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We performed a prospective, randomized, open study in 109 outpatients under chronic anticoagulation with acenocoumarine, presenting with International Normalized Ratios (INRs) > or = 6.0 and no or minor bleeding. All the patients withheld one dose of acenocoumarine; in addition, a treated group also received 1 mg oral vitamin K1. We aimed at a post-intervention INR < 6.0, with a target zone of 2.0-4.0. The INRs were lowered from a mean of 8.1 +/- 1.7 to 4.9 +/- 2.5 in the controls (P = 0.0000) and from 8.4 +/- 2.4 to 3.3 +/- 3 in the treated patients (P = 0.0000). There were no differences in the percentage of patients with post-intervention INRs < 6.0 or within the therapeutic zone. One-third of the treated patients and only 2% of the controls reached INRs < 2.0 (P = 0.0003). Oral vitamin K1 offered no advantage to the simple discontinuation of one dose of acenocoumarine. A substantial number of treated patients were consequently exposed to under-anticoagulation.

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BACKGROUND AND OBJECTIVES: Difficulties in identifying the coexistence of neutralizing anti-factor VIII antibodies (anti-fVIII) and lupus anticoagulant (LA) are mainly due to the interference of LA on anti-fVIII assays. Our aim was to reveal the presence of anti-fVIII using a system that is not affected by LA. DESIGN AND METHODS: We developed an enzyme-linked immunosorbent assay (ELISA) method that uses phospholipid-free recombinant factor VIII as the antigen. A monoclonal anti-fVIII was tested as a positive control, excluding non-specific binding by using two unrelated monoclonal antibodies. The ELISA was performed on hemophilic plasmas with anti-fVIII and negative LA (n=12) or without inhibitors (n=12). Two hemophilic plasmas with LA and presumably anti-fVIII were also assayed. Positive LA (n=12) and normal (n=10) plasmas were tested as negative controls. RESULTS: All (12/12) plasmas with anti-fVIII and 5/12 hemophilic plasmas without inhibitors were positive; LA and normal plasma controls were negative. INTERPRETATION AND CONCLUSIONS: Results presented here show that LA does not interfere with the anti-fVIII ELISA: However, the assay detects both neutralizing and non-neutralizing anti-fVIII antibodies, therefore a neutralizing effect must be confirmed through functional tests.

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Urinary excretion of aluminium after a successful transplant can reverse pre-transplant aluminium intoxication. We have evaluated the time course of urinary aluminium excretion and its correlation with several parameters of renal function and mineral metabolism in 49 patients (33 men and 16 women) with a wide range of pre-transplant serum aluminium concentrations, performing sequential determinations at pre-transplant time and at 7, 30, 60, and 90 post-transplant days. Mean serum aluminium at pre-transplant was 54.5+/-46.8 microg/l decreasing progressively to 28.7+/-24.4 microg/l at 90 days (P<0.0002), paralleling the decrease in serum creatinine. Urinary aluminium decreased from 63.0+/-77.9 to 52.4+/-55.9 microg/l at 90 days (P<0.0001). The maximum urinary aluminium/creatinine was 1.8+/-2.7 at 7 days and was associated with the greatest fractional excretion of sodium (4.7+/-5.1%), and the lowest tubular reabsorption of phosphate (55.7+/-25.1%). The fractional excretion of aluminium was also greatest at day 7 (1.1+/-0.9%) when serum creatinine was still elevated (3.6+/-2.3 mg/dl). At each period of time after transplantation fractional excretion of aluminium was similar in all patients despite disparate serum aluminium concentrations. Fractional excretion of aluminium was highest in those patients who developed post-Tx acute tubular necrosis (0.7+/-0.5 vs 1.5+/-1.0%, P=0.008). We found a direct positive correlation (r=0.43; P<0.002) between urinary aluminium and urinary phosphate. Basal levels and sequential changes in serum PTH, calcium, and phosphate did not correlated with fractional excretion of aluminium. These findings suggest: (i) urinary aluminium remains elevated during prolonged periods after transplant and is probably a marker of pre-transplant tissue aluminium accumulation; (ii) post-transplant fractional excretion of aluminium seems to correlated positively with other evidences of renal tubular dysfunction. Early post-transplant tubular malfunction could significantly enhance urinary aluminium elimination.

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Aluminium intoxication exerts profound effects on secondary hyperparathyroidism in chronic renal failure and could influence the evolution of post-transplant parathyroid function. We have evaluated 44 patients after successful renal transplantation, sequentially from day 0 up to day 90 from the beginning of graft function, determining serum and urinary aluminium, PTH (intact molecule) and several other parameters of mineral metabolism. Patients were grouped according to their basal serum aluminium: Group LA (n = 25) had serum aluminium less than 40 micrograms/l (mean 21 +/- 10 micrograms/l), and Group HA (n = 19) had serum aluminium greater than 40 micrograms/l (mean 100 +/- 43 micrograms/l). This latter group also had greater urinary aluminium excretion during the study period. Evolution of renal function was similar in both groups. Group LA had increased pre-transplant iPTH (353 +/- 416 pg/ml vs 175 +/- 94, P = 0.05). Seven days after regaining renal function both groups showed a marked decrease in iPTH and then a continued decline up to day 90 with mean serum values of the hormone showing no further differences between groups. The incidence of hypercalcaemia was similar in both groups but no patients in Group HA developed hypercalcaemia at post-transplant day 7 while 12% in Group LA did so. Urinary phosphate excretion and the incidence of post-transplant hypophosphataemia were similar in both groups. These findings suggest: (a) patients with more aluminium intoxication have lower values of pre-transplant iPTH and they correct parathyroid function in a different way than non-intoxicated patients in early post-transplant days; (b) they have lower and later incidence of hypercalcaemia.

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Foram estudados 51 casos de infecçäo urinária, considerando-se diversos fatores, tais como: agente etiológico, localizaçäo da infecäo, fatores predisponentes, sexo, idade e raça. O diagnóstico da infecçäo do trato urinário (ITU) foi baseado no exame bacteriológico, sendo considerado positivo quando a amostra de urina, colhida com auxílio de cateter, apresentava acima de 10 elevado à quinta potência bactérias/ml. Dos animais examinados, quatro cäes apresentaram infecçäo mista, totalizando 55 microorganismos isolados. Escherichia coli foi a mais frequentemente isolada (35,3 por cento), seguida de Staphylococcus sp (23,5 por cento), Proteus mirabilis (15,7 por cento), Streptococcus sp (13,7 por cento), Klebsiella sp (9,8 por cento), Pseudomonas aeruginosa (3,9 por cento), Enterobacter cloacae (2,0 por cento), Citrobacter freundii (2,0 por cento) e Providencia rettgeri (2,0 por cento). Quanto à sensibilidade dos germes isolados frente a diversos agentes antimicrobianos, a norfloxacina e a gentamicina mostraram-se eficazes no tratamento de microorganismos Gram-negativos, enquanto a cefalotina e a nitrofurantoina foram mais eficazes contra bactérias Gram-positivas. Os animais que apresentaram maior frequência de ITU pertenciam às raças Cocker Spaniel e Pastor Alemäo, envolvendo mais machos do que fêmeas com predominância de pielonefrites. Embora as infecçöes urinárias tivessem sido observadas em todas as idades, houve um predomínio nos cäes de média idade. Observou-se ainda que a urolitíase foi um fator pré-disponente ou adjacente de ITU, envolvendo germes como Staphylococcus sp e Proteus mirabilis naqueles casos com pH urinário alcalino

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