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

The current concepts of normal fat absorption and the entero-hepatic circulation of bile acids are being reviewed with emphasis on the steps which are clinically important. Based on an understanding of normal physiology, diseases associated with steatorrhea can be classified according to pathogenetic mechanisms. In some diseases the pathogenesis of the steatorrhea is not understood. Malabsorption of fat and bile salts can have characteristic consequences such as nutritional deficiencies, diarrhea, hyperoxaluria with nephrolithiasis, and cholelithiasis. For quantitative assessment of steatorrhea chemical analysis of fecal fat is necessary.
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PMID:[Absorption and malabsorption of fat and bile acids (author's transl)]. 89 17

In a group of 57 children with urolithiasis hypomagnesaemia was found in 15 cases (26.3%). All children but one with abnormally low serum magnesium levels had recurrent or bilateral nephrolithiasis or nephrocalcinosis. Prevalence of hyperoxaluria and hypercalciuria, marked severity of the clinical features, abnormality of Ca metabolism and its responsiveness to MgO treatment were demonstrable in Mg deficiency.
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PMID:Magnesium deficiency in children with urolithiasis. 100 96

Hyperoxaluria is frequently seen in patients with inflammatory bowel disease, or after resection of the ileum. It is assumed to be responsible for the development of nephrolithiasis, nephrocalcinosis (oxalate nephrosis) and progressive renal impairment in these patients. Steatorrhea may aggravate the severity of hyperoxaluria. A 60-year-old male underwent massive resection of the jejunum and ileum 10 years prior to admission, due to strangulation of the small bowel, with occlusion of the superior mesenteric artery. He remained well except for steatorrhea which developed two-and-a-half years prior to admission, when microhematuria, proteinuria and oxaluria developed progressively. Since that time, the nephrolithiasis, nephrocalcinosis and renal failure have continued to worsen despite therapy with oxalate restriction and oxalate-binding agents. A renal biopsy, performed late in the clinical course, showed severe changes in the renal parenchyma. The decline in renal function proved irreversible. The unusual metabolic consequences of massive resection of the small intestine and their mechanisms are discussed.
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PMID:Hyperoxaluria, nephrolithiasis, nephrocalcinosis and renal failure after massive resection of the small intestine: report of a case. 136 95

Abnormal dietary habits that lead to hypercalciuria, hyperoxaluria, hypereruricosuria, and hypocitraturia do not always result in nephrolithiasis. A concept is emerging according to which, to account for renal stone formation in the face of the aforementioned biochemical disorders, one must search for underlying conditions in patients with the disease. Work carried out over the past few years and reviewed herein definitely supports this idea and includes the following processes: 1) interleukin-1 production by monocytes to augment the impact of dietary hypercalciuria; 2) disturbed activation of pyridoxine to pyridoxal 5'-phosphate to aggravate dietary hyperoxaluria; 3) abnormal intestinal transport of citrate to aggravate dietary hypocitraturia; 4) molecular abnormalities of glycoprotein inhibitors to aggravate the promotive effect of the diet on urinary crystallization; and 5) renal tubular lesions to favor particle retention and stone formation. This article reviews the most recent literature and discusses the author's "powder keg and tinderbox" theory of idiopathic calcium stone disease.
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PMID:Renal stone disease in the 1990s: the powder keg and tinderbox theory. 136 43

A small group of patients with nephrolithiasis who forms mixed (calcium oxalate and uric acid) calculi presents particular problems in their clinical management. In 3,158 stones analyzed in our laboratory, we found 158 mixed calculi in 86 of the patients. In this work, the clinical and biochemical results obtained from 27 patients with mixed stones were compared with those from 27 control patients with calcium oxalate renal lithiasis. A significant difference was found in oxalate and citrate urinary elimination (mean +/- SD) in mixed stone formers versus pure calcium oxalate stone formers: oxaluria (mg/24 h: 38 +/- 15 vs. 28 +/- 12; p less than 0.01) and citraturia (mg/24 h: 214 +/- 139 vs. 437 +/- 303; p less than 0.01). Citraturia was decreased in a high proportion (77%) in mixed stone formers, and only a reduced percentage of them (23%) presented normal values, although in the low limit of normality. As treatment and prophylactic measure, we proposed oral administration of citrates in mixed stone patients because citrate inhibits spontaneous nucleation of calcium salts and crystal growth, and it also increases the urinary pH with a consequent increase in uric acid solubility.
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PMID:Hypocitraturia as a pathogenic risk factor in the mixed (calcium oxalate/uric acid) renal stones. 158 30

To better understand the pathogenesis of nephrolithiasis, we developed a new animal model that closely mimics human calcium oxalate stone disease. Rats were treated with a regimen that combines moderate hyperoxaluria (produced by 10 days of feeding with 3% ammonium oxalate) with mild proximal tubular injury/dysfunction (produced by 8 daily injections of gentamicin sulfate -40 mg./kg.). This combined treatment caused a marked increase in the incidence of calcium oxalate crystals and stones over that seen in animals treated with oxalate or gentamicin alone. Using a semiquantitative scoring system for estimating the abundance of crystals in coronal sections of kidneys, we found that 63% of animals receiving gentamicin plus oxalate showed "moderate" numbers of crystal, as compared to 8% of animals receiving oxalate alone; and the majority of the crystals occurred in the papilla, a pattern similar to that seen in human stone disease. Untreated rats and rats treated with gentamicin alone did not exhibit calcium oxalate crystals or stones. Despite the abundance of crystals and stones, animals receiving gentamicin plus oxalate retained relatively normal renal function as judged by creatinine clearance. Thus, the model has several advantages over preexisting models of nephrolithiasis. Crystal and stone deposition develop rapidly (within 14 days). The pattern of deposition resembles that seen in human stone disease and renal function remains relatively normal. These findings indicate that this model of nephrolithiasis may prove useful for studies of the pathogenesis of stone disease. Moreover, they suggest that renal tubular injury and/or dysfunction may produce conditions conducive to the formation and growth of calcium oxalate stones.
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PMID:A new model of nephrolithiasis involving tubular dysfunction/injury. 194 7

Nephrolithiasis is a heterogeneous disorder, with varying chemical composition and pathophysiologic background. Although kidney stones are generally composed of calcium oxalate or calcium phosphate, they may also consist of uric acid, magnesium-ammonium phosphate, or cystine. Stones develop from a wide variety of metabolic or environmental disturbances, including varying forms of hypercalciuria, hypocitraturia, undue urinary acidity, hyperuricosuria, hyperoxaluria, infection with urease-producing organisms, and cystinuria. The cause of stone formation may be ascertained in most patients using the reliable diagnostic protocols that are available for the identification of these disturbances. Effective medical treatments, capable of correcting underlying derangements, have been formulated. They include sodium cellulose phosphate, thiazide, and orthophosphate for hypercalciuric nephrolithiasis; potassium citrate for hypocitraturic calcium nephrolithiasis; acetohydroxamic acid for infection stones; and D-penicillamine and alpha-mercaptopropionylglycine for cystinuria. Using these treatments, new stone formation can now be prevented in most patients.
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PMID:Etiology and treatment of urolithiasis. 196 46

The active transport of conjugated bile acids by the ileum is responsible for the enterohepatic circulation of bile acids, a physiological process that ensures an ample supply to the intestine of these key biological surfactants, irrespective of the rate of their biosynthesis from cholesterol. The ileal bile acid transport system is a high capacity, low affinity secondary active Na+ co-transport system that differs in substrate specificity from that present in the hepatocyte. Ileal transport is homeostatically regulated by feedback inhibition of the bile acids that are transported. The enterohepatic circulation is responsible for the concentration profile present in the intestine--high concentrations in the small intestine and low concentrations in the large intestine. Loss of ileal absorption, when mild, leads to a sequence of events that result in increased concentrations in the large intestine causing diarrhea. Severe bile acid malabsorption causes decreased concentrations in the small intestine which in turn lead to fat maldigestion and fat malabsorption. The increased passage of fatty acids into the colon contributes to diarrhea. Fat maldigestion and malabsorption also causes increased absorption of dietary oxalate from the colon which causes hyperoxaluria and contributes to nephrolithiasis. In cholestatic liver disease, inappropriate upregulation of ileal bile acid transport is likely to cause retention of hepatotoxic endogenous bile acids. In familial hypercholesterolemia, efficient bile acid absorption contributes to downregulation of LDL receptors and the maintenance of elevated plasma cholesterol levels; upregulation of bile acid transport during bile acid sequestrant therapy could diminish its efficacy. Efforts are in progress to develop a suitable bile acid analogue to be administered orally for conditions of bile acid deficiency in the small intestine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biological and medical aspects of active ileal transport of bile acids. 206 93

The incidence and prevalence of urolithiasis in the Czechoslovak Socialist Republic is as high as in other countries of Central and Western Europe, and lower than in the Scandinavian countries. Apart from its high incidence, urolithiasis is characterized by its high tendency to recurrence. New knowledge of its pathogenesis helps to diagnose metabolic disorders responsible for increased excretion of concretion-producing substances and/or for deficiency in protective factors. In case of calcium oxalate lithiasis, with the highest incidence, attention is to be paid to its various forms of hypercalciuria, and, more recently, to moderate hyperoxaluria, and as regards protective factors, to magnesium, citrates, pyrophosphates and mucopolysaccharides. The determination of the type of metabolical disorder in patients with lithiasis enables to modify the diet and/or medication leading to causal prophylaxis against recurrence, i.e. metaphylaxis. At our Prague urological clinic, a consultation centre for lithiatic patients has been in operation since 1977. Long-term experience has shown that it has been successful especially in preventing recurrence or a in a substantial reduction in recurrence in 94% of the followed-up patients. Although the centre's activity is demanding both on the personnel and laboratory, even first sufferers from ilthiatic attacks should take advantage of it. At this early stage, such patients were found to have a metabolic disorders in 60%. In the past 7 years of treating nephrolithiasis and ureterolithiasis, new methods have been introduced which substantially improve the results and are less invasive than a classical operation. Among others, they comprise percutaneous endoscopic methods of disintegration and concrement extraction from the kidney and ureter, uteroscopy and extracorporeal shock-wave lithotripsy. It is to be expected that these methods will replace classical operations at a rate of 90%.
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PMID:[Urolithiasis. Review of present knowledge of epidemiology, pathogenesis, metaphylaxis and treatment]. 266 71

Despite the frequency and morbidity of nephrolithiasis in autosomal dominant polycystic kidney disease (ADPKD), this association has not been subject to a detailed study. One hundred fifty-one of 751 ADPKD patients seen at the Mayo Clinic between 1976 and 1986 had nephrolithiasis. Seventy-four had passed calculi or had stones surgically removed. Stone analysis was available in 30 patients: uric acid, calcium oxalate, calcium phosphate, and struvite were present in 56.6%, 46.6%, 20%, and 10%, respectively. Calculi were observed in 71 of 79 patients with excretory urograms available for review. Faintly opaque and bull's eye stones, probably containing uric acid, were present in 12.7% and 14.1% of these patients, respectively. Precaliceal tubular ectasia was observed in 15.5%. Ninety-seven patients had preserved renal function (serum creatinine less than 1.5 mg/dL) at the initial evaluation. Six were excluded because they had other known causes of stone disease. The most common metabolic abnormality in the remaining 91 patients was hypocitric aciduria (ten of 15 patients with measurements). The urine pH in the first voided morning specimens (5.66 +/- 0.05) was significantly lower than that of an unselected control population (5.92 +/- 0.03, P less than 0.001). Hyperuricosuria, hyperoxaluria, and hypercalciuria were observed in six of 32 (18.8%), six of 31 (19.4%), and three of 39 (9.7%) patients with preserved renal function. The composition of the stones, the frequency of hypocitric aciduria, and the low urine pH (possibly related to the defect in excretion of ammonia described in ADPKD), suggest that metabolic, along with mechanical, factors are responsible for the frequent occurrence of nephrolithiasis in this disease.
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PMID:The association of nephrolithiasis and autosomal dominant polycystic kidney disease. 335 68


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