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Case analysis of purple urine-bag syndrome at a long-term care service in a community hospital.
BACKGROUND: Purple urine-bag syndrome (PUBS) is a rare phenomenon in which the contents of urine bags turn purple or blue following patient catheterization. The condition often causes care givers tremendous distress. We investigated the prevalence and possible causes of PUBS for a group of elderly patients. METHODS: A total of 157 patients featuring urine catheterization, 13 of whom exhibiting PUBS were analyzed with regards to age, functional status, duration of catheterization, number of daily medications, living location, feeding route, bowel habits, and the pattern of use of a urinary catheter. Urine samples were cultured from all the PUBS patients participating. RESULTS: Two men who underwent cystostomy and 11 women who underwent urethral catheterization who exhibited PUBS were observed for this study. The age, duration of catheterization, number of daily medications feeding pattern and functional status between the group exhibiting PUBS and the group of patients without PUBS demonstrated no significant differences. A total of 69.2% of the PUBS-affected patients, as compared to 43.1% of the non-PUBS patients, lived in nursing homes, and 84.6% of the PUBS-affected patients were constipated, as were 66% of the non-PUBD subjects. In total, 72.7% of PUBS patients were reported to be using a laxative suppository, compared with 41% of the non-PUBS group, whereas 92.3% of PUBS patients were catheterized using a plastic (PVC) foley, as compared to 70.8% of the non-PUBS patients. The pH for 12 out of 13 PUBS patients' urine was > or = 7. Escherichia coli, Provendicia var. spp., Proteus mirabilis, Klebsiella pneumoniae were the common pathogens isolated from the urine samples provided by our PUBS patients. CONCLUSION: We found that PUBS was more likely associated with the female gender, alkaline urine, constipation, institutionalization, the use of a plastic (PVC) urinary catheter, and certain bacteria such as Provendicia var. spp., Escherichia coli, Proteus mirabilis, and Klebsiella pneumoniae.
[Effect of oral sorbent, AST-120, on serum concentration of indoxyl sulfate in uremic rats].
Indoxyl sulfate is a metabolite of tryptophan. Indole is synthesized in intestine from tryptophan by intestinal bacteria. The absorbed indole is converted to indoxyl sulfate through indoxyl in liver. Serum concentration of indoxyl sulfate is markedly increased as an inhibitor of drug-binding in uremic patients as compared with healthy subjects. Since indoxyl sulfate is bound to serum albumin, it cannot be removed efficiently by hemodialysis, and it tends to accumulate in uremic serum. To determine if oral sorbent, AST-120, could adsorb indole in intestine and then decrease serum concentration of indoxyl sulfate, it was administered to nephrectomized uremic rats. Serum concentration of indoxyl sulfate was markedly decreased in uremic rats fed with oral sorbent as compared with control uremic rats. However, serum concentrations of creatinine and urea nitrogen were not significantly decreased in the uremic rats fed with oral sorbent as compared with the control uremic rats. Serum concentration of tryptophan was not decreased but rather increased in the uremic rats fed with oral sorbent as compared with the control uremic rats. Concentration of indoxyl sulfate in bile of a uremic rat was much lower than that in the uremic serum, suggesting that the adsorption of indoxyl sulfate in intestine is not a major mechanism of decreasing the serum concentration of indoxyl sulfate. These results demonstrate that oral sorbent, AST-120, can decrease serum concentration of indoxyl sulfate in uremia due to adsorption of indole in intestine.
[Pernicious anemia with indicanuria].
A 67-year-old female was diagnosed as having classical pernicious anemia. Laboratory data included low serum vitamin B12 concentrations, abnormal deoxyuridine suppression test, methylmalonic aciduria, atrophic gastritis, positive anti-intrinsic factor antibody and Schilling test results typical of pernicious anemia. During hospitalization it was incidentally noted that her urine was green colored. Jaffe' reaction and Obermayer reaction for indicanuria were both positive. Dark purple crystalline material was obtained by centrifugation of her urine. The crystalline substance was soluble in methanol and its absorbance curve was identical to that of authentic indoxylsulphate potassium salt. Daily output of this substance was nearly 50 times normal. There was no increase in urinary excretion of monoamino-monocarboxyl amino acides. The exact reason for her indicanuria was not clear, although abnormal bacterial growth in the intestine remained as a possibility.
[Study on the uremic protein binding inhibitors as uremic toxin: toxic effect on erythroid colony formation, lymphocyte blast formation and renal function].
Certain uremic metabolites are recognized to have high affinity to serum protein and some of them have been identified as hippuric acid (HA), quinolinic acid (QA) and indoxyl sulfate (IS). Cell toxicity and effect on renal function of these substances were examined by means of erythroid colony formation, lymphocyte blast formation and isolated perfused rat kidney. These substances inhibited the binding of diphenylhydantoin to albumin, depending on the concentration of the substances. At the same concentration of 10 mg/dl, IS was most potent and QA was the second. QA and IS suppressed the erythroid colony formation, depending on the concentration of QA and IS. On the other hand, HA had no suppressive effect even at the higher concentration. The suppressive effect of QA and IS were attenuated by increasing erythropoietin concentration. QA and IS had strong suppressive effect of lymphocyte blast formation and interleukin 2 production at the concentration of uremic serum. However, they did not suppress the increase of intracellular calcium concentration of lymphocytes after stimulation by mitogen. This might indicate the possibility that these substances act not only on cell surface but on intracellular protein. HA and IS inhibited para-aminohippurate secretion and QA suppressed tubular reabsorption of sodium in isolated perfused rat kidney. These results show that the uremic protein binding inhibitors may influence renal regulation of fluid and electrolyte homeostasis. It is concluded that some of the protein binding inhibitors have toxic effects on cell function of various tissues and play a role in pathophysiology of uremia.
Determination of indoxyl sulfate in plasma of patients with renal failure by use of ion-pairing liquid chromatography.
Using our newly developed ion-pairing reversed-phase liquid-chromatographic method for assay of indoxyl sulfate, we measured its concentration in plasma of normal subjects and patients in various degrees of renal failure. Response was linear over the range of 50 to 25 000 pmol of indoxyl sulfate injected into the chromatograph. We demonstrated the specificity of the assay for azotemic plasma by using enzymatic conversion with a sulfatase. For a moderately above-normal indoxyl sulfate concentration in azotemic plasma of 134 mumol/L (29 mg/L), the within-day CV was 1.6%, the day-to-day CV 2.8%. Mean analytical recovery was 101.0% (CV = 2.8%). Over a range of 29 to 192 mg of creatinine per liter of plasma (x), indoxyl sulfate (y) concentration (in mumol/L) was positively correlated (y = 1.30x + 0.43). This method should prove valuable for further study of uremic toxins.
[Does Giardia lamblia favor the proliferation of intestinal bacteria?].
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Accumulation of indoxyl sulfate, an inhibitor of drug-binding, in uremic serum as demonstrated by internal-surface reversed-phase liquid chromatography.
We quantified indoxyl sulfate in uremic serum by using internal-surface reversed-phase high-performance liquid chromatography. Its concentrations were markedly increased in chronic hemodialysis patients, and were significantly but weakly correlated with the concentrations of creatinine and beta 2-microglobulin in these patients' serum, and with the duration of their hemodialysis treatment. Indoxyl sulfate could not be removed effectively by conventional hemodialysis because of its strong binding to serum albumin. Equilibrium dialysis demonstrated that indoxyl sulfate inhibited the binding of salicylate to albumin, and that 3-carboxy-4-methyl-5-propyl-2-furanpropionic acid inhibited the binding of indoxyl sulfate to albumin. In conclusion, indoxyl sulfate was markedly accumulated in uremic serum, and inhibited drug binding.
[New aspects of the pathogenesis and therapy of alcoholic delirium (author's transl)].
Clinically, and especially biochemically, alcoholic delirium corresponds closely to an incipient but reversible exogenous hepatic coma. The blood levels of ammonia in particular, free phenols and lactate are greatly increased. These same metabolites increase slightly in the blood of persons with healthy livers after a single alcohol loading. The treatment of alcoholic delirium consists of optimal sedation with Distraneurin, which appears to have no side effects on the liver. There is even a lowering of the raised lactate level in the blood after a single administration of Distraneurin. Ammonia and phenols are reduced by ammonia-lowering aminoacids, lactulose and bifidum milk. Most important, however, is strict abstention from alcohol, which alone brings about a rapid improvement of pathological biochemical and morphological liver findings.
Some biochemical aspects of clinical Johne's disease in cattle.
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Determination of urinary constituents in solutions by least-squares resolution of ultraviolet spectrums.
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[New biochemical findings in mongolism].
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The effect of hormones and vitamin B6 on urinary excretion of metabolites of the kynurenine pathway.
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[Indicanuria in liver cirrhosis].
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[Diagnosis of the stagnant loop syndrome].
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[Letter: Urinary diagnostics in precancerous conditions?].
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