Why Chronic Kidney Disease So Often Ends in Heart Problems

• CKD reflects progressive injury to the kidney’s filtering units — As individual filters are damaged, the remaining healthy ones compensate by increasing their workload to preserve overall filtration. This adaptive response allows you to feel relatively normal for long periods, even as structural damage continues to accumulate beneath the surface.

However, over time, the added strain wears down the remaining filters, leading to a steady decline in the kidneys’ total filtering capacity. Unlike acute kidney injury, which develops rapidly and may resolve, chronic kidney disease progresses gradually over months or years and is generally irreversible.⁴

• Clinicians assess CKD using two core markers of function and structure — The first is the estimated glomerular filtration rate (eGFR), which represents how much blood your kidneys filter each minute. It serves as a practical indicator of overall filtering efficiency. An eGFR below 60 signals reduced kidney function, while lower than 15 signals kidney failure.

The second marker is albumin leakage into the urine, measured as the albumin-to-creatinine ratio. Albumin is a blood protein that healthy kidneys retain within the bloodstream. When it appears in the urine, it indicates damage to the filtration barrier, allowing larger molecules to pass through when they should not.

Together, eGFR and albumin levels provide a clearer picture of how much filtering capacity remains and how compromised the kidney structure has become, helping clinicians gauge disease severity and progression risk.⁵

• CKD progresses through five defined stages — Stages 1 and 2 reflect early disease, where kidney function remains near normal but laboratory testing reveals evidence of strain or mild structural injury. At this point, symptoms are uncommon.

Stages 3a and 3b indicate moderate loss of function, during which waste products begin to accumulate more noticeably and blood pressure regulation becomes more difficult. Some people begin to experience fatigue or swelling in the legs, hands, or face.

Stage 4 represents severe impairment, where the kidneys struggle to meet the body’s metabolic demands and symptoms become more pronounced. Stage 5, also known as kidney failure, occurs when the kidneys can no longer maintain fluid, electrolyte, and waste balance without external support, making dialysis or transplantation necessary for survival.⁶

• Declining kidney function disrupts systems far beyond filtration — As kidney function declines, the effects extend well beyond filtration alone. Impaired regulation of sodium, potassium, phosphorus, and acid-base balance places strain on nerves, muscles, and the cardiovascular system. Hormonal disruptions interfere with blood pressure control, red blood cell production, and bone remodeling.⁷

• The study focused on circulating extracellular vesicles (EVs) — Think of extracellular vesicles as tiny envelopes that cells use to send instructions to distant organs. When your kidneys are healthy, these messages maintain normal function. In people with CKD, EVs circulating in the blood differed from those in healthy individuals not by number or size but by their molecular cargo and biological effects on heart cells.

• CKD-derived EVs were enriched with a distinct set of microRNAs — These microRNAs act like dimmer switches for your genes — they can turn down the activity of specific proteins your heart needs to contract properly. The damaged kidney sends microRNAs that essentially turn off your heart’s ability to pump effectively.

• These microRNAs originate primarily from kidney cells rather than from the heart or other tissues — The researchers traced the precursor forms of microRNAs back to kidney tissue in both human patients and animal models. This establishes a direct kidney-to-heart communication pathway that explains how CKD can initiate cardiac injury even when heart disease has not yet been diagnosed.

• EVs isolated from the blood plasma of CKD patients were directly cardiotoxic — When these CKD-derived EVs were exposed to heart muscle cells, they significantly reduced cell viability and triggered apoptosis, a regulated form of cell death. In addition to promoting cell loss, these vesicles interfered with the ability of heart muscle cells to contract properly, a fundamental requirement for maintaining normal cardiac output.

• CKD-derived EVs disrupt calcium handling inside cardiomyocytes — Cardiomyocytes are heart muscle cells responsible for generating the force needed to pump blood throughout your body. Calcium ions control the contraction and relaxation cycle of the heart muscle, and precise regulation is essential for coordinated beating.

Heart cells treated with EVs from CKD patients struggled to handle calcium normally. Calcium signals in these cells rose more weakly and cleared more slowly, which interfered with the timing and strength of contraction. This resulted in changes that mirror early functional features of heart failure even before symptoms appear.

• Reducing circulating EVs led to improvement in heart function — Cardiac contraction strengthened while markers of fibrosis (pathological scar tissue buildup that stiffens heart muscle) and hypertrophy (abnormal thickening and enlargement of heart muscle cells) declined. Researcher Uta Erdbrügger, M.D., an internal medicine physician-scientist with the University of Virginia School of Medicine’s Division of Nephrology, noted:

“Kidney and heart disease can develop silently, so they are often discovered only after damage has already been done. Our findings can help to identify patients at risk for heart failure earlier, enabling earlier treatment and improved outcomes.”⁹

• Diabetes — Persistently elevated blood glucose damages the delicate filtering structures inside the kidneys, thickening and scarring the glomerular membranes that separate waste from blood.

As this barrier becomes compromised, albumin begins to leak into the urine, a key marker of early kidney damage. About one in three people with diabetes also have chronic kidney disease, making it the leading cause of kidney failure in the United States.^10,11

• High blood pressure — High blood pressure places constant mechanical stress on the small blood vessels that supply the kidneys. Over time, this pressure damages vessel walls, reduces blood flow to filtering units, and accelerates scarring within kidney tissue.

As kidney function declines, fluid and sodium regulation becomes less precise, which can further raise blood pressure and increase strain on remaining healthy tissue. Approximately one in five people with high blood pressure develop kidney disease.¹²

• Nonsteroidal anti-inflammatory drugs (NSAIDs) — Regular or long-term use of NSAIDs such as ibuprofen or naproxen can impair kidney function by reducing blood flow to the kidneys and interfering with protective prostaglandin signaling.

These medications blunt pain and inflammation by altering enzyme activity, but in doing so they also limit the kidneys’ ability to adapt to stress, dehydration, or reduced circulation. Over time, repeated exposure can contribute to chronic injury, particularly in people with existing risk factors such as aging, hypertension, or diabetes.^13,14

• Kidney stones — Recurrent kidney stones can contribute to CKD through repeated obstruction, inflammation, and localized tissue injury. Stones can block urine flow, raise pressure within the kidney, and trigger inflammatory responses that damage surrounding structures. When stone formation occurs frequently or remains untreated, the cumulative impact can scar kidney tissue and reduce overall filtration capacity.¹⁵

• Obesity — Excess body weight places additional metabolic demands on the kidneys. Obesity is associated with insulin resistance, chronic low-grade inflammation, altered lipid metabolism, and increased filtration workload, all of which strain kidney tissue over time.

To compensate for increased metabolic needs, the kidneys often filter more blood than normal, a state known as hyperfiltration. While this initially maintains balance, prolonged hyperfiltration accelerates wear on filtering units and increases the risk of progressive decline.^16,17,18

1. Restore a healthy sodium-to-potassium balance — Blood pressure regulation depends heavily on the balance between sodium and potassium rather than sodium alone. Aggressively cutting salt often disrupts metabolic signaling, raises insulin levels, and increases physiological stress, which undermines blood pressure control. The real issue isn’t salt itself, but where it comes from.

Most people get their sodium from ultraprocessed foods, which are stripped of potassium, a mineral necessary to counterbalance sodium. Replacing these with whole, unprocessed foods such as ripe fruit, root vegetables, and well-cooked greens helps restore mineral balance and reduce renal workload.

2. Optimize your vitamin D levels — Vitamin D helps regulate the hormonal system that controls blood pressure and fluid balance. When vitamin D levels remain low, this system becomes overstimulated, increasing vascular tension and kidney strain.

Regular sun exposure remains the most effective way to maintain healthy vitamin D levels. However, avoid peak hours (10 a.m. to 4 p.m.) if you consume linoleic acid (LA) from vegetable oils. This polyunsaturated fat builds up in your skin and oxidizes quickly, increasing your risk of skin damage.

Cut these oils from your diet for at least six months before getting peak sun exposure. Get your vitamin D levels tested at least twice a year and aim for a level between 60 and 80 ng/mL (150 to 200 nmol/L). If you don’t get regular sunlight, consider supplementing with vitamin D3 to maintain healthy levels year-round.

3. Maintain daily movement — Regular movement improves circulation, stabilizes blood sugar, and reduces pressure on the kidney’s filtering units. An hour of moderate activity, such as walking, cycling, or swimming, supports these processes without overtaxing the system. If you’re just beginning, starting with 10-minute sessions can still provide benefits. Every bit of movement supports healthier kidneys.

4. Pay attention to your oxalate intake — If you have a history of kidney stones, moderating oxalate intake helps reduce recurrence risk. Foods particularly high in oxalates include spinach, almonds, peanut butter, sweet potatoes, and figs. Regular exposure to large amounts of these compounds increases the likelihood that oxalates will concentrate in the urine.

Combining oxalate-containing foods with calcium-rich options limits absorption in the digestive tract. Calcium binds to oxalate in the gut, forming an insoluble compound that is eliminated in stool rather than filtered through the kidneys. Dairy products and low-oxalate greens such as kale serve this role effectively.

Preparation methods also influence oxalate load. Boiling high-oxalate foods draws oxalates into the cooking water, which should be discarded before consumption. Adequate hydration further lowers risk by diluting oxalates, reducing their ability to crystallize and form stones.

5. Reduce excess phosphorus intake — Phosphorus from processed foods places additional filtering demands on the kidneys. Phosphate additives used in packaged foods, colas, and fast-food meats are absorbed efficiently and accumulate quickly when kidney function begins to decline.

This disrupts calcium balance and triggers hormonal changes that strain kidney tissue. Choosing fresh foods and avoiding ingredients labeled with phosphate or phosphoric acid lowers this burden. When phosphorus levels rise, limiting dairy intake also becomes important due to its high absorbable phosphorus content.¹⁹

6. Stay well-hydrated with pure water — Hydration supports kidney function by diluting waste products and reducing stone formation risk. Thirst provides a reliable guide to your hydration levels, while urine color offers an additional indicator. Pale yellow urine reflects adequate hydration, while darker shades signal the need for increased fluid intake.

7. Address recurrent urinary tract infection (UTI) without antibiotics — Repeated UTIs have been associated with faster kidney decline. At the same time, frequent antibiotic use stresses kidney tissue and alters microbial balance. Non-antibiotic approaches deserve consideration when appropriate, especially in people with existing kidney vulnerability.²⁰

One alternative treatment worth considering is methylene blue. Learn more about it in “Benefits and Side Effects of Methylene Blue — A Comprehensive Guide.”

8. Screen early if risk factors are present — High blood pressure, diabetes, obesity, and family history all increase the likelihood of kidney disease. Simple blood and urine tests that measure eGFR and urine albumin reveal early damage long before symptoms appear. Detecting changes at this stage gives you the opportunity to address kidney issues before irreversible damage.