Use of ultrasound to confirm guidewire position in hemodialysis catheter implantation.

INTRODUCTION: Hemodialysis is the most used dialysis modality in Brazil for the treatment of end-stage chronic kidney disease and severe acute kidney injury. Non-tunneled, short-term, double-lumen catheters allow immediate vascular access in patients without a definitive vascular access for dialysis treatment. Implantation is performed using the Seldinger technique, traditionally based on anatomical landmarks or with puncture under direct visualization by ultrasonography. Confirmation of the placement of the catheter is usually made with a chest X-ray after the end of the procedure. OBJECTIVE: To describe the use of ultrasonography to confirm the proper positioning of the guidewire during catheter implantation in real time, ensuring the desired path. METHODS: We used the Seldinger technique for catheter implantation. The confirmation of the position of the guidewire occurred after the introduction of 50 cm of this wire, as described in the aforementioned technique. A convex transducer was placed longitudinally below the xiphoid process to visualize the guidewire in the inferior vena cava, or transversely at the same location to visualize it in the cavoatrial junction or right ventricle, using the two-dimensional mode of the ultrasound device. After viewing the guidewire, the catheter implantation proceeded. RESULTS AND DISCUSSION: The technique was performed in 1549 patients, and regarded 2596 catheter implantations over a period of 5 years and 9 months. The only complication observed was local hematoma, occurring in 0.1% of cases. CONCLUSION: Confirmation of guidewire position with ultrasonography during catheter implantation is recommended because it is safe, low cost and ensures correct catheter direction.

Disseminated Paracoccidioidomycosis in a Kidney Transplant Recipient.

Paracoccidioidomycosis (PCM) is an endemic fungal infection in Latin America, which manifests as an acute or chronic form and is more frequent in adult males. It is caused by Paracoccidioides brasiliensis or Paracoccidioides lutzii, which are thermodimorphic fungi. The disease can present as a severe and disseminated form involving the lungs, skin, lymph nodes, spleen, liver, and lymphoid organs of the gastrointestinal tract. Most of the primary infections are subclinical, and the cell-mediated immune response contains the infection. It is rare in transplant patients, and there are few cases described in the literature. In solid organ transplant patients, it usually results from the reactivation of a latent infection, manifesting itself after a few years of transplantation with frequent pulmonary and skin involvement. PCM is an endemic infection in Brazil; however, as it is not classified as a notifiable disease, there is no accurate database on its incidence, and case reports are important sources of information. Clinical disease in kidney transplant patients is rare and has a high mortality rate. In this scope, the present clinical case reports the challenges of the clinical management of disseminated PCM caused by Paracoccidioides brasiliensis in a kidney transplant recipient who used immunosuppressive drugs and was treated with Itraconazole.

Role of FGF23 in Pediatric Hypercalciuria.

BACKGROUND: This study explored the possible role of FGF23 in pediatric hypercalciuria. METHODS: Plasma FGF23 was measured in 29 controls and 58 children and adolescents with hypercalciuria: 24 before treatment (Pre-Treated) and 34 after 6 months of treatment (Treated). Hypercalciuric patients also measured serum PTH hormone, 25(OH)vitD, phosphate, calcium, creatinine, and 24 h urine calcium, phosphate, and creatinine. RESULTS: There were no differences in age, gender, ethnicity, or body mass index either between controls and patients, or between Pre-Treated and Treated patients. Median plasma FGF23 in controls was 72 compared with all patients, 58 RU/mL (p = 0.0019). However, whereas FGF23 in Pre-Treated patients, 73 RU/mL, was not different from controls, in Treated patients it was 50 RU/mL, significantly lower than in both controls (p < 0.0001) and Pre-Treated patients (p = 0.02). In all patients, there was a correlation between FGF23 and urinary calcium (r = 0.325; p = 0.0014). Treated patients had significantly lower urinary calcium (p < 0.0001), higher TP/GFR (p < 0.001), and higher serum phosphate (p = 0.007) versus Pre-Treated patients. CONCLUSIONS: Pharmacological treatment of hypercalciuric patients resulted in significantly lower urinary calcium excretion, lower serum FGF23, and elevated TP/GFR and serum phosphate concentration, without significant changes in PTH. Further studies are indicated. This trial is registered with Clinical Registration Number RBR 8W27X5.

Longitudinal study of bone mineral density in children with idiopathic hypercalciuria.

Children with idiopathic hypercalciuria (IH) may have a reduced bone mineral density (BMD), which could impact on bone health in adulthood. There is currently no strong evidence for a preferred treatment of such children. The aim of our study was to evaluate the BMD z-score before and after treating children and adolescents with IH with potassium citrate and thiazides. The study consisted of a historical cohort of 80 pediatric patients who were evaluated between October 1989 and November 2010. Bone scanning and densitometry measurements were made with dual-emission X-ray absorptiometry. Lumbar-spine BMD (g/cm(2)) and BMD z-score were evaluated before and after treatment. The t test and Mann-Whitney U test were used for statistical analysis. Forty-three boys and 37 girls were followed for a median time of 6.0 years. Median calcium excretion before and after treatment was 5.0 and 2.6 mg/kg/24 h, respectively. The BMD z-score changed significantly from -0.763 ± 0.954 (mean ± SD) to -0.537 ± 0.898 (p < 0.0001) before and after treatment, respectively. The BMD z-score of the patients improved with treatment, suggesting a beneficial effect and potential need for treatment. However, the lack of a control group points to the need for future studies to corroborate this outcome.

Bone disease in pediatric idiopathic hypercalciuria.

Idiopathic hypercalciuria (IH) is the leading metabolic risk factor for urolithiasis and affects all age groups without gender or race predominance. IH has a high morbidity with or without lithiasis and reduced bone mineral density (BMD), as described previously in pediatric patients as well as in adults. The pathogenesis of IH is complex and not completely understood, given that urinary excretion of calcium is the end result of an interplay between three organs (gut, bone and kidney), which is further orchestrated by hormones, such as 1,25 dihydroxyvitamin D, parathyroid hormone, calcitonin and fosfatonins (i.e., fibroblast growth-factor-23). Usually, a primary defect in one organ induces compensatory mechanisms in the remaining two organs, such as increased absorption of calcium in the gut secondary to a primary renal loss. Thus, IH is a systemic abnormality of calcium homeostasis with changes in cellular transport of this ion in intestines, kidneys and bones. Reduced BMD has been demonstrated in pediatric patients diagnosed with IH. However, the precise mechanisms of bone loss or failure of adequate bone mass gain are still unknown. The largest accumulation of bone mass occurs during childhood and adolescence, peaking at the end of the second decade of life. This accumulation should occur without interference to achieve the peak of optimal bone mass. Any interference may be a risk factor for the reduction of bone mass with increased risk of fractures in adulthood. This review will address the pathogenesis of IH and its consequence in bone mass.

Efeitos da acidose metabólica sobre o tecido ósseo: evidências clínicas e experimentais / Effects of metabolic acidosis on the bone: clinical evidence and experimentai

A acidose metabólica é considerada um componente comum a diversas doenças. Inúmeros estudos descreveram a participaçâo do tecido ósseo na manutençâo da homeostase ácido básica. Entretanto, os efeitos do tamponamento ósseo sobre o osso propriamente dito nâo estâo bem estabelecidos. A acidose metabólica altera a composiçâo do osso através de açâo fisico química direta, além de estimular a reabsorçâo óssea mediada por células. Este artigo revisa algumas evidências experimentais e clínicas sobre a participaçâo do osso como sistema de tamponamento dos distúrbios do equilibrio ácido básico. Os efeitos que o osso, agindo como tampâo, exerce sobre sua própria composiçâo celular e estrutura também sâo discutidos.