Kumar et. al publishes in Kidney International Reports

Dietary Oxalate Induces Urinary Nanocrystals in Humans

KIR_Graphical Abstract

Nanocrystal Paper


Crystalluria is thought to be associated with kidney stone formation and can occur when urine becomes supersaturated with calcium, oxalate, and phosphate. The principal method used to identify urinary crystals is microscopy, with or without a polarized light source. This method can detect crystals above 1 μm in diameter (microcrystals). However, analyses of calcium oxalate kidney stones have indicated that crystallite components in these calculi are 50–100 nm in diameter. Recent studies have suggested that nanocrystals (<200 nm) elicit more injury to renal cells compared to microcrystals. The purpose of this study was to determine whether (i) urinary nanocrystals can be detected and quantified by nanoparticle tracking analysis (NTA, a high-resolution imaging technology), (ii) early-void urine samples from healthy subjects contain calcium nanocrystals, and (iii) a dietary oxalate load increases urinary nanocrystal formation.

Mitchell et. al publishes review in AJP Renal

Dietary Oxalate and Kidney Stone Formation 

Dietary Oxalate and Kidney Stone Formation Review


Dietary oxalate is plant-derived and may be a component of vegetables, nuts, fruits, and grains. In normal individuals, approximately half of urinary oxalate is derived from the diet and half from endogenous synthesis. The amount of oxalate excreted in urine plays an important role in calcium oxalate stone formation. Large epidemiological cohort studies have demonstrated that urinary oxalate excretion is a continuous variable when indexed to stone risk. Thus, individuals with oxalate excretions >25 mg/day may benefit from a reduction of urinary oxalate output. The 24-h urine assessment may miss periods of transient surges in urinary oxalate excretion, which may promote stone growth and is a limitation of this analysis. In this review we describe the impact of dietary oxalate and its contribution to stone growth. To limit calcium oxalate stone growth, we advocate that patients maintain appropriate hydration, avoid oxalate-rich foods, and consume an adequate amount of calcium.

Patel et. al publishes in Redox Biology

Oxalate induces mitochondrial dysfunction and disrupts redox homeostasis in a human monocyte derived cell line

Graphical Abstract

Oxalate and THP-1 Monocyte Paper


Monocytes/macrophages are thought to be recruited to the renal interstitium during calcium oxalate (CaOx) kidney stone disease for crystal clearance. Mitochondria play an important role in monocyte function during the immune response. We recently determined that monocytes in patients with CaOx kidney stones have decreased mitochondrial function compared to healthy subjects. The objective of this study was to determine whether oxalate, a major constituent found in CaOx kidney stones, alters cell viability, mitochondrial function, and redox homeostasis in THP-1 cells, a human derived monocyte cell line. THP-1 cells were treated with varying concentrations of CaOx crystals (insoluble form) or sodium oxalate (NaOx; soluble form) for 24 h. In addition, the effect of calcium phosphate (CaP) and cystine crystals was tested. CaOx crystals decreased cell viability and induced mitochondrial dysfunction and redox imbalance in THP-1 cells compared to control cells. However, NaOx only caused mitochondrial damage and redox imbalance in THP-1 cells. In contrast, both CaP and cystine crystals did not affect THP-1 cells. Separate experiments showed that elevated oxalate also induced mitochondrial dysfunction in primary monocytes from healthy subjects. These findings suggest that oxalate may play an important role in monocyte mitochondrial dysfunction in CaOx kidney stone disease.