Although neither zinc nor zirconium is ferromagnetic, their alloy ZrZn2 exhibits ferromagnetism below 35 K.

Occurrence
Zinc makes up about 75 ppm (0.0075%) of Earths crust, making it the 24th most abundant element. Typical background concentrations of zinc do not exceed 1 μg/m3 in the atmosphere; 300 mg/kg in soil; 100 mg/kg in vegetation; 20 μg/L in freshwater and 5 μg/L in seawater. The element is normally found in association with other base metals such as copper and lead in ores. Zinc is a chalcophile, meaning the element is more likely to be found in minerals together with sulfur and other heavy chalcogens, rather than with the light chalcogen oxygen or with non-chalcogen electronegative elements such as the halogens. Sulfides formed as the crust solidified under the reducing conditions of the early Earths atmosphere. Sphalerite, which is a form of zinc sulfide, is the most heavily mined zinc-containing ore because its concentrate contains 60–62% zinc.Other source minerals for zinc include smithsonite (zinc carbonate), hemimorphite (zinc silicate), wurtzite (another zinc sulfide), and sometimes hydrozincite (basic zinc carbonate). With the exception of wurtzite, all these other minerals were formed by weathering of the primordial zinc sulfides.Identified world zinc resources total about 1.9–2.8 billion tonnes. Large deposits are in Australia, Canada and the United States, with the largest reserves in Iran. The most recent estimate of reserve base for zinc (meets specified minimum physical criteria related to current mining and production practices) was made in 2009 and calculated to be roughly 480 Mt.
Inhibition of cyclooxygenases therefore rather selectively damages the renal papillae, increasing the risk of renal papillary necrosis.NSAIDs caused no adverse effects on renal function in healthy dogs subjected to anesthesia. Most healthy kidneys contain enough physiologic reserve to compensate for this NSAID-induced decrease in blood flow. However, those subjected to additional injury from phenacetin or paracetamol may progress to analgesic nephropathy. Phenacetin and paracetamol
It is unclear how phenacetin induces injury to the kidney. Bach and Hardy have proposed that phenacetins metabolites lead to lipid peroxidation that damages cells of the kidney.Paracetamol is the major metabolite of phenacetin and may contribute to kidney injury through a specific mechanism. In cells of the kidney, cyclooxygenases catalyse the conversion of paracetamol into N-acetyl-p-benzoquinoneimine (NAPQI). NAPQI depletes glutathione via non-enzymatic conjugation with glutathione, a naturally occurring antioxidant. With depletion of glutathione, cells of the kidney become particularly sensitive to oxidative damage. Diagnosis
Diagnosis is traditionally based on the clinical findings above in combination with excessive analgesic use. It is estimated that between 2 and 3 kg each of phenacetin or aspirin must be consumed before evidence of analgesic nephropathy becomes clinically apparent.Once suspected, analgesic nephropathy can be confirmed with relative accuracy using computed tomography (CT) imaging without contrast. One trial demonstrated that the appearance of papillary calcifications on CT imaging was 92% sensitive and 100% specific for the diagnosis of analgesic nephropathy. Treatment
Treatment of analgesic nephropathy begins with the discontinuation of analgesics, which often halts the progression of the disease and may even result in normalization of kidney function.