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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of the kidney in states of hyperoxaluria and hypercalciuria was investigated in seven patients with hyperoxaluria after jejunoileal bypass (JIB) and six patients with idiopathic hypercalciuria (IHC). Eight apparently healthy persons formed a control group. Besides hyperoxaluria, the patients with JIB displayed an elevated plasma concentration of oxalate and the oxalate clearance was increased and higher than creatinine clearance, indicating a net tubular secretion of oxalate. The JIB patients had lower 24-h urinary excretions of calcium, phosphate, magnesium and citrate and higher serum parathyroid hormone (PTH) than controls, indicating increased secretion of PTH to compensate for calcium malabsorption. IHC patients exhibited increased fasting urinary calcium even though their serum values were similar to those in the controls. These results indicate a reduced tubular calcium reabsorption, which was most pronounced in patients with highest PTH values. We conclude that hyperoxaluria in JIB patients is associated both with intestinal hyperabsorption and with enhanced tubular secretion of oxalate, and that in some patients with IHC hypercalciuria is due to reduced tubular reabsorption of calcium.
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PMID:Hyperoxaluria or hypercalciuria in nephrolithiasis: the importance of renal tubular functions. 212 87

Enteric hyperoxaluria due to malabsorption syndromes has been well documented to cause renal calculi and chronic tubulointerstitial renal damage. Rarely, in the setting of intestinal bypass operations for morbid obesity, enteric hyperoxaluria has produced acute renal failure. We report two patients who suffered acute deterioration of renal function associated with increased intestinal absorption and renal excretion of oxalate associated with steatorrhea. One patient had a large portion of his small bowel resected many years prior to the onset of the renal failure and the second patient had chronic pancreatitis causing steatorrhea. Both patients had renal biopsy documentation of the acute nature of the tubular damage produced by oxalate deposition. The mechanisms of their deterioration of renal function may relate to sudden increases in steatorrhea in association with episodes of volume depletion. Enteric hyperoxaluria may be an easily overlooked and potentially preventable etiology of acute renal dysfunction.
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PMID:Acute deterioration of renal function associated with enteric hyperoxaluria. 222 62

We have evaluated the urinary excretion of promoting (calcium, phosphorus, uric acid, oxalate) and inhibiting (citrate, magnesium, glycosaminoglycans) factors of crystallization in subjects with idiopathic hypercalciuria and calcium urolithiasis and in a control group. The examined children had a free diet and were drug free for the last 2 weeks. They were not affected by malabsorption, D-RTA, urinary tract infection, or urinary tract malformation (factors interfering with urinary excretion of citrate and oxalate). In the patients with calcium urolithiasis, the daily urinary excretion of oxalate was significantly higher (p less than 0.01), and the urinary excretion of citrate was significantly lower (p less than 0.001) than in the subjects with idiopathic hypercalciuria and in the control group. Among the subjects with idiopathic hypercalciuria, those aged 4-9 years had a significantly reduced, though in the normal range, urinary excretion of citrate as compared with those aged 10-15 years (362 +/- 189 and 503 +/- 198 mg/g creatinine/24 h, respectively; p less than 0.01). Our data show that hypocitruria may play an important role in the pathogenesis of urolithiasis in children with idiopathic hypercalciuria. In these cases, the urinary citrate excretion was not inversely related to age, as has been suggested by other authors.
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PMID:Promoters and inhibitors of calcium urolithiasis in children. 225 56

Jejunoileal bypass (JIB) has been widely performed for treatment of excessive obesity. Formation of calcium oxalate stones is a common side effect. Since, under physiological conditions, the intestinal absorption of calcium and that of oxalate are interrelated, intestinal oxalate and calcium absorption were measured in the present study by isotope techniques in 19 JIB patients and 20 healthy controls. The JIB patients showed pronounced hyperoxaluria and markedly increased absorption of oxalate, with a urinary excretion of 14C-oxalate of 29 +/- 19% (controls 6.2 +/- 3.7%; p less than 0.001). There was a strong correlation between the intestinal absorption and urinary excretion of oxalate in the JIB patients (r = 0.72; p less than 0.001). Furthermore, their oxalate kinetics was altered, with continued urinary excretion of 14C-oxalate for up to 48 hours. The JIB patients also had reduced calcium absorption (36 +/- 9.1% vs. 47 +/- 9.0%; p less than 0.001) and patients with malabsorption of calcium and low urinary calcium had the highest intestinal absorption and urinary excretion of oxalate. It is concluded that hyperoxaluria in JIB patients is due to a significant extent to hyperabsorption of oxalate.
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PMID:Intestinal absorption of oxalate and calcium in patients with jejunoileal bypass. 259 24

Urinary oxalate concentrations were measured in 45 patients with quiescent Crohn's disease, four patients with chronic pancreatitis and five healthy subjects after a normal oxalate (150 g/day) diet, after a high-fat (150 g/day), normal oxalate diet and after and after a high-oxalate (500 mg/day) diet. Urinary oxalate concentrations were significantly (P less than 0.05) higher in patients with Crohn's disease and steatorrhoea, but not in those with chronic pancreatitis, after administrating a high-oxalate diet compared with healthy subjects. Mean oxalate values were 19.1 mg/24 h in controls compared with 65.8 mg/24 h in Crohn's disease patients. A direct correlation (r = 0.37, P less than 0.01) was established between faecal rats and urinary oxalate after oval oxalate load: this correlation (r = 0.43, P less than 0.01) is closer when only patients with Crohn's disease are considered. The study, therefore, confirmed a correlation between steatorrhoea and hyperoxaluria in patients with Crohn's disease; however, the high percentage of false positive results limits the use of urinary oxalate concentrations as a reliable indicator of lipid malabsorption. It is concluded that, at present, measurement of urinary oxalate cannot be recommended as a valid alternative to the Van de Kamer method for diagnosing lipid malabsorption.
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PMID:Urinary oxalate recovery after oral oxalic load: an alternative method to the quantitative determination of stool fat for the diagnosis of lipid malabsorption. 262 29

A 54 years old white woman and a 38 years old white man with short-bowel disease are reported. Both of them were submitted to surgical procedures for urinary oxalate calculi. They presented malabsorption syndrome with steatorrhea and severe malnutrition. The patients received parenteral nutrition. The woman had also cholelithiasis and acute pancreatitis. The clinical and laboratory data are presented and the pathophysiology of short-bowel disease with emphasis on bile salts depletion, the effect of bile salts on colon oxalate absorption, and intestinal loss of water is commented. The management of short-bowel disease and the use of cholesteramine and the supplementary diet is discussed.
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PMID:[Physiopathology of the short bowel: apropos of 2 cases]. 263 97

Hyperoxaluria and hypercalciuria are common features of renal calcium stone disease. The purpose of the present investigation was to examine the relationships between the intestinal absorption and the renal handling of oxalate and calcium in patients with idiopathic renal stone disease and in patients with enteric hyperoxaluria following jejunoileal bypass (JIB), in comparison with healthy controls. Hyperoxaluria was associated with a higher frequency of both stone episodes and stone operations than a lower urinary oxalate concentration. Patients with idiopathic stone disease showed increased intestinal uptake of both oxalate and calcium, which was probably of importance for their propensity to form calcium oxalate-containing stones. Hyperoxaluria in patients with JIB was found to be a result of hyperabsorption of oxalate, and these patients displayed altered oxalate kinetics with continued urinary excretion of orally administered 14C-oxalate for more than 48 hours. The prolonged excretion is assumed to be due to a prolonged absorption and/or an increased oxalate pool. Malabsorption of calcium and low fasting urinary calcium excretion in the JIB patients were associated with high tubular reabsorption of calcium, the latter presumably attributable to a compensatory increase in circulating parathyroid hormone (PTH). In most recurrent renal stone formers the urinary calcium concentration was increased, with an inverse relationship to serum PTH, indicating intestinal hyperabsorption of calcium. A subgroup of hypercalciuric patients showed increased urinary calcium due to reduced tubular reabsorption of calcium. It is suggested that this is a renal defect resulting in a compensatory rise in PTH. Two different mechanisms of similar prevalence might explain enhanced secretion of PTH in normocalcaemic stone disease, namely reduced calcium absorption and a renal defect in the form of reduced tubular reabsorption of calcium. Glycosaminoglycans efficiently inhibit calcium oxalate crystal growth by binding to the surface of calcium oxalate crystals. In this study the binding was dependent on ionic strength. Higher affinity to the crystals may be the reason why highly charged glycosaminoglycans were more efficient inhibitors of calcium oxalate crystal growth. A calcium-containing organic marine hydrocolloid with the capacity to bind oxalate in vitro was shown to reduce enteric hyperoxaluria. In addition to biochemical effects considerable improvements in diarrhoeal symptoms were reported.
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PMID:Oxalate metabolism in renal stone disease with special reference to calcium metabolism and intestinal absorption. 266 21

The formation of a neobladder by the transformation of sections of the terminal ileum has become an important alternative to supravesical urinary diversion. The discussion about the optimal urosurgical technique however has, so far ignored the problems of consecutive enteric defunctionalization and deficiency symptoms resulting from the anatomical shortening of the ileum. The analysis of experimental investigations and functionally comparable syndromes, such as Crohn's disease, permits an insight into the pathophysiological consequences. These relate to disorders in the bile acid and vitamin B12 metabolism and to the potential induction of a secondary hyperoxaluria, with a subsequent oxalate calculus diathesis. Further more, the reduction of the absorption area in the ileum can lead to calcium and vitamin D malabsorption with the development of intestinal osteopathy. These pathophysiological relationships must be taken into account in the long-term medical care of patients with ileal neobladder. The preventive and therapeutic measures are described.
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PMID:[Ileocystoplasty and enteropathies]. 276 94

Studies in 24 recurrent oxalate stone-formers have shown that values for urinary calcium excretion for this group on at-home diets vary significantly (P less than 0.001) more than values for creatinine excretions. By placing stone-formers on controlled in-hospital diets and measuring their calcium excretions, we were able to predict probable outpatient hypercalciuria (greater than 7.5 mmol/day) with a sensitivity of 95% and a specificity of 95%. In this study, the renal loss of calcium during low-calcium diets was proportional to the absorptive hypercalciuria during high-calcium diets. Calcium loading experiments in fasted stone-formers and normal subjects indicated that citrate, at citrate:calcium molar ratios ranging from 0.12 to 1, stimulated urinary calcium excretion more than did calcium carbonate loading alone. In addition, citrate also significantly (P less than 0.05) increased the excretion of urinary oxalate by two normal subjects for a given load of calcium oxalate. Malabsorption of citrate and possibly other hydroxycarboxylic acids may thus predispose to oxalate nephrolithiasis by promoting calcium and oxalate absorption.
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PMID:Effect of citrate on the urinary excretion of calcium and oxalate: relevance to calcium oxalate nephrolithiasis. 291 May 76

Common variable hypogammaglobulinemia (immunodeficiency), a disorder characterized by late-onset immunoglobulin deficiency and lack of humoral immunity, has a variable association with bronchiectasis, cholelithiasis, nodular lymphoid hyperplasia, gastrointestinal neoplasia, megaloblastic anemia, and malabsorption. The patient described in this report had all of the above except neoplasia. In addition, he had calcium oxalate renal stones probably secondary to his malabsorption. The first case demonstrating the beneficial effect of home hyperalimentation in patients with severe malabsorption refractory to other treatments is described. Home hyperalimentation overnight allows the patient freedom for daily activities while also being more cost-effective than in-hospital parenteral nutrition.
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PMID:Home hyperalimentation for common variable hypogammaglobulinemia with malabsorption secondary to intestinal nodular lymphoid hyperplasia. 311 40


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