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Query: UMLS:C0020500 (hyperoxaluria)
 912 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

389 consecutive renal stone formers (275 males, 114 females) were investigated in an out-patient stone clinic. Renal tubular acidosis (RTA) was found in 83 patients (22%). Proximal RTA was twice as common as the distal tubular type. The acidification defects were exclusively of the incomplete form with normal basal blood acidbase status. Main diagnoses besides RTA were primary hyperparathyroidism (3.5%), medullary sponge kidney (3.5%), infection induced stones (3%), urate stones (2%), intestinal disorder (1.5%) and cystinuria (0.5%). The metabolic evaluation was mainly based on 24 h urine sampling on a free diet. In 248 patients (64%) no distinct abnormality was considered to be primarily responsible for stone formation. Clinical and biochemical analysis of these so-called idiopathic stone formers disclosed a male preponderance (80%) and, compared to a non-stone-forming control group, a higher urinary calcium excretion, yet with a considerable overlap between the two groups. Hyperuricosuria and hyperoxaluria were rare findings. The conclusion of the study is given as a proposal for clinical classification and ambulatory investigation of renal stone formers.
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PMID:Ambulatory diagnostic evaluation of 389 recurrent renal stone formers. A proposal for clinical classification and investigation. 684 37

Clinical and biochemical data were obtained from 50 patients in whom stones form and 20 controls to set up and test a screening procedure for detecting metabolic abnormalities related to the formation of urinary calculi and to provide a preliminary estimate of the frequency of these disorders in our area. A comparison between patients in whom stones form and controls in terms of the quantitative biochemical parameters evaluated (serum calcium, uric acid and inorganic phosphate, and urine calcium, uric acid, inorganic phosphate, oxalic acid, xanthine and alpha-amino-nitrogen) showed a significant difference only with respect to excretion of urinary oxalate by adults, which was higher in patients in whom stones form. Metabolic disorders were detected in 15 adult patients with stones. Of these patients 9 had isolated hyperoxaluria, 3 had incomplete renal tubular acidosis, 1 had idiopathic hypercalciuria, 1 had heterozygous cystinuria and 1 had idiopathic hypercalciuria associated with heterozygous cystinuria. These results suggest a high frequency of metabolic abnormalities in patients in whom stones form in our area, so that the wider use of the screening used here may benefit a large number of patients with preventive and therapeutic measures.
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PMID:Metabolic factors in urolithiasis: a study in Brazil. 742 May 93

The aetiology of nephrolithiasis was investigated in 32 north Indian children (25 boys, 7 girls, mean age 7.9 +/- 3.3 years). An underlying disorder was detected in 16 (50%) patients and included idiopathic hypercalciuria (8 patients), hyperoxaluria (3 patients) and renal tubular acidosis, primary hyperparathyroidism and hyperuricosuria (1 patient each). Magnesium ammonium phosphate calculi were found in 2 patients with recurrent urinary tract infections, 1 of whom had a duplex pelvic collecting system. In 16 patients (50%) a cause for renal calculi was not identified. Our findings suggest that an underlying disorder is present in a large proportion of children with nephrolithiasis where appropriate treatment may be beneficial.
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PMID:Aetiology of nephrolithiasis in north Indian children. 757 12

To elucidate the frequency and clinical picture of renal tubular acidosis-1 (RTA-1) in nephrolithiasis, the acid-loading test was performed in 474 patients with calcium-containing stones. RTA-1 was detected in a total of 11 patients (6 men and 5 women, 2.3%). The incidence of RTA-1 in female patients tended to be higher than in male patients (3.2 vs. 1.9%). One male patient had the complete form, the others had incomplete form. There was a tendency that RTA-1 patients were younger than non-RTA-1 patients in men, and the former were older than the latter in women. The percentages of positive family history and positive past history were 27 and 45%, respectively. Stones were single in 7 cases and multiple in 4 cases. They were unilateral in 10 cases, and bilateral in 1 case. Hypercalciuria was detected in 2 of the 11 cases, hyperuricosuria was present in none of the 11 cases, and hyperoxaluria in 2 of 8 cases examined. Stones were composed of calcium oxalate in 2 cases, calcium phosphate in 2, and calcium oxalate mixed with calcium phosphate in 3.
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PMID:Incidence and clinical features of renal tubular acidosis-1 in urolithiasis. 846 Apr 53

About 80% of all renal stones contain calcium oxalate and/or calcium phosphate as their main crystalline components. The most important risk factors for increases in calcium oxalate crystallization are low urine volume, hyperoxaluria and hypocitraturia. Hypercalciuria, however, is of secondary importance as a cause of increased crystallization: whereas calcium and oxalate crystallize in a 1:1 ratio, the molar concentration ratio in urine amounts to about 10:1 in favor of calcium. Therefore, increases in urinary calcium will not be followed by a rise in crystallization as long as oxalate remains constant, whereas even the slightest increases in urinary oxalate immediately cause more crystals to precipitate. Thus, low calcium diet is not only unnecessary but is contraindicated since it may cause secondary hyperoxaluria (increased intestinal oxalate absorption) and osteopenia (negative calcium balance). On the other hand, overconsumption of animal protein (meat, poultry, fish) induces more pronounced hyperoxaluria and hypocitraturia and contributes to an overall negative calcium balance. It is, however, only by the interplay of "bad" dietary habits with underlying abnormalities such as up-regulation of calcitriol production, incomplete renal tubular acidosis or defective macromolecular crystallization inhibitors, that people become recurrent calcium renal stone formers.
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PMID:[Diagnostic markers in calcium nephrolithiasis--current and traditional ideas with a new look]. 857 Oct 96

The first episode of nephrolithiasis provides an opportunity to advise patients about measures for preventing future stones. Low fluid intake and excessive intake of protein, salt and oxalate are important modifiable risk factors for kidney stones. Calcium restriction is not useful and may potentiate osteoporosis. Diseases such as hyperparathyroidism, sarcoidosis and renal tubular acidosis should be considered in patients with nephrolithiasis. A 24-hour urine collection with measurement of the important analytes is usually reserved for use in patients with recurrent stone formation. In these patients, the major urinary risk factors include hypercalciuria, hyperoxaluria, hypocitraturia and hyperuricosuria. Effective preventive and treatment measures include thiazide therapy to lower the urinary calcium level, citrate supplementation to increase the urinary citrate level and, sometimes, allopurinol therapy to lower uric acid excretion. Uric acid stones are most often treated with citrate supplementation. Data now support the cost-effectiveness of evaluation and treatment of patients with recurrent stones.
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PMID:Prevention of recurrent nephrolithiasis. 1059 18

When hypercalcemia is detected in a kidney stone formation, an intact parathyroid hormone measurement should be made. Detection of hyperparathyroidism (HPT) is important to prevent further stone episodes and to avoid the complications of high serum calcium in other organ systems. Stones in patients with HPT often contain apatite salts in addition to calcium oxalate because parathyroid excess may create a renal tubular acidosis. The calculi seen in patients with sarcoidosis, another hypercalcemic state that may cause stone formation, however, are usually pure calcium oxalate. Excess generation of 1,25-dihydroxyvitamin D results in intestinal hyperabsorption of calcium and secondary hyperoxaluria.
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PMID:Kidney stones as a manifestation of hypercalcemic disorders. Hyperparathyroidism and sarcoidosis. 1077 70

Annual incidences of kidney stones are about 0.1-0.4% of the population, and lifetime prevalences in the USA and Europe range between 8 and 15%. Kidney stones occur more frequently with increasing age and among men. Within ten years, the disease usually recurs in more than 50% of patients. Nowadays, about 85% of all kidney stones contain calcium salts (calcium oxalate and/or calcium phosphate) as their main crystalline components. Because human urine is commonly supersaturated with respect to calcium salts as well as to uric acid, crystalluria is very common, i.e. healthy people excrete up to ten millions of microcrystals every day. Recurrent stone formers appear to excrete lower amounts or structurally defective forms of crystallization inhibitors which allows for the formation of large crystal aggregates as precursors of stones. Alternatively, crystal adhesion to urothelial surfaces may be enhanced in stone formers. Medical treatment of renal colic is based on nonsteroidal antiinflammatory drugs, because prostaglandins appear to play a crucial role in the pathophysiology of pain during ureteral obstruction. In addition, centrally acting analgesics such as pethidine-HCl may be required in many cases. The administration of high amounts (3-4 liters/day) of intravenous fluids should be abandoned, since it may raise intraureteral pressure whereby pain increases and kidney pelvis or fornices may rupture. All first-stone formers should undergo a simple basic evaluation, including stone analysis (x-ray diffraction or infrared spectrometry), serum values of ionized calcium (alternatively: total calcium and albumin) and creatinine, urinalysis and repeated measurements of fasting urine pH in order to detect urinary acidification disorders or low urine pH. In high-risk patients with as first stone episode (i.e. strongly positive family history, inflammatory bowel disease, short-bowel syndrome, nephrocalcinosis, bilateral stones, hypercalcemia, renal tubular acidosis, airline pilots) as well as in all recurrent stone formers, an extended metabolic evaluation should be performed. Two 24-hurines should be collected on free-choice diet not prior to three months after stone passage or urological intervention. Analysis includes measurements of volume, creatinine, calcium, oxalate, uric acid and citrate; sodium and urea as markers of salt and protein consumption are optional but clinically very helpful. Since hypercalciuria is of much less importance than increases in urinary oxalate, therapeutic efforts should primarily focus on lowering urinary oxalate excretion. Sufficient calcium intake, i.e. 1200 mg per day, is crucial, because it allows for binding of oxalate at the intestinal level whereby increases of urinary oxalate (reciprocal hyperoxaluria) can be avoided. Excess intake of flesh protein (meat, fish, poultry) is lithogenic since it increases urinary calcium, oxalate and uric acid, and lower citrate. On the other hand, a diet rich in alkali (vegetables, fruit) is associated with a lower risk of stone formation. A "common sense diet" containing sufficient amounts of fluids, 1200 mg of calcium per day and reduced amounts of flesh protein as well as salt is able to reduce the 5-year stone recurrence rate in calcium stone formers by 50%. The scientific evidence for drug treatment (thiazides, alkali citrate) is rather poor: the most widely quoted randomized thiazide trial included only 42 patients of whom 36% left the protocol prematurely, whereas 36-48% of patients included in three randomized studies with alkali citrate suffered from undesirable side-effects; nevertheless, citrate therapy reduced the stone recurrence rate by 38%, compared with 22% in patients on placebo treatment (p < 0.0005).
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PMID:[Pathophysiology, diagnosis and conservative therapy in calcium kidney calculi]. 1264 86

The purpose of the present review is to provide an update about the most common risk factors or medical conditions associated with renal stone formation, the current methods available for metabolic investigation, dietary recommendations and medical treatment. Laboratory investigation of hypercalciuria, hyperuricosuria, hyperoxaluria, cystinuria, hypocitraturia, renal tubular acidosis, urinary tract infection and reduction of urinary volume is based on the results of 24-hr urine collection and a spot urine for urinary sediment, culture and pH. Blood analysis for creatinine, calcium and uric acid must be obtained. Bone mineral density has to be determined mainly among hypercalciurics and primary hyperparathyroidism has to be ruled out. Current knowledge does not support calcium restriction recommendation because it can lead to secondary hyperoxaluria and bone demineralization. Reduction of animal protein and salt intake, higher fluid intake and potassium consumption should be implemented. Medical treatments involve the use of thiazides, allopurinol, potassium citrate or other drugs according to the metabolic disturbances. The correction of those metabolic abnormalities is the basic tool for prevention or reduction of recurrent stone formation.
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PMID:Renal stone disease: Causes, evaluation and medical treatment. 1711 7

This retrospective survey examines the etiology of nephrocalcinosis (NC) in 40 patients (26 boys), over an 8-year period. The median age at onset of symptoms and presentation was 36 months and 72 months, respectively. Clinical features included marked failure to thrive (82.5%), polyuria (60%) and bony deformities (52.5%). The etiology of NC included distal renal tubular acidosis (RTA) in 50% patients and idiopathic hypercalciuria and hyperoxaluria in 7.5% each. Other causes were Bartter syndrome, primary hypomagnesemia with hypercalciuria, severe hypothyroidism and vitamin D excess. No cause for NC was found in 12.5% patients. Specific therapy, where possible, ameliorated the biochemical aberrations, although the extent of NC remained unchanged. At a median (range) follow up of 35 (14-240) months, glomerular filtration rate (GFR) had declined from 82.0 (42-114) ml/min per 1.73 m2 body surface area to 70.8 (21.3-126.5) ml/min per 1.73 m2 body surface area (P = 0.001). Our findings confirm that, even with limited diagnostic facilities, protocol-based evaluation permits determination of the etiology of NC in most patients.
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PMID:Etiology of nephrocalcinosis in northern Indian children. 1728 94


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