Hyponatremia and Hypernatremia in Kidney Disease: What You Need to Know

When your kidneys start to fail, they don’t just stop filtering waste-they also lose their ability to keep your sodium levels in check. That’s when problems like hyponatremia and hypernatremia creep in. These aren’t just lab numbers gone wrong. They’re silent threats that can lead to falls, confusion, fractures, and even death-especially in people with chronic kidney disease (CKD).

What Exactly Are Hyponatremia and Hypernatremia?

Hyponatremia means your blood sodium is below 135 mmol/L. Hypernatremia means it’s above 145 mmol/L. Sodium isn’t just table salt-it’s the main electrolyte that controls fluid balance in and around your cells. When sodium drops too low, water floods into your brain cells. When it rises too high, your cells shrink. Both can wreck your nervous system.

In healthy people, kidneys adjust urine output to keep sodium steady. But in CKD, that system breaks down. By stage 4 or 5 (GFR under 30 mL/min), your kidneys can’t make enough dilute urine to flush out extra water-or enough concentrated urine to hold onto water when you’re dehydrated. That’s why both low and high sodium levels become common.

Why Kidney Disease Makes Sodium Problems Worse

Your kidneys don’t just filter blood-they fine-tune it. In early CKD (stages 1-2), your kidneys still work well enough to handle normal salt and water intake. But they need to produce more urine to do it. As kidney function drops, that buffer disappears.

By stage 3, your kidneys start struggling to excrete excess sodium. If you eat a salty meal, that salt stays in your body longer than it should. In advanced CKD, your kidneys can’t make urine that’s very dilute or very concentrated. This means even small changes in water intake-like drinking an extra glass of tea or skipping a meal-can swing your sodium levels dangerously.

Plus, many CKD patients take diuretics. Thiazides (like hydrochlorothiazide) are common for high blood pressure, but they’re risky in CKD. Below a GFR of 30, they barely work-and they’re notorious for causing hyponatremia. Loop diuretics (like furosemide) are safer in late-stage CKD, but they still need careful dosing.

Types of Hyponatremia in Kidney Disease

Not all low sodium is the same. There are three types, and kidney disease affects them differently:

• Hypovolemic hyponatremia (15-20% of cases): You lose both water and sodium, but lose more sodium. This happens with vomiting, diarrhea, or salt-wasting kidney conditions like Addison’s disease or overuse of diuretics.
• Euvolemic hyponatremia (60-65% of cases): Your total body water goes up, but your sodium stays normal. This is the most common type in CKD. Your kidneys can’t get rid of extra water, so it builds up. Thiazide diuretics are a big reason why.
• Hypervolemic hyponatremia (15-20% of cases): You have too much total fluid-swelling in your legs, belly, or lungs. This happens when heart failure or advanced CKD causes fluid overload. The extra water dilutes your sodium.

The key to fixing hyponatremia is knowing which type you have. Treating them the same can be deadly.

Why Hyponatremia Is So Dangerous in CKD

Low sodium isn’t just a lab result. It’s a red flag for serious problems.

Studies show CKD patients with hyponatremia have a nearly 2x higher risk of dying than those with normal sodium. In older adults, it’s linked to:

• 35% higher chance of osteoporosis
• 28% prevalence of gait instability (vs. 12% in normal sodium)
• 1.8x higher risk of falls
• 1.7x higher risk of fractures
• Cognitive decline-3 studies found hazard ratios between 1.35 and 2.17

Hospitalized CKD patients with hyponatremia have 28% higher death rates than those with normal levels. And if sodium drops during hospitalization? Mortality spikes even more.

Here’s the twist: The very advice meant to protect CKD patients can make hyponatremia worse. Many doctors tell patients to cut sodium, potassium, and protein to protect their kidneys. But cutting protein and salt reduces solute load, which lowers urine output. That makes it harder for your kidneys to excrete water-even if you’re drinking too much. In Japan, where solute restriction is aggressive, hyponatremia is more common in CKD patients than in Western countries.

Hypernatremia: The Overlooked Threat

Most people focus on low sodium. But high sodium is just as dangerous-and often missed.

Hypernatremia happens when you lose too much water or take in too much salt. In CKD, it’s often caused by:

• Not drinking enough fluids (especially in elderly patients with reduced thirst sensation)
• Diabetes insipidus (kidneys can’t respond to ADH)
• Excess salt intake (rare, but possible with processed foods or IV fluids)

When sodium rises, your brain cells shrink. That can cause seizures, coma, or brain bleeding. The fix? Slow, controlled water replacement. Don’t correct it faster than 10 mmol/L in 24 hours. Too fast, and your brain swells. That’s just as deadly as osmotic demyelination from too-slow correction of hyponatremia.

How to Manage Sodium Disorders in CKD

There’s no one-size-fits-all fix. Treatment depends on your stage of CKD, your symptoms, and what’s causing the imbalance.

For Hyponatremia:

• Fluid restriction: Most common first step. For early CKD, limit to 1,000-1,500 mL/day. For advanced CKD, drop to 800-1,000 mL/day.
• Stop thiazide diuretics: If you’re on them and have GFR under 30, ask your doctor to switch to a loop diuretic.
• Correct sodium slowly: Never raise sodium by more than 4-6 mmol/L in 24 hours. Faster correction risks osmotic demyelination syndrome-a rare but devastating brain injury.
• Watch for salt-wasting: If you’re losing sodium in urine despite low intake, you may need 4-8 grams of salt per day. This is rare but critical to catch.

For Hypernatremia:

• Replace water gradually: Use oral fluids if possible. IV fluids only if severely dehydrated.
• Target correction rate: No more than 10 mmol/L per day. Faster = brain swelling risk.
• Check for medications: Lithium, demeclocycline, or certain antipsychotics can cause water loss.

And avoid vaptans (like tolvaptan). These drugs block ADH to help flush water-but they don’t work well in advanced CKD and can cause liver damage. The European Medicines Agency warns against using them in stage 4-5 CKD.

What Patients and Families Need to Know

Managing sodium in CKD isn’t just about medicine. It’s about daily choices.

Many patients get confused by conflicting advice: “Eat low sodium!” but also “Drink enough water!” The truth? It’s a tightrope walk. Too little salt can cause hyponatremia. Too much water can too. Too little water can cause hypernatremia.

Studies show it takes 3-6 sessions with a renal dietitian for patients to understand this balance. Elderly patients-70-75% of advanced CKD cases-struggle the most. They forget to drink. They think “no salt” means no flavor. They skip meals and don’t realize they’re not getting enough solutes to make urine.

One common mistake? Cutting salt so hard that you reduce your protein and fluid intake. That lowers your urine output, trapping water in your body. You end up with hyponatremia-even though you thought you were doing everything right.

Integrated care helps. When nephrologists, dietitians, pharmacists, and primary care doctors work together, hospitalizations for sodium disorders drop by 35%.

New Tools and Future Directions

There’s hope on the horizon.

In 2023, the FDA approved a new sodium monitoring patch for CKD patients. It measures sodium in your skin fluid continuously and matches serum levels with 85% accuracy. No more frequent blood draws.

Researchers are also studying the gut-kidney axis. Early data suggests your intestines may help compensate for failing kidneys by adjusting sodium absorption. If proven, this could lead to new dietary or probiotic therapies.

The 2024 KDIGO guidelines are expected to push for personalized fluid targets-not a one-size-fits-all limit. Your ideal water intake may depend on your residual kidney function, not just your stage of CKD.

With 850 million people worldwide living with CKD-and that number rising fast-getting sodium right isn’t optional. It’s essential.

Key Takeaways

• Hyponatremia and hypernatremia are common, dangerous, and often missed in CKD.
• Low sodium is more frequent than high sodium, but both can kill.
• Thiazide diuretics are a major cause of hyponatremia in CKD-switch to loop diuretics if GFR is below 30.
• Fluid restriction is key, but too little salt can make hyponatremia worse.
• Correct sodium slowly: no more than 4-6 mmol/L/day for low sodium, no more than 10 mmol/L/day for high sodium.
• Team-based care (nephrologist + dietitian + pharmacist) cuts hospitalizations by 35%.
• New monitoring patches and research into gut-kidney links are changing how we manage this.