What Medications Cause Low GFR?

October 8, 2025 •

5 min read

According to the National Kidney Foundation, over-the-counter pain relievers like nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most common culprits for drug-induced kidney damage. Understanding what medications cause low GFR is vital for preventing potentially reversible kidney problems, especially in individuals with existing kidney disease or other risk factors.

Quick Summary

A decline in glomerular filtration rate can be caused by various medications, including NSAIDs, blood pressure drugs, certain antibiotics, and contrast dyes. Risk is often higher with underlying kidney conditions, so it is important to understand how different drug classes can impact kidney function.

Key Points

NSAIDs reduce GFR: Nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen can lower GFR by constricting renal blood vessels, a risk that increases with long-term use, high doses, or existing kidney problems.
ACE inhibitors cause initial GFR drop: While beneficial long-term for blood pressure and kidney disease, ACE inhibitors and ARBs cause an initial, reversible drop in GFR by affecting intraglomerular hemodynamics.
Diuretics increase dehydration risk: Often prescribed for high blood pressure, diuretics can lead to volume depletion, which reduces blood flow to the kidneys and decreases GFR.
Certain antibiotics are nephrotoxic: Aminoglycosides and some other antibiotics can directly damage renal tubular cells or cause an allergic inflammation (interstitial nephritis), leading to a decline in GFR.
Contrast dye can cause acute kidney injury: Used in imaging, iodinated radiocontrast dye can temporarily harm kidney function, particularly in individuals with pre-existing kidney disease or diabetes.
Risk factors amplify harm: Patient factors such as older age, diabetes, dehydration, and existing CKD significantly increase the risk of developing medication-induced low GFR.

The kidneys play a crucial role in maintaining overall health by filtering waste and excess fluids from the blood. The glomerular filtration rate (GFR) is a key measure of this function, indicating how well the tiny filtering units (glomeruli) of the kidneys are working. When certain medications are introduced, they can interfere with this delicate process, leading to a decline in GFR. This drug-induced nephrotoxicity can occur through several different mechanisms, affecting the kidneys in both acute and chronic ways.

How Medications Affect Glomerular Filtration

Medications can cause a low GFR by disrupting the kidney's normal function in several ways:

Altered Intraglomerular Hemodynamics: The kidney naturally regulates blood flow through the glomeruli by controlling the constriction and dilation of the blood vessels. Medications that interfere with this autoregulation, such as NSAIDs, ACE inhibitors, and ARBs, can reduce blood flow and pressure within the glomerulus, causing a drop in GFR.
Tubular Cell Toxicity: Some drugs are toxic to the renal tubular cells, which are responsible for reabsorbing water and other nutrients. This direct toxicity can impair the cells' function, leading to acute tubular necrosis. Examples include aminoglycoside antibiotics and certain chemotherapy agents.
Inflammation (Interstitial Nephritis): A drug can trigger an allergic or hypersensitivity reaction in the kidneys, causing inflammation in the interstitial space surrounding the tubules. This can be caused by drugs like NSAIDs, certain antibiotics, and proton pump inhibitors (PPIs).
Crystal Nephropathy: Certain drugs can precipitate in the renal tubules, forming crystals that obstruct urine flow. This blockage and the associated inflammation can lead to kidney injury. Common culprits include some antibiotics, antivirals, and older laxatives.
Rhabdomyolysis: A rare but serious side effect of some medications, like statins, can cause skeletal muscle injury. This releases myoglobin into the bloodstream, which is toxic to the kidneys and can cause tubular obstruction and acute kidney failure.

Common Medication Classes That Cause Low GFR

Several classes of medications are known to cause a decrease in GFR. These include both prescription and over-the-counter drugs.

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

NSAIDs like ibuprofen (Advil, Motrin) and naproxen (Aleve) are common causes of low GFR, especially with chronic or high-dose use. They work by inhibiting cyclooxygenase (COX) enzymes, which also reduces the production of renal prostaglandins. These prostaglandins are normally responsible for vasodilation in the kidneys, so their inhibition can lead to unopposed vasoconstriction, decreased renal blood flow, and a lower GFR.

ACE Inhibitors and Angiotensin Receptor Blockers (ARBs)

ACE inhibitors (e.g., lisinopril) and ARBs (e.g., losartan) are crucial for managing hypertension and heart disease. However, they cause a reversible drop in GFR by dilating the efferent arterioles of the glomerulus, which lowers the pressure required for filtration. While a small, controlled decrease is expected and often beneficial long-term, a significant drop requires monitoring and possible dose adjustment, particularly in patients with existing kidney disease.

Diuretics

Often called "water pills," diuretics like furosemide (Lasix) and hydrochlorothiazide can decrease GFR by causing volume depletion and dehydration. This reduction in circulating volume can decrease renal blood flow and, subsequently, GFR. Loop diuretics, in particular, can decrease effective circulating volume through venodilation or diuresis and may cause a decrease in renal blood flow and glomerular filtration rate.

Certain Antibiotics

Aminoglycosides: Antibiotics such as gentamicin can cause direct tubular cell toxicity, leading to acute tubular necrosis. The risk is higher with prolonged therapy and higher trough levels.
Vancomycin: This antibiotic can cause acute interstitial nephritis or acute tubular necrosis.
Sulfonamides: These can cause crystal nephropathy and acute interstitial nephritis.

Iodinated Radiocontrast Dye

Used in imaging procedures like CT scans, iodinated contrast dye can cause contrast-induced nephropathy (CIN), characterized by a decline in kidney function within 48 to 72 hours of exposure. The risk is highest in those with pre-existing kidney disease, diabetes, or dehydration.

Immunosuppressants

Calcineurin inhibitors, such as cyclosporine and tacrolimus, are used to prevent organ rejection. They can cause a dose-dependent vasoconstriction of the afferent arterioles, leading to reduced GFR and potentially chronic interstitial nephritis.

Proton Pump Inhibitors (PPIs)

Commonly used for acid reflux, PPIs like omeprazole have been linked to acute interstitial nephritis, an unpredictable allergic reaction that can affect kidney function.

Comparison of Nephrotoxic Drug Classes


Drug Class	Mechanism of Action	Risk Factors	Potential Reversibility
NSAIDs	Inhibit vasodilatory prostaglandins, leading to renal vasoconstriction.	Chronic use, high doses, existing CKD, dehydration, elderly patients.	Often reversible upon discontinuation.
ACE Inhibitors/ARBs	Alter intraglomerular hemodynamics by dilating efferent arterioles.	Advanced CKD, bilateral renal artery stenosis, volume depletion.	Reversible, especially with dose adjustment or discontinuation.
Diuretics	Cause intravascular volume depletion and decrease renal blood flow.	High doses, dehydration, heart failure, cirrhosis.	Reversible with correction of volume status.
Aminoglycoside Antibiotics	Direct tubular cell toxicity.	Prolonged therapy, high trough concentrations, existing CKD.	Reversible, but requires careful monitoring.
Contrast Dye	Direct tubular cell toxicity and impaired renal blood flow.	Pre-existing CKD, diabetes, heart failure, older age.	Often reversible within 4 weeks.

Factors Increasing the Risk of Drug-Induced Low GFR

Certain patient-specific factors increase the susceptibility to drug-induced kidney damage:

Pre-existing Chronic Kidney Disease (CKD): Patients with compromised kidney function are at significantly higher risk.
Age: Individuals over 60 years old are more vulnerable.
Intravascular Volume Depletion: Dehydration, heart failure, or diuretic use can all increase risk.
Diabetes: Diabetic nephropathy is a major risk factor for contrast-induced kidney injury.
Exposure to Multiple Nephrotoxins: Using multiple drugs with the potential for kidney toxicity increases the overall risk.

How to Minimize Risk

If you have concerns about kidney function, consider these preventative measures:

Consult Your Healthcare Provider: Discuss all medications, including over-the-counter options, with your doctor or pharmacist.
Monitor Renal Function: Regular blood tests to check GFR and serum creatinine are crucial, especially when starting a new medication known to affect the kidneys.
Maintain Adequate Hydration: Staying well-hydrated is essential, particularly when taking diuretics or before receiving contrast dye.
Adjust Dosing: Your doctor may need to adjust the dose of a medication based on your GFR.
Use Alternatives When Possible: In some cases, a less nephrotoxic alternative can be used, such as acetaminophen for pain relief instead of an NSAID, especially for long-term use.

Conclusion

While many medications can cause a decrease in GFR, understanding the risks and mechanisms is key to protecting kidney health. For at-risk individuals, close monitoring, collaboration with healthcare providers, and minimizing exposure to multiple nephrotoxic agents are essential strategies. Patients taking medications like NSAIDs, ACE inhibitors, diuretics, or certain antibiotics should be aware of the potential impact on their kidneys. Open communication with your doctor can ensure that the benefits of your medication outweigh the risks to your renal function.

For more information on safe medication use with kidney disease, please visit the National Kidney Foundation's guide.

Frequently Asked Questions

For individuals concerned about kidney health, acetaminophen (Tylenol) is generally considered a safer option for pain relief than NSAIDs like ibuprofen or naproxen, especially with long-term use.

No, you should not stop taking ACE inhibitors or ARBs without consulting your doctor. A small, initial drop in GFR is expected and often part of the long-term kidney-protective benefit. Your doctor will monitor your kidney function to determine if a dose adjustment is necessary.

Dehydration reduces the total blood volume, leading to decreased blood flow to the kidneys. This makes the kidneys more susceptible to damage from nephrotoxic drugs, as their ability to compensate for toxic effects is diminished.

Yes, taking multiple nephrotoxic drugs simultaneously increases the risk of kidney injury. The combination of drugs like NSAIDs and certain antibiotics, for instance, can have a synergistic toxic effect on the kidneys.

Contrast-induced nephropathy is a form of acute kidney injury caused by the contrast dye used in imaging tests. People with pre-existing kidney disease, diabetes, heart failure, or dehydration are at higher risk.

PPIs like omeprazole have been linked to acute interstitial nephritis, a form of kidney inflammation. This is generally an unpredictable allergic reaction and not related to dose.

No, many cases of drug-induced low GFR, especially if detected early, are reversible upon discontinuation of the offending medication. However, chronic use of certain drugs or high-risk situations can lead to permanent damage.