Vitamin renal stones

A number of reports have suggested that high intakes of vitamin C are associated with increased excretion of oxalate however, much of the oxalate may be the result of nonenzymic formation from ascorbate under alkaline conditions, occurring either in the bladder or after collection, and thus not a risk factor for renal stone formation (Chalmers et al., 1986). Gerster (1997) suggested that people who are recurrent oxalate stone formers should, as a matter of pmdence, restrict their intake of vitamin C to 100 mg per day, but noted that the risk of stone formation in the population at large is inversely related to vitamin C intake. 

EXCESS There is concern about the possibility that certain susceptible individuals may develop renal stones or hemolytic anemia from megadoses of vitamin C. 

A8. Anonymous, Renal stones, magnesium, and vitamin Bg in rats. Nutr. Rev. 19, 306-308 (1961). 

Chronic megadoses of vitamin C may precipitate formation of calcium oxalate renal stones, oxalate nephropathy, and renal failure. The amount required to cause this is variable from 2 to 8gday . Bone oxalate deposits have also been reported. Esophageal and dental erosion are possible with tablet ingestion. Heinz body hemolytic anemia has been seen in premature infants. 

B. Hyperparathyroidism is the likely cause of all of the patient s symptoms. Increased parathyroid hormone leads to bone demineralization, increased calcium uptake from the intestine, increased blood levels of calcium, decreased calcium ion excretion by the kidney, and increased phosphate excretion in the urine. Increased blood calcium levels caused renal stones, while bone demineralization progressed to osteopenia. The patient s intake of calcium and vitamin D are not excessive. Calcitonin acts to decrease bone demineralization. Muscle weakness and depression reflect the widespread role of calcium ion in many physiologic processes. 

Up to 5% of the population are at risk from the development of renal oxalate stones. The risk is from both ingested oxalate and that formed endogenously, mainly from the metabolism of glycine. A number of reports have suggested that people consuming high intakes of vitamin C excrete more oxalate in the urine. However, no pathway for the formation of oxalate from ascorbate is known, and it seems that the oxalate is formed non-enzymically under alkaline conditions either in the bladder or after collection, and hence high vitamin C intake is not a risk factor for renal stone formation. 

Mega vitamin intake of vitamin C may result in diarrhea due to intestinal irritation. Since ascorbic acid is partially metabolized and excreted as oxalate, renal oxalate stones may form in some patients. 

Hypercalcemia can result from an excessive intake of vitamin D. Prolonged immobilization can also result in hypercalcemia, as bone resorption increases with this immobilization, especially where there is concurrent renal failure (where the kidneys cannot excrete the excess calcium). Sudden, severe hypercalcemia results in vomiting, coma, and possibly death. Prolonged hypercalcemia can result in the formation of kidney stones and in the calcification of soft tissues, such as the eye. Stone formation and caiciheahon are more likely to occur with concurrent hyperphosphatemia. 

As intestinal absorption of calcium increases, urinary calcium excretion also increases. When the latter exceeds 300 mg/d, formation of calcium phosphate or calcium oxalate stones (urolithiasis) may occur. Hypercalciuria may result from decreased reabsorption of calcium due to a renal tubular defect or from increased intestinal absorption of calcium. Hypercalciuria may be due to an intrinsic defect in the intestinal mucosa or secondary to increased synthesis of 1,25-(OH)2D in the kidney. Disordered regulation of 1,25-(0H)2D synthesis is relatively common in idiopathic hypercalciuria. Treatment usually includes reduction in dietary calcium. Increased vitamin D intake, hyperparathyroidism, and other disorders can also cause hypercalciuria and urolithiasis. 

Adverse effects of oral calcium and vitamin D supplementation include hypercalcemia and hypercalciuria, especially in the hy-poparathyroid patient, in whom the renal calcium-sparing effect of parathyroid hormone is absent. Hypercalciuria may increase the risk of calcium stone formation and nephrolithiasis in susceptible patients. One maneuver to help prevent calcium stones is to maintain the calcinm at a low normal concentration. Monitoring 24-hour urine collections for total calcium concentrations (goal <300 mg/24 h) may also minimize the occurrence of hypercalciuria. The addition of thiazide dinretics for patients at risk for stone formation may result in a reduc-tionof both urinary calcium excretion and vitamin D requirements." ... 

Another concern is the fear that, since the vitamin is metabolised mainly via ethanedioic (oxalic acid), a high dose might lead to the formation of kidney stones. While there is no clear evidence that this occurs, and the phenomenon has been described as a myth, the commonsense advice is for those prone to recurrent stone formation or suffering from any renal impairment to avoid high doses which also exacerbate acidosis in chronic renal disease and renal tubular acidosis. Sustained hyperoxaluria has been found only rarely to accompany an excessive ingestion of vitamin C. 

D3 supplementation (4000 lU/day) for 12 months in patients with low-risk of prostate cancer [36 ]. No adverse events were also observed with vitamin D supplementation in kidney stone formers [37 ], in patients with depression [38 -] or in HIV-infected individuals being treated with efavirenz [39 ]. The administration of paricalcifol for 8 weeks in patients with metastatic breast cancer was not also associated with any serious adverse events [40 ]. Supplementation with calcitriol (0.5 ig daily) for 8 weeks to reduce proteinuria in patients with IgA nephropathy was not associated with hypercalcaemia, but renal calculus was reported in one patient [Tl ]. 

Renal tubular acidosis Disorder of membrane iranspm ot hydrogen ion arrd bicatbon ate by kidney tubules. Inability of kidney to excrete an add urine persistent meta boltc acidosis results kidney stones increased urinery calcium and phosphate osteomalacia, potassium depletion. Oral administration ni sodium bicarbonate or citrate supplemental potassium and/or calcium untl body states repleted possibfy vitamin D therapy. 

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