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Transient acantholytic dermatosis, also known as Grover's disease, is an acquired dermatological condition characterised by the sudden emergence of pruritic, erythematous papules, or vesicles, primarily affecting the trunk. It is observed most commonly in men older than 50 years. Histology typically demonstrates a pattern of focal acantholysis within the epidermis, dyskeratotic cells including corps ronds and grains, and a variable perivascular lymphocytic infiltrate in the upper dermis. While its aetiology is not well understood, recognised triggers include excessive heat, sweating, sun exposure, and certain drugs, such as chemotherapy agents. More recently, isolated reports of Grover's disease and Grover-like skin eruptions have been described in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and following COVID-19 vaccination. We report the case of a 65-year-old man who presented to secondary care with a nine-day history of an intensely pruritic rash over his chest and back. On internal medical workup, he was found to have SARS-CoV-2 infection and rapidly deteriorated due to coronavirus disease 2019 (COVID-19)-associated pneumonia, necessitating a 10-day hospital admission for supportive care. Diagnostic workup of his skin lesions confirmed transient acantholytic dermatosis (Grover's disease), which resolved following a course of oral corticosteroids. This case underscores the rare but significant association between Grover's disease and COVID-19, contributing valuable insights to the evolving body of literature on cutaneous lesions associated with SARS-CoV-2 infection, and highlighting the importance of considering SARS-CoV-2 screening as part of the diagnostic workup for patients presenting with Grover-like skin eruptions.

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INTRODUCTION: CorMatrix is an acellular extracellular matrix that acts as a biological scaffold and remodels into site-specific tissue. We used it for the (re)construction of arteriovenous fistulas. METHODS: In this prospective pilot case study, we used CorMatrix in six patients. We included patients who required vascular access reconstruction due to thrombosis of unsalvageable arteriovenous fistulas, patients with high-flow arteriovenous fistulas and patients with microvasculature in which autologous arteriovenous fistulas did not mature, requiring reconstruction with a graft. We sutured the CorMatrix plate into a tubular shape and then constructed arterial and venous anastomoses. RESULTS: There were no periprocedural complications, CorMatrix-related infections, bleeding or limb swelling after the procedures. CorMatrix was first punctured after 8-10 weeks. In five patients, a percutaneous angioplasty due to CorMatrix stenosis was performed; in one patient, a stent was placed due to refractory stenosis. We observed eight thromboses during the observation period (four in one patient). Perianastomotic stenosis of CorMatrix and interdialytic hypotension were the causes of the thrombosis in five patients, cephalic arch stenosis in two patients and thromboembolism to the brachial artery and arteriovenous fistula in one patient. Thrombendarteriectomy was successful in 87.5% of patients, and one patient required arteriovenous fistula reconstruction. After a median observation period of 12.5 (range 4-23) months, all arteriovenous fistulas were patent, with a median brachial artery flow of 1450 (range 700-1700) mL/min. CONCLUSION: Arteriovenous fistula (re)construction with CorMatrix seems to be feasible and safe, with a relatively high incidence of neointimal hyperplasia, predominantly at venous anastomoses, but additional clinical studies are needed.

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AIMS: We evaluated the impact of hemodialysis on mortality and hospital readmission in patients with cardiorenal syndrome. METHODS: All patients were NYHA IV functional class and underwent laboratory testing, echocardiography, and cardiac functional testing. Hemodialysis was indicated in patients with progressive decline of kidney function and consequent failure to titrate heart failure medication as well as in patients with hypervolemia that was resistant to conservative treatment with more than 4 annual hospitalizations due to heart failure and/or concomitant chronic kidney disease stage III - IV. Patients were treated with low-efficacy bicarbonate hemodialysis with permanent central venous catheter used as vascular access. RESULTS: Since 2004, 67 patients were started on hemodialysis because of cardiorenal syndrome. Hospital readmission rate due to heart failure decreased (1 year before dialysis vs. 1 year after dialysis: 0.79 ± 1.32 vs. 0.22 ± 0.65 hospitalizations per year, p = 0.001) together with the duration of annual hospital stay (11.4 ± 21.4 vs. 3.7 ± 10.4 days, p = 0.011). 1-, 2-, 3-, 4- and 5-year survival for our patients was 81%, 61%, 52%, 47%, and 39%, respectively. CONCLUSIONS: Chronic renal replacement therapy with hemodialysis and strict uremic, electrolyte, and volume control may be more beneficial for patients with advanced heart failure with preserved or reduced LVEF than ultrafiltration alone. We have observed better survival of terminal cardiorenal patients treated with hemodialysis than in the general NYHA IV population, with lower hospital readmission rate and less hospitalized days for heart failure.
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BACKGROUND: Ultrasound-guided percutaneous endovascular treatment of arteriovenous fistula (AVF) or graft failure is an alternative to radiologically-guided angioplastic methods. Its main advantages are that it can be used with open or percutaneous access, using no contrast media and no radiation. The aim of this study was to analyze the results of ultrasound-guided endovascular treatment of arteriovenous access failure. MATERIAL AND METHODS: Preoperative ultrasound was used to determine the degree of stenosis and the size of balloon used in angioplasty. Angioplasty was performed as open procedure or by using a 4 - 6 French percutaneous sheath. Indications for angioplasty were significant stenosis of native vein or polytetrafluoroethylene (PTFE) graft with or without AVF thrombosis. Stenosis was considered significant if it narrowed the lumen of AVF for more than 50% and changed the shape of the flow curve. Balloon inflation was controlled by ultrasound. Procedural success was assessed with repeated postprocedural ultrasound. RESULTS: In the period from August 2012 until August 2016, 228 ultrasound-guided open or percutaneous transluminal angioplasties (PTA) were performed (61% men, mean age 66.6 ± 12.0 years), success rate was 93%. In 19 (8%) cases, ultrasound-guided PTA was used in conjunction with surgical reconstruction of arteriovenous fistula/graft and in 27 (12%) cases with thromboendarterectomy. Main complications were recoil, phlebitic vein rupture, and guidewire false route in thrombotic vessels. The main cause of access failure was perianastomotic stenosis (25%). 46% of patients required repeated PTA after the first one (after a mean time of 20.8 ± 22.8 weeks, mean number of repeated PTA 2.1 ± 1.7). Repeated PTA was done intentionally as stepped dilatation or because of rethrombosis/restenosis. Ultrasound-guided stent placement was done in 8% of PTA. CONCLUSIONS: Ultrasound-guided endovascular treatment of arteriovenous fistula or graft is a feasible and safe method of reestablishing or maintaining a functional vascular access.
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A well-functioning vascular access is essential for successful haemodialysis in patients with end-stage kidney failure. Sometimes, when we have exploited all conventional ways of vascular access salvage, we have to find a unique solution to preserve it.

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BACKGROUND: Incidence of drug-drug interactions (DDIs) increases with complexity of treatment and comorbidities, as in heart failure (HF). This randomized, double-blind study evaluated the intervention of the pharmacist on prevalence of clinically relevant DDIs (NCT01855165). METHODS: Patients admitted with HF were screened for clinically relevant DDIs, and randomized to control or intervention. All attending physicians received standard advice about pharmacological therapy; those in the intervention group also received alerts about clinically relevant DDIs. Primary endpoint was DDI at discharge and secondary were re-hospitalization or death during follow-up. RESULTS: Of 213 patients, 51 (mean age, 79 ± 6 years; male, 47%) showed 66 clinically relevant DDIs and were randomized. For intervention (n=26) versus control (n=25), the number of patients with and the number of DDIs were significantly lower at discharge: 8 vs. 18 and 10 vs. 31; p=0.003 and 0.0049, respectively. Over a 6 month follow-up period, 11 control and 9 intervention patients were re-hospitalized or died (p>0.2 for all). No significant differences were seen between control and intervention for patients with eGFR <60 mL/min/1.73 m(2) (78%) for re-hospitalization or death (10 vs. 7; p=0.74). CONCLUSIONS: Pharmacist intervention significantly reduces the number of patients with clinically relevant DDIs, but not clinical endpoints 6 months from discharge.

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BACKGROUND: Autosomal dominant polycystic kidney disease (ADPKD) is a genetically heterogeneous disorder caused by mutations in at least two different loci. Prior to performing mutation screening, if DNA samples of sufficient number of family members are available, it is worthwhile to assign the gene involved in disease progression by the genetic linkage analysis. METHODS: We collected samples from 36 Slovene ADPKD families and performed linkage analysis in 16 of them. Linkage was assessed by the use of microsatellite polymorphic markers, four in the case of PKD1 (KG8, AC2.5, CW3 and CW2) and five for PKD2 (D4S1534, D4S2929, D4S1542, D4S1563 and D4S423). Partial PKD1 mutation screening was undertaken by analysing exons 23 and 31-46 and PKD2 . RESULTS: Lod scores indicated linkage to PKD1 in six families and to PKD2 in two families. One family was linked to none and in seven families linkage to both genes was possible. Partial PKD1 mutation screening was performed in 33 patients (including 20 patients from the families where linkage analysis could not be performed). We analysed PKD2 in 2 patients where lod scores indicated linkage to PKD2 and in 7 families where linkage to both genes was possible. We detected six mutations and eight polymorphisms in PKD1 and one mutation and three polymorphisms in PKD2. CONCLUSION: In our study group of ADPKD patients we detected seven mutations: three frameshift, one missense, two nonsense and one putative splicing mutation. Three have been described previously and 4 are novel. Three newly described framesfift mutations in PKD1 seem to be associated with more severe clinical course of ADPKD. Previously described nonsense mutation in PKD2 seems to be associated with cysts in liver and milder clinical course.

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