The specific kidney injuries induced by analgesics are renal papillary necrosis and chronic interstitial nephritis.

[4] Risk factors for poor prognosis include recurrent urinary tract infection and persistently elevated blood pressure.

[6] The scarring of the small blood vessels, called capillary sclerosis, is the initial lesion of analgesic nephropathy.

It is currently thought that the kidney toxicities of NSAIDs and the antipyretics phenacetin and paracetamol may combine to give rise to analgesic nephropathy.

Kidney blood flow is a complex, tightly regulated process that relies on a number of hormones and other small molecules, such as prostaglandins.

Thus the innermost structures of the kidney, known as the renal papillae, are especially dependent on prostaglandin synthesis to maintain adequate blood flow.

[10] Bach and Hardy have proposed that phenacetin's metabolites lead to lipid peroxidation that damages cells of the kidney.

Once suspected, analgesic nephropathy can be confirmed with relative accuracy using computed tomography (CT) imaging without contrast.

[17] One trial demonstrated that the appearance of papillary calcifications on CT imaging was 92% sensitive and 100% specific for the diagnosis of analgesic nephropathy.

They include aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs),[19] as well as the antipyretics paracetamol (known as acetaminophen in the United States) and phenacetin.

Introduced in the late 19th century, phenacetin was once a common component of mixed analgesics in parts of Europe, Australia, and the United States.

Data from Switzerland, for example, demonstrated a decline in the prevalence of analgesic nephropathy among people with end-stage kidney disease, from 28% in 1981 to 12% in 1990.