Renal damage crystal deposition

Acute gout could cause urate uropathy, whereby uric acid crystals are deposited within the renal tubules, causing intrinsic renal damage. 

ACUTE INTRATUBULAR CRYSTAL DEPOSITION CAUSING PERMANENT RENAL DAMAGE IN THE PIG... 

Animals may develop subacute toxicity if enough plant material is ingested to produce hypocalcemia and kidney damage, but no so much that the animal dies. With larger or more prolonged exposures, animals may experience larger deposits of calcium oxalate crystals that result in renal fibrosis or renal failure which can ultimately lead to death. 

The major effects of hyperphosphatemia are related to the development of hypocalcemia (caused by phosphate inhibition of renal la-hydroxylase) and its related consequences, as well as vascular and organ damage resulting from the deposition of calcium-phosphate crystals. Extravascular calcification can result in band keratopathy, red eye, pruritus, and periarticular calcification, especially in renal failure patients (see Chap. 44). In addition, soft-tissue calcifications in the conjunctiva, skin, heart, cornea, lung, gastric mucosa, and kidney have been observed, primarily in chronic renal failure patients." Hyperphosphatemia associated with chronic renal disease may result in renal osteodystrophy because of overproduction of parathyroid hormone. This condition is discussed in detail in Chap. 44. 

This study has shown that deposition of crystals in the renal tubules even for short periods, can produce irreversible damage, not only locally, but also affecting other parts of the nephron. It is hoped that this experiment, together with a long term study now underway, will provide a model for crystal nephropathy in man. 

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