Biomedical subjects

D Teta

Publications and source records attributed to D Teta.

7 recordsLinked to original sources

PubMed2006

[Chronic renal failure: what diet?].

A low protein diet has been traditionally advocated in patients with chronic renal failure (CRF), in order to slow its progression. However, CRF is often associated with malnutrition, aggravating its prognosis, especially in elderly patients. In severe CRF, the spontaneous reduction of appetite coupled with additional restrictions regarding sodium, potassium and phophates may further impact on nutrition status. The potential benefit of a low protein diet is therefore questionable. We only recommend a moderately restricted protein diet (0,8 g/kg/day) in selected patients with no sign of malnutrition. This strategy, if applied, must be supported by a multidisciplinary approach involving a nephrologist and a specialised dietician. Additional dietary restrictions are not justified, except in particular situations.

Diet, Protein-Restricted↗

PubMed2006

[Malnutrition on dialysis: the end of a fatality].

Protein-energy malnutrition in patients treated with haemodialysis (HD) is a complex, multifactorial and prevalent problem, starting well ahead of the dialysis program. It is associated with an increased morbidity and mortality. Uraemic patients are relatively resistant to nutrients because of metabolism abnormalities. Prevention of malnutrition is therefore more efficient than treatment per se. Classical supplementation including oral nutritional supplements, intradialytic parenteral nutrition and enteral nutrition remain efficient, if applied for a sufficient time. A global approach coupling supplementation and strategies designed to optimise metabolism abnormalities should increase treatment efficacy and improve the outcome and quality of life of these patients.

Humans↗

PubMed2006

[Obesity: what impact on renal function?].

The increasing prevalence of obesity is a major public health concern, affecting more than one third of the Swiss population. The renal effects of obesity per se, independent of hypertenison or diabetes, though, are less known. Obesity is positively correlated with proteinuria and the development of glomerulomegaly and focal segmental glomerulosclerosis. The pathophysiology of the obesity-associated kidney disease is complex, including hemodynamic and physical factors and increased synthesis of vasoactive and fibrogenic substances by adipose tissue. The most important therapeutic approach is weight reduction. Angiotension converting enzyme (ACE) inhibition is effective in reducing proteinuria, but longer follow-up is required to determine the long term benfits of ACE inhibition.

Humans↗

PubMed2003

A young man with a renal colic.

We report the case of a 35-year-old man with no cardiovascular morbidity, presenting with acute flank pain, microscopic haematuria and normal blood pressure. Initially diagnosed as a ureteral colic, the patient was recovered 6 weeks later with severe hypertensive crisis. Further investigations revealed a massive renal infarction secondary to medial fibromuscular dysplasia (FMD). Several aspects of this presentation are intriguing. Renal infarcts are usually seen in older patients having cardiac problems and/or major atheromatous plaques. In addition, FMD is mainly observed in young females and rarely progresses to renal artery occlusion. Furthermore, in this case, FMD remained silent until the acute renal infarction occurred, despite a significant kidney size reduction at the time of diagnosis. Finally, the observation of a delayed hypertensive response to a major renovascular insult provides incentives to discuss possible pathophysiological mechanisms involved in renovascular hypertension.

Adult↗

PubMed1999

Effects of acidosis on leptin secretion from 3T3-L1 adipocytes and on serum leptin in the uraemic rat.

Marked hyperleptinaemia and metabolic acidosis are common findings in patients with chronic renal failure. In animal models, both leptin administration and acidosis reduce food intake. However, leptin causes loss of body fat, while acidosis induces muscle wasting. Whether a low pH and leptin production are related has not been studied. Leptin secretion was measured in cultured 3T3-L1 adipocytes exposed to acid or control pH for up to 96 h. In addition, serum leptin was compared between acidotic and bicarbonate-treated uraemic Wistar rats using the remnant model. Leptin levels in the culture medium were decreased at an acid pH of 7.1 compared with a control pH of 7.5 at 96 h (562+/-78 and 831+/-103 pg.48 h(-1). well(-1) respectively; mean+/-S.E.M.; P=0.037). Similarly, serum leptin in uraemic rats was found to be lower in the acidotic group than in the bicarbonate-treated group, although this observation fell just short of statistical significance (1273+/-171 compared with 2059+/-376 pg/ml; P=0.07). In conclusion, acidosis decreases leptin secretion from cultured adipocytes. Accordingly, acidotic uraemic rats seem to exhibit lower serum leptin levels than their bicarbonate-supplemented counterparts. This study is the first report providing a link between acidosis and leptin levels.

3T3 Cells↗

PubMed1991

[Focal cerebral necrosis caused by intraventricular chemotherapy with methotrexate].

A 60 year old white woman progressively developed radicular pain and weakness in both legs. A meningeal carcinomatosis was diagnosed, and an intrathecal chemotherapy with methotrexate (M.T.X.) was begun. A catheter was placed in the frontal horn of the right lateral ventricle. One month later, the patient progressively developed inattentiveness and confusion. The examination showed an abulic-hypokinetic syndrome, and a left hemiparesis. A C.T. scan showed a hypodensity in the frontal-lobe white matter on the right, with contrast enhancement surrounding the region of the catheter. Results of cytologic, bacterial and fungal studies of cerebrospinal fluid were negative. The catheter was removed. The patient was treated with prednisone and she improved. This complication is very rare, and is noticed in only 0.6% of patients who had intraventricular M.T.X. therapy. The cause of this syndrome is a displacement of the catheter into parenchyma. This syndrome is distinct from the other complications (meningoencephalitis, leukoencephalopathy, myelopathy).

Brain↗

PubMed1990

[Reversible ophthalmoplegia, cerebellar syndrome and vigilance disorders following phenytoin poisoning].

A 20-year-old man developed marked ophthalmoplegia and cerebellar symptoms after suicidal intoxication with phenytoin (maximal plasmatic level 73.6 mg/l). Symptoms of toxicity completely resolved with supportive care and with activated charcoal. The clinical picture of acute phenytoin intoxication is reviewed. The most common disorders are ataxia, nystagmus and mental status changes, but ophthalmoplegia is rare.

Adult↗