Improved methodology to induce hyperoxaluria without treatment using hydroxyproline

Abstract

The use of hydroxyproline (HP) to generate hyperoxaluria in the rat is a problem because it is impossible to separate the effect of oxalate on renal injury from the effects of HP and the large array of metabolic intermediates formed when HP is converted to oxalate. Previously, the Dahl salt-sensitive (SS) and Brown Norway (BN) rat strains were studied to determine genetic control of resistance or susceptibility to HP-induced renal injury and crystal deposition. To develop a better model to induce hyperoxaluria without causing injury from HP metabolites, animals were fed a diet containing various levels of added oxalate (0, 1, 2, 3, or 5%). After 5 weeks rats were killed and the kidneys were removed for microscopic evaluation of tubule changes and crystal deposition. The 3 and 5% oxalate-fed groups had a substantial increase in urine oxalate, about 50 and 140 µmol/g body weight over controls, respectively. Both the SS and BN 3% oxalate-fed animals showed only slightly elevated tubule area and no crystal deposition. However, BN animals fed 5% oxalate had a dramatic increase in their percent tubule areas compared to control BN rats and treated SS rats. Crystal deposition in the kidneys was only observed in the 5% oxalate-fed groups. The BN kidneys demonstrated a threefold higher crystal deposition compared to oxalate-fed SS rats. We conclude that oxalate-supplemented food is a better method of producing hyperoxaluria in the rat than using HP which may introduce metabolic intermediates injurious to the kidney.

Oral administration of indigenous oxalate degrading lactic acid bacteria and quercetin prevents calcium oxalate stone formation in rats fed with oxalate rich diet

“…In concordant with previous reports (Wiessner et al, 2011), the oxalate and calcium level in urine was significantly elevated in rats fed with KOx. Urinary oxalate and calcium excretion were increased to 3.86 and 3 fold in rats fed with KOx than control rats at the end of the experimental period.…”

“…Other chemicals and De Man Rogosa media (MRS) were purchased from Himedia, India. The experimental diet containing 5% potassium oxalate (KOx) was purchased from National Institute of Nutrition (NIN), Tarnaka, Jamai-Osmania, Hyderabad, India (Wiessner, Garrett, Hung, Wille, & Mandel, 2011).…”

Steatorrhea and Hyperoxaluria Occur after Gastric Bypass Surgery in Obese Rats Regardless of Dietary Fat or Oxalate

“…In a thorough study of escalating potassium oxalate concentration in rodent chow, Wiessner and colleagues 25 detected an increase in urinary oxalate levels in control rats when dietary oxalate supplementation exceeded 2%. To avoid this confounder, we chose 1.5% potassium oxalate in our chow, and indeed urinary oxalate excretion in control animals remained low and constant throughout the study (range 3.75–5.05 μmol/day, Figure 5) regardless of fat content.…”

Recombinant Lactobacillus plantarum expressing and secreting heterologous oxalate decarboxylase prevents renal calcium oxalate stone deposition in experimental rats

“…The experimental diet containing 5% potassium oxalate was procured from National Institute of Nutrition (NIN, Hyderabad, India). Hyperoxaluria and calcium oxalate crystal were induced in a rat model as described elsewhere [ 18 ]. Urinary and serum biochemical parameters were measured in semi automated photometer 5010 V5 + (Robert Riele GmbH, Germany) using commercially available kits [Additional file 2 ].…”