Calcium oxalate crystal deposition in the kidney: identification, causes and consequences

Abstract

Calcium oxalate (CaOx) crystal deposition within the tubules is often a perplexing finding on renal biopsy of both native and transplanted kidneys. Understanding the underlying causes may help diagnosis and future management. The most frequent cause of CaOx crystal deposition within the kidney is hyperoxaluria. When this is seen in native kidney biopsy, primary hyperoxaluria must be considered and investigated further with biochemical and genetic tests. Secondary hyperoxaluria, for example due to enteric hyperoxaluria following bariatric surgery, ingested ethylene glycol or vitamin C overdose may also cause CaOx deposition in native kidneys. CaOx deposition is a frequent finding in renal transplant biopsy, often as a consequence of acute tubular necrosis and is associated with poorer long-term graft outcomes. CaOx crystal deposition in the renal transplant may also be secondary to any of the causes associated with this phenotype in the native kidney. The pathophysiology underlying CaOx deposition is complex but this histological phenotype may indicate serious underlying pathology and should always warrant further investigation.

A Sodium Oxalate-Rich Diet Induces Chronic Kidney Disease and Cardiac Dysfunction in Rats

“…Oxalate nephropathy is a rare condition affecting patients, and it is caused by either inherited enzymatic deficiencies (primary hyperoxaluria) or exogenous sources, such as dietary consumption of products rich in oxalate, as well as via other substances that may metabolize into oxalate within the body, such as vitamin C (secondary hyperoxaluria) [14,15]. Stricto sensu, our model mimicked secondary hyperoxaluria, since sodium oxalate was facilitated through the rats' diets.…”

Incidence and Importance of Calcium Deposition in Kidney Biopsy Specimens

“…The pathogenesis of calcification in the renal tubules is not fully understood. Presumptions are that hypercalciuria is a risk factor for tubular calcification in the form of calcium phosphate and that hyperoxaluria is the primary risk factor for CaOx deposition, similar to the pathogenesis of nephrolithiasis [6]. However, studies in patients with small bowel resection and malabsorption leading to hyperoxaluria have CaOx deposits in the inner medullary collecting ducts [13], but no such depositions are found in specimens from idiopathic CaOx stone formers [14].…”

“…In contrast to calcium phosphate deposition, the presence of birefringent CaOx deposition in the kidneys has been observed in patients with excess intestinal absorption of oxalate due to gastric bypass, malabsorption, ethylene glycol toxicity, or impaired metabolism as in primary hyperoxaluria. In addition to kidneys, CaOx deposits can be found in many different tissues [5, 6].…”

Primary hyperoxaluria: the adult nephrologist's point of view

“…These patients should be referred to a specialist metabolic clinic (if available) or a specialist centre for workup, as Dent disease should also be considered. In many centres this may lead to a kidney biopsy to obtain a histological diagnosis and this might show features of oxalosis [ 7 ]. These include calcium oxalate crystals, often best appreciated in polarised light, and sometimes features of acute inflammation not expected in cases with bland urinary sediment.…”