A lot of IgAN patients complain about having headaches, often very severe and persistent ones. How to treat them is a problem: our literature advises against using aspirin, acetaminophen (Tylenol, etc.) or ibuprofen.

There is an entire class of kidney disease called "analgesic nephropathy" resulting from the use (or overuse) of analgesics like aspirin, acetaminophen, and ibuprofen. Most cases of analgesic nephropathy, at least in the United States, come from combination products containing phenacetin. The Handbook of Non-Prescription Drugs notes: "The potential for abuse of this compound and the incidence of toxicity . . . have prompted the FDA advisory review panel to recommend removing phenacetin from nonprescription drug products." Questions about the other three drugs remain, however.

Aspirin destroys the ability of blood platelets to synthesize thromboxane A₂, which causes platelets to clump together. Interfering with its production inhibits platelet aggregation, thus making aspirin useful in preventing strokes and heart attacks. But aspirin is implicated in the development of Reye's Syndrome, a potentially fatal neurologic disorder that can attack young adults and children. It can also damage the lining of the stomach. Those who take large daily doses of aspirin, such as people with arthritis, often use highly buffered aspirin, which reduces erosion of the gastrointestinal tract but contains large amounts of sodium, which should be avoided by those on low-sodium diets. According to the Handbook of Non-Prescription Drugs, aspirin alone is not believed to cause analgesic nephropathy, but "it may worsen or perpetuate the progression of papillary necrosis and renal dysfunction."

Like aspirin, acetaminophen is both an analgesic and antipyretic (used in bringing down fevers). As it has gained favor in the U. S., however, there has also be growing concern that its ready availability, combined with the public's lack of appreciation of the dangers of acetaminophen toxicity, may "produce a new health hazard." Acetaminophen can damage the kidneys (and has been linked to analgesic nephropathy), but it is toxic primarily to the liver. Chronic poisoning is aggravated by alcohol consumption; acute poisoning can produce fatal necrosis of the liver. Because of its easy availability, it is often the drug of choice for young people attempting suicide. (They will survive the night, but unless antidoted will die within days from liver failure.) Since problems with the liver's clearance of immune complexes from the body may be implicated in the development of IgAN, drugs that are hepatotoxic (toxic to the liver) may be every bit as dangerous to an IgAN patient as drugs that are nephrotoxic (toxic to the kidneys).

Ibuprofen is stronger than aspirin and its effects last longer. Like aspirin, it reduces platelet aggregation and increases the time it takes blood to clot (an effect greatly enhanced by drinking alcohol). Ibuprofen also cuts down on renal prostaglandin synthesis; it can cause sodium and water retention and decrease kidney function. Glomerular filtration rate declined in patients with mild kidney impairment who took 1,200 mg/day of ibuprofen for one week.

This may seem like a lot of ibuprofen, but it is less than the recommended daily dosage for menstrual cramps. Those with kidney disease, high blood pressure, diabetes, lupus, asthma, heart disease, or a history of aspirin sensitivity should avoid ibuprofen. One review of the medical literature noted: "It is unquestionable that ibuprofen can cause renal damage, including functional acute renal failure, water and electrolyte disorders, and interstitial nephritis." The same study further noted that those most at risk for kidney damage were people who had a low volume of blood in their veins, such as those who'd lost blood in an accident, or who had weak hearts.

Analgesics interfere with prostaglandin production. In healthy people, prostaglandins have little effect on kidney function; but in people whose kidneys are impaired, particularly when the flow of blood to the organ is reduced (by cirrhosis of the liver, heart failure, or low blood volume), they are important to maintaining renal function. The effects of different prostaglandins are conflicting: some are vasodilators and inhibit platelet aggregation, while others are vasoconstrictors and promote platelet aggregation. From the kidneys' point of view, however, analgesics likes aspirin, acetaminophen and ibuprofen seem to interfere with the production of "good" prostaglandins as well as of the "bad" ones that contribute to kidney damage.

We don't know how much harm analgesics may do to the kidneys of IgAN patients because there have been no studies on this subject. It seems prudent, however, to act on the assumption that damage is likely to develop earlier and be more widespread in kidneys already injured by glomerulonephritis than in healthy kidneys.

The Network has guidelines for treating headache pain with hydrotherapy, breathing and relaxation techniques, and homeopathy, none of which requires using anything toxic to the kidneys. For more information see "Headache Treatments."

1. American Pharmaceutical Association & National Professional Society of Pharmacists, Handbook of Non-Prescription Drugs, 8th ed., p. 204.

2. Ibid.

3. Ibid., p. 203.

4. JFE Mann, et al., "Ibuprofen as An Over-the-Counter Drug: Is There A Risk for Renal Injury?" Clinical Nephrology, v. 39, no. 1 (1993), p. 4.

5. Handbook of Non-Prescription Drugs, p. 202.

6. Mann, p. 1.

7. Ibid., p. 5.

[Reprinted from Network News, No. 5 (October 1995)]