STEC colitis mimicking acute severe colitis with life-threatening consequences: a case report.

Acute colitis is a common feature of infection with Shiga-toxin producing Escherichia coli (STEC) and can mimic acute severe ulcerative colitis. Early recognition is important as there is a risk of developing Shiga toxin-induced haemolytic uremic syndrome (STEC-HUS), defined by the triad of microangiopathic haemolytic anemia, thrombocytopenia and organ damage. In severe cases STEC-HUS can cause severe neurological complications and can be fatal. We present a patient with a medical history of refractory ulcerative colitis, where making the diagnosis of STEC-HUS was challenging since the initial clinical presentation was difficult to differentiate from a flare of ulcerative colitis. This case illustrates that STEC induced colitis can mimic acute severe ulcerative colitis. This finding is of utmost clinical importance because of the potential life-threatening complications of STEC-HUS. Therefore it should be excluded promptly in patients with acute severe ulcerative colitis by using multiplex-PCR assay on a faecal sample.

Use of the modified meek technique for the coverage of extensive burn wounds.

INTRODUCTION: Autologous split thickness skin grafting using meshing technique remains the preferred option for the management of deep dermal and full thickness burns. The limited donor site availability seen in patients with extensive burns, however, restricts use of the mesh grafting technique for skin expansion. Meek micrografting was developed to allow for greater expansion, and, therefore, more reliable treatment of extensive burns. This study aimed to present our outcomes using the Meek micrografting technique and identify risk factors for graft failure. METHODS: A retrospective review of patients admitted to our large academic hospital who were treated with the Meek micrografting technique from 2013 to 2022 was conducted. Patient demographics, surgical characteristics and outcomes were reported. Regression analyses were performed to identify factors that influence graft take and reoperation rate. RESULTS: A total of 73 patients with a mean age of 45.7 ± 19.9 years and mean burn size of 60.0 ± 17.8%TBSA, with 45.3 ± 14.9% TBSA being third degree burns, received Meek transplantation. The mean graft take after removal of the pre-folded polyamide gauze at the tenth post-operative day was 75.8 ± 14.7%. Pre-treatment with use of an allograft, longer waiting time between admission and Meek grafting and transplantation over a dermal matrix were identified as positive predictors for graft take, while age was established as a negative predictor. CONCLUSION: By examining the outcomes of the Meek micrografting technique in extensive burn wounds we identified that preconditioning of the wound bed, through allograft or negative pressure wound therapy application, positively correlates with improved outcomes, including higher graft take. At the same time, older age was seen to negatively correlate with graft take. Overall, Meek transplantation displays a favorable safety profile with promising outcomes. Future prospective studies and clinical trials can optimize the procedure and help establish it as the golden standard for extensive and complex burns.

PRECISION: the Belgian molecular profiling program of metastatic cancer for clinical decision and treatment assignment.

PRECISION is an initiative from the Belgian Society of Medical Oncology (BSMO) in collaboration with several stakeholders, encompassing four programs that aim to boost genomic and clinical knowledge with the ultimate goal to offer patients with metastatic solid tumors molecularly guided treatments. The PRECISION 1 study has led to the creation of a clinico-genomic database. The Belgian Approach for Local Laboratory Extensive Tumor Testing (BALLETT) and GeNeo studies will increase the number of patients with advanced cancer that have comprehensive genotyping of their cancer. The PRECISION 2 project consists of investigator-initiated phase II studies aiming to provide access to a targeted drug for patients whose tumors harbor actionable mutations in case the matched drug is not available through reimbursement or clinical trials in Belgium.

Pathogenic neurofibromatosis type 1 (NF1) RNA splicing resolved by targeted RNAseq.

Neurofibromatosis type 1 (NF1) is caused by loss-of-function variants in the NF1 gene. Approximately 10% of these variants affect RNA splicing and are either missed by conventional DNA diagnostics or are misinterpreted by in silico splicing predictions. Therefore, a targeted RNAseq-based approach was designed to detect pathogenic RNA splicing and associated pathogenic DNA variants. For this method RNA was extracted from lymphocytes, followed by targeted RNAseq. Next, an in-house developed tool (QURNAs) was used to calculate the enrichment score (ERS) for each splicing event. This method was thoroughly tested using two different patient cohorts with known pathogenic splice-variants in NF1. In both cohorts all 56 normal reference transcript exon splice junctions, 24 previously described and 45 novel non-reference splicing events were detected. Additionally, all expected pathogenic splice-variants were detected. Eleven patients with NF1 symptoms were subsequently tested, three of which have a known NF1 DNA variant with a putative effect on RNA splicing. This effect could be confirmed for all 3. The other eight patients were previously without any molecular confirmation of their NF1-diagnosis. A deep-intronic pathogenic splice variant could now be identified for two of them (25%). These results suggest that targeted RNAseq can be successfully used to detect pathogenic RNA splicing variants in NF1.

Hyperhomocysteinemia: a trigger for complement-mediated TMA?

A 34-year-old man of North African descent was referred to the emergency department because of malignant hypertension (220/113 mmHg), acute visual disturbances and acute kidney failure (serum creatinine 14.0 mg/dL). Blood analysis was compatible with thrombotic microangiopathy (TMA). Kidney biopsy confirmed this diagnosis with histological changes including intimal edema, arteriolar thrombi, and severe tubulointerstitial damage. Fundoscopy showed hypertensive retinopathy stage IV. Subsequent biochemical screening revealed normal complement testing and a marked elevation in homocysteine concentration (161 µmol/L; normal value 7-15 µmol/L). Other secondary causes of TMA were excluded. Further genetic testing for cobalamin C (cblC) deficiency showed no pathogenic mutations in the MMACHC gene. However, a homozygous c.665C>T polymorphism (NM_005957.4) in the methylenetetrahydrofolate reductase (MTHFR) gene was found explaining the severe hyperhomocysteinemia due to reduced activity of MTHFR. Additional genetic testing for alternative complement pathway proteins showed mutations in the genes encoding factor H and factor B, both categorized as possibly pathogenic using mutation prediction software. This is the first described case of TMA in a patient with severe hyperhomocysteinemia caused by a genetic defect other than cblC. We postulate that endothelial damage due to hyperhomocysteinemia and hypertension could have triggered the TMA episode in this patient with two possible predisposing pathogenic mutations in the alternative complement pathway. Furthermore, our case demonstrates the need for complete full diagnostic testing in patients with TMA.

Surveillance recommendations for patients with Lynch syndrome and FAP : a monocentric study.

BACKGROUND AND STUDY AIMS: The most important causes of hereditary colorectal cancer are Lynch syndrome (LS) and the adenomatous polyposis syndromes (familial adenomatous poly- posis syndrome or FAP, attenuated FAP or AFAP and MUTYH associated polyposis syndrome or MAP). The aim of this study was to investigate whether all patients with a hereditary syndrome within one center receive uniform advice regarding surveillance and treatment. PATIENTS AND METHODS: A retrospective analysis was performed of all electronic patient health records of patients with LS, FAP, AFAP and MAP who received genetic counselling or were followed by a health care specialist at the University Hospital in Ghent. RESULTS: Data from 122 patients were collected. For all patients, recommendations from the medical genetics department were highly consistent. Adherence to their recommendations was good within the center for the management of colon polyps. There was a lack of consistency in the screening and surveillance advice for other tumors in departments other than gastroenterology. Only 33 patients had systematic follow-up consultations to check results and organize surveillance. CONCLUSION: Previously, small studies have suggested that patients with hereditary gastrointestinal cancer syndromes infrequently have surveillance as specified in the guidelines. This study shows almost uniform recommendations and good adherence for surveillance of the colon, but incomplete or contradictory advice for surveillance of other organs. The need for an integrated approach from a multidisciplinary team will only increase in the future, because more families with hereditary cancer are likely to be found due to the increased use of next generation sequencing in cancer diagnostics.

How GDPR Enhances Transparency and Fosters Pseudonymisation in Academic Medical Research.

The European General Data Protection Regulation (GDPR) has dotted the i's and crossed the t's in the context of academic medical research. One year into GDPR, it is clear that a change of mind and the uptake of new procedures is required. Research organisations have been looking at the possibility to establish a code-of-conduct, good practices and/or guidelines for researchers that translate GDPR's abstract principles to concrete measures suitable for implementation. We introduce a proposal for the implementation of GDPR in the context of academic research which involves the processing of health related data, as developed by a multidisciplinary team at the University Hospitals Leuven. The proposal is based on three elements, three stages and six specific safeguards. Transparency and pseudonymisation are considered key to find a balance between the need for researchers to collect and analyse personal data and the increasing wish of data subjects for informational control.

Routine histopathological examination after female-to-male gender-confirming mastectomy.

BACKGROUND: The number of transmen seeking gender-confirming surgery has risen steadily throughout the last decade. Pathologists are increasingly confronted with transmale mastectomy specimens. It is not clear whether routine histopathological examination is useful. This study explored the possible benefit of routine investigation through detailed description of lesions encountered in mastectomy specimens after female-to-male gender-confirming surgery. METHODS: Breast tissue from a cohort of transmen was reviewed. The presence of benign and malignant breast lesions was recorded. The number of terminal duct-lobule units (TDLUs) per ten low-power fields (LPFs) was quantified. Information on hormone therapy and morphometry was retrieved for selected patients. RESULTS: The cohort included 344 subjects with a mean age of 25·8 (range 16-61) years at the time of surgery; the age at surgery decreased significantly over time. Older individuals presented with a significantly higher number of breast lesions. The number of TDLUs per LPF was lower in heavier breasts, but did not correlate with age. Breast lesions, either benign or malignant, were present in 166 individuals (48·3 per cent). Invasive breast cancer was found in two (0·6 per cent); one tumour was an unexpected finding. The number of breast lesions encountered on histopathological examination increased significantly when more tissue blocks were taken. CONCLUSION: The discovery of an unexpected breast cancer in a 31-year-old transman emphasizes the importance of thorough routine histopathological examination of mastectomy specimens. The number of tissue blocks taken should be based on age and breast weight.

Incorporating PARP-inhibitors into clinical routine: A tailored treatment strategy to tackle ovarian cancer.

DNA repair mechanisms play a key role in oncogenesis and cancer progression in women with BRCA mutation-positive (BRCAm) ovarian cancer (OC). The BRCA1/2 and poly(ADP-ribose) polymerase (PARP) proteins are considered the foremost mediators among the various components of double-strand and single-strand repair, respectively. A series of new therapeutic drugs that target PARP have been developed for BRCAm OC. This class of agents provokes tumour-specific cytotoxicity with minimal side effects by inducing synthetic lethality, of which they are the first clinical example. The European Medicines Agency granted accelerated licensing approval for the first-in-class-drug that inhibits PARP, olaparib (Lynparza™, AstraZeneca). Olaparib can be used as a monotherapeutic maintenance treatment in patients with platinum-sensitive relapsed (germline and/or somatic) BRCAm high-grade serous epithelial ovarian, fallopian tube or primary peritoneal cancer responsive to platinum-based chemotherapy. Seen in light of these recent events, this review article will focus on (a) how PARP-inhibitors exploit cancer-specific defects in the homologous recombination repair apparatus and (b) how BRCA testing is implemented in routine clinical care.

Mycobacterium genavense infection in a solid organ recipient: a diagnostic and therapeutic challenge.

Renal transplant recipients are highly susceptible to infections caused by uncommon pathogens because of their immunocompromised state. We report a case of disseminated Mycobacterium genavense infection in a patient with a combined renal and cardiac transplant. Diagnosing M. genavense infections remains a challenge because of the absence of specific clinical symptoms in combination with the difficulties of culturing the organism using standard mycobacterial culture procedures. This clinical case demonstrates the importance of molecular techniques as part of the initial work-up in order to rapidly establish the diagnosis.

Inflammation and the bone-vascular axis in end-stage renal disease.

UNLABELLED: Bone loss and vascular calcification coincide in patients with end-stage renal disease, similar as to what is observed in the general population. In the present bone biopsy study, we provide further evidence that (micro-)inflammation may represent a common soil for both diseases. INTRODUCTION: Vascular calcification is a common complication of end-stage renal disease (ESRD) and is predictive of subsequent cardiovascular disease and mortality. Mounting evidence linking bone disorders with vascular calcification has contributed to the development of the concept of the bone-vascular axis. Inflammation is involved in the pathogenesis of both disorders. The aim of the present study was to evaluate the relationship between aortic calcification, inflammation, and bone histomorphometry in patients with ESRD. METHODS: Parameters of inflammation and mineral metabolism were assessed in 81 ESRD patients (55 ± 13 year, 68 % male) referred for renal transplantation. Static bone histomorphometry parameters were determined on transiliac bone biopsies performed during the transplant procedure. Aortic calcification was quantified on lateral lumbar X-rays using the Kauppila method. RESULTS: Aortic calcification, low bone turnover, and low bone area were observed in 53, 37, and 21 % of patients respectively. Inflammatory markers were found to be independently associated with aortic calcification (hsIL-6) and low bone area (TNF-α). Low bone area associated with aortic calcification, independent of age, diabetes, and inflammation. CONCLUSIONS: Low bone area and inflammation associates with aortic calcification, independent of each other and traditional risk factors. Our data emphasize the role of (micro-)inflammation in the bone-vascular axis in CKD.

BRCA1, BRCA2 and PALB2 mutations and CHEK2 c.1100delC in different South African ethnic groups diagnosed with premenopausal and/or triple negative breast cancer.

BACKGROUND: Current knowledge of the aetiology of hereditary breast cancer in the four main South African population groups (black, coloured, Indian and white) is limited. Risk assessments in the black, coloured and Indian population groups are challenging because of restricted information regarding the underlying genetic contributions to inherited breast cancer in these populations. We focused this study on premenopausal patients (diagnosed with breast cancer before the age of 50; n = 78) and triple negative breast cancer (TNBC) patients (n = 30) from the four South African ethnic groups. The aim of this study was to determine the frequency and spectrum of germline mutations in BRCA1, BRCA2 and PALB2 and to evaluate the presence of the CHEK2 c.1100delC allele in these patients. METHODS: In total, 108 South African breast cancer patients underwent mutation screening using a Next-Generation Sequencing (NGS) approach in combination with Multiplex Ligation-dependent Probe Amplification (MLPA) to detect large rearrangements in BRCA1 and BRCA2. RESULTS: In 13 (12 %) patients a deleterious mutation in BRCA1/2 was detected, three of which were novel mutations in black patients. None of the study participants was found to have an unequivocal pathogenic mutation in PALB2. Two (white) patients tested positive for the CHEK2 c.1100delC mutation, however, one of these also carried a deleterious BRCA2 mutation. Additionally, six variants of unknown clinical significance were identified (4 in BRCA2, 2 in PALB2), all in black patients. Within the group of TNBC patients, a higher mutation frequency was obtained (23.3 %; 7/30) than in the group of patients diagnosed before the age of 50 (7.7 %; 6/78). CONCLUSION: This study highlights the importance of evaluating germline mutations in major breast cancer genes in all of the South African population groups. This NGS study shows that mutation analysis is warranted in South African patients with triple negative and/or in premenopausal breast cancer.

The effect of anastomosis time on outcome in recipients of kidneys donated after brain death: a cohort study.

Whether warm ischemia during the time to complete the vascular anastomoses determines renal allograft function has not been investigated systematically. We investigated the effect of anastomosis time on allograft outcome in 669 first, single kidney transplantations from brain-dead donors. Anastomosis time independently increased the risk of delayed graft function (odds ratio per minute [OR] 1.05, 95% confidence interval [CI] 1.02-1.07, p < 0.001) and independently impaired allograft function after transplantation (p = 0.009, mixed-models repeated-measures analysis). In a subgroup of transplant recipients, protocol-specified biopsies at 3 months (n = 186), 1 year (n = 189), and 2 years (n = 153) were blindly reviewed. Prolonged anastomosis time independently increased the risk of interstitial fibrosis and tubular atrophy on these protocol-specified biopsies posttransplant (p < 0.001, generalized linear models). In conclusion, prolonged anastomosis time is not only detrimental for renal allograft outcome immediately after transplantation, also longer-term allograft function and histology are affected by the duration of this warm ischemia.

Sclerostin Serum Levels and Vascular Calcification Progression in Prevalent Renal Transplant Recipients.

CONTEXT: Vascular calcification (VC) is prevalent and progressive in renal transplant recipients (RTRs). Recent cross-sectional data suggest that activated Wnt signaling contributes to VC. OBJECTIVE: The objective was to investigate whether circulating levels of the Wnt antagonist sclerostin associate with progression of VC. DESIGN: This was a post hoc analysis of the longitudinal observational Brussels Renal Transplant Cohort study. SETTING: The setting was a tertiary care academic hospital. PATIENTS: Coronary artery calcification and aorta calcification were measured by multislice spiral computerized tomography in 268 prevalent RTRs (age, 53 ± 13 y; 61% male) at baseline and remeasured in 189 patients after a median follow-up of 4.4 years. Baseline serum sclerostin levels were assessed on stored blood samples. Regression analysis was performed to identify determinants of baseline VC and progression. MAIN OUTCOME MEASURE: The main outcome measure was progression of VC. RESULTS: VC was present in up to 84% of participants at baseline. Almost half of the patients showed progression of VC, according to Hokanson criteria. The cross-sectional analysis at baseline demonstrated a direct association between sclerostin levels and VC score in univariate analysis, which became inverse after adjustment for age, gender and PTH level. Remarkably, a lower sclerostin level was identified as an independent determinant of a higher baseline aorta calcification score in the final regression model. Moreover, baseline sclerostin levels showed an inverse association with VC progression, at least after adjustment for traditional risk factors. CONCLUSIONS: Serum sclerostin levels inversely associated with VC burden and progression in prevalent RTRs after adjustment for traditional risk factors. Our data corroborate previous findings in nontransplanted chronic kidney disease patients and support the notion that sclerostin may be up-regulated in the vascular wall during the VC process as part of a local counterregulatory mechanism directed to suppress VC. Additional clinical and experimental data are required for confirmation.

Next generation sequencing to determine the cystic fibrosis mutation spectrum in Palestinian population.

An extensive molecular analysis of the CF transmembrane regulator (CFTR) gene was performed to establish the CFTR mutation spectrum and frequencies in the Palestinian population, which can be considered as an understudied population. We used a targeted Next Generation Sequencing approach to sequence the entire coding region and the adjacent sequences of the CFTR gene combined with MLPA analysis of 60 unrelated CF patients. Eighteen different CF-causing mutations, including one previously undescribed mutation p.(Gly1265Arg), were identified. The overall detection rate is up to 67%, and when we consider only CF patients with sweat chloride concentrations >70 mEq/L, we even have a pickup rate of 92%. Whereas p.(Phe508del) is the most frequent allele (35% of the positive cases), 3 other mutations c.2988+1Kbdel8.6Kb, c.1393-1G>A, and p.(Gly85Glu) showed frequencies higher than 5% and a total of 9 mutations account for 84% of the mutations. This limited spectrum of CF mutations is in agreement with the homozygous ethnic origin of the Palestinian population. The relative large portion of patients without a mutation is most likely due to clinical misdiagnosis. Our results will be important in the development of an adequate molecular diagnostic test for CF in Palestine.

Fatal visceral ischemia as a complication of intra-aortic balloon placement.

We present a case of visceral ischemia due to an anatomic versus balloon length mismatch. An 80-year-old women underwent elective coronary artery bypass graft surgery. The direct post-operative period was complicated by low cardiac output, not responding to inotropic or vasopressor drugs. An intra-aortic balloon pump (IABP) was inserted during an explorative rethoracotomy. The first 3 days, an improvement of the hemodynamic function was seen. During this period, hepatic dysfunction, renal failure with need for hemodialysis and rising values of serum lactate were seen. A computed tomography (CT) of the chest and abdomen showed splenic infarction, ascites and signs of gastric and intestinal ischemia. The IABP was blocking the celiac trunk, the superior mesenteric artery and the renal arteries and was immediately removed. The patient died shortly after due to multiple organ failure. To prevent ischemic complications in smaller patients, we advise a follow-up CT after placement of the IABP.

A vestibular schwannoma in a patient with Birt-Hogg-Dube syndrome.

Birt-Hogg Dubé syndrome is an autosomal dominant disease with variable clinical expression. It is characterized by cutaneous manifestations, renal tumors and lung cysts. Other tumors, such as adrenal tumors and tumors originating from the neural crest cells such as meningioma and neurothekeoma have also been described. This syndrome is caused by germline mutations in the folliculin (FLCN) gene located on chromosome 17p. We report, for the first time, a patient with BHDS and a history of a vestibular schwannoma in adolescence. The diagnosis of BHDS was confirmed, by identifying a nonsense mutation in exon 10 of the FLCN gene. A vestibular schwannoma also originates from neural crest cells, just as other neural tumors, previously encountered in patients with BHDS. The reported mutations cause a truncation of the protein, folliculin. The exact role of folliculin is still undetermined. Two different theories suggest the effect of tumorigenesis. One is that folliculin plays an important role in the AMPK-mTOR pathway which leads to proliferation of cells when activated. The other is that the folliculin acts as a possible tumor suppressor gene, since there is a high frequency of second hits in the FLCN-gene. In order to confirm a possible relation of BHDS and neural crest tumors, further research is necessary in the tumorigenesis of the folliculin gene.

Retrospective observational study on the incidence of incisional hernias after colorectal carcinoma resection with follow-up CT scan.

BACKGROUND: Incisional hernia (IH) is the most frequent complication after colorectal carcinoma (CRC) resection. The incidence depends on the method of follow-up, where ultrasound yields a significant number of additional hernias compared to clinical examination alone. Not many studies have evaluated the value of computed tomography (CT) to diagnose IH. METHODS: The CorreCT study is a retrospective cohort study of IH after CRC surgery by clinical examination and by CT, as reported in the medical files. Additional independent reviewing of all CTs by two radiologists was performed. RESULTS: From the oncological database (2004-2008) of the hospital, 598 patients with CRC were identified. The data of 448 consecutive patients who underwent surgery were analyzed. Tumors were resected by laparotomy in 366 patients (81.7 %), by laparoscopy in 76 patients (17.0 %) and by laparotomy after conversion in 6 patients (1.3 %). A clinical follow-up by the surgeon in 282 patients (62.9 %) with a mean duration of 33 months, yielded 49 patients with IH (17.4 %). The mean time of IH diagnosis (T1) was 19 months. Only 16 patients (33 %) underwent a hernia repair. For 363 patients (81.0 %), CT follow-up was available for a mean period of 30 months. In 84 patients (23.1 %), an IH was diagnosed with a mean T1 of 21 months. The review of all CTs by two independent radiologists yielded additional IH in 19 and 21 patients, respectively, increasing the IH rate to 29.1 and 29.7 %, respectively, and with a decrease in mean T1 to 14 months. The inter-observer agreement between the radiologists had a Kappa-statistic of 0.73 (95 % CI 0.65-0.81). For those patients with disagreement between the radiologists, a final agreement was made during an additional reviewing session of both radiologists, increasing the IH rate to 35.0 %. Comparing clinical follow-up, routine CT follow-up, and reassessed CT follow-up we found a statistically significant difference between the three methods of IH detection (p < 0.0001). CONCLUSION: CT follow-up can identify significantly more IH than clinical examination alone, in particular if the radiologist focuses on IH development. Furthermore, we showed that focused CT evaluation diagnosed IH 7 months earlier than routine CT and 5 months earlier than clinical follow-up alone.

Effect of clinical examination and anatomical location on native arteriovenous fistula maturation rate in high risk patients.

BACKGROUND: Maximal use of native arteriovenous fistulas (AVFs) for patients on hemodialysis therapy remains a clinical challenge. Primary failure rates remain high with risk factors such as female gender, diabetes mellitus, lower arm AVF and higher age. We wondered if a strategy of careful clinical examination prior to AVF creation and a preference towards an upper arm AVF in case of doubt about the quality of the vein in patients with any of the above mentioned risk factors, would lead to better maturation rates. METHODS: The records of all patients who received an AVF between January 2005 and December 2009 at our University Hospitals Leuven were studied retrospectively. Demographic data, comorbidity, fistula characteristics, fistula maturation and fistula complications were recorded and analyzed. RESULTS: Of 344 patients enrolled, 156 (45.3%) received a lower arm AVF and 188 (54.7%) an upper arm AVF. Two hundred and seventy-six (80.2%) fistulas had a normal maturation. Lower arm AVF was a significant risk factor for non-maturation in this series (73.1% versus 86.2% ; p = 0,0024). Female gender, diabetes and high age were not, but female gender showed a significant difference in distribution in upper arm versus lower arm fistulas (62.40% versus 37.6% ; p = 0,0218). CONCLUSIONS: Careful clinical examination prior to upper or lower arm AVF creation together with the integration of risk assessment in the planning of AVF is worthwhile. A preference towards upper arm fistulas if major risk factors are -present can improve overall maturation rates and lead to the same maturation rates as in the overall dialysis population. Therefore, the presence of risk factors for non-maturation should not lead to the underuse of native AVFs.

Post-streptococcal glomerulonephritis: not an extinct disease!

We present the case of a 29-year-old type 1 diabetic patient with the diagnosis of acute post-streptococcal glomerulonephritis. The incidence of this textbook example of acute glomerulonephritis has dropped dramatically in the developed world during the past decades due to the more widespread use of antibiotics. However, the present case illustrates that it is not an extinct disease and that clinicians should be aware of this entity. Particular attention is needed for the fact that the clinical context in which the disease occurs may be different from the classical "post-angina" presentation.