Diabetes is the most common cause of renal failure. In the United States, it accounts for roughly 44% of all new cases of end-stage kidney disease, the point at which kidneys can no longer sustain life without dialysis or a transplant. High blood pressure is the second leading cause at about 28%, and the two conditions together explain more than seven out of ten cases.
How Diabetes Damages the Kidneys
Both type 1 and type 2 diabetes can lead to kidney failure, though type 2 accounts for the vast majority of cases simply because it is far more common. The damage happens gradually. Persistently high blood sugar injures the tiny filtering units inside each kidney, causing them to leak protein into the urine and slowly lose their ability to clean the blood.
This process, called diabetic nephropathy, unfolds over years. In the earliest stage, the kidneys may actually filter faster than normal, masking the problem. Within a few years the internal structures begin to thicken and scar. Small amounts of protein start spilling into the urine, a sign detectable with a simple urine test long before symptoms appear. As damage accumulates, larger amounts of protein leak out, blood pressure rises, and the kidneys’ filtering rate steadily drops. By the time someone feels noticeably unwell, a significant portion of kidney function is already gone.
The progression from early protein leakage to kidney failure varies widely. Some people with diabetes never develop serious kidney disease, while others reach end-stage disease within 15 to 20 years. Tight blood sugar control, blood pressure management, and certain medications that protect the kidneys can slow or even stall the decline at each stage.
High Blood Pressure as the Second Leading Cause
Uncontrolled high blood pressure is responsible for about 28% of new kidney failure cases in the U.S. The mechanism is straightforward: elevated pressure constricts and damages the small blood vessels that supply the kidneys. With reduced blood flow, the kidneys gradually lose their filtering capacity. They become less able to remove waste and excess fluid from the body, and that extra fluid in the bloodstream pushes blood pressure even higher, creating a self-reinforcing cycle that accelerates the damage.
What makes this cause especially tricky is that high blood pressure rarely produces symptoms on its own. Many people don’t know their blood pressure is elevated until organ damage has already begun. And because diabetes and high blood pressure frequently coexist, the combined strain on the kidneys is greater than either condition alone.
Other Notable Causes
Glomerulonephritis, a group of diseases that inflame the kidney’s filtering units, is the third most common cause, accounting for about 6% of new kidney failure cases. It can result from autoimmune conditions, infections, or causes that are never clearly identified. Some forms respond well to treatment while others progress despite therapy.
Polycystic kidney disease is the most significant genetic cause. Fluid-filled cysts gradually enlarge the kidneys and destroy healthy tissue over decades. Because it is inherited, it tends to cluster in families and is typically diagnosed earlier in life than diabetes or blood pressure-related kidney disease. The U.S. Renal Data System groups it alongside diabetes, hypertension, and glomerulonephritis as one of the four major categories used to classify kidney failure.
Acute vs. Chronic Kidney Failure
The causes above all describe chronic kidney disease, where damage accumulates over months or years. Acute kidney injury is a separate situation: kidney function drops suddenly, often over hours or days, and the causes are different. The most common triggers are prolonged low blood flow to the kidneys (from severe dehydration, blood loss, or a major drop in blood pressure), overwhelming infection (sepsis), and exposure to substances toxic to kidney tissue, including certain antibiotics, contrast dyes used in imaging scans, and common pain relievers like ibuprofen or naproxen when used heavily.
The key difference is that acute kidney injury is often reversible if the underlying cause is treated quickly. Chronic kidney disease, by contrast, involves permanent structural damage. However, repeated episodes of acute injury can contribute to chronic disease over time.
Who Is Most at Risk
Age is the single strongest demographic factor. About 34% of adults aged 65 and older have some degree of chronic kidney disease, compared with 12% of those aged 45 to 64 and just 6% of adults under 45. Women are slightly more affected than men (14% vs. 12%).
Race and ethnicity also play a role. Roughly 20% of non-Hispanic Black adults have chronic kidney disease, compared with about 14% of Hispanic adults, 14% of non-Hispanic Asian adults, and 12% of non-Hispanic White adults. These disparities reflect differences in rates of diabetes and high blood pressure, access to healthcare, and possibly genetic factors that influence kidney vulnerability.
Global Differences in Causes
The dominance of diabetes and high blood pressure as leading causes holds true across most developed countries, and the U.S. has experienced some of the most rapid increases in kidney disease from both type 2 diabetes and hypertension. In parts of Asia and sub-Saharan Africa, however, the picture looks different. Glomerulonephritis and kidney diseases of unknown origin are more prevalent there, driven by higher rates of infections, environmental exposures, and limited access to early treatment for conditions that would be caught sooner in wealthier healthcare systems.
Catching Kidney Damage Early
Because the most common causes of kidney failure are silent for years, screening is the only way to catch damage before it becomes irreversible. The tests are simple: a urine sample that measures protein leakage and a blood test that estimates how well the kidneys are filtering.
Current guidelines from the American Diabetes Association recommend that everyone with type 2 diabetes get both tests at least once a year, regardless of how they feel. For people with type 1 diabetes, annual screening should start five years after diagnosis. If early kidney damage is detected, testing frequency increases to two to four times per year depending on how advanced the disease is.
For people without diabetes, routine screening is recommended if you have high blood pressure, a family history of kidney disease, or other risk factors. Protein in the urine (specifically an elevated albumin-to-creatinine ratio between 30 and 300 mg/g) is the earliest measurable sign of diabetic kidney damage. Catching it at this stage opens the widest window for treatment to slow progression and, in many cases, preserve enough kidney function to avoid ever needing dialysis.