Heart and kidneys form such a close tandem When one fails, sooner or later it drags the other down with it. However, this cardiorenal connection remains largely unknown to many people: most patients with chronic kidney disease are unaware they have it and, at the same time, are unaware that their main threats are not only dialysis or transplantation, but also heart attack, stroke, or heart failure.
Understanding how kidney and heart health are related It is key to getting ahead of problems: detecting the disease before it shows up, controlling risk factors, choosing the right treatments (both pharmacological and lifestyle) and avoiding that vicious cycle in which heart failure worsens kidney function and kidney damage accelerates the deterioration of the cardiovascular system.
The dangerous connection between the heart and kidneys
Around half a million people worldwide live with kidney disease And tens of thousands in countries like Spain live with some degree of chronic kidney disease. When this damage is severe, the risk of cardiovascular events (heart attack, stroke, peripheral artery disease) increases tenfold. Most strikingly, more than half of all deaths in patients with chronic kidney disease are due to cardiovascular causes, far exceeding infections or other complications.
Cardiologists and nephrologists have been warning for years That, from stage III of chronic kidney disease (when the glomerular filtration rate falls below approximately 60%), the person enters fully into the territory of “vascular morbidity”: more heart attacks, more cerebrovascular disease, more problems in the arteries of the legs and, in general, a cocktail of vascular complications that are concentrated in those who have damaged kidneys.
This relationship is not unidirectionalA heart patient with heart failure may experience kidney deterioration due to reduced blood and oxygen reaching the renal tissue. Simultaneously, anemia, high cholesterol, and especially the high blood pressure typical of kidney failure, directly harm the heart. This creates what is known as “cardiorenal dominance”: a constant interplay between these two organs where any prolonged disruption ultimately damages both.
The link is further strengthened if we add the metabolic componentThe combination of cardiovascular disease, kidney deterioration and factors such as diabetes or obesity has led to talk of “cardio-renal-metabolic syndrome (CKM)”, a scenario in which multiple problems overlap (metabolic, hemodynamic, inflammatory and hormonal) that drive a cycle of progressive damage.
How kidneys and heart work and why they are needed
The heart is the “pump” that propels the blood to the entire body to carry oxygen and nutrients to every cell. The kidneys, located on either side of the spine in the back of the abdomen, act as a complex filtering plant: they purify the blood of waste products, regulate the balance of water and salts, produce hormones that control blood pressure, and help in the formation of red blood cells.
Each kidney is approximately the size of a fist It contains thousands of microscopic filtering structures. Blood pumped by the heart arrives through a renal artery; this blood is distributed through small vessels where substances are “selected” to determine which are eliminated and which are returned to the bloodstream. Under normal conditions, approximately 180 liters of blood are filtered each day, producing between 1 and 2 liters of urine, which carries waste products such as creatinine, urea, ammonia, sodium, potassium, and phosphorus.
Proteins and blood cells should not pass into the urineWhen these symptoms appear, it’s a sign that the kidneys are damaged. Furthermore, the kidneys produce hormones that regulate blood pressure and erythropoietin, which is key for red blood cell production. Therefore, persistent kidney dysfunction can eventually lead to hypertension, anemia, and mineral imbalances that put a strain on the heart.
The heart, for its part, needs an elastic blood vessel system to work without overexertion. If the arteries become rigid or filled with plaque (atherosclerosis), the pressure that the left ventricle must overcome increases, and it responds by hypertrophying (thickening). This left ventricular hypertrophy, so common in kidney patients, ends up impairing cardiac function and facilitating the development of heart failure, arrhythmias, and coronary events.
Cardiorenal syndrome: when they fail at the same time
Cardiorenal syndrome describes the scenario in which A primary failure in the heart or kidney triggers a cascade that ultimately damages the other organ. This interaction is explained by several well-known mechanisms.
On one hand there are hemodynamic and circulatory problemsIf the heart doesn’t pump strongly enough (for example, in acute or chronic heart failure), less blood flow reaches the kidneys. Less blood flow means less oxygen and nutrients, which progressively damages kidney tissue.
Hormonal compensation systems are also activatedespecially the renin-angiotensin-aldosterone system and the sympathetic nervous system. In the short term, these mechanisms help maintain blood pressure and blood flow to vital organs, but when they persist chronically, they promote hypertension, sodium and water retention, fibrosis of the heart muscle, and pathological remodeling of the arteries.
Chronic inflammation and oxidative stress are another pillar of this connectionIn chronic kidney disease, numerous inflammatory markers (C-reactive protein, fibrinogen, interleukins, tumor necrosis factor, adhesion molecules, etc.) are elevated, and substances that would normally be eliminated by the kidneys accumulate. This “inflammatory soup” accelerates atherosclerosis, damages the vascular endothelium, and contributes to arterial stiffness and heart deterioration.
In addition to all this, there are shared classic risk factors due to both conditions: high blood pressure, diabetes, dyslipidemia, smoking, obesity, sedentary lifestyle, and advanced age. When these factors remain uncontrolled for years, they eventually cause structural and functional damage to both the kidneys and the heart, leading to simultaneous kidney and heart failure.
Types of cardiorenal syndrome
To better organize this complex interaction Several types of cardiorenal syndrome have been described depending on which organ is affected first and whether the problem is acute or chronic:
- Type 1: acute cardiac decompensation (e.g., acute heart failure or extensive heart attack) that causes a sudden worsening of kidney function.
- Type 2: chronic heart disease (long-standing heart failure) that gradually impairs kidney function.
- Type 3: acute renal failure that secondarily triggers cardiac damage, with arrhythmias, decompensation or even heart failure.
- Type 4 (classically described although it slips in your list): established chronic kidney disease that generates cardiac remodeling, accelerated atherosclerosis and heart failure.
- Type 5: a systemic disease (such as diabetes, severe sepsis, autoimmune disorders) that simultaneously affects the heart and kidneys.
In clinical practice, many patients fit into more than one type throughout its evolution. A common example would be a person with diabetes and CKD who suffers an acute coronary syndrome, experiences worsening kidney function during hospitalization, and is left with chronic heart failure: several types of cardiorenal syndrome converge here at the same time.
Chronic kidney disease: the silent enemy of the heart
Chronic kidney disease (CKD) has a nasty habit of progressing silently.In its early stages, it doesn’t usually cause noticeable symptoms; it’s often detected incidentally, in a blood test that shows elevated creatinine or a simple urine test that indicates the presence of protein. Sometimes, the only clue is high blood pressure that’s difficult to control.
As glomerular filtration decreases and stages 3, 4, and 5 are enteredThe risk of cardiovascular death skyrockets. With moderate CKD (stage 3), the risk of dying from cardiac causes doubles; in more advanced stages (stage 4 and pre-dialysis), it triples or more. The paradox is that many of these patients do not die from kidney failure in the strictest sense, but from a heart attack, stroke, or sudden death before even needing dialysis or a transplant.
To complicate matters further, heart attacks in people with CKD They often present atypically: less chest pain, less pronounced electrocardiographic changes (for example, without clear ST-segment elevation), and vaguer symptoms. Furthermore, cardiologists sometimes avoid contrast studies for fear of further kidney damage, which can delay the diagnosis of blocked coronary arteries until a serious event occurs.
The end-stage renal failure (ESRF) phase, in which dialysis or transplantation is required.This is preceded by a long period of progressive decline in glomerular filtration. During this time, cardiovascular disease gains ground: more rapid atherosclerosis, left ventricular hypertrophy, arterial stiffness, arrhythmias, and a very high percentage of heart failure.
The figures are conclusiveBetween 40 and 70% of people starting dialysis already have signs of cardiovascular disease, and approximately 40% of deaths in dialysis patients are due to cardiac causes. Cardiovascular mortality is between 5 and 10 times higher than in the general population, even after adjusting for age, diabetes, and other factors.
Cardiovascular risk factors in kidney disease
In CKD, classic risk factors coexist with other more specific ones. of kidney damage. The traditional risk factors are those known to everyone: age, hypertension, diabetes, smoking, high LDL cholesterol, low HDL cholesterol, and obesity. But in kidney disease, “non-traditional” factors are added that also contribute to atherosclerosis and heart damage.
Among these non-classical factors, the following stand out: The chronic inflammation already mentioned, oxidative stress, hyperhomocysteinemia, anemia, alterations in calcium-phosphorus metabolism (leading to calcifications in blood vessels and heart valves), endothelial dysfunction, intense activation of the renin-angiotensin system and the sympathetic nervous system, as well as sodium and water retention.
In addition, microalbuminuria or mild proteinuria is very common in CKDThis refers to the presence of small amounts of albumin in the urine that can go unnoticed without specific testing. These “small leaks” of protein are an early marker of kidney damage, but they are also strongly associated with increased cardiovascular risk, left ventricular hypertrophy, increased carotid intima-media thickness, and signs of ischemia.
Several studies have shown that the mere presence of microalbuminuria This translates into a significant increase in the risk of heart attack, stroke, or cardiovascular death, even in people without diabetes. In certain high-risk groups, having microalbuminuria can double the overall mortality rate compared to those without it.
This has led to consideration of renal function and albuminuria. as top-level prognostic markers in cardiology. Today it is known that the further the glomerular filtration rate falls below 60 ml/min/1,73 m², the greater the probability of having cardiovascular events of all kinds, from acute coronary syndrome to heart failure or stroke.
Left ventricular hypertrophy and vascular remodeling
Left ventricular hypertrophy (LVH) is one of the hallmarks of heart disease in patients with CKD. The heart responds to pressure overload (hypertension, stiffness of large arteries, aortic stenosis) and volume overload (fluid retention, anemia, hyperdynamic circulation by arteriovenous fistula in dialysis) by thickening its walls.
In relatively early stages of kidney disease A slight increase in left ventricular mass and alterations in diastolic function (the heart relaxes less effectively) are already detected. Echocardiographic studies show that the prevalence of LVH increases as glomerular filtration rate decreases and can exceed 70% in patients starting dialysis, with a predominance of concentric hypertrophy.
This remodeling is not innocent.Left ventricular hypertrophy (LVH) decreases ventricular compliance, raises filling pressures, and promotes the development of pulmonary edema in the face of any fluid overload. It also increases the oxygen demand of the myocardium in the context of coronary arteries with atherosclerosis or stiffness, which predisposes to ischemia, even without critical epicardial coronary lesions.
In parallel, the major arteries undergo an intense remodeling processThe walls become more rigid, thicken, and calcifications appear in both the intima (classic atherosclerosis) and the media, which are very typical of chronic kidney disease. The consequence is an increase in pulse pressure and a more abrupt arrival of the pressure wave to the ventricle, which worsens left ventricular hypertrophy and subendocardial ischemia.
These structural alterations result in a high risk of arrhythmias.especially in patients on hemodialysis, where the combination of myocardial fibrosis, abrupt changes in volume and electrolytes, and LVH is associated with sudden death in a significant percentage of cases.
Recent findings: kidney gallbladders that damage the heart
Recent research has shed more light on “toxic dialogue” between the kidney and the heart. A study from the University of Virginia and Mount Sinai has shown that damaged kidneys release small particles called extracellular vesicles into the bloodstream, which act as messengers between cells.
In people with chronic kidney diseaseThese vesicles transport non-coding microRNAs capable of directly affecting cardiac tissue. In experimental models, blocking or reducing the circulation of these vesicles improved heart function and slowed the progression to heart failure, suggesting that the diseased kidney sends active “signals” that worsen the condition of the myocardium.
Blood plasma analysis of patients with CKD They have identified elevated concentrations of these pathological vesicles compared to healthy individuals, reinforcing the idea that the kidney is not merely a bystander, but a direct actor in heart damage. In the future, this could allow for the development of blood tests to detect patients at higher risk of heart failure and the design of targeted therapies that block these harmful messengers.
This type of finding is part of a new way of understanding precision medicine.: to identify very specific biomarkers that allow the treatment to be tailored to each patient profile, something especially valuable in complex diseases such as CKD combined with heart failure.
Diagnosis: how the heart-kidney axis is assessed
To detect cardiorenal syndrome and CKD with cardiovascular impact A combination of simple and more sophisticated tests is used. For the kidneys, blood tests measure creatinine and allow for estimation of the glomerular filtration rate using validated formulas (such as those derived from MDRD or Cockcroft-Gault, now adjusted and calibrated), avoiding the need to collect urine for 24 hours in most cases.
Urine provides a lot of informationThe detection of albuminuria or proteinuria, even if mild, is a warning sign of both early kidney damage and increased cardiovascular risk. In some cases, the albumin/creatinine ratio is measured in a single urine sample, which facilitates screening in primary care and cardiology clinics.
In the cardiac part, biomarkers and imaging tests are used.Blood tests using high-sensitivity troponins, natriuretic peptides (BNP or NT-proBNP), and other markers can indicate myocardial damage or ventricular overload. Electrocardiograms and, especially, echocardiograms allow for the assessment of systolic and diastolic function, the presence of left ventricular hypertrophy (LVH), valvular calcifications, or signs of pulmonary hypertension.
When coronary artery disease is suspectedStress tests, stress echocardiography, perfusion scans, or coronary computed tomography are used. In patients with advanced CKD, the need for iodinated contrast must be balanced with the risk of worsening kidney function, requiring careful planning. Coronary catheterization remains the gold standard for studying the coronary arteries when there is a high suspicion of CKD.
In summary, cardiorenal evaluation should be performed jointly.The cardiologist must always look at creatinine, GFR and albuminuria; the nephrologist, on the other hand, cannot limit himself to the kidney and must systematically assess the state of the heart and vascular tree of his patients.
Treatment: Protect both kidneys and heart
The treatment of cardiorenal syndrome and CKD with high cardiovascular risk It pursues three main objectives: to slow the progression of kidney damage, to minimize cardiac events, and to cut off the mechanisms that feed the vicious cycle between both organs.
Lifestyle measures are a true cornerstoneMaintaining blood pressure within recommended ranges (usually below 130/80 mmHg in most kidney patients), controlling weight, quitting smoking, moderating alcohol, moving daily, and following a diet rich in fruits, vegetables, and legumes but low in salt (around 3 g of salt per day) are steps that influence the heart, kidneys, and brain.
Regarding drugs, the inhibitors of the renin-angiotensin system ACE inhibitors and ARBs have been the cornerstone of kidney and heart protection for decades: they reduce blood pressure, decrease proteinuria, slow the progression of CKD, and promote partial regression of LVH. Their use, when not contraindicated, is associated with lower mortality and fewer hospitalizations for heart failure.
In recent years, SGLT2 inhibitors have emerged strongly.Initially used to treat type 2 diabetes, large clinical studies have shown that drugs such as dapagliflozin, empagliflozin, and canagliflozin not only lower glucose levels but also significantly reduce the risk of progression of kidney disease and major cardiovascular events, including hospitalizations for heart failure.
In trials with thousands of patientsAdministering SGLT2 inhibitors on top of standard treatment (including ACE inhibitors or ARBs) achieved reductions of nearly 40% in the combined endpoint of major renal impairment, initiation of dialysis, or death from renal or cardiovascular causes. Interestingly, this benefit was observed in both people with and without diabetes.
Other pillars of the approach include diureticsThese include essential fluid volume adjustment and relief of congestion in heart failure without overburdening the kidneys; beta-blockers, which reduce mortality in heart failure and after myocardial infarction; mineralocorticoid antagonists (such as spironolactone or eplerenone) when tolerated; and new cardiorenal axis modulators being tested in clinical trials (such as ziltivekimab, which targets specific inflammatory pathways).
In cases where kidney function falls to very low levels Renal replacement therapy may be necessary: hemodialysis, peritoneal dialysis, or transplantation. The choice of technique and the timing of initiation should consider not only renal parameters but also the cardiac status, since sudden changes in volume or pressure during dialysis can decompensate a fragile heart.
Prevention: manage blood pressure, blood sugar, and lifestyle
The most effective way to protect both the heart and the kidneys It’s about not waiting for advanced disease to appear. Screening and rigorous monitoring in people with risk factors is key: those with hypertension, diabetes, obesity, smokers, patients with a history of heart attack, stroke, or peripheral vascular disease… all of them should have regular checks of creatinine, GFR, and albuminuria.
High blood pressure has rightfully earned the nickname “silent killer”. Because it often doesn’t cause symptoms but gradually damages the walls of the arteries in the kidneys, heart, and brain. Keeping it under control through lifestyle changes and medication when necessary prevents the development of chronic kidney disease and drastically reduces the risk of heart attack, heart failure, and stroke.
Poorly controlled diabetes is now the leading cause of CKD in many countriesGood glycemic control (with proper diet, exercise and adjusted medication, including drugs with proven cardiorenal benefit such as SGLT2 or GLP-1 analogues when indicated) delays the onset of kidney damage for many years and makes life much less complicated for the heart.
Furthermore, prevention involves small daily decisions.: reduce salt intake, avoid self-medication with drugs that are potentially toxic to the kidneys (such as certain anti-inflammatories taken chronically), attend regular check-ups and do not ignore symptoms such as leg swelling, disproportionate fatigue, difficulty breathing or changes in the amount of urine.
The underlying message is clearProtecting cardiovascular health from an early age and closely monitoring kidney function in those with accumulated risk factors can prevent many of the most serious heart-kidney complications. Integrating the perspectives of cardiologists and nephrologists, utilizing new therapies with proven benefits, and maintaining a healthy lifestyle make all the difference in life expectancy and, above all, quality of life. [related url=”https://www.cultura10.com/principales-partes-y-sistemas-del-cuerpo-humano/”]