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Biomedical subjects

O M Wrong

Publications and source records attributed to O M Wrong.

At least 19 recordsLinked to original sources
PubMed1994

Dent's disease; a familial proximal renal tubular syndrome with low-molecular-weight proteinuria, hypercalciuria, nephrocalcinosis, metabolic bone disease, progressive renal failure and a marked male predominance.

We describe a familial form of renal Fanconi syndrome characterized by hypercalciuria, low-molecular-weight proteinuria, nephrocalcinosis and slowly progressive renal failure. Males are much more severely affected than females. The patients studied included 15 males and 10 females, and five families with up to three generations involved. Studies of the two largest families described here have already shown that their disease is inherited on the X-chromosome. The series contains the two unrelated patients originally described by Dent and Friedman in 1964 as 'hypercalcuric rickets'.

Adolescent↗
PubMed1993

Immune-related potassium-losing interstitial nephritis: a comparison with distal renal tubular acidosis.

Six patients with immune-related potassium-losing interstitial nephritis (IRPLIN) are described, and compared with 34 patients with immune-related distal renal tubular acidosis (IRdRTA) and 24 with familial distal renal tubular acidosis (FdRTA). Close similarities were found between IRPLIN and IRdRTA. In our experience, both syndromes are confined to postpubertal women, and are characterized by systemic features of autoimmune disease and a chronic interstitial nephritis which is probably immune-mediated and responsible for the functional tubular defects of the two syndromes. In IRPLIN, a renal potassium-losing state is the main consequence (probably mediated at least in part by renin and aldosterone hypersecretion secondary to renal sodium-losing), and urinary acidification is normal or minimally disturbed; consequently there is no systemic acidosis, and the syndrome is not complicated by nephrocalcinosis or renal bone disease. In IRdRTA, the renal tubular lesion also usually causes potassium depletion, but the most prominent tubular fault is a defect in urinary acidification, which commonly causes metabolic acidosis and often leads to nephrocalcinosis and bone disease. Familial dRTA, in contrast, is equally prevalent in the two sexes and presents at an earlier age than IRPLIN and IRdRTA. Patients with FdRTA and IRdRTA have a similar urinary acidification defect and propensity to acidosis, nephrocalcinosis and bone disease. FdRTA is frequently complicated by renal potassium-losing, but hypokalaemia is less common and less profound than in IRdRTA and IRPLIN, suggesting that immune-related interstitial nephritis has a particular tendency to cause renal potassium-losing.

Acidosis, Renal Tubular↗
PubMed1990

The effect of lactulose, pectin, arabinogalactan and cellulose on the production of organic acids and metabolism of ammonia by intestinal bacteria in a faecal incubation system.

An in vitro faecal incubation system was used to study the metabolism of complex carbohydrates by intestinal bacteria. Homogenates of human faeces were incubated anaerobically with added lactulose, pectin, the hemicellulose arabinogalactan, and cellulose, both before and after subjects had been pre-fed each carbohydrate. Fermentation of added substrate was assessed by the production of short-chain fatty acids (SCFA) and suppression of net ammonia generation over 48 h of incubation. Control faecal homogenates to which carbohydrate was not added yielded an average increment of SCFA of 43 mmol/l, equivalent to 172 mmol/kg in the original stool. The addition of lactulose, pectin and arabinogalactan each increased the yield of SCFA by a similar amount, averaging 6.5 mmol/g carbohydrate or 1.05 mol/mol hexose equivalent; organic acid yield was not increased by pre-feeding these substances for up to 2 weeks. Acetate was the major SCFA in all samples at all times and, after pre-feeding with extra carbohydrate, butyrate concentrations exceeded propionate in all samples. Faecal homogenates incubated with cellulose showed no greater SCFA production than controls over the first 48 h, but there was a slight increase when samples from two subjects pre-fed cellulose were incubated for 14 d. Net ammonia generation was markedly suppressed by addition of lactulose to faecal incubates with an initial period of net bacterial uptake of ammonia. Pectin and arabinogalactan also decreased ammonia generation, but the reductions were not significant unless subjects were pre-fed these materials; cellulose had no effect on ammonia generation.

Adult↗
PubMed1986

Comparison of 2-mercaptopropionylglycine and D-penicillamine in the treatment of cystinuria.

We have compared 2-mercaptopropionylglycine (MPG) with D-penicillamine in its capacity to reduce the urinary excretion of cystine by patients with cystinuria. Satisfactory ion-exchange chromatographic methods for the measurement of urinary MPG, D-penicillamine, cystine and the cysteine-disulfides of the two drugs have been developed, and we have established the time course of the excretion of these substances after oral intake of each drug. MPG was found to be approximately one and a half times as effective as D-penicillamine, both in reducing urinary excretion of free cystine and in the amounts of mixed disulfide which appeared in the urine.

Adult↗
PubMed1985

The contribution of endogenous urea to faecal ammonia in man, determined by 15N labelling of plasma urea.

To establish the role of endogenous urea as a source of faecal ammonia, the plasma urea of two healthy men was labelled with 15N at a constant level for several days and its 15N enrichment was compared with that of faecal ammonia and total nitrogen. Faeces collected after one complete gastrointestinal transit from the onset of plasma labelling had ammonia 15N enrichments which were only 8.5 +/- 1.2% and total nitrogen enrichments which were 6.8 +/- 0.7% of the plasma urea 15N enrichment. These results show that endogenous urea is not the main precursor of faecal ammonia, which is probably derived by bacterial deamination from the protein of dietary residues, intestinal secretions and shed epithelial cells. The minor contribution of endogenous urea to faecal ammonia suggests that the lumen of the large bowel is not the main site of endogenous urea hydrolysis. The similar labelling of faecal total nitrogen and ammonia nitrogen supports other evidence that these faecal nitrogen fractions are in a constant state of exchange.

Adult↗
PubMed1984

Domestic metallic mercury poisoning.

In a family exposed to metallic mercury vapour two patients had acrodynia, one had the nephrotic syndrome, and one person remained well. Recognition of the variable manifestations of the disease and prevention of further exposure were the most important aspects of management. Recovery appeared to be complete as blood mercury levels fell to normal. Urinary mercury levels were too variable to be reliable as indications of progress.

Accidents, Home↗
PubMed1984

Treatment of chronic renal failure with dietary fiber.

We have tested the hypothesis that dietary fiber, by inhibiting colonic bacterial ammonia generation and increasing fecal nitrogen excretion, might decrease hepatic urea synthesis and thereby reduce plasma urea in patients with chronic renal failure. Six and 8 week courses of two different hemicelluloses, arabinogalactan and ispaghula, reduced mean plasma urea in uremic subjects by 11% and 19% respectively. Ispaghula also reduced the rate of rise of plasma creatinine to zero and, in one formal balance study, increased fecal nitrogen excretion by 39%. Experiments in vitro showed that ispaghula depressed anaerobic fecal bacterial net ammonia generation by 30%, and adsorbed neither urea nor ammonia. The reduction in plasma urea caused by dietary fiber is likely to be due to inhibition of colonic bacterial production of ammonia; such therapy could conceivably alleviate some of the symptoms of uremia and postpone dialysis in patients with endstage renal disease.

Adolescent↗