Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020500 (hyperoxaluria)
 912 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The chances of stone formation occurring through a free particle mechanism were calculated using the approach of Finlayson and Reid [1]. For these calculations we used new data on nephron dimensions, supersaturation and crystal growth rates in urine, and also incorporated the size increasing effect of crystal agglomeration. The calculations were performed assuming different levels of oxalate excretion, simulating the diurnal variation and acute hyperoxaluria following a dietary load. In addition urinary flow conditions were varied according to changes in daily urinary volume. It is shown that during the normal transit time of urine through the nephron, particles can obtain a size big enough to be retained in the nephron. This is mainly due to the size-increasing effect of the agglomeration process. The precipitable amount of oxalate present is not limiting for the maximum attainable particle size. However, acute increases in oxalate excretion do pose a risk because supersaturation is reached earlier in the nephron and consequently the crystal particles are allowed more time to increase in size. In conclusion, the present calculations demonstrate that during the normal transit time through the kidney, crystalline particles can be formed which are large enough to be retained because of their size and thus form the nidus of a stone. The highest risk is encountered at the end of those collecting ducts where crystals formed in nephrons with a long loop of Henle meet and agglomerate.
Kidney Int 1994 Sep
PMID:Calcium oxalate nephrolithiasis, a free or fixed particle disease. 799 6

The present study was carried out to investigate the relation between erythrocyte oxalate flux rate and the pathogenesis of calcium oxalate renal stone disease having hyperoxaluria as the main risk factor. Male albino rats were made hyperoxaluric by feeding them diets viz. vitamin B6 deficient, vitamin B6 deficient + 51.7% galactose or fructose (serving as a sole source of carbohydrate), along with their respective pair-fed controls for 4 weeks. After 28 days of feeding, oxalate excretion was in the order of vitamin B6 deficient + galactose > galactose control > vitamin B6 deficient + fructose > vitamin B6 deficient > fructose control/vitamin B6 control. Whereas, transmembrane oxalate flux rate was in the order of vitamin B6 deficient > vitamin B6 deficient + galactose > vitamin B6 deficient + fructose > vitamin B6 control > galactose control > fructose control. No significant correlation (r = 0.304) was found between the urinary oxalate excretion and erythrocyte oxalate flux rates of various groups of rats. The study indicates that increase in oxalate excretion does not concomitantly increase the transmembrane oxalate flux in red blood cells.
Biochem Mol Biol Int 1993 Sep
PMID:A comparative study of erythrocyte oxalate flux rate and urinary oxalate excretion in hyperoxaluric rats. 826 Sep 49

The study describes the indications and results of combined liver/kidney transplantation in eight patients suffering from end-stage hepato-renal diseases. The causes of primary renal failure were hyperoxaluria type I (2/8), diabetic nephropathy (2/8), glomerulonephritis (2/8), congenital pyelonephritis (1/8), and polycystic kidneys (1/8). Only five of these patients were on chronic dialysis prior to transplantation. The indication for kidney transplantation in the other three patients was low GFR (< 20 mL/min) and the anticipation of further deterioration of the renal function after liver transplantation as a result of cyclosporine toxicity. The end-stage liver diseases were chronic active hepatitis (4/8) and alcoholic cirrhosis (2/8). There was no evidence for liver failure in two patients undergoing combined transplants for primary hyperoxaluria. The 1-year patient survival rate is 75 per cent, and at that time, kidney and liver function were found to be within normal range. In conclusion, excellent long-term patient survival, as well as kidney and liver graft function, can be achieved in patients suffering from complex end-stage disease of both organs who undergo combined liver and kidney transplantation.
Am Surg 1993 Sep
PMID:The role of combined liver/kidney transplantation in end-stage hepato-renal disease. 836 68

Presentation of the analytical results from the patients seen for lithiasic disease (LD) over a two-year period at the Hospital Reina Sofia, Tudela. This Hospital covers a homogeneous Health Area including 22 villages and a population of 76,000 people. The clinical cases of 785 patient diagnosed with LD between May 1988 and 1990 May are analyzed. Microhaematuria in fresh urine is detected in 64.20% patients and crystalluria in 33.37%. Significant bacteriuria is present in 5.73% of total patients with prevalence of E. coli in 42.4%. Only 2 cases of hyperparatiroidism were diagnosed during the study period but later another two cases of HPT were detected in bone injuries studied due to rheumatic disease. No normocalcemic HPT cases were diagnosed among suspected cases. The metabolic studies were of little use in our experience, maybe because of non-availability of basic analytical determinations such as citraturia. Nevertheless, higher values of urinary volume, calciuria and uricemia and lower values of magnesemia and magnesiuria were found in lithiasic patients that in control ones. Neither oxaluria or the remaining analytical parameters provide differential data. Hypercalciuria higher than 300 mg in seen in 28.6% of studied patients and in 12.5% of the control group.
Actas Urol Esp 1995 Sep
PMID:[Epidemics of urinary calculi in la Ribera de Navarra (II). Analytic studies]. 866 30

Urolithiasis is one of the most frequent causes of morbidity in developed countries and its incidence is close to 5%. In our experience, 67.4% of urinary stones contain calcium oxalate as the main component, and hyperoxaluria plays an important role in the pathophysiology of this type of stone. The mechanisms responsible for the increment in urinary excretion of oxalate could involve oxalic acid synthesis. This increase could be due either to an increment of its endogenous formation or to an exogenous load of its precursors. Furthermore, an increased intestinal oxalate absorption is a frequent cause of hyperoxaluria and urolithiasis. Ingestion of oxalate rich foods, imbalance in the supply of other nutrients that influence oxalic acid absorption and GI disorders with malabsorption and/or decreased degradation of intraluminal oxalate can increase intestinal oxalate transport and cause hyperoxaluria. In this article we review the physiological mechanisms that control the oxalate pool: endogenous synthesis, exogenous supply, intestinal absorption and renal excretion of oxalic acid. We analyze the causes and the pathophysiological mechanisms that increase urinary oxalate excretion. We describe a protocol for the biochemical study of patients with hyperoxaluria and the therapeutic measures to reduce urinary oxalate are reviewed. Finally, possible research that may provide further insight into oxalate metabolism in patients with hyperoxaluria are discussed.
Arch Esp Urol 1996 Sep
PMID:[Hyperoxaluria and renal calculi]. 902 8

Urolithiasis and/or nephrocalcinosis due to hereditary diseases are a rare event which must be kept in mind of physicians who take care of children (10 to 40% of all causes of lithiases) as well as of adults (less than 15% of all causes of lithiases) since a specific management is usually required. The most frequent inborn disorders are idiopathic hypercalciuria, distal tubular acidosis, cystinuria and hyperoxaluria. Stone formation is always secondary to an increased urine concentration of promotors, i.e. calcium, oxalate, phosphate, cystine, xanthine. One of the most informative diagnosis investigation is infrared spectrophotometry which can identify stone composition. When such a technique is not available, biochemical investigations should be adapted to both personal and family history. In addition to high fluid intake (2 to 3 L/m2/24 h) sometimes associated with alcalinisation, the management of hereditary stone disease requires specific procedure. In all cases, the long-term renal prognosis is related to both primary disease and therapeutic compliance.
Rev Prat 1997 Sep 15
PMID:[Hereditary diseases causing kidney calculi]. 936 14

In order to assess the significance of the intestinal absorption of oxalate from food for the hyperoxaluria of the individual patient, an oxalate absorption test has been developed using doubly 13C-labelled oxalate and a gas chromatographic selected ion monitoring mass spectrometric assay. This test has been applied to volunteers and patients with urinary stones. The percentage of dose absorbed (range 1-48%) could be determined with a coefficient of variation of 15.2%. The assay to measure doubly 13C-labelled oxalate in the presence of unlabelled oxalate in urine, using the homologue malonic acid as internal standard, is described.
J Chromatogr B Biomed Sci Appl 1998 Sep 25
PMID:Mass spectrometric-selected ion monitoring assay for an oxalate absorption test applying [13C2]oxalate. 982 49

Interstitial calcium oxalate (CaOx) crystals can be found in primary oxalosis and in secondary hyperoxaluria. In a rat model for nephrolithiasis, we investigated whether such crystals can be removed by the surrounding interstitial cells. CaOx crystals were induced by a crystal-inducing diet based on ethylene glycol (EG) and ammonium chloride (CID). Both lithogenic compounds were added to the drinking water. After 9 days, the animals received normal drinking water for 2 days. Using this CID, only the interstitial crystals are retained. Subsequently, half of the population remained on normal drinking water (normo-oxaluria), whereas the other half received a low dose of EG alone (chronic hyperoxaluria). The rats were killed at regular times thereafter. The results showed that the kidney-associated oxalate significantly declined during normo-oxaluria, but remained high during chronic hyperoxaluria. Interstitial cells positive for the leukocyte common antigen (CD45; which identifies all types of leukocytes), the ED1 antigen (which is specific for monocytes and macrophages), and the major histocompatibility class II antigen (MCHII), respectively, had increased in number, with minor differences between both rat populations. The cells around the interstitial crystals were mostly positive for ED1. Multinucleate giant cells were regularly observed. These cells were positive for CD45 and ED1 and sometimes also for MCHII. The crystals in these cells were moderately positive for acid phosphatase and carbonic anhydrase II. It is concluded that interstitial CaOx crystals can be removed under normo-oxaluric conditions and that, in all likelihood, macrophages and multinucleate giant cells are involved in that process.
Am J Kidney Dis 2000 Sep
PMID:Role of macrophages in nephrolithiasis in rats: an analysis of the renal interstitium. 1097 95

Urolithiasis, the process of formation of stones in the kidney and the urinary tract, is the major clinical manifestation of hyperoxaluria. Crystal deposition, as indicated by increased stone-forming constituents in urine, such as calcium, oxalate and uric acid, and decreased concentration of inhibitors, such as magnesium and glycosaminoglycans, was observed in pyridoxine-deficient hyperoxaluric rats. Renal tubular damage was indicated by increased excretion of enzymes such as alkaline phosphatase, lactate dehydrogenase, gamma-glutamyl transferase, beta-glucuronidase and N-acetyl glucosaminidase. Fibrinolytic activity was found to be reduced. Administration of pentacyclic triterpenes such as lupeol and its structural analogue betulin to hyperoxaluric rats minimised the tubular damage and reduced the markers of crystal deposition in the kidneys. In this connection, lupeol was found to be more effective than betulin.
Fitoterapia 2000 Sep
PMID:Control of urinary risk factors of stones by betulin and lupeol in experimental hyperoxaluria. 1144 2

Secondary hyperoxaluria is due either to increased intestinal oxalate absorption or to excessive dietary oxalate intake. Certain intestinal diseases like short bowel syndrome, chronic inflammatory bowel disease or cystic fibrosis and other malabsorption syndromes are known to increase the risk of secondary hyperoxaluria. Although the urinary oxalate excretion is usually lower than in primary hyperoxaluria, it may still lead to significant morbidity by recurrent urolithiasis or progressive nephrocalcinosis. A clear distinction between primary and secondary hyperoxalurias is important. As correct classification may be difficult, appropriate diagnostic tools are needed to delineate the metabolic background as a basis for optimal treatment. We developed an individual approach for the evaluation of patients with suspected secondary hyperoxaluria. First, 24 h urines are examined repeatedly for lithogenic (e.g. calcium, oxalate, uric acid) and stone-inhibitory (e.g. citrate, magnesium) substances, and the patients are asked to fill in a dietary survey form. Urinary saturation is calculated using the computer based program EQUIL2, and the BONN-Risk-index is determined. The measurement of plasma oxalate and of urinary glycolate helps to distinguish between primary and secondary hyperoxalurias. If secondary hyperoxaluria is suspected, the stool is examined for Oxalobacter formigenes, an intestinal oxalate degrading bacterium, as lack or absence may lead to increased intestinal oxalate absorption. The last diagnostic step is to study the intestinal oxalate absorption using [13C2]oxalate. Depending on the results, various therapeutic options are available: 1) a diet low in oxalate, but normal or high in calcium, 2) a high fluid intake (>1.5 L/m2/d), 3) medications to increase the urinary solubility, 4) specific therapeutic measures in patients with malabsorption syndromes, depending on the underlying pathology, and 5) intestinal recolonization of Oxalobacter formigenes or the treatment with other oxalate degrading bacteria.
Front Biosci 2003 Sep 01
PMID:Diagnostic and therapeutic approaches in patients with secondary hyperoxaluria. 1295 11


<< Previous 1 2 3 4 5 6 Next >>