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Pathogenetic mechanisms of diabetic nephropathy
No full textDiabetes is the leading cause of ESRD because diabetic nephropathy develops in 30 to 40% of patients. Diabetic nephropathy
does not develop in the absence of hyperglycemia, even in the presence of a genetic predisposition. Multigenetic predisposition
contributes in the development of diabetic nephropathy, thus supporting that many factors are involved in the
pathogenesis of the disease. Hyperglycemia induces renal damage directly or through hemodynamic modifications. It induces
activation of protein kinase C, increased production of advanced glycosylation end products, and diacylglycerol synthesis. In
addition, it is responsible for hemodynamic alterations such as glomerular hyperfiltration, shear stress, and microalbuminuria.
These alterations contribute to an abnormal stimulation of resident renal cells that produce more TGF-1. This growth factor
upregulates GLUT-1, which induces an increased intracellular glucose transport and D-glucose uptake. TGF-1 causes
augmented extracellular matrix protein deposition (collagen types I, IV, V, and VI; fibronectin, and laminin) at the glomerular
level, thus inducing mesangial expansion and glomerular basement membrane thickening. However, low enzymatic degradation
of extracellular matrix contributes to an excessive accumulation. Because hyperglycemia is the principal factor
responsible for structural alterations at the renal level, glycemic control remains the main target of the therapy, whereas
pancreas transplantation is the best approach for reducing the renal lesions
[Gout and chronic kidney disease: specific diagnostic and therapeutic features]
No full textIn the last decades, the increase in life expectancy, changes in diet and lifestyle have resulted in raising of incidence and prevalence of gout in all countries. The phenotype of patients with gout has changed a lot over the years: more and more frequently they have several co-morbidities such as hypertension, cardiovascular disease, diabetes, obesity, chronic kidney disease (CKD) and metabolic syndrome that influence the progression and challenge the therapeutic management. The management of gout in CKD patients demands more attention and specific features in diagnosis and therapeutic approach. This article summarizes the most recent published evidences on how to best diagnose and treat the gouty patients with CKD, how to better manage medications for the treatment of acute gouty flares and for the chronic hyperuricemia management
Renal lesions in patients with type 2 diabetes: A puzzle waiting to be solved
Full text linkThree hundred sixty-six million people worldwide will be living with diabetes mellitus (DM) by 2030 ([1, 2]; http://www.idf.org/global-diabetes-plan-2011-2021). Prospectively, 75–150 million of these patients will develop a diabetic nephropathy (DN) or a non-diabetic renal disease (NDRD), either isolated or superimposed on DN [3, 4]. To date, the differential diagnosis between ND and NDRD remains a challenge that nephrologists are trying to win [5]
There is a choice for immunosuppressive drug nephrotoxingcity: Is it time to change?
No full textThe central issue in organ transplantation remains suppression
of allograft rejection. Thus, development of
immunosuppressive drugs is the key to successful allograft
function. New immunosuppressive drugs were
introduced on the basis of their ability to reduce the
incidence of acute rejection and to demonstrate shortterm
outcomes at least equivalent to those achieved
with the use of established immunosuppressive therapy.
Although short-term renal allograft survival has
improved since the introduction of calcineurin inhibitors
(CNIs), long-term renal allograft survival remains
a major concern, with chronic allograft nephropathy
(CAN) being the principal cause of renal allograft loss
after the first year. CAN has traditionally been viewed
as the result of repeated low-grade immune responses
directed against allogeneic tissue, but recent evidence
indicates that nonimmunological or alloantigen-independent
factors also contribute to its pathogenesis.
CNI nephrotoxicity occurs soon after initiation of therapy,
is more clearly dose-dependent. This scenario
presents a clear need for new strategies that produce
adequate immunosuppression to prevent acute rejection
and simultaneously reduce adverse effects associated
with CNI-related therapies. To obtain significant
long-term improvement in renal allograft outcomes, it
may be necessary to adopt new immunosuppressive
regimens that rely less on CNIs
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
The relevance of experimental models in the pathogenetic investigation of primary IgA nephropathy
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