Managing the Kidney when the Heart is Failing
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Their main function is to act as a filter system that removes waste products and excess fluid from the body. Over time, high blood pressure harms renal blood vessels The nephrons in the kidneys are supplied with a dense network of blood vessels, and high volumes of blood flow through them. Damaged kidney arteries do not filter blood well. Kidneys have small, finger-like nephrons that filter your blood. Each nephron receives its blood supply through tiny hair-like capillaries, the smallest of all blood vessels.
When the arteries become damaged, the nephrons do not receive the essential oxygen and nutrients — and the kidneys lose their ability to filter blood and regulate the fluid, hormones, acids and salts in the body. Damaged kidneys fail to regulate blood pressure. The role of ultrafiltration remains controversial, and it is currently recommended only for diuretic-resistant patients as it has not been associated with better outcomes. The occurrence of AKI during HF is associated with substantially greater short- and long-term mortality.
The incidence of heart failure HF has been steadily increasing and will further increase due to the ageing of the general population and the availability of better treatment. HF often coexists with other comorbidities, which are the main determinants of prognosis. The coexistence of renal and cardiac disease can be today defined as cardiorenal syndrome CRS. CRS is classified into five subtypes, considering which organ is affected first and whether it is affected acutely or chronically Table Table AKI leading to acute cardiac dysfunction.
CKD leading to chronic cardiac dysfunction. Chronic cardiac dysfunction: LV remodelling, diastolic and systolic dysfunction, cardiomyopathy, CAD. Systemic condition leading to both heart and renal dysfunction. This broad range in incidence is also attributable to the different timeframe used to ascertain renal impairment Cruz, Inconsistent definitions for AKI during HF limit standardization of data and make epidemiologic studies difficult.
The timeframe used to recognize CRS type 1 should be limited to the period in which a direct pathophysiological linkage between HF and AKI is presumed. CRS type 1 is associated with poor clinical outcomes, hospital readmission, and increased healthcare expenditure Bagshaw et al. The risk of death seems to be proportional to the severity of AKI; however, even small and transient changes in serum creatinine SCr appear to influence the risk Gottlieb et al. Moreover, patients with end-stage renal disease have an increased risk of progression. The pre-existence of chronic conditions such as chronic HF or chronic kidney disease CKD are independent risks for poor outcomes Hillege et al.
Renin—angiotensin—aldosterone system RAAS , sympathetic nervous system SNS , and non-osmotic arginine vasopressin AVP release are the neurohormonal adaptive mechanisms, mainly acting through salt-water retention and vasoconstriction. Drugs usually administered during HF, such as diuretics, angiotensin-converting enzyme inhibitors ACEIs and angiotensin receptor blockers ARBs , can also contribute to kidney dysfunction. They are responsible for the renal haemodynamic changes, which in turn may precipitate AKI. Recently, the role of inflammation in the progression of HF has been investigated.
It may play a role not only in distant organ damage, such as AKI, but also in further damaging cardiomyocytes. Systemic hypoperfusion consequent to reduction in cardiac output results in neurohormonal activation. This condition simulates intravascular volume depletion, in response to which baroreceptors activate adaptive mechanisms. Both these effectors act synergistically, increasing systemic vascular resistance to compensate for the initial decrease in ejection fraction EF. Sympathetic stimulation contributes to sodium reabsorption, both directly and indirectly through a positive feedback on the juxtaglomerular apparatus, which finally increases renin release.
ATII, aldosterone, and SNS also have a long-term trophic effect on cardiomyocytes and renal tubular cells, promoting cell hypertrophy, apoptosis, and tissue fibrosis Burns and Thomas, Non-osmotic release of AVP is an appropriate response to intravascular hypovolaemic state, which is a stronger stimulus than the osmotic on AVP release. The clinical implication of this physiologic mechanism is the development of hyponatraemia due to both diuretic therapy and free-water retention caused by AVP.
The action of AVP on principal cells of collecting ducts is mediated by V 2 receptors located on the basolateral membrane. The interaction between AVP and V 2 receptors induce the expression of the water channels aquaporin 2 AQP2 on the apical membrane, thus increasing collecting duct free-water permeability. Moreover, AVP also leads to vasoconstriction and cardiac hypertrophy through the V 1a receptor.
Central venous pressure CVP and jugular venous pressure JVP were both found to be associated with impaired renal function Mullens et al. This effect seems to be related to the increased pressure in renal veins which is back transmitted by the increased CVP. Animal experimental data showed that increased renal venous pressure decreases renal blood flow RBF and glomerular filtration rate GFR through a vasoconstriction of afferent and efferent arterioles Dilley et al. Moreover, RBF is determined by the abdominal perfusion pressure which is inversely related to intra-abdominal pressure IAP.
It was associated with worse renal function at baseline while its reduction was strongly correlated with the improvement of kidney function Mullens et al. Many drugs commonly prescribed for the treatment of AHF can also contribute to further damage of kidney function. Patients with AHF are in a narrow therapeutic management window.
Diuretics are the cornerstone in the treatment of AHF Aspromonte et al. These agents may resolve congestion providing a rapid relief from symptoms, but overdiuresis can cause arterial underfilling and worse kidney function. These agents have proven efficacy in improvement of outcomes in stabilized HF, however they have to be avoided during CRS type 1 and only after clinical stabilization can they cautiously be titrated Hillege et al. During AHF, renal perfusion is strictly dependent on neurohormonal activation, which maintains GFR through vasoconstriction of both afferent and efferent arteriole.
This is mostly important in conditions where renal reserve is impaired, such as previous kidney injuries or with ageing Chronopoulos et al. In such conditions GFR can be normal, due to overworking of residual functional nephrons whose activity is strictly dependent on constant activation of RAAS.
Managing chronic heart failure patient in chronic kidney disease.
The ability to response to an extra stimulus would require a further activation of RAAS to maintain GFR that these nephrons cannot achieve. The contribution of nephrotoxic medications to development of AKI has an important role in all hospitalized patients and it is even more relevant in the setting of AHF where kidney is more vulnerable because of the haemodynamic impairment.
Even if the route of administration was not included in the prognostic score system, some data support a higher risk of AKI after IA administration above the level of the renal arteries than after intravenous IV administration Stacul et al. Immune-mediated mechanisms have also been implicated in the development of CRS type 1 Gullestad and Aukrust, ; Frantz et al.
Abnormality in balance between inflammatory and anti-inflammatory cytokines suggests the existence of immune dysregulation in patients with HF Aukrust et al. The inflammation is a consequence of ischaemic cell damage related to hypoperfusion and it is further amplified after reperfusion. Moreover, during AHF, blood flow is shunted away from the splanchnic region to preserve perfusion in the brain, heart, and kidney. Gut ischaemia can be responsible for paracellular absorption of lipopolysaccharide LPS and systemic endotoxaemia may occur as a consequence Ronco et al.
Inflammation seems to be more than just an accompanying feature during HF since it may have a role in organ damage and in particular in AKI Friedewald and Rabb, ; Cantaluppi et al. Recently, it has been demonstrated that plasma-induced apoptosis, capsase 3 and 8 activities, and interleukin IL -6 levels were significantly higher in CRS type 1 patients when compared to healthy controls and to patients with AHF but without renal impairment Virzi et al. Inflammation also appears to play a role in fluid redistribution increasing the vascular permeability and interfering with the mechanism of lymphatic reabsorption Cotter et al.
Inflammation can therefore concur to the pathogenesis not only of pulmonary and peripheral oedema, but also of kidney interstitial oedema which can contribute to reduction in GFR. CRS type 1 is the final effect of interaction between complex pathogenic factors and once it begins, it is difficult to abort. In CRS type 1, the cardiac event is primal and the preventive approach is aimed at reducing the risk of acute decompensation. One-third of the patients hospitalized for AHF have de novo AHF precipitated by pneumonia, hypertension, atrial fibrillation, or acute cardiac ischaemia.
The remaining two-thirds have chronic HF which acutely decompensates usually because of non-compliance with diet restriction or with medications. Preventive strategies in the first group include implementation of lifestyle modifications and optimization of blood pressure control through drugs that block RAAS or beta-adrenergic blockers McCullough et al.
In this case, a decrease of GFR can even be protective in the long term Ruggenenti and Remuzzi, In fact, the reduction of the glomerular intracapillary pressure as a consequence of RAAS blocking reduces proteinuria, which in turn reduces the risk of glomerulosclerosis Apperloo et al. However, a persistent progressive increase in SCr should be cautiously evaluated and any cause of renal hypoperfusion, such as AHF, should be excluded. Prompt withdrawn is recommended if AHF or any other cause of volume depletion is suspected.
Prevention strategies such as adequate IV volume expansion with either sodium chloride or sodium bicarbonate solution are strongly recommended. However, adequate fluid loading is not easily achievable in patients with AHF, because of fluid overload. N -acetylcysteine can have an additive preventive effect in addition to adequate IV fluid loading. Another mainstay of prevention is recognition of patients at risk of developing CRS type 1 Cruz, In addition to scoring systems, renal biomarkers could be useful to predict the risk of AKI.
Increased levels of molecules involved in tubular damage might precede a reduction in GFR. However, there are no specific recommendations for the treatment of CRS type 1. Diuretics, inotropic agents, vasopressors, vasodilators, and mechanical devices can all be used in AHF according to the clinical presentation. Management of patients with CRS type 1 should be different from the standard treatment of HF since many drugs used in AHF can further compromise renal function. Vasodilators such as nitroglycerine and nitroprusside can exacerbate renal injury by precipitating hypotension.
In particular, a significant deterioration in renal function with nesiritide has been described Sackner-Bernstein et al. The expected effect on kidney function is related to the improvement in haemodynamics, though the risk of renal damage secondary to the side effect of MCS, such as haemolysis, should also be taken into account Mao et al. Diuretics are an essential component of the treatment of AHF since they promote natriuresis and reduce volume overload leading to relief from symptoms. Aggressive diuresis may be necessary to achieve clinical outcome, but overdiuresis can possibly lead to hypovolaemia and precipitate CRS type 1.
Biomarker-guided therapy and the use of bioelectric impedance vector analysis BIVA to assess hydration status could be helpful to monitor diuretic therapy and avoid unwanted iatrogenic complications during the treatment of AHF Aspromonte et al.
Their natriuretic effect is impaired because of the reduced amount of sodium that reaches the collecting ducts as a consequence of increased proximal reabsorption. Even if a high level of natriuretic peptides NPs can be a consequence of reduced renal clearance, monitoring of NPs can be helpful in assessment of changes in volume status and target diuretic therapy McCullough et al.
In the setting of AHF, IV loop diuretics such as furosemide should be preferred because of their fast action. Their diuretic effect appears after 30—60 minutes, however clinical improvement of dyspnoea can occur even faster because of their vasoactive effect. The optimal regimen for diuretic dose is unclear regarding both mode of administration and dosing. Intermittent administration can lead to salt retention during the interval in which the plasmatic concentration is low, the so-called rebound sodium retention Ellison, This is important especially in conditions of renal impairment where the ability of the kidney to clear a diuretic is prolonged and the true pharmacokinetics are less predictable.
Diuretic dose should be individualized to the clinical response. In patients with severe AHF, renal responsiveness to loop diuretics may be decreased so that the natriuretic response is reduced and delayed compared to normal subjects. In this setting, more frequent or continuous administration can increase diuretic effect. In patients with CKD in which less diuretic reaches the site of action, a higher dose is necessary to obtain relevant diuretic response, but the natriuretic effect is not delayed Brater, A high dose of diuretics has been found to be associated with adverse clinical outcomes including AKI, progression of HF, and death in multiple studies Bagshaw et al.
In fact, severe AHF may require a higher dose of diuretics with the aim of overcoming diuretic resistance. Many factors seem to contribute to diuretic resistance, and when it is established it may be difficult to reverse Elliso, Chronic use of furosemide can cause hypertrophy and hyperplasia of distal tubular cells thiazide sensitive secondary to the increased delivery of distal sodium so-called braking phenomenon ; however, in the setting of AHF, the increased sodium reabsorption at proximal tubular cells secondary to neurohormonal early breaking activation also plays a determinant role Aspromonte et al.
Hyponatraemia and hypoalbuminaemia can also have an additive effect. A recent randomized controlled trial that compared continuous infusion of furosemide versus bolus injection and low dose equal to pre-existing oral dose versus high dose 2. High dose resulted in greater net fluid loss, weight loss, and relief from dyspnoea after 72 hours, but at the expense of a significant more frequent transient AKI. However, there was no difference in SCr or in clinical outcome after 60 days from randomization Felker et al. Thiazides and potassium-sparing diuretics can be used in addition to the loop diuretics, to antagonize the late breaking effect McMurray et al.
Metolazone is an exception because it retains its efficacy in patients with renal insufficiency Paton and Kane, ; Ernst and Moser, When the combination of loop diuretic and thiazide is used, close monitoring of electrolytes is required because of the risk of hypokalaemia. Recently a non-selective, oral V 2 receptor antagonist tolvaptan was investigated in patients hospitalized for symptomatic HF. It was administrated in addition to the standard therapy and even if no effect on long-term mortality and HF-related morbidity was found, it showed promising results in term of short-term outcomes.
Currently tolvaptan is approved in the United States for the treatment of hyponatraemia in HF, in cirrhosis, and in the syndrome of inappropriate antidiuretic hormone secretion, while in Europe it is allowed only for the last indication. No data are available about its effect with renal impaired function. The theoretic advantage of UF is that fluid overload is treated by a slow, continuous, and controlled fluid removal rather than by a rapid, intermittent, and uncontrolled way such as with diuretic therapy.
As a consequence, neurohormonal activation could be better controlled as well as electrolyte balance and acid—base metabolism. Application of this technology has been limited by the need for high flow rates, large extracorporeal blood volumes, and large-bore central venous catheters. Although potentially attractive, the results regarding the superiority of UF compared to diuretics are still controversial. No SCr differences were observed between the groups. Change in body weight was similar in the two groups after 96 hours although UF was associated with higher adverse events, including kidney failure, bleeding complications, and IV catheter-related complications Bart et al.
It is associated with adverse clinical outcomes, including increased mortality, rehospitalization, and increased healthcare expenditures. Multiple pathophysiologic mechanisms have been implicated, including neurohormonal activation, venous congestion, inflammation, effects of pharmacologic therapy for HF RAAS antagonists and diuretics , and nephrotoxic exposure. Prevention is of paramount importance, consisting of avoiding acute decompensation of chronic HF, and, among patients already presenting with AHF, prompt recognition of those at increased risk for AKI.
Among patients with established AKI, diuretics remain the cornerstone of therapy. IV administration by bolus or continuous infusion appears to be equally efficacious. The role of UF remains controversial, and it is currently recommended only for diuretic-resistant patients. Apperloo, A.
Also on the A to Z Guide:
A short-term antihypertensive treatment-induced fall in glomerular filtration rate predicts long-term stability of renal function. Kidney Int , 51, —7. Find this resource:. Aspromonte, N. Role of bioimpedance vectorial analysis in cardio-renal syndromes. Semin Nephrol , 32, 93—9. Management and monitoring of haemodynamic complications in acute heart failure. Heart Fail Rev , 16 6 , — Metabolic and toxicological considerations for diuretic therapy in patients with acute heart failure.
Expert Opin Drug Metab Toxicol , 7, — Aukrust, P. Cytokine network in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.
Am J Cardiol , 83, — Bagshaw, S. Nephrol Dial Transplant , 25, — Bart, B. Ultrafiltration in decompensated heart failure with cardiorenal syndrome.
N Engl J Med , , — Brater, D. Diuretic therapy. High blood pressure : High blood pressure also known as hypertension occurs when blood is pushed through the arteries at an increased pressure. When blood pressure is too high, the walls of the arteries can become weakened and also cause complications such as stroke or heart attack. Complications that develop from chronic kidney disease, as well as the underlying conditions that cause chronic kidney disease, can put you at risk for cardiovascular disease.
The following are complications that develop from renal disease and can lead to cardiovascular disease:. Anemia : Anemia is when your body does not have enough red blood cells. The kidneys manufacture a hormone called erythropoietin , which tells the bone marrow to make more red blood cells. If your kidneys are damaged, your erythropoietin levels can fall, and your body will not make enough red blood cells. Several studies have shown that anemia can be related to cardiovascular disease. Red blood cells contain a protein called hemoglobin, which helps transport oxygen throughout the body.
If a body is not getting enough oxygen, the heart is not getting enough oxygen either. Without adequate oxygen to the heart muscles, a person may be susceptible to a heart attack. Anemia can also cause the heart to pump more blood in order to circulate enough oxygen throughout the body. As the heart works harder, the muscle in the left lower chamber of the heart can develop thick walls. This is a condition called left ventricular hypertrophy LVH.
LVH can increase the chance of heart failure. High blood pressure: The kidneys make renin, which is an enzyme that helps control blood pressure.
Heart disease & chronic kidney disease (CKD)
When blood pressure is too low, healthy kidneys release renin to stimulate different hormones that increase blood pressure. Damaged kidneys may release too much renin, which can lead to high blood pressure. High blood pressure increases the risk of heart attack, congestive heart failure and stroke.
High homocysteine levels : Homocysteine is an amino acid normally found in blood. Healthy kidneys regulate the amount of homocysteine in the blood and remove any excess. But damaged kidneys cannot remove the extra homocysteine. High levels of homocysteine have been linked to the build up of plaque in the blood vessels, which can lead to cardiovascular diseases such as atherosclerosis when fatty material deposited along the artery walls gets hard and blocks the blood flow and coronary artery disease.
High levels of homocysteine may also damage the lining of the blood vessels, making a person prone to blood clots which increase the risk of stroke and heart attack. Calcium-phosphate levels : Different studies have suggested a link between the calcium and phosphorus levels in patients undergoing dialysis and the hardening of the coronary arteries. Healthy kidneys help keep calcium and phosphorus levels in balance. But damaged kidneys cannot do this. Often, there is too much phosphorus and calcium in the blood. When this happens, there is a risk for coronary artery disease. Diabetes and high blood pressure are the two leading causes of kidney disease.
Here is how each can affect your heart and lead to cardiovascular disease:. Diabetes : Diabetes is a condition where excess sugar remains in the bloodstream. This sugar can damage the blood vessels not only in the kidneys but elsewhere in the body, including the major blood vessels that feed the muscles of the heart. High blood pressure : Not only is high blood pressure a complication from diabetes, it is also a cause of kidney disease. Too much pressure can weaken the walls of the blood vessels, which can lead to a stroke.
Whether your cardiovascular disease is caused by complications of your kidney disease or by the underlying cause of your kidney disease, it's important to be aware of the impact it can have on your overall health.