Why does chf cause renal failure

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Anaemia has diverse causes in HF, including reduced renal function with lower erythropoietin production and blunted response, bone marrow suppression in HF, iron deficiency, and not unimportantly, haemodilution due to excessive venous congestion which in some series is the most prevalent cause. When present there is a stepwise increase in the risk of HF hospitalizations and mortality from normo-, to micro- and macro-albuminuria.

In addition to increased glomerular permeability, decreased re-absorption in the tubules due to tubular damage likely further contributes to the development of albuminuria. Tubular damage is now increasingly recognized in patients with acute and chronic HF. In addition, increased congestion may be associated with tubular damage. Most of the research focusing on tubular damage markers in acute HF has been focused on the identification of patients at risk of WRF.

In non-HF patient populations, tubular damage markers are sensitive and specific markers of severe AKI. Recent reports have indicated that blood urea nitrogen BUN could be an even better prognosticator that resembles some form of GFR. However, BUN has been associated with factors beyond glomerular filtration, such as neurohormonal activation and haemodynamic status, which could be the reason for the fact that it retains powerful prognostic information even after controlling for GFR.

Since renal dysfunction in patients with HF is a mechanistically heterogeneous disorder, it is logical to assume that prognosis and treatment may also differ. Unfortunately, phenotyping patients with renal dysfunction has proved a challenging endeavour since no gold standard exists by which HF-induced renal dysfunction can be differentiated from intrinsic renal parenchymal disease. However, in the absence of a gold standard, it is impossible to determine if these markers are actually identifying mechanistically distinct types of renal dysfunction.

Additional research within this domain is warranted. HF patients with severe renal dysfunction have been excluded from randomized clinical trials of current evidence-based treatments. Recently, the effect of evidence-based treatments on the slope of eGFR was reported for most evidence-based therapies. For device therapy, such as biventricular pacing or left ventricular assist devices, two devices that improve cardiac output and possibly RBF, eGFR has been reported to increase at least transiently in responders.

However, both treatments failed to provide renal benefit. Finally, therapies that modulate congestion may also influence renal function. Loop diuretics are the cornerstone of the treatment of symptoms and signs of congestion in acute and chronic HF. However, their effect on renal function is poorly understood and studied, and observational data are strongly confounded by indication, since patients with more severe HF and renal dysfunction are prescribed more loop diuretics.

The study did show that, although post-discharge outcomes were similar, higher loop diuretics dosages were associated with more fluid and weight loss but a higher incidence of WRF. Approach to the heart failure patients with renal dysfunction. Since ultrafiltration directly reduces venous congestion, it could directly influence renal function by reducing renal venous pressure.

Until we know more, with the current available evidence, we have highlighted possible treatment decisions based on changes in renal function and response to diuretics in Figure 4. By no means should this figure serve as guideline, but it might serve to suggest a possible course of action in response to deterioration of renal function in different situations.

In the next 10 years, research will need to focus on further characterizing why some patients with impaired renal function and WRF fair pretty well, while others struggle to survive. Studies should be conducted that differentiate between true and pseudo-WRF, and how we can possibly early distinguish between both, possibly via markers of tubular or glomerular damage, or yet to be discovered markers or imaging modalities.

It is clear that renal dysfunction does not mean the same thing in each patient, and we need strategies to determine the individual response. If possible, we need treatment options that can prevent significant deteriorations in renal function, since more severe renal dysfunction is associated with persistent reduction in GFR and structural renal damage. Furthermore, in acute HF we need strategies that improve diuretic response in patients that are most likely to benefit from the therapy, without compromising renal function.

To do so, we need more information on the changes in haemodynamics, cardiorenal connectors, renal function and structure during and possibly before hospitalization. Additionally, in both acute and chronic HF, we need more information on whether specifically targeting renal function with therapies alters prognosis. In chronic HF, where the incidence of severe renal dysfunction is increasing, we need evidence-based treatments or strategies that are specifically designed and executed in HF patients with low GFR, an area now underdeveloped.

We also need more information on how modulation of congestion in patients with chronic HF may alter renal function and structure, since the importance of venous congestion in the chronic situation remains poorly understood.

Finally, to help determine where progress is made or needed, researchers should embark on a voyage to redesign and define the cardiorenal syndrome in HF with evidence of the last 10 years. It should highlight possible pathophysiologic patient trajectories and treatment options, and also highlight dynamics in cardiac and renal function once simultaneous deterioration in heart and renal function has been diagnosed. It could also include specific research questions and areas of interest and uncertainties, and look forward to what is needed in the next 10 years.

The cause of renal dysfunction is multifactorial, but reduced renal perfusion and venous congestion are prominent factors, which are probably mediated and modified by a multitude of cardiorenal connectors. New evidence suggests that not all deteriorations in renal function during treatment are a bad sign, but we are still unable to identify beforehand which patients will respond and this is a challenge for the near future.

Finally, although much has been learned on the interaction between heart and kidney in HF, we need more dedicated epidemiologic, mechanistic, and controlled trials in HF patients with reduced renal function. To facilitate this, a new, updated classification of cardiorenal syndromes is needed which incorporates recent evidence and highlights areas of interest and areas of uncertainties where progress is wanted. Ultimately, this should lead to preventive and treatment strategies that can preserve renal function in patients with HF.

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In both controlled and uncontrolled studies of CHF, the correction of the anemia with erythropoietin EPO and oral or intravenous IV iron has been associated with improvement in many cardiac and renal parameters and an increased QoL. EPO itself may also play a direct role in improving the heart unrelated to the improvement of the anemia--by reducing apoptosis of cardiac and endothelial cells, increasing the number of endothelial progenitor cells, and improving endothelial cell function and neovascularization of the heart.

The opposite also is true. Patients who have heart failure or who suffer a heart attack can develop kidney problems — either acute kidney injury or chronic kidney disease.

When a person develops both heart and kidney problems, the condition sometimes is referred to as cardiorenal syndrome. In the case of a heart attack, a number of factors can contribute to a subsequent decline in kidney function. The stress of a heart attack can result in hormonal changes within the body, and that can have a negative effect on how well the kidneys work.

Changes in heart function may lead to kidney damage by decreasing the blood supply to the kidneys.