of the ear lobe complicated with nephrosis syndrome and malignant lymphoma: a case report].

Here we report a rare case of Merkel cell carcinoma complicated with nephrosis and malignant lymphoma. A 79-year-old male, who had undergone rectectomy due to colorectal cancer about 10 years previously, was diagnosed as Merkel cell carcinoma of the left ear lobe with lymph node metastases. Tumor resection and lymph node dissection were performed. A year later, follow-up PET-CT revealed a small hot spot at the ileocecum without apparent tumor formation based on examination by colonoscopy. The patient received 56 Gy of radiation. Two months later, he developed new-onset nephrosis followed by renal failure, and was referred to our hospital (Cr 4.26 mg/dL, UA 13.5 mg/dL, Alb 2.1 g/dL). Further examination negated the possibility of vasculitis, collagen disease, or myeloma kidney. Since his renal function continued to decline, causing uremic symptoms, he was hospitalized and underwent hemodialysis soon after referral. Abdominal CT scan revealed an ileocecal mass with multiple abdominal lymphadenopathy, which was later diagnosed as diffuse large B-cell lymphoma (stage IV) by tumor biopsy. Corticosteroid therapy (prednisolone 60 mg/day) was soon initiated with no response. Local skin redness and blister formation at the left shoulder emerged gradually, which strongly suggested a local recurrence of Merkel cell carcinoma. Despite the use of rituximab, the patient's general condition deteriorated without any sign of recovery. Three months after the start of dialysis, we discontinued dialysis therapy due to his poor health status, and eventually he died of cachexia. Autopsy revealed triple cancers: rectal cancer, Merkel cell carcinoma, and malignant lymphoma. In addition to the case report, we will summarize and discuss former similar case reports in the literature.

Neonatal diagnosis of a patient with hypoparathyroidism, sensorineural deafness and renal dysplasia (HDR) syndrome associated with cerebral infarction.

Hypoparathyroidism, sensorineural deafness and renal dysplasia syndrome (HDRS) is comprised of a triad of conditions. It is an autosomal dominant condition caused by mutations in the GATA3 gene, located at 10p15, a critical region in the development of the embryonic parathyroid glands, inner ear, and kidneys. Here we describe the case of a patient with all three components of HDR syndrome diagnosed in the neonatal period who presented with cerebral infarction, hypocalcemia, and renal anomalies. Upon chromosomal microarray he was found to have an interstitial deletion at 10p, which produced a partial deletion in the GATA3 gene.

Reduced B lymphoid kinase (Blk) expression enhances proinflammatory cytokine production and induces nephrosis in C57BL/6-lpr/lpr mice.

BLK, which encodes B lymphoid kinase, was recently identified in genome wide association studies as a susceptibility gene for systemic lupus erythematosus (SLE), and risk alleles mapping to the BLK locus result in reduced gene expression. To determine whether BLK is indeed a bona fide susceptibility gene, we developed an experimental mouse model, namely the Blk+/-.lpr/lpr (Blk+/-.lpr) mouse, in which Blk expression levels are reduced to levels comparable to those in individuals carrying a risk allele. Here, we report that Blk is expressed not only in B cells, but also in IL-17-producing γδ and DN αß T cells and in plasmacytoid dendritic cells (pDCs). Moreover, we found that solely reducing Blk expression in C57BL/6-lpr/lpr mice enhanced proinflammatory cytokine production and accelerated the onset of lymphoproliferation, proteinuria, and kidney disease. Together, these findings suggest that BLK risk alleles confer susceptibility to SLE through the dysregulation of a proinflammatory cytokine network.

Two distinct WT1 mutations identified in patients and relatives with isolated nephrotic proteinuria.

Wilms' tumor type 1 gene (WT1) encodes a zinc-finger transcription factor that plays a key role during genitourinary development and in adult kidney. Mutations in exons 8 and 9 are associated with Denys-Drash Syndrome, whereas those occurring in the intron 9 donor splice site are associated with Frasier Syndrome. Familial cases of WT1 mutations are rare with only few cases described in the literature, whereas cases of WT1 mutations associated with isolated nephrotic proteinuria with or without focal segmental glomerular sclerosis (FSGS) are even rarer. Exons 8 and 9 of WT1 gene were analyzed in two non-related female patients and their parents. Patient 1, who presented with isolated nephrotic proteinuria and histologic pattern of FSGS, is heterozygous for the mutation c.1227+4C>T. This mutation was inherited from her mother, who had undergone kidney transplant due to FSGS. Patient 2 is heterozygous for the novel c.1178C>T transition inherited from her father. The putative effect of this nucleotide substitution on WT1 protein is p.Ser393Phe mutation located within the third zinc-finger domain. The patient and her father presented, respectively, isolated nephrotic proteinuria and chronic renal failure. These data highlight the importance of the inclusion of WT1 gene mutational analysis in patients with isolated nephrotic proteinuria, especially when similar conditions are referred to the family.

Co-occurrence of 22q11 deletion syndrome and HDR syndrome.

22q11 deletion syndrome is one of the most common chromosomal deletion syndromes and is usually caused by a 1.5-3.0 Mb deletion at chromosome 22q11.2. It is characterized by hypocalcemia resulting from hypoplasia of the parathyroid glands, hypoplasia of the thymus, and defects of the cardiac outflow tract. We encountered a Japanese boy presenting with an unusually severe phenotype of 22q11 deletion syndrome, including progressive renal failure and severe intellectual disabilities. Diagnostic testing using fluorescent in situ hybridization revealed deletion of the 22q11 region, but this did not explain the additional complications. Copy number analysis was therefore performed using whole genome single nucleotide polymorphism (SNP) assay, which identified an additional de novo deletion at 10p14. This region is the locus for hypoparathyroidism, deafness, and renal dysplasia (HDR) syndrome caused by haploinsufficiency of GATA3. Together, these two syndromes sufficiently explain the patient's phenotype. This is the first known case report of the co-occurrence of 22q11 deletion syndrome and HDR syndrome. As the two syndromes overlap clinically, this study indicates the importance of carrying out careful clinical and genetic assessment of patients with atypical clinical phenotypes or unique complications. Unbiased genetic analysis using whole genome copy number SNP arrays is especially useful for detecting such rare double mutations.

Experimentally induced puromycine aminonucleoside nephrosis (PAN) in rats: evaluation of angiogenic protein platelet-derived endothelial cell growth factor (PD-ECGF) expression in glomeruli.

BACKGROUND: In experimentally induced puromycine aminonucleoside nephrosis (PAN) animal models, nephrotic syndrome with minimal change disease and focal and segmental sclerosis-like nephritis similar to that in human is demonstrated; however, the real mechanism of PAN is not yet elucidated. Platelet derived endothelial cell growth factor (PD-ECGF), an endothelial mitogen protein, is believed to take part in microvessel formation and in stimulation of angiogenesis and its expression has not been totally demonstrated in PAN rats yet. In this study, we aimed to examine PD-ECGF expression in acute and chronic PAN induced in rats and find out the association between its expression and the stages of angiogenesis in kidney. METHODS: For the experiment, twenty-four Male Wistar Albino rats were used and divided into four groups; control group (n = 6), pre-proteinuria group (n = 6), acute group (n = 6) and chronic group (n = 6). We compared statistically all data by One-way ANOVA Test followed by Dunn Multiple Comparison Test. RESULTS: Proteinurea levels in control and pre-proteinuria groups were not statistically different; however, it was remarkably higher in the acute nephrosis group and significantly greater in the chronic nephrosis group than control group (p < 0.0025). In pre-proteinuria group, the serum albumin and creatinine clearances also did not significantly differ from the control group. On the other hand, in the acute and chronic nephrosis groups, serum albumin and creatinine clearances progressively decreased (p < 0.05). In our immunohistochemical studies, we showed elevated PD-ECGF expression in glomeruli of acute and chronic PAN rats. Microscopic and ultrastructural appearances of the glomeruli of acute and chronic PAN showed various sequential steps of angiogenesis, macrophages and immature capillaries with primitive lumens and apoptotic endothelial cells in the increased mesangial matrix. CONCLUSIONS: It is reported that acute and chronic PAN progressively increase PD-ECGF expression and following induction of angiogenesis in the affected glomeruli.

Infantile nephrotic syndrome with microcephaly and global developmental delay: the Galloway Mowat Syndrome.

The authors present the first case of Galloway Mowat Syndrome (GMS), a rare disorder comprising of nephrotic syndrome in association with microcephaly, from India. An 11-mo-old girl with microcephaly, developmental delay and nystagmus presented with nephrotic syndrome. The perinatal and neonatal periods had been uneventful. The renal biopsy revealed mesangial proliferation with IgM deposition, while MRI of the brain showed hypomyelination. Molecular diagnosis by polymerase chain reaction (PCR) did not reveal any pathogenic sequences in the exons and the flanking intronic regions of the NPHS2 gene and LAMB2 gene. The infant responded to prednisolone. GMS must be suspected whenever microcephaly and global developmental delay occurs in association with nephrotic syndrome, as this is important for prognostication and genetic counseling. The genetics of GMS remains an enigma and further research is required to delineate the pathogenesis of this disorder.

Acute kidney injury due to osmotic nephrosis following intraoperative placement of an intraperitoneal antiadhesive barrier.

In recent years, a common strategy for the prevention of postsurgical intra-abdominal adhesions has been intrasurgical placement of adhesion barriers into the peritoneal cavity. Osmotic agents, such as various polysaccharides, frequently are used as antiadhesive materials. The effects of these materials on kidney function have not yet been studied. We report a case of an individual with pre-existing chronic kidney disease who developed acute kidney injury after surgical placement of an antiadhesive barrier of macromolecular polysaccharides. A kidney biopsy, performed because of persistent kidney failure, showed tubular cell lesions compatible with osmotic nephrosis lesions. This case suggests that use of polysaccharide-containing antiadhesive barriers can induce severe kidney damage. Such barriers should be used with caution in patients with abnormal kidney function to prevent irreversible damage.

Presumed atypical HDR syndrome associated with Band Keratopathy and pigmentary retinopathy.

This report describes presumed atypical hypoparathyroidism, deafness, and renal dysplasia (HDR) syndrome associated with unexpected ocular findings. The patient had exotropia, bilateral band keratopathy, and pigmentary retinopathy, including attenuated retinal vessels and atrophy of the retinal pigment epithelium. Even though the calcific plaques were successfully removed, visual acuity in both eyes gradually decreased and electroretinography was extinguished.

Absence of hypoalbuminemia despite nephrotic proteinuria in focal segmental glomerulosclerosis secondary to polycythemia vera.

In addition to displaying geographic variation, focal segmental glomerulosclerosis (FSGS) has become the commonest cause of the nephrotic syndrome seen in adults in recent years. Secondary FSGS in particular, is observed when glomerular workload is increased. Polycythemia vera (PV) is a hematological disease characterized by abnormal proliferation in the erythroid series. The number of case reports belonging to glomerulonephritis secondary to PV is limited. In the literature, there are few reports of FSGS. One study pointed out that the presence of normoalbuminemia was detected in patients with FSGS secondary to hyperfiltration when there was nephrotic proteinuria. Here, we report a case of FSGS following a course with normoalbuminemia despite nephrotic range proteinuria developing secondary to PV. Our case is the first report in the literature with thes characteristics.

[Questionnaire for assessing the risk of venous thromboembolism in hospitalized surgical and non-surgical patients in the 4th Hungarian antithrombotic guideline entitled "Risk reduction and treatment of venous thromboembolism"]. / Vénásthromboembolia-kockázati kérdôív kórházban kezelt sebészeti és nem sebészeti betegek részére "A thromboemboliák kockázatának csökkentése és kezelése" címu, 4. magyar antithromboticus irányelvben.

A large proportion of hospitalized surgical and medical patients are at risk for venous thromboembolism. Depending on the type of surgical intervention, venous thrombosis develops in 15-60% of surgical patients without prophylaxis. Although venous thromboembolism is most often considered to be associated with recent surgery or trauma, 50 to 70% of symptomatic thromboembolic events and 70 to 80% of fatal pulmonary embolisms occur in nonsurgical patients. International and national registries show that the majority of at-risk surgical patients actually received the appropriate thromboembolic prophylaxis. However, despite of international and national recommendations, prophylaxis was not provided for a large proportion of at-risk medical patients. The rate of medical patients receiving prophylaxis should be increased, and appropriate thrombosis prophylaxis should be offered to at-risk medical patients. The thrombosis risk assessment is an important tool to identify patients at increased risk for venous thromboembolism, to simplify decision making on prophylaxis administration, and to improve the adherence to guidelines. When the risk is recognized, if there is no contraindication, prophylaxis should be ordered. The 4th Hungarian Antithrombotic Guideline entitled "Risk reduction and treatment of thromboembolism" calls attention to the importance of risk assessment and for the first time it includes and recommends risk assessment models for hospitalized surgical and medical patients. The risk assessment models are presented and the evidence based data for the different risk factors included in these models are reviewed.