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Featured researches published by T. Drüeke.


The Lancet | 1980

EFFECT OF PARATHYROIDECTOMY ON LEFT-VENTRICULAR FUNCTION IN HÆMODIALYSIS PATIENTS

T. Drüeke; J. Fleury; Y. Toure; P. De Vernejoul; M. Fauchet; P. Lesourd; C. Le Pailleur; Jean Crosnier

The effect of parathyroidectomy on left-ventricular function was evaluated in chronic-haemodialysis patients with advanced hyperparathyroidism. Radionuclide angiocardiography (22 patients) and ultrasound echography (8 patients) revealed a significant increase in left-ventricular ejection fraction 1--2 weeks after parathyroidectomy. This improvement was associated with an augmented cardiac index (radionuclide method) and with an increase in mean velocity of circumferential myocardial fibre shortening (echocardiography). Circulating blood volume and erythrocyte space, as well as arterial blood-pressure, had changed little after parathyroidectomy, whereas plasma calcium, phosphate, and immunoreactive parathyroid hormone were significantly lower after surgery. Thus, correction of severe hyperparathyroidism led to a significant improvement in cardiac performance.


BMJ | 1977

Congestive cardiomyopathy in uraemic patients on long term haemodialysis.

T. Drüeke; C. Le Pailleur; B Meilhac; C Koutoudis; Johanna Zingraff; J. Di Matteo; Jean Crosnier

Five uraemic patients who developed progressive cardiac failure with clinical evidence of congestive cardiomyopathy at the start or during haemodialysis treatment were studied. The diagnosis of cardiomyopathy, for which there was no apparent cause, was confirmed by angiocardiographic and haemodynamic studies. These showed a significant increase in left ventricular end-diastolic volume over normal values obtained in 12 patients without uraemia. The mean velocity of myocardial fibre shortening was significantly decreased, as was the index of normalised rigidity. Three of the five patients presented the complete picture of the disease. The other two also had considerable ventricular dilatation and a decreased index of normalised rigidity but normal ejection fraction and only moderately decreased myocardial contractility indices. This suggests that there may be primary involvement of normalised heart muscle rigidity followed by secondary changes in myocardial contractility in uraemic patients with congestive cardiomyopathy.


Nephron | 1981

Left Ventricular Function in Hemodialyzed Patients with Cardiomegaly

T. Drüeke; C. Le Pailleur; M. Sigal-Saglier; Johanna Zingraff; Jean Crosnier; J. Di Matteo

Left ventricular function was investigated in 21 chronic hemodialysis patients with cardiomegaly not due to major pericardial effusion. Angiographic and hemodynamic studies were performed in all, and


Nephron | 1987

Effect of Calcitriol in the Control of Plasma Calcium after Parathyroidectomy

F. Clair; L. Leenhardt; Agnès Bourdeau; Johanna Zingraff; D. Robert; C. Dubost; E.F. Sachs; T. Drüeke

Severe, prolonged hypocalcemia in observed in some, but not all, hemodialysis patients after parathyroidectomy performed because of uncontrolled hyperparathyroidism. The aim of the present study was to investigate whether calcitriol and calcium supplementation in the immediate period after parathyroidectomy (days 1-14) was of more help in the control of plasma calcium than calcium supplementation alone. Fourteen hemodialysis patients were enrolled in a prospective, randomized, double-blind and placebo-controlled study. From the day after parathyroidectomy, 7 patients received calcitriol and the remaining 7 a placebo using incremental doses adjusted to the degree of hypocalcemia (up to 4 micrograms/day for calcitriol). Plasma calcium, phosphorus, alkaline phosphatase and immunoreactive parathyroid hormone levels before parathyroidectomy were comparable in both patients groups, as was the lowest plasma calcium achieved after parathyroidectomy. The decrease in plasma calcium after parathyroidectomy was related to plasma alkaline phosphatase and to the number of osteoclasts and osteoblasts on bone biopsy surface before parathyroidectomy. The mean decrement of plasma calcium (days 3-9) as compared to that before parathyroidectomy was less pronounced in calcitriol-treated than in placebo-treated patients (0.25 +/- 0.06 versus 0.45 +/- 0.05 mM, mean +/- SEM, p less than 0.025). Treatment with placebo was interrupted before day 14 because of persistent severe hypocalcemia in 4 of 7 patients, whereas calcitriol treatment was continued in all 7 patients up to 14 days. Patients on calcitriol treatment required less mean calcium supplements (days 1-9) than patients receiving placebo (37.4 +/- 3.2 versus 49.4 +/- 3.7 g, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)


Nephron | 1989

Dialysis-Related Amyloidosis in the Sternoclavicular Joint

Johanna Zingraff; T. Drüeke; T. Bardin

Dr. J. Zingraff, INSERM Unité 90, Hôpital Necker, 161, rue de Sèvres, F-75743 Paris Cedex 15 (France) Dear Sir, In a recent letter to the Editor of this journal, Sethi et al. [1] report 2 cases of ß2-microglobulin (ß2-M) amyloidosis of the sternoclavicular joint (SCJ) in hemodialysis patients, presenting as acute osteoarthritis. No evidence of bacterial infection could be demonstrated histologi-cally, but unfortunately it appears that the biopsy material has not been cultured. The authors also claim that, to the best of their knowledge, the involvement of the SCJ has not been previously described with dialysis amyloid. However, the presence of ß2-M amyloid deposits in the SCJ in 9 chronic hemodialysis patients has recently been reported by our group at the 20th meeting of the American Society of Nephrology (Washington, D.C., December 1987) and at the 4th meeting of the British Society of Rheumatology (London, UK, November 1987). Our preliminary findings have been published in abstract form [2]. In our study, amyloid deposits of the SCJ had been systematically sought during neck surgery in 22 hemodialysis patients. Of the 22 subjects included in the study, 13 had been on chronic hemodialysis for more than 10 years. Eight of them (62%) had amyloid deposits in their SCJ biopsy that reacted with an anti ß2-M antibody, stressing the high incidence of ß2-M amyloidosis in patients undergoing hemodialysis for a long period of time. The 2 cases reported by Sethi et al. had both been on hemodialysis for at least 10 years (10 and 15 years, respectively). Hence their observations are in line with the prevalence of ß2-M amyloidosis in our patients. However, in our experience, the finding of SCJ amyloidosis was not associated with local inflammatory signs in any case, in contrast to the clinical presentation of the patients of Sethi et al. Thus, the authors’ assumption of a causal relationship between ß2-M amyloidosis and the occurrence of acute arthritis remains questionable. Moreover, the absence of patent, acute inflammation of other joints, though massively involved [3], during ß2-M amyloidosis rather pleads against such a hypothesis. However, clinically latent, micro-inflammatory processes, may be involved in the pathogenesis of this serious complication of long-term hemodialysis. References Sethi, D.; Maher, E.R.; Cary, N.R.B.: Dialysis amyloid presenting as acute arthritis. Nephron 50:73–74 (1988). Zingraff, J.; Bardin, T.; Noel, L.-H.; Dubost, C; Kuntz, D.; Drüeke, T.: Occurrence of ß2microglobulin (ß2-M) amyloid deposits in sternoclavicular synovium of chronic hemodialysis patients (Abstract). Kidney int. 35:242 (1988).


The Lancet | 1986

ERYTHROPOIETIN TREATMENT IN ANAEMIC PATIENTS ON HAEMODIALYSIS

B. Zins; T. Drüeke; J. Zingraff; Lynda Bererhi; Henri Kreis; C. Naret; S. Delons; J.-P. Castaigne; F. Peterlongo; Nicole Casadevall; B. Varet


The Lancet | 1991

Lack of haemodialysis-associated amyloidosis

Johanna Zingraff; Thomas Bardin; Laure-Hélène Noël; T. Drüeke


Contributions To Nephrology | 1986

Cardiomyopathy in Patients on Maintenance Haemodialysis

T. Drüeke; C. Le Pailleur


The Lancet | 1988

DESFERRIOXAMINE, ANAEMIA, AND HAEMODIALYSIS

A.C. Grant; K.B. Modi; R.S.C. Rodger; A.I. Macdougall; B.J.R. Junor; T. Drüeke; Carlo Basile


The Lancet | 1994

Dietary salt and blood pressure

T. Drüeke

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Johanna Zingraff

Necker-Enfants Malades Hospital

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C. Le Pailleur

Necker-Enfants Malades Hospital

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Jean Crosnier

Necker-Enfants Malades Hospital

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J. Di Matteo

Necker-Enfants Malades Hospital

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Agnès Bourdeau

Necker-Enfants Malades Hospital

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B. Zins

Necker-Enfants Malades Hospital

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C. Dubost

Necker-Enfants Malades Hospital

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Carlo Basile

Necker-Enfants Malades Hospital

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D. Robert

Necker-Enfants Malades Hospital

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E.F. Sachs

Necker-Enfants Malades Hospital

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