Contributions to nephrology
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In the US and Europe, approximately 90% of heart failure (HF) hospitalizations are due to symptoms and signs of sodium and fluid excess. Congestion is associated with HF progression. According to data from large national registries, approximately 40% of hospitalized HF patients are discharged with unresolved congestion, which may contribute to unacceptably high rehospitalization rates. ⋯ Clinical studies of ultrafiltration have shown that removal of isotonic fluid relieves symptoms of congestion, improves cardiac filling pressures and exercise capacity, and restores diuretic responsiveness in patients with diuretic resistance, concomitantly with favorable effects on pulmonary function, ventilatory efficiency, and neurohormonal activation. Ultrafiltration has been shown to reduce rehospitalizations in a randomized controlled trial of patients with decompensated HF. Future larger controlled clinical trials should evaluate the effect of ultrafiltration on survival.
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Since 1984 reports of renal involvement in AIDS patients have been presented in the literature. Different forms of renal disease were noted in the AIDS population including those related to systemic and local renal infections, tubulointerstitial disease, renal involvement by neoplasm and glomerular disease including collapsing glomerulopathy (CG). HIV-associated nephropathy (HIVAN) has been demonstrated to be more severe in the black population. ⋯ In a rat model of CG developed by our group, the injection of serum from CG patients resulted in proteinuria, glomerular tuft retraction and podocyte damage at the ultrastructural level (visceral epithelial cell foot-process effacement). No ultrastructural or light microscopy abnormalities were seen in rats injected with serum from non-collapsing FSGS or healthy subjects. Based on the experience of our group, circulating factors play a dominant role in the pathogenesis of idiopathic CG.
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All aspects of current treatment of acute kidney injury (AKI), including renal replacement therapy (RRT), are basically supportive. Emergent RRT is indicated in the management of AKI with refractory pulmonary edema, hyperkalemia or metabolic acidosis, or when uremic symptoms or signs develop. More aggressive practitioners use prophylactic RRT inpatients with sustained anuria, persistent oliguria with progressive azotemia and a probable glomerular filtration rate < 10 ml/min, or to prevent uncontrolled positive fluid balance in patients with AKI. ⋯ The approach to RRT dosing in AKI is more evidence-based. Outcomes in single-center studies of higher intensity versus standard RRT (intermittent and/or continuous) have been in consistent. However, two large multicenter negative randomized trials have shifted the weight of evidence towards suggesting provision of an effectively delivered standard dose of RRT in AKI, rather than seeking to increase RRT intensity.
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Sepsis is the most common cause of acute kidney injury (AKI). There has been a growing body of evidence demonstrating the association between worsening of kidney function during sepsis and the risk of short- and long-term mortality. AKI in sepsis is associated with poor outcome and independently predicts increased mortality. ⋯ The expanding population of patients with sepsis and AKI, and the associated excess mortality provide a strong basis for further research aimed at addressing more rigorously all potentially modifiable factors to reduce this burden to patients and health care systems. Better insights into bidirectional and synergistic pathways linking sepsis and AKI might open the window for new therapeutic approaches that interrupt this vicious circle. Here, we discuss the rationale for and the current understanding of the bidirectional relationship between AKI and sepsis.
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Acute kidney injury (AKI) is associated with a heavy burden of morbidity and mortality, despite advances in intensive care and the management of high-risk patients. Numerous clinical trials have failed to ameliorate the outcomes of AKI. ⋯ Similarly, a multidisciplinary dialogue is making progress towards standardization of the clinical trial endpoints to prove efficacy and effectiveness in AKI research. Taken together with the increasing availability of timely, sensitive, and specific novel biomarkers of kidney damage, we are poised to use these tools to conduct successful clinical trials of agents for the prevention and treatment of this devastating clinical syndrome.