Genetic and dietary influences on urinary oxalate excretion

Several genes contribute to the development of calcium oxalate nephrolithiasis as it is a polygenic disease. To explore the influence of genetic factors on oxalate excretion we have examined the distribution of oxalate excretions in 101 normal individuals who consumed self-selected diets. The distribution was apparently trimodal, consistent with the existence of three classes of oxalate excretors reflecting two allelic genes determining high and low oxalate excretion occurring with frequencies of 0.32 and 0.68 respectively. The pattern of inheritance in eight families was compatible with the expression of a pair of codominant alleles. A comparison of the distribution of excretory classes among the 101 normal individuals with that of 101 calcium oxalate stone formers suggests that high oxalate excretion may be associated with a 4-fold increased risk of stone disease and intermediate excretion with a 1.6-fold increase. Control of dietary factors influencing oxalate excretion apparently improved the discrimination between excretory classes in 17 individuals but the intra-individual variability in oxalate excretion was not reduced in four of nine individuals in whom this parameter was evaluated. More stringent dietary control than that applied in this study may be required before more extensive genotyping of individuals is attempted. Received: 4 February 1997 / Accepted: 22 October 1997     

Distribution of organic matrix in calcium oxalate renal calculi

Summary The quantity of protein and carbohydrate comprising the matrix of calcium oxalate monohydrate (COM) renal stones was found to decrease with distance from the surface of the stone. The average organic concentration of stones 3 to 30 mm in diameter ranged from 5.7% at the surface to 2.7% at the core. This concentration gradient suggests matrix involvement in a “growth front” on stone surfaces with migration of organic material from the “older” interior. The matrix distribution was not readily correlated with density variations or with the presence of hydroxyapatite or calcium oxalate dihydrate. Surface matrix concentrations were greater than amounts predicted by physical adsorption. Electron microscopy confirmed the presence of the organic-rich surface layer and also suggested that increase in stone size occurs predominantly by crystal growth with microcrystal aggregates as growth centers.     

Increased protein intake on controlled oxalate diets does not increase urinary oxalate excretion

High animal protein intake is a risk factor for calcium oxalate stone disease. The effect of dietary protein on the urinary excretion of calcium, acid and citrate is well established. However, its effect on oxalate excretion is unclear, due in part to an inadequate control of dietary oxalate intake in previous studies. This relationship warrants clarification due to the proposed important role of the metabolism of amino acids in endogenous oxalate synthesis. In this study, 11 normal subjects consumed controlled oxalate diets containing 0.6, 1.2 and 1.8 g protein/kg body weight/day. The analysis of 24 h urine collections confirmed that as protein intake increased, urinary calcium and glycolate increased and urinary pH and citrate decreased. The increased glycolate excretion was due in part to an increased hydroxyproline, but not glycolate consumption. Total daily urinary oxalate excretion did not change. When indexed to creatinine there was a small but significant decrease in oxalate excretion. This is most likely due to hyperfiltration. These results indicate that as dietary protein intake increases, the catabolism of diet-derived amino acids is not associated with an increased endogenous oxalate synthesis in normal subjects.     

Vitamin D repletion does not alter urinary calcium excretion in healthy postmenopausal women

OBJECTIVE

To evaluate, in a posthoc analysis of a previous study, whether vitamin D repletion in postmenopausal women with insufficient vitamin D increases urinary calcium excretion, as vitamin D therapy might contribute to hypercalciuria and calcium stones in susceptible individuals, and the effect of vitamin D on the risk of urolithiasis warrants attention.

SUBJECTS AND METHODS

We recruited 18 women at ≥5 years after menopause who had vitamin D insufficiency (serum 25(OH)‐vitamin D, 16–24 mg/dL). We excluded women with a history of urolithiasis and kidney disease. Women had one calcium absorption study when vitamin D‐insufficient, received vitamin D therapy, and completed a second calcium absorption study when vitamin D‐replete. We fed subjects meals that mirrored the nutrient composition from self‐reported 7‐day diet diaries. To measure calcium absorption, we collected urine for 24 h during both visits.

RESULTS

We achieved vitamin D repletion in all women (25(OH)‐vitamin D before and after treatment, 22 and 63 mg/dL, respectively; P < 0.001). The mean calcium intake was 832 mg/day. Residual urine specimens were available for 16 women, allowing a measurement of 24‐h urinary calcium. Calcium excretion did not change after vitamin D therapy (212 before vs 195 mg/day after; P = 0.60). Of four women with hypercalciuria (>247 mg/day), calcium excretion decreased in three (377–312 mg/day, not significant).

CONCLUSION

Vitamin D supplementation did not increase the urinary calcium excretion in healthy postmenopausal women. Many stone formers are at risk of premature bone loss, vitamin D insufficiency, or both. Based on the present results we suggest a study of patients with hypercalciuria and nephrolithiasis to determine the risks of vitamin D therapy.     

Effect of two sports drinks on urinary lithogenicity

The effect of commercial oral rehydration solutions (“sports drinks”) relative to water on risk of nephrolithiasis has not been studied previously. We studied the effect of two sports drinks, Performance (Shaklee Corp., Pleasanton, CA, USA) and Gatorade (Gatorade, Chicago, IL, USA) on urinary chemistry and measures of lithogenicity in non-stone formers. Performance has a pH of 4.3, and contains 21 mmol/L of sodium, 5.3 mmol/L of potassium, 0.8 mmol/L of calcium, and 19.5 mmol/L of citrate. Gatorade pH ranges from 2.9 to 3.2, and contains 20 mmol/L of sodium, 3.2 mmol/L of potassium, negligible calcium, and 13.9 mmol/L of citrate. Subjects drank 946 ml (32 oz) of tap water daily for 3 days, and recorded diet history. This was followed by a second 3-day experimental period during which subjects drank 946 ml (32 oz) of sports drink daily, duplicating diets from part 1. In each 3-day period, urine was collected for 24 h during days 2 and 3. Urine chemical analysis was performed, and supersaturations of calcium oxalate, calcium phosphate and uric acid were calculated. Nine subjects completed the study using Performance, ten used Gatorade. Urine volumes and creatinine excretions were not different during the control and experimental periods. Performance increased mean citrate excretion by 170 mg/day (95% CI 57–284 mg/day; P = 0.01) and increased urine pH by 0.31 (95% CI 0.03–0.59; P = 0.03). Gatorade did not significantly change urinary citrate excretion or pH. Neither drink caused significant differences in the excretion of sodium and calcium or any supersaturation value. Ingestion of Performance, but not Gatorade, led to an increase in mean urinary citrate excretion and pH as compared to water. The increase in citrate is likely to be a clinically significant effect. pH is an important determinant of alkali load in beverages containing organic anions. Performance, with more citrate and a higher pH than Gatorade, could represent a superior alternative to water for reducing urinary lithogenicity. Most sports drinks with significant carbohydrate content however may contain too many calories, and fructose, to be preferred beverages for stone prevention. Presented at the annual meeting of the ROCK Society (Research on Calculous Kinetics), 16 June 2006, Vail, CO, USA.     

Acute kidney injury in donors of donation after brain plus cardiac death does not affect recipients' short-term prognosis in transplantation

Objective To investigate the clinical efficacy of renal transplantation from donors of donation after brain and cardiac death(DBCD) complicated with acute kidney injury (AKI), and summarize the clinical experience of evaluation and application. Methods The clinical data of the 45 DBCD donors and 80 recipients in the First People's Hospital of Foshan from September 2011 to September 2015 were retrospectively analyzed. DBCD donors were classified into the AKI group (n=26)and non-AKI group (n=19) according to the serum creatinine level and urine output when the donors were admitted to the intensive care unit (ICU) in this hospital. A total of 80 recipients were divided into the AKI group (n=46) and non-AKI group (n=34) correspondingly. The condition of the donors before organ procurement between the two groups was compared, and the incidence of various complications, the 1 years survival rates of recipients and graft after renal transplantation were compared between the two groups. Results Among 45 donors, 26 cases(57.8%) suffered from AKI. The serum creatinine of donors was significantly higher in the AKI group than that in the non-AKI group (P＜0.01). The incidence of delayed graft function (DGF) in AKI group and non-AKI group was 21.7% and 8.8% respectively (P＞0.05). After 1 years, the serum creatinine of the recipients in AKI group was significantly higher than that in non-AKI group [(134.9±63.4) μmol/L vs (106.6±28.2) μmol/L, P＜0.05], but the survival rates of recipients and grafts did no differ between the two groups (both P＞0.05). Conclusions The donors combined with AKI do not have a worse effect on the incidence of DGF, the 1-year survival rates of recipients and grafts after transplantation. So, the donors with AKI for transplantation can widen the origin of kidney grafts.     

Effects of <Emphasis Type="Italic">Lactobacillus casei</Emphasis> and <Emphasis Type="Italic">Bifidobacterium breve</Emphasis> on urinary oxalate excretion in nephrolithiasis patients

It had been suggested that lactic acid bacteria (LAB) may degrade oxalate in the intestinal lumen, reducing urinary oxalate excretion. We aimed to evaluate the effect of a LAB mixture containing Lactobacillus casei (LC) and Bifidobacterium breve (BB) (LC + BB) upon urinary oxalate reduction in stone-forming (SF) patients without hyperoxaluria under conditions of an oxalate-rich diet. After an oxalate restriction period (7 days washout), 14 SF patients consumed an oxalate-rich diet during 4 weeks (200 mg/day) and a lyophilized LC + BB preparation was given t.i.d. after meals during the last 2 weeks. Twenty-four-hour urine samples were collected for determination of oxalate, calcium, magnesium, citrate, sodium, potassium and creatinine at baseline, after 2 weeks (DIET) and 4 weeks (DIET + LC + BB). The mean urinary oxalate excretion was significantly higher after DIET versus baseline (27 ± 8 vs. 35 ± 11 mg/24 h), but the mean decrease was not significant between DIET + LC + BB and DIET periods (35 ± 11 vs. 33 ± 10 mg/24 h). Seven out of 14 patients presented a reduction in oxaluria after LC + BB versus DIET, being the reduction higher than 25% in 4, and up to 50% in 2 of them. The latter two patients were those who had presented the greatest increase in oxaluria in response to dietary oxalate. In conclusion, this mixture of L. casei and B. breve was shown to possess a variable lowering effect upon urinary oxalate excretion that may be dependent on dietary oxalate intake.