1,721,118 research outputs found
Dialysate and replacement fluid composition for CRRT.
No full textContinuous renal replacement therapies (CRRTs) are increasingly used in order to maintain normal or near-normal acid-base balance in intensive care unit (ICU) patients. Acid-base balance is greatly influenced by the type of dialysis employed and by the administration route of replacement fluids. In continuous veno-venous hemofiltration, buffer balance depends on losses with ultrafiltrate and gain with replacement fluid, while in techniques such as continuous veno-venous hemodiafiltration, clinicians should balance the role of the dialysate. The type of buffer greatly influences not only acid-base correction, but also clinical outcome. Lactate or bicarbonate fluids are currently used, but recent studies suggest that bicarbonate-buffered replacement fluids can improve acid-base status and reduce cardiovascular events better than lactate fluids. The buffer concentration should exert a buffer load that may compensate for deficits, for losses in the buffer process, and for extracorporeal losses and should therefore usually be supraphysiological. However, the dialysate buffer or electrolyte concentration need always to be balanced with that of the replacement fluids employed. Both fluids should contain electrolytes in concentrations aiming for a physiologic level and taking into account preexisting deficits or excess and all input and losses. Clinicians should be aware that in CRRTs the quality control for sterility, physical properties, individualized prescription and balance control are vitally important
Osteocalcin (BGP) Radioimmunoassay and Radiological Findings in Renal Osteodystrophy Assessment
No full textHighlights from the 60th national meeting of the Italian Society of Nephrology: celebrating the role of the nephrologist
No full textProteinuria in the prognosis of IgA nephropathy. Aucella F, Netti GS, Piemontese M, Cincione IR, Infante B, Gesualdo L.
No full textIgA Nephropathy (IgAN) is the most common lesion causing primary glomerulonephritis in the world. The main clinical predictors of progression are: elevated blood pressure, high histological score and proteinuria. Although elevated serum creatinine concentration at diagnosis, increased excretion of cytochines, age at onset, obesity and genetic factors may all influence clinical outcome, it is quite clear that proteinuria is the hallmark of renal damage in IgAN. Patients with IgAN and little or no proteinuria (3 g/day. The product of duration (years) and urinary protein excretion (g/day) at the time of renal biopsy is more significantly correlated with progression. So, this so called proteinuria index may be a useful predictor for glomerular and interstitial histopathological changes and the fate of renal function in IgAN. The progression of IgAN may be slowed by antihypertensive and antiproteinuric therapy, such as angiotensin converting enzyme inhibitors and/or angiotensin II receptor blockers, that can minimize secondary glomerular injury. Proteinuria has been shown to be an adverse prognostic factor in IgAN, with a strong relationship between proteinuria and prognosis and established importance of remission. Consequently, targeting proteinuria may be a valid surrogate for individualized kidney protective therapy
Quantitative ultrasound technique at the phalanges in discriminating between uremic and osteoporotic patients.
No full textMolecular and genetic basis of inherited nephrotic syndrome.
No full textNephrotic syndrome is an heterogeneous disease characterized by increased permeability of the glomerular filtration barrier for macromolecules. Podocytes, the visceral epithelial cells of glomerulus, play critical role in ultrafiltration of plasma and are involved in a wide number of inherited and acquired glomerular diseases. The identification of mutations in nephrin and other podocyte genes as causes of genetic forms of nephrotic syndrome has revealed new important aspects of the pathogenesis of proteinuric kidney diseases and expanded our knowledge of the glomerular biology. Moreover, a novel concept of a highly dynamic slit diaphragm proteins is emerging. The most significant discoveries in our understanding of the structure and function of the glomerular filtration barrier are reviewed in this paper
The genetic background of uremic secondary hyperparathyroidism.
No full textMany studies have shown how gene mutations and genetic polymorphisms could influence secondary uremic hyperparathyroidism (HPTH), modulating parathyroid (PT) function and hyperplasia. Parathyroid hormone (PTH) gene expression and hormone secretion is regulated mainly by serum calcium, with a post-transcriptional effect, and by vitamin D with a transcriptional effect. PT cells retain the ability to proliferate and to apoptose. Hyperphosphatemia, hypocalcemia and vitamin D deficiency all stimulate PT cell proliferation. In the early stage of chronic uremia, PT proliferation is polyclonal, as in diffuse hyperplasia, whereas nodular hyperplasia growth is monoclonal with an increasingly recognized genetic background. HPTH has been associated with a number of familial diseases, such as multiple endocrine neoplasia-type 1 (MEN1), multiple endocrine neoplasia-type2A (MEN2A), neurofibromatosis type1 (NF1) and HPTH with multiple ossifying jaw fibromas (HPT-JT Syndrome). The genes involved in these diseases have been also investigated in secondary HPTH (sHPTH). Moreover, in sporadic and secondary uremic HPTH, clonal rearrangement and/or oncogene overexpression, gene deletions and tumor suppressor gene inactivation have been reported. However, each condition shows different patterns of genetic abnormalities. Finally, PT function modulation by genetic polymorphisms of vitamin D and calcium receptors and of the PTH gene is reviewed
Liquid chromatography-tandem mass spectrometry method as the golden standard for therapeutic drug monitoring in renal transplant
No full textL'ultrasonografia quantitativa, nuova tecnica per lo studio della patologia ossea nell'uremia
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