I. Analgesic nephropathy and non-steroidal anti-inflammatory drugs
Analgesic nephropathy (also known as analgesic nephropathy) is chronic interstitial kidney damage caused by long-term massive abuse of analgesics (mainly non-steroidal antipyretic and analgesic drugs), and can develop renal papillary necrosis and interstitial nephritis, and renal failure can occur in the late stage.
Non-steroidal anti-inflammatory drugs are a large class of drugs with anti-inflammatory, antipyretic and analgesic effects, excluding corticosteroids, which have been used for the treatment of patients with rheumatic diseases for up to a century. Due to the effectiveness and relative safety of these drugs, some of them have been classified as over-the-counter (OTC) drugs in China and western countries. There is more awareness of the gastrointestinal mucosal damage caused by this class of drugs, but the nephrotoxicity of the drugs is often overlooked. Some studies have reported that the risk of acute kidney injury in those who apply NSAIDs is about three times higher than in those who do not. NSAID drugs that have been shown to cause analgesic nephropathy include aspirin, finasteride, salicylamide, acetaminophen, indomethacin (anti-inflammatory pain), ibuprofen (fenpropathrin, aniracetam, efaproxiral), pautazone, neproxen, mefenamic acid, diclofenac (fotarine), sudoxicam, etc. It is generally believed that analgesic nephropathy can occur when analgesics are taken continuously for more than three years and the cumulative dose of analgesics exceeds 2 to 3 kg. A study showed that in a group of patients who took oral NSAIDs for various reasons (including rheumatoid arthritis, gouty arthritis, etc.) with a cumulative dose of more than 1000 capsules, 24.4% of the patients had renal papillary necrosis confirmed by intravenous pyelogram, ultrasound and CT.
II. Risk factors for analgesic nephropathy
The risk of acute kidney injury (AKI) due to NSAID is influenced by the type of NSAID and the dose administered. The incidence of kidney damage varies among different types of NSAIDs, with indomethacin causing the highest incidence of AKI, while aspirin is relatively low, and naproxen, diclofenac sodium, ibuprofen, and piroxicam are between indomethacin and aspirin. In addition to the factors of NSAID, the following are also risk factors for AKI due to NSAID.
1. Advanced age (>60 years)
The elderly, especially those over 60 years of age, have reduced renal physiological function and increased dependence on prostaglandins, so the risk of renal damage should be paid more attention to the use of NSAID in the elderly.
2.Insufficient effective circulating blood volume
In patients with cirrhotic ascites, congestive heart failure, hypotension, dehydration, and unclosed arterial catheter, the effective circulating blood volume decreases, resulting in excessive activation of renin angiotensin stimulation and increasing the nephrotoxicity of NSAIDs, which may lead to AKI.
3.Basic kidney disease
The use of NSAID in patients with pre-existing renal diseases (such as renal vascular disease, glomerulonephritis, nephrotic syndrome, urinary tract obstruction, diabetic nephropathy, etc.) is likely to induce AKI, and studies have confirmed that the incidence of elevated serum creatinine, decreased renal function, serum uric acid and anemia is significantly higher in older adults with underlying renal disease than in those without underlying renal disease.
4. Combination of drugs
When NSAID is combined with diuretics, β-blockers, aminoglycoside antibiotics and angiotensin-converting enzyme inhibitors, the incidence of AKI is significantly higher.
III. Clinical manifestations
Analgesic nephropathy can occur at any age, and is particularly common in the elderly. The clinical manifestations are varied, and sometimes the symptoms are mild and non-characteristic. Early polyuria, nocturia and thirst may occur, followed by mild to moderate renal insufficiency, manifested by a mild increase in serum creatinine and urea nitrogen, and patients may be asymptomatic or have only a slight decrease in urine output, while anemia symptoms often appear earlier and are more severe than in the azotemia phase of other nephropathies. Finasteride and the finasteride metabolite acetaminophen tend to cause renal papillary necrosis, and patients present with sudden onset of severe azotemia, hematuria, and renal colic.
IV. Treatment
The key to the treatment of this disease is early diagnosis, timely discontinuation of drugs, and protection of renal function. Adequate fluid intake should be ensured to maintain a 24-hour urine volume of more than 2000ml, thus promoting the excretion of drugs and reducing the renal damage of drugs. Pay attention to the prevention of infection, once the infection is found, antibiotics with low nephrotoxicity should be actively used to avoid aggravating renal damage. High-dose corticosteroids help the recovery of renal disease, and dialysis treatment is performed when necessary in severe patients. For early diagnosed, light patients, renal function can recover on its own within one year after stopping the drug, and the prognosis is good; in severe cases, permanent renal damage can occur, and even develop into end-stage renal failure.
V. A few words of advice
In order to avoid the occurrence of analgesic nephropathy as much as possible, the following issues should be noted when using NSAIDs.
1. strictly grasp the indications and contraindications for the use of NSAIDs, prevent abuse, and avoid long-term use in large doses as much as possible.
2, in the presence of the above risk factors should be used with caution NSAID, and adjust the drug dose.
3, use varieties and dosage forms with few adverse reactions.
4, avoid the simultaneous use of two or more NSAIDs, otherwise not only the therapeutic effect does not increase, but also increase adverse reactions.
5, avoid the combined use of other nephrotoxic drugs.
6, monitor renal function before and 2 weeks after NSAID administration. If blood creatinine ≥ 177 μmol/L, discontinue NSAID; if blood creatinine is between 133 and 177 μmol/L before medication, pay attention to close monitoring to prevent renal damage from occurring.