12 research outputs found

    The history of clinical renal transplant

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    After pioneeristic clinical and experimental work done by Jaboulay and Carrel in Lyon at the begining of the XX century, it was only in 1936 that Yu Yu Voronoy in Ukraine and then in 1945 Landsteiner and Hufnagel in Boston, USA, transplanted human kidneys. In 1955 Murray reported the first successful homotransplantation in identical twins and he later received the Nobel Prize in 1990 for this achievement. These milestones associated to the broadening of knowledge in the field of tissue typing, allowed the diffusion of kidney and other organ transplantation

    Reduction of oxaluria after an oral course of lactic acid bacteria at high concentration

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    Background. Hyperoxaluria is a major risk factor for renal stones, and in most cases, it appears to be sustained by increased dietary load or increased intestinal absorption. Previous studies have shown that components of the endogenous digestive microflora, in particular Oxalobacter formigenes, utilize oxalate in the gut, thus limiting its absorption. We tested the hypothesis of whether oxaluria can be reduced by means of reducing intestinal absorption through feeding a mixture of freeze-dried lactic acid bacteria. Methods. Six patients with idiopathic calcium-oxalate urolithiasis and mild hyperoxaluria (>40 mg/24 h) received daily a mixture containing 8 × 1011 freeze-dried lactic acid bacteria (L. acidophilus, L. plantarum, L. brevis, S. thermophilus, B. infantis) for four weeks. The 24-hour urinary excretion of oxalate was determined at the end of the study period and then one month after ending the treatment. The ability of bacteria to degrade oxalate and grow in oxalate-containing media, and the gene expression of Ox1T, an enzyme that catalyzes the transmembrane exchange of oxalate, also were investigated. Results. The treatment resulted in a great reduction of the 24-hour excretion of oxalate in all six patients enrolled. Mean levels ± SD were 33.5 ± 15.9 mg/24 h at the end of the study period and 28.3 ± 14.6 mg/24 h one month after treatment was interrupted compared with baseline values of 55.5 ± 19.6 mg/24 h (P < 0.05). The treatment was associated with a strong reduction of the fecal excretion of oxalate in the two patients tested. Two bacterial strains among those used for the treatment (L. acidophilus and S. thermophilus) proved in vitro to degrade oxalate effectively, but their growth was somewhat inhibited by oxalate. One strain (B. infantis) showed a quite good degrading activity and grew rapidly in the oxalate-containing medium. L. plantarum and L. brevis showed a modest ability to degrade oxalate even though they grew significantly in oxalate-containing medium. No strain expressed the Ox1T gene. Conclusions. The urinary excretion of oxalate, a major risk factor for renal stone formation and growth in patients with idiopathic calcium-oxalate urolithiasis, can be greatly reduced with treatment using a high concentration of freeze-dried lactic acid bacteria. We postulate that the biological manipulation of the endogenous digestive microflora can be a novel approach for the prevention of urinary stone formation

    Family recurrence and oligo-anuria predict uremic restless legs syndrome

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    Objectives\u2002-\u2002 To determine clinical and laboratory predictors of restless legs syndrome (RLS) in patients with end-stage kidney disease (ESKD) undergoing long-term hemodialysis (HD). Materials and Methods\u2002-\u2002 One hundred and sixty-two consecutive patients were assessed. History of sleep disturbances, neurological examination, clinical, and laboratory data were collected. Patients with and without RLS were compared, and a logistic regression model described the relations between independent predictors and RLS. Results\u2002-\u2002 Fifty-one patients (32%) currently had RLS (RLS+). RLS+ vs RLS- patients were more frequently women (49% vs 29%, P\u2003=\u20030.012), had first-degree relative with RLS (22% vs 6%, P\u2003=\u20030.004), insomnia (59% vs 36%, P\u2003=\u20030.007), peripheral neuropathy (41% vs 21%, P\u2003=\u20030.006), and low residual diuresis (92% vs 68% with below 500\u2003ml/24\u2003h, P\u2003=\u20030.001). Low (OR\u2003=\u20038.71, CI\u2003=\u20032.27-33.41; P\u2003=\u20030.002) and absent (OR\u2003=\u20034.96, CI\u2003=\u20031.52-16.20; P\u2003=\u20030.008) residual diuresis, peripheral neuropathy (OR\u2003=\u20034.00, CI\u2003=\u20031.44-11.14; P\u2003=\u20030.008), and first-degree relative with RLS (OR\u2003=\u20033.82, CI\u2003=\u20031.21-12.13; P\u2003=\u20030.023) significantly predicted RLS in ESKD patients undergoing HD. Conclusion\u2002-\u2002 Positive family history for RLS together with reduced/absent residual renal function and peripheral neuropathy predicts the risk for RLS in ESKD patients undergoing HD. Longitudinal studies are warranted to correlate RLS occurrence with genetic and environmental factors

    Group I nonreciprocal inhibition in restless legs syndrome secondary to chronic renal failure

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    BACKGROUND: Neurophysiological investigations disclosed spinal cord hyperexcitability in primary restless legs syndrome (p-RLS). Uremic RLS (u-RLS) is the most common secondary form, but its pathophysiological mechanisms remain unsettled. Aim of this study was to explore spinal cord excitability by evaluating group I nonreciprocal (Ib) inhibition in u-RLS patients in comparison with p-RLS patients and healthy subjects. METHODS: Eleven u-RLS patients undergoing long-term hemodialysis treatment, nine p-RLS patients and ten healthy subjects were studied. Soleus H reflex latency (HR-L), H(max)/M(max) ratio, and Ib inhibition were evaluated. Ib inhibition was tested measuring the amplitude changes in soleus H reflex following stimulation of the synergist gastrocnemius medialis (GM) nerve at rest. Nerve conduction studies were performed in the uremic patients. RESULTS: The H(max)/M(max) ratio did not differ in the three groups. The u-RLS patients showed a normal Ib inhibition comparable with the healthy group, whereas the p-RLS group had evidence of a reduced active inhibition compared with both u-RLS patients (P = 0.04) and controls (P = 0.007), prominently at 5 ms (P = 0.007) and at 6 ms (P = 0.02) of conditioning-test interval. Neurophysiological examination disclosed abnormalities ranging from higher HR-L to clear-cut polyneuropathy in most u-RLS patients. CONCLUSIONS: Unlike p-RLS patients, u-RLS patients had normal Ib inhibition, suggesting a regular supraspinal control of Ib spinal interneurons. Subclinical peripheral nerve abnormalities were detected in most uremic patients. Peripherally disrupted sensory modulation may represent the major pathophysiological determinant of uremic RLS
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