Idiopathic Stone Research Articles

Etiological and clinical patterns of childhood urolithiasis in Iraq

This study was conducted to evaluate the etiological and clinical characteristics of urolithiasis in Iraqi children. From 1999 to 2004, 204 children with renal calculi were evaluated. The age range of the patients was 4 months to 14 years, 61.3% of the patients were under 5 years. Male to female ratio was 2.8:1. The mean age at onset of symptoms was 3.2 years, and stone disease was diagnosed at a mean of 3.5 years. Hematuria (44.6%) and pain (28.4%) were the main clinical presentation. Of the 204 patients 45.1% had a family history of stones. Consanguinity was recorded in 72%; 75.5% had metabolic disorders. Stones were located at multiple sites in 80 patients, or 39.2%; 58 of these 80, or 72.5%, had metabolic disorders. Multiple stones were present in 47 (23%); 72.3% were related to metabolic disorders. In 126 patients, or 61.8%, both kidneys were involved equally. Bladder stones were found in 11.3%. Staghorn calculi occurred in 29 patients, or 14.2%; 27 of these had recurrent urinary tract infection (UTI). Nephrocalcinosis was diagnosed in 7, or 3.4%; all had metabolic disorders. Etiology of stone formation was established in 189 patients, or 92.6%, whereas 15, or 7.4%, had idiopathic stones. Metabolic disorders were the commonest cause in 106 patients (52%); 52 patients were classified as infective (25.5%). Anatomical defects were present in 25 (12.2%) and 6 children (2.9%) with primary endemic bladder calculi. Coexisting UTI was common (36.8%) in the metabolic group. We concluded that urolithiasis is a serious problem among Iraqi children, with early onset of presentation. Metabolic disorders were the major causes, but can be masked by associated UTI. Proper management of UTI with a careful metabolic assessment of young stone formers is valuable in combating urolithiasis.

Long-term potassium citrate therapy and bone mineral density in idiopathic calcium stone formers

Several authors have described an association between idiopathic calcium (Ca) stone disease and bone mass reduction. Hypocitraturia is a frequent feature of urolithiasis, and alkaline citrate has been recommended as one of the choice treatments in this disease. Some evidence exists as to the positive effect of potassium (K) citrate therapy on bone mass. The aim of this work was the longitudinal evaluation of bone mineral density (BMD) changes in a group of Ca oxalate stone formers treated with K citrate for two years. Enrolled patients were 120; 109 subjects completed the study (51 males and 58 females). A metabolic study and distal radius BMD measurements were conducted both at baseline (BAS) and at the end of the study (END). BMD (0.451 +/- 0.081 vs 0.490 +/- 0.080 g/cm2), T-score (-1.43 +/- 1.02 vs -0.90 +/- 1.04), net gastrointestinal alkali absorption (40.37 +/- 50.57 vs 61.26 +/- 42.26 mEq/day), urinary citrate (2.53 +/- 1.15 vs 3.10 +/- 1.44 mmol/day) and K (58.93 +/- 22.28 vs 65.45 +/- 23.97 mmol/day) excretion significantly increased from BAS to END. Urinary Ca excretion remained unchanged from BAS to END (5.16 +/- 2.74 vs 5.57 +/- 2.85 mmol/ day). Our results indicate that long-term treatment with K citrate increases forearm BMD in idiopathic Ca stone formers. It seems probable that the alkali load provided by this drug reduces bone resorption by a buffering of the endogenous acid production. K citrate appears to be a further therapeutic opportunity for the management of osteoporosis in Ca stone formers.

Idiopathic urinary stone disease: possible polygenic aetiological factors

About 12% of men and 5% of women of Western European descent develop at least one urinary stone during their lifetime. The incidence is somewhat less in individuals of sub-Saharan African or Asian descent, although there is a high incidence in the Middle Eastern countries. Calcium oxalate is a major constituent of about 70% of these stones. They are of multifactorial origin, with both genetic and environmental factors involved. The genetic factors influence different components of a highly complex system whereby calcium oxalate, which has a very low solubility in water, remains in solution. When the system is perturbed, the calcium oxalate crystallizes, the crystals aggregate and stones form. The genetic factors operate through mechanisms that are less obvious than the environmental ones such as the patient's state of hydration and dietary effects on the concentrations of the relevant ionic species. It is now generally accepted that the crystallization process begins in the distal ducts of the kidney by adhesion of calcium and oxalate to the epithelial surfaces of the tubule cells and their internalization. The calcium oxalate crystal becomes detached, with some incorporated organic materials forming a microlith. This process of microlith formation could arise either because of genetically determined alterations in the surface properties of the cells, or in the composition and/or concentration of substances in the urine that inhibit crystal nucleation and/or aggregation. The microliths pass through the collecting tubules more slowly than calcium oxalate in simple physical solution, aggregating until they reach the pelvicalycial system, where they grow into stones and pass down the ureters. It has been suggested that a shift in the crystal form from the mono-hydrate to the di-hydrate form reduces the likelihood of such adhesion, and that molecular inhibitors of crystallization operate by favouring the dihydrate form.1 Calcium oxalate urolithiasis had, … Address correspondence to Dr R.W.E. Watts, Renal Section, Division of Medicine, Imperial College, London, Hammersmith Campus, Du Cane Road, London W12 0NN

Developments in stone prevention

This review focuses on new developments in stone prevention. Unfortunately, no major progress in this field has happened. There is a worldwide lack of randomized and controlled trials, which could confirm our theoretical assumptions and preventive concepts in stone disease. With these preconditions in mind, this review presents the current knowledge of metabolic influences causing the symptom "stone" and the effective measures against it. Modern lifestyle, dietary habits and obesity emerge to be the promoters of idiopathic stone disease. Cross-sectional studies showed significant correlations between these factors and kidney stones with direct implications on our preventive concepts: normalization of body mass index, adequate physical activity, balanced nutrition and sufficient circadian fluid intake. Modern diets containing a lot of animal protein, refined carbohydrates and salt act on the metabolism like an acid load. To overcome these disadvantageous effects, a sufficient supply of potassium and alkali is required. Last but not least, calcium should not be restricted. There is clear evidence from clinical and experimental research that a normal or a high calcium supply is appropriate in calcium stone disease. Only in absorptive hypercalciuria calcium restriction remains beneficial in combination with thiazide and citrate therapy. Up to 85% of all stone patients could anticipate lower risk of stone recurrence with elementary reorientation of their lifestyle and dietary habits. Normalizing the major risk factors is easy and cheap. About 15% of patients forming stones require additional specific pharmacological prevention. The specific measures to avoid recurrence of the stone disease are precisely defined.

STONE FORMATION IS PROPORTIONAL TO PAPILLARY SURFACE COVERAGE BY RANDALL'S PLAQUE

Randall's plaques are common in calcium oxalate (CaOx) stone formers (SF). Plaque coverage correlates directly with urine calcium excretion and inversely with urine volume. We hypothesize that plaque coverage should increase proportionally with increasing stone number. We measured plaque areas in idiopathic CaOx stone formers and nonstone formers (NSF), and identified significant relationships with quantified stone histories. A total of 13 SFs and 4 control NSFs underwent nephroscopic papillary mapping with representative still images and MPEG (Moving Pictures Experts Group) movies used to identify plaque and papillary borders. Stone histories were obtained through patient interviews, and from medical records and radiographs. The relationship of plaque coverage to clinical stone events was assessed by general multivariate linear modeling. Log transformation normalized the distribution of percent plaque coverage and stone number. Plaque surface area in SFs differed significantly from that in NSFs (p <0.0001). The duration of stone disease and the log transformed percent plaque coverage correlated significantly with the number of stones (0.677 and 0.620, p = 0.003 and 0.008, respectively). On multivariate analysis and correcting for the duration of stone disease total percent plaque coverage correlated significantly with the number of stones (R = 0.496, p = 0.05). Disease duration and plaque coverage did not correlate significantly (p = 0.257). Percent plaque coverage directly correlates with the number of stones formed even when corrected for the duration of stone disease. However, plaque coverage does not correlate with the duration of stone disease. These results support the hypothesis that the pathogenesis of CaOx stones begins with Randall's plaques.

Rôle possible de la carence en vitamines A et E dans les lithiases idiopathiques chez l’homme

The purpose of our study is to compare the status of vitamin A and E enters a group of male patients aged 30–40 years and having idiopathic lithiasis in the other whose origin of the lithiasis is awarded to a hypercalciuria and/or hypercalciuria and/or hyperoxaluria. Reference values were established from a normal subjects aged 30–40 years and having no history of nephrolithiasis. Our results showed that the mean levels of vitamin A was significantly lower in idiopathic renal stone-formers than metabolic stone-formers ( p < 0.001). Compared to control group, the status of vitamin A was found lower only in idiopathic renal stone patients ( p < 0.05). On the contrary, the mean levels of vitamin E were found similar in the two patient groups, but significantly lower compared to control group. These results suggested that idiopathic renal stone genesis could be generated by vitamin A deficiency.

(Patho)physiological implications of the novel epithelial Ca2+ channels TRPV5 and TRPV6.

The epithelial Ca(2+) channels TRPV5 and TRPV6 constitute the apical Ca(2+) entry mechanism in active Ca(2+) (re)absorption. These two members of the superfamily of transient receptor potential (TRP) channels were cloned from the vitamin-D-responsive epithelia of kidney and small intestine and subsequently identified in other tissues such as bone, pancreas and prostate. These channels are regulated by vitamin D as exemplified in animal models of vitamin-D-deficiency rickets. In addition, the epithelial Ca(2+) channels might be involved in the multifactorial pathogenesis of disorders ranging from idiopathic hypercalciuria, stone disease and postmenopausal osteoporosis. This review highlights the emerging (patho)physiological implications of these epithelial Ca(2+) channels.

Pediatric Urolithiasis: Developing Nation Perspectives

We evaluated epidemiology, etiology, dietary and urinary risk factors, and the composition of calculi in pediatric stone formers in Pakistan. This retrospective study includes 1,440 children treated between 1987 and 2000. Case records were reviewed for demographics, etiology and clinical symptoms. Dietary and urinary risk factors were analyzed prospectively in idiopathic stone formers. Stone composition was analyzed by infrared spectroscopy. There were 1,075 males and 365 females for a male-to-female ratio of 3:1. The peak age for renal and bladder stones was 6 to 10 and 1 to 5 years, respectively. Overall 795 stones (55%) were renal, 198 (14%) were ureteral and 447 (31%) were vesical. Bladder stones were present in 60% of cases in the mid 1980s but decreased to 15% in the mid 1990s. The clinical symptoms were abdominal pain in 511 patients (51%) and fever in 193 (19.5%). There were anatomical abnormalities in 96 patients (12%), metabolic abnormalities in 206 (25%), infection stones in 60 (7%) and idiopathic stones in 444 (55%). Urinary analysis in idiopathic stone formers revealed hypercalciuria in 17 (11%), hyperoxaluria in 62 (40%), hyperuricosuria in 41 (27%) and hypocitruria in 97 (63%). Diet involved a low intake of protein in 60 cases (44%), calcium in 45 (33%), potassium in 105 (77%) and high oxalate in 75 (55%). The composition was calcium oxalate in 362 stones (47%), ammonium hydrogen urate in 210 (27%) and struvite in 49 (6.4%). Stones recurred in 30 patients (2%). The pattern of calculous disease changed from a predominantly lower tract site in the mid 1980s to the upper tract in the mid 1990s. Stone composition, urinary risk factors and dietary analysis suggest that diet, dehydration and poor nutrition are the main causative factors of stone disease.

Prevention of Spinal Bone Loss by Potassium Citrate in Cases of Calcium Urolithiasis

We determine if potassium citrate treatment stabilizes spinal bone density among patients with recurrent calcium oxalate nephrolithiasis. We studied a group of 16 men and 5 women with stones taking potassium citrate from 11 to 120 months. They represented all patients from the Stone Clinic who took potassium citrate alone for at least 11 months. L2-L4 bone mineral density data before and after potassium citrate treatment were retrieved retrospectively and analyzed. In the combined group L2-L4 bone mineral density increased significantly by 3.1% over mean duration of 44 months. Z score, corrected for age matched normal values, increased significantly by 3.8%. Urinary pH, citrate and potassium increased significantly during treatment but urinary calcium did not change. Potassium citrate, a commonly used drug for the prevention of recurrent nephrolithiasis, may avert age dependent bone loss. Spinal bone density increased in most patients when it normally decreases.

前頭葉内巨大脳石症の1例

前頭葉内巨大脳石症の1例

Effect of Dietary Intake on Urinary Oxalate Excretion in Calcium Oxalate Stone Formers in Their Forties

Purpose: To examine the influence of dietary intake on urinary oxalate excretion in calcium oxalate stone formers in their forties.Patients and Methods: Dietary intake was recorded by using the dietary–record method in 58 idiopathic stone formers in their forties. The patients collected their urine for 24 h at home and their urinary oxalate excretion was measured. The relationship between the dietary intake of various nutrients and urinary oxalate excretion was examined by mono– and multivariate analysis.Results: The intake of animal fat was correlated with urinary oxalate excretion by monovariate analysis, but that of total protein, animal protein, calcium and carbohydrate were not. By multivariate analysis, the intake of animal fat was correlated with urinary oxalate excretion and the intake of calcium was inversely correlated with urinary oxalate excretion.Conclusion: The intake of animal fat was positively and the intake of calcium was negatively correlated with the urinary oxalate excretion in stone formers in their forties. It was shown that animal fat plays an important role in urinary oxalate excretion.

Urinary Exertion Of Calcium By Urinary Stone Disease Patients And Normal

To compare the urinary excretion of calcium by subjects in a known area of high incidence of urinary stone disease, and a known area of low incidence, 12 adult male patients with idiopathic calcigerous urinary stone disease in south-East Nigeria and 55 similar patients from Scotland, United Kingdom were analyzed thirty-six healthy subjects in Nigeria and 30 in Scotland were also analyses as controls. Twenty-four hour urinary excretion of calcium was higher in patients from Scotland (6.81 +0.48mmols/24 hours). It was also higher in control from Scotland (5.96+0.61 mmol/24 hours), than in controls from Nigeria (2.33+0.21mmols/24 hours), and the difference was statistically significant (P (Nig J Surg Res 2000;2:1-5) KEY WORDS: Calcigerous stone, disease, calcium excretion Nigeria, Scotland.

Hyperoxaluria in Idiopathic Calcium Nephrolithiasis: What are the Limits?

The object of this study was to investigate the role for measurement of 24-h renal oxalate excretion in the evaluation of idiopathic calcium stone formers. Renal excretion rates of oxalate and creatinine were measured in 24-h urines in 46 consecutive male recurrent idiopathic calcium stone formers and 61 healthy males. Furthermore, day-to-day variation in renal oxalate excretion in 10 male recurrent stone formers and 10 healthy males were evaluated by measuring 24-h oxalate excretion on 5 different days in each individual. Concentrations of oxalate in urine were measured using an enzymatic method without ascorbate interference. The cumulative frequency distribution curves of 24-h renal oxalate excretion rates of stone formers and controls were congruent, and there were no statistically significant differences in oxalate excretion rates between stone formers and controls. Mean 24-h oxalate excretion (95%-confidence intervals) was 0.22 (0.18-0.25) mmol and 0.21 (0.18-0.24) mmol in stone formers and controls, respectively (p = 0.9). The day-to-day variation study did not reveal any differences in renal oxalate excretion pattern between stone formers and controls, and the presence of intermittent hyperoxaluria could not be confirmed. The oxalate excretion rates were generally low. In our region, there appear to be no differences in 24-h renal excretion rates of oxalate between male recurrent idiopathic calcium stone formers and healthy males, and the syndrome of mild hyperoxaluric calcium nephrolithiasis could not be identified in our population of idiopathic stone formers. Hence, a limit of abnormal oxalate excretion that distinguishes an idiopathic stone former from a non-stone former could not be defined in our population. Therefore, the value of routine measurement of urinary oxalate in idiopathic urolithiasis is difficult to accept, and cannot be recommended.

Diagnostic and therapeutic aspects of recurrent renal stone disease

Recurrent renal stones occur in 7.5% ofCaucasian men and 3% of all women. Even withincreasing urbanisation, renal calculi are reported inless than I% of black South African men and women. Four hundred recurrent stone formers were studied at the metabolic stone clinic using routine and special tests. The appropriate therapy for each subgroup is outlined and studies on various different treatments are presented. In addition, lithogenic risk factors were studied in normal black and white subjects and in black stone formers, in order to clarify the low incidence in the black population. Patients were classified according dietary andmetabolic lithogenic risk factors. 10% of stoneformers had pure dietary factors. The percentage ofstone formers in each of the various metabolicsubgroups was as follows: Renal hypercalciuria 12%, Absorptive hypercalciuria 10%, Mild metabolichyperoxaluria 20%, Hypocitraturia 50%. Successfultherapy in terms of preventing further stoneformation was reported using indapamide, calciumcarbonate and potassium citrate in renal hypercalciuria,mild metabolic hyperoxaluria and hypo-citraturia respectively. Black volunteer subjects hadsignificantly higher 24hr urinary sodium excretionand significantly lower 24hr urinary calcium, citrateand cystine excretion than white volunteer subjects. Twenty-four hours urinary values in black stoneformers were found to be approaching those levelsfound in white. As urbanisation occurs in the black population, the incidence of urolithiasis would be expected to increase. We conclude that a detailed metabolic work-up is essential in the elucidation of the various metabolic risk factors. in so-called idiopathic CaOx stone formers. It allows appropriate, specific and highly cost-effective therapy aimed at the prevention of recurrence. [Erratum appears in AJN, 2017; 20(1):200.]

Ammonium acid urate crystal formation in adult North American stone-formers

Although ammonium acid urate (AAU) stones are endemic in Asia, pure AAU calculi have almost disappeared from industrialized countries and clinical pathophysiologic relevance of sporadic stones containing AAU crystals is currently unknown. We reviewed 1,396 crystallographic stone analyses performed in our institution over a 10-year period. Prevalence of stones containing AAU crystals and predominantly AAU stones were 3.1% and 0.2%, respectively. In more than two thirds of cases, AAU crystals represented less than 10% of stone crystal composition. No pure AAU stone was found. According to crystalline predominance, 42%, 35%, and 12% of these calculi were uric acid, infectious, and calcium oxalate stones, respectively. AAU crystals were detected as discrete intercrystalline or peripheral deposits in 74.4% of stones. In only one calculus was AAU crystals detected in the nucleus. The hospital charts of 37 patients who presented with 43 calculi containing AAU crystals were also reviewed. The mean age was 53.1 ± 16.6 years. Fifty-seven percent of calculi were upper urinary tract stones and 43% were bladder stones. Upper urinary tract calculi were more frequently uric acid stones, followed by infectious and calcium oxalate stones. Lower urinary tract calculi were more frequently infectious stones, followed by uric acid stones. Upper urinary tract stones were passed spontaneously in 13 patients and removed surgically in nine patients. Nine of these subjects were idiopathic recurrent stone formers who had passed other calculi with no trace of AAU crystal. Fifty-seven percent of lower urinary tract stones were associated with documented bladder dysfunction. In conclusion, although AAU-containing urolithiases are occasionally seen in our population, predominantly or primarily AAU stones are exceptional. AAU crystal formation usually appears as a minor and secondary phenomenon of no primary pathophysiologic relevance in stone formation.

Epidemiological profile, mineral metabolic pattern and crystallographic analysis of urolithiasis in Kuwait.

This study was conducted to determine the epidemiological profile of urolithiasis in Kuwaiti patients and the associated metabolic abnormalities favouring stone formation in this patient population. Between 1986 and 1994, a total of 421 Kuwaiti patients were studied in Al-Amiri renal stone laboratory. The mineral composition of stones was determined using a combination of stereoscopic microscopy and infrared spectrophotometry. Mineral metabolic screen (MMS) was available in 306 (72.7%) of those patients. The average annual incidence of new stone formation in Kuwaiti patients was 23.9 per 100,000 population. The incidence was only 6.9 per 100,000 population in those from pediatric age group, 33.4 in adults and 73.6 in the elderly. The frequency of new stone formation was higher among males as compared to females at different age groups. Calcium oxalate (CaO) constituted 72.1% of renal stones encountered in adults as compared to only 52.1% and 40.7% in elderly and pediatric age groups. Eighty four patients had recurrent and/or high stone load. Detailed family history was available in 57 of those 84 patients and was suggestive of strong family aggregation of stone disease in 30 (53%) patients. The proportion of urate stones was 15.4% of all stones formed and constituted a major cause of renal stones in children (24.1%), adults (14.4%) and elderly (12.5%). Cystine stones were found in 10 patients (2.4%). Hyperuricemia was detected in 1/3 of patients from pediatric age group. In adults, 89 (38.4%) of 232 patients had abnormal MMS, of which hyperuricosuria with or without hyperuricemia accounted for 79.8% of those abnormalities. In elderly patients, metabolic disorders were detected in 7 (17.5%) of the 40 patients. In the latter group, all except one, had hyperuricosuria with or without hyperuricemia. Cystinuria, distal renal tubular acidosis (d-RTA) and hyperparathyroidism constituted 6.6% of metabolic abnormalities in the patients studied. Primary abnormalities of upper and lower urinary tract was detected in 6% of adult patients as compared to 47% in children and 30% in the elderly. In conclusion; the incidence rate of new stone former in Kuwait is significantly lower from that reported in Europe and USA. This latter finding and the high familial aggregation of urolithiasis in our area constitute a cogent argument against the role of hot climate in the pathogensis of urolithiasis and are in favour of genetic predisposition. Isolated hyperuricosuria was detected in 17% of idiopathic CaO stone formers. The latter finding is of practical importance since red-meat is a common food item in our area and restriction of purine-intake may help to decrease the frequency of urate and CaO stone formation in predisposed patients.

In vitro degradation of oxalic acid by human feces.

Oxalic acid-degrading bacteria have been isolated from human faces. Therefore, the possibility exists that oxalic acid in food is degraded in human intestine by such bacteria, and absorption and excretion of oxalic acid is reduced. It may be possible that patients who form idiopathic stones have fewer oxalic acid-degrading bacteria than healthy controls. The purpose of this study is to examine the possibility that oxalic acid in food is degraded in the human intestine. Nineteen patients with calcium stones and 13 healthy subjects were included in the study. Samples of feces were diluted with Barber medium containing 1 g/L of oxalic acid dihydrate, and 1%, 0.1% and 0.01% suspensions were prepared. These solutions were incubated under anaerobic conditions at 37 degrees C for seven days. The degradation of oxalic acid was estimated by the decrease of oxalic acid in the medium. The feces of almost all persons with or without calculi degraded oxalic acid to some degree. Incomplete or no oxalic acid degradation was found in 15 of the 19 stone-forming patients and in five of the 13 stone-free controls. Large numbers of oxalic acid-degrading bacteria were observed less often in the feces of stone-formers than in the feces of stone-free controls.

Anomalous phospholipid n-6 polyunsaturated fatty acid composition in idiopathic calcium nephrolithiasis.

Anomalies in the erythrocyte transport of anions and cations have been described in idiopathic calcium oxalate nephrolithiasis and seem to play a pathogenetic role in this disease. In consideration of the hypothesis that the complex array of ion flux cell abnormalities is an epiphenomenon of an anomaly in the composition of cell membranes, this study investigated cell-membrane lipid composition. In idiopathic calcium oxalate renal stone formers, in which ion transport abnormalities were present, and in healthy control subjects, plasma and erythrocyte membrane lipid composition, the erythrocyte oxalate exchange, and Na/K/2Cl cotransport activity were evaluated. Furthermore, in stone formers, the effect of a 30-day fish-oil diet supplementation on plasma lipids, erythrocyte oxalate exchange, oxaluria, and calciuria was investigated. The effect of archidonic acid released by phospholipase A2 on anion-carrier phosphorylation and activity in erythrocytes was evaluated as well. Patients had a lower content of linoleic and higher concentration of archidonic acids in both plasma and erythrocyte membrane phospholipids, and an increased archidonic/linoleic acid ratio. The archidonic acid level correlated with the erythrocyte oxalate exchange and sodium cotransport activity. Fish-oil supplementation lowered calcium and oxalate urine excretion, and normalized the erythrocyte oxalate exchange. Phospholipase A2 increased the erythrocyte anion-carrier protein phosphorylation and the oxalate exchange. This study shows that idiopathic calcium nephrolithiasis in the patient group reported here is characterized by a systemic defect in phospholipid archidonic acid levels that might provide an answer to the link between genetic background, dietary habits, and renal lithiasis.

Effect of dietary intake on urinary oxalate excretion in calcium renal stone formers.

To investigate the influence of dietary intake on urinary oxalate excretion in calcium renal-stone formers. Dietary intake was monitored by using the dietary-record method in 60 idiopathic stone formers. The patients collected their urine for 24 h at home and their urinary oxalate excretion rate was determined. The relationship between the daily intake of various nutrients and urinary oxalate excretion was examined by both monovariate and multivariate analyses. By monovariate analysis, the intake of carbohydrate, total protein and fat were significantly correlated with urinary oxalate excretion, but the intake of calcium and body surface area were not. In addition, the intake of total protein was highly correlated with that of fat. By multivariate analysis, the intake of carbohydrate and fat were significantly related to urinary oxalate excretion, and the intake of calcium was inversely correlated with urinary oxalate excretion, but the intake of total protein showed no significant correlation. The intake of carbohydrate and fat was positively and the intake of calcium was inversely correlated with urinary oxalate excretion in stone formers and, taken together, these findings suggested that fat plays an important role in urinary oxalate excretion and that protein has a minimal effect.

Erythrocyte transmembrane flux and renal clearance of oxalate in idiopathic calcium nephrolithiasis

An anomaly in erythrocyte oxalate transport has been reported in patients with idiopathic calcium oxalate nephrolithiasis. Even if clinical and experimental evidence suggests a causal role of this cellular anomaly in calcium nephrolithiasis, a definitive answer to this fundamental question is still lacking. We approached this problem by searching for a possible relationship between the erythrocyte oxalate self-exchange anomaly and the renal clearance of this anion in stone formers. In 10 idiopathic calcium-oxalate renal stone formers, and 10 healthy subjects we evaluated the erythrocyte oxalate flux rate, and the renal fractional clearance of oxalate by a recently described enzymathic procedures for plasma oxalate determination. With respect to controls, stone formers had higher oxalate flux rate in erythrocytes, and higher oxalate renal fractional clearance with a significant direct correlation between the two parameters. These data are compatible with a membrane transport abnormality within the kidney of these stone formers, and the existence of a common defect of the oxalate transport shared by both erythrocytes and tubular renal cells. The latter may be crucial in the pathogenesis of calcium oxalate nephrolithiasis, by modifying the renal handling of oxalate.