Renal calcium phosphate and oxalate deposition in prolonged vitamin B₆ deficiency: studies on a rat model of urolithiasis

Abstract

Objective To determine the effect on kidney oxalate-salt deposition of a prolonged diet which induced vitamin B 6 deficiency in adult rats, as there are reports of the pathogenic involvement of vitamin B 6 deficiency in the formation of renal calcium oxalate calculi. Materials and methods The study comprised 24 6-month-old male albino Wistar rats; 12 were fed with a purified vitamin B 6 -deficient diet and the others provided with the same diet but supplemented with 6 mg/kg of vitamin B 6 . After 12 weeks, all rats were killed, and their kidneys fixed in formalin and routinely processed to paraffin for morphological examination; some fragments were fixed in glutaraldehyde and prepared for ultrastructural examination. From each rat consecutive sections of both kidneys were cut and stained with haematoxylin and eosin, periodic-acid Schiff, Sirius red and the Von Kossa method for calcium. Sections were examined in polarized light and by electron microscopy. Results The histopathological and ultrastructural features of the kidney of vitamin B 6 -deficient rats were those of tubular-interstitial nephritis, characterized by tubular atrophy, interstitial fibrosis and chronic inflammatory infiltration. Oxalate and phosphate crystals were present in the papillary and parenchymal connective tissue. Ultrastructural features confirmed severe tubular epithelial lesions and the presence of an interstitial and intraepithelial inflammatory infiltrate; there was mild interstitial fibrosis. None of these features were apparent in the kidney of control rats. Conclusions Histopathological and ultrastructural data indicate that a prolonged vitamin B 6 -deficient diet may contribute to the formation and deposition of calcium phosphate and oxalate crystals, which lead to severe damage of the renal parenchyma. This phenomenon may occur not only in growing rats, which have more active protein metabolism and consequently higher vitamin B 6 requirements, but also in adult rats.

Endogenous oxalogenesis after acute intravenous loading with ethylene glycol or glycine in rats receiving standard and vitamin B6‐deficient diets

“…Therefore, loading with ethylene glycol in the presence of vitamin B6 deficiency augmented urinary oxalate and glycolate excretion in this study suggesting that metabolic conversion rate (7.2%) of ethylene glycol (20 mg) given to vitamin B6‐deficient rats is almost equal to that (6.1%) of glycolate (20 mg) given to normal rats 12 . Histopathological and ultrastructural data indicate that prolonged vitamin B6 deficiency may contribute to the formation and deposition of calcium phosphate and oxalate crystals, which can severely damage the renal parenchyma 55 …”

Effects of different dietary amounts of LCPUFA n3 and vitamin B6 on lipid composition and antioxidant defences in rat kidney

“…Although these morphologic alterations were not further investigated in this framework, they are similar to those found in similar dietary conditions. The B 6 deficiency, in fact, induces tubular-interstitial nephritis, characterized by tubular atrophy, interstitial fibrosis and chronic inflammatory infiltration [21].…”

Dietary Therapy in Idiopathic Nephrolithiasis

“…High intakes of ascorbic acid causes a rise in oxaluria, 61-72 but up to 1500 mg/d this effect is negligible and does not increase the risk of kidney stones. 73,74 Pyridoxine enters the oxalic acid metabolism, and a deficiency of this vitamin could lead to an increase in the endogenous production of oxalate 75 ; conversely, a supplementation of pyridoxine could reduce oxaluria. 76 A high vitamin B 6 intake (over 40 mg/d) was associated with a reduced risk of stones in women 74 but not in men.…”