Atypical presentation of systematic nocardiosis and successful treatment with meropenem.
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Biomedical subjects
Publications and source records attributed to K Farrington.
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PURPOSE: To report the previously undescribed development of thrombotic thrombocytopenic purpura (TTP) in a human immunodeficiency virus (HIV)-positive child and discuss the differential diagnosis. PATIENT AND METHODS: Our patient was a 9-year-old boy with vertically acquired HIV infection and a previous history of immune thrombocytopenic purpura (ITP). Initial presentation, difficulty in diagnosis, clinical course, and subsequent outcome are described. RESULTS: Rapid resolution of TTP following plasmapheresis was seen. CONCLUSIONS: Recognition of this treatable though potentially fatal complication in severely ill HIV-infected children requires a high degree of suspicion in view of its diverse clinical manifestations. The long-term outcome may be relatively good.
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Blood urea and serum creatinine levels are important factors in deciding when to start dialysis. Recently, in the assessment of dialysis adequacy, emphasis has shifted from reliance on these parameters to use of kinetic methods. We therefore applied urea kinetic modelling (UKM) to 63 consecutive chronic renal failure (CRF) patients at the time dialysis commenced and compared the results to those obtained after 6 months of dialysis treatment. Mean normalised urea clearance (daily KT/V) at the commencement of dialysis (KTi/V) was 0.15 +/- 0.05, a level indicative of underdialysis in regularly dialysed patients. After 6 months, mean daily KT/V was 0.35 +/- 0.12 in patients subsequently established on CAPD, and 0.49 +/- 0.08 in those subsequently haemodialysed (both p < 0.001 compared to mean KTi/V). Serum creatinine levels on commencing dialysis were similar to those after 6 months treatment by either mode. Mean age (p < 0.01) and co-morbidity index (p < 0.05) were higher, and mean KTi/V lower (p < 0.05) in the 6 patients who died during a mean follow-up period of 10 +/- 4.5 months than in survivors. Hospitalisation rates during follow-up (excluding admissions for access surgery and training) correlated with age (r = 0.332, p < 0.01), co-morbidity index (r = 0.351, p < 0.01) and KTi/V (r = -0.302, p < 0.05). Blood urea and serum creatinine levels on commencing dialysis were the same in those who died and in survivors and did not correlate with hospitalisation rates. Diabetics started dialysis with a similar mean KTi/V to non-diabetics but with a lower mean serum creatinine (p < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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We studied 43 CAPD patients for 4 months during the change from a high-calcium dialysis fluid (Baxter PD1) to a low-calcium fluid (Baxter PD4), which also contained low magnesium (0.25 mmol/l) and high lactate concentrations (40 mmol/l). Serum calcium fell significantly as did the incidence of hypercalcaemia, whilst the proportion of patients taking calcium-containing phosphate binders increased. There was a non-significant increase in serum i-PTH levels but the proportion with i-PTH > 150 pg/ml (normal range 10-65 pg/ml) increased significantly. There was a significant fall in serum magnesium level and seven patients developed hypomagnesaemia. Serum bicarbonate increased significantly and progressively and 17 patients were alkalotic at 4 months, five severely (bicarbonate 35-40 mmol/l). One patient developed recurrent episodes of painful subcutaneous and periarticular calcification, which may have been related to the alkalosis. Initial serum bicarbonate levels correlated significantly with dialysis adequacy assessed by daily Kt/V (r = 0.458, P = 0.002). The relationship to adequacy was abolished during the period of use of the high-lactate dialysis fluid. Use of low-magnesium CAPD fluids must be supported by regular monitoring of serum magnesium levels. The high lactate concentration in such fluids may not be appropriate and is potentially hazardous when individualization of dialysis dose demands the use of relatively high exchange volumes. Low serum bicarbonate levels in CAPD patients reflect inadequate dialysis, which use of these fluids serves to mask.
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Urea kinetic modelling (UKM) has been proposed as a tool for auditing the adequacy of CAPD and a total fractional daily urea cleared volume (Kt/V) of 0.25 suggested as the minimum adequate level. At the start of CAPD the kidneys contribute significantly to the total clearance and Kt/V often falls below 0.25 as renal function declines. We performed 3-monthly UKM measurements in 56 CAPD patients. These results were used to individualize exchange volume and frequency in an attempt to achieve a Kt/V > 0.25 and compensate for declining renal function in all patients over a study period of 1 year. The mean Kt/V was maintained over 0.29 over the study period. During this time the residual renal component of Kt/V fell significantly from 0.09 (SD +/- 0.07) to 0.06 +/- 0.08 (P < 0.001) while the dialysis component increased significantly from 0.20 +/- 0.05 to 0.24 +/- 0.05 (P < 0.005). This was achieved by increasing the mean daily exchange volume from 8.12 +/- 1.22 to 10.39 +/- 2.68 litres (P < 0.001). After a year, 15 patients had Kt/V < or = 0.25 despite maximum practical exchange volumes. Twelve patients dropped out of the study due to death (4), transplantation (2), and transfer to haemodialysis (6 patients, of whom 4 had frank uraemic toxicity). In most CAPD patients it is possible to compensate for declining renal function by increasing exchange volume, at least over 1 year. However, CAPD was unable to provide Kt/V > 0.25 in 40% of patients, despite individualization of the dialysis prescription.
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Kinetic analysis was performed in all 58 patients undergoing standard CAPD. The urea distribution volume was estimated from anthropomorphic measurements (Watson formulae). Normalized protein catabolic rate (NPCR), daily protein leak (PL), urea and creatinine Kt/Vs, clearances and peritoneal mass transfer coefficients (Kp) were calculated from measurements on serum, 24-h urine and PD fluid effluent. The mean total (renal+PD) daily creatinine and urea Kt/Vs (KT/V) were 0.31 (range 0.15-0.79) and 0.31 (0.18-0.65). There was no relationship between KT/V and serum urea or Kp. The strongest determinant of the urea KT/V was the residual renal urea clearance (KrU)(R = 0.79, P < 0.001) which decreased with time on dialysis (R = -0.38, P < 0.005). There was a significant correlation between the hospital admissions per year and both the urea and creatinine KT/V and KrU (R = -0.30, -0.32, P < 0.05). Patients with urea KT/V < 0.25 (n = 22) had more hospital admissions/year than those with KT/V > 0.25 (mean of 2.6 versus 1.5, P < 0.05). NPCR correlated with urea KT/V (R = 0.62, P < 0.001) but not with serum albumin or the PL. Patients identified by UKM to be less well dialysed have a lower residual renal function and are more likely to be hospitalized. Undernutrition in CAPD patients appears to be related to underdialysis rather than protein loss.
The efficiency of haemodialysis may be limited by recirculation of blood between venous and arterial needles. Recirculation can be detected directly using a saline dilution method but is most commonly calculated from the urea concentrations of simultaneous samples from venous and arterial lines and a peripheral vein (three-sample method). The methods detect markedly different rates of recirculation in similar study populations. To investigate the possibility that the methods detect different phenomena, we performed both tests on 16 haemodialysis patients at various extracorporeal blood flow rates (Qb). The saline dilution method showed no recirculation in any of the patients, whereas the three-sample method indicated recirculation in all patients. The three-sample method indicated a mean recirculation fraction of 12.5% (SD 6.1) and was not influenced by changing Qb, suggesting that it was not detecting fistula recirculation. The three-sample method detects a solute concentration difference between arterial blood and peripheral blood during dialysis. There appears to be a disequilibrium between a central pool, represented by the arterial sample, and a poorly perfused peripheral pool, relatively isolated from the dialysis process, represented by the peripheral venous sample. The three-sample method for detecting recirculation should be abandoned.
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Twelve patients with chronic renal failure (CRF) requiring dialysis, 7 of whom were hypercalcaemic, were treated with 24,25-dihydroxycholecalciferol [24,25(OH)2D3; 10 micrograms daily for 3 months] or placebo and the treatment then crossed over for a further 3 months. Treatment with 24,25(OH)2D3 was associated with small but significant increments in the fractional rates of absorption of calcium (p less than 0.01) and phosphate (p less than 0.05) measured by a combined radioisotope test, but even during treatment, the absorption of both calcium and phosphate remained subnormal. A significant fall in immunoreactive parathyroid hormone (i-PTH) levels occurred during treatment (p less than 0.05) in the absence of significant changes in plasma ionised calcium and plasma phosphate levels. In 7 patients, treatment with 24,25(OH)2D3 converted parathyroid glands which were non-suppressible by calcium infusion before treatment to suppressible ones (greater than 50% suppression of i-PTH levels) at similar levels of ionised calcium. 24,25(OH)2D3 may have a role in the treatment of renal osteodystrophy, especially in patients with hypercalcaemic hyperparathyroidism.
Thirty-three cases of infective endocarditis presenting during a 6.5 year period to a district general hospital were analysed retrospectively. The annual incidence was 22 cases per million population. Twenty-two cases had pre-existing cardiac disease, mainly valvular disease-usually rheumatic (nine cases) and prosthetic valves (10 cases). Recognizable precipitants such as recent surgery were uncommon. Two cases presented after deliberate drug overdose possibly due to depression exacerbated by systemic disease. Symptoms were usually non-specific. All but two cases had murmurs and most were pyrexial. Splinter haemorrhages and clubbing were seen in about 20% of cases. Viridans-type streptococci were the commonest infecting organisms (14 cases). Staphylococcal infection (six cases) was confined to intravenous drug abusers and patients with prosthetic valves. Five cases were culture negative. Cardiac failure was present in 13 cases at presentation and developed in seven others during treatment. Acute valve replacement was necessary in eight cases, and late replacement in three. Renal impairment (plasma urea > 8 mmol/l and/or plasma creatinine > 120 mumol/l) occurred in 19 cases during the course of their illness. Embolic phenomena occurred in 12 patients and mostly involved the central nervous system. In the 8 fatal cases, the cause of death was cardiac failure in six, cerebrovascular accident in one, and myocardial infarction in one. Four of the six patients who subsequently died of cardiac failure had been referred for surgery. Both those who were not referred had coexisting medical problems. Factors associated with increased mortality were age, male sex, cardiac failure (P < 0.01), renal impairment (P < 0.05), and embolic phenomena (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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