Urine lipids in patients with a history of filariasis

The presence of lipids in postprandial urine was assessed in 116 patients with a history of filariasis and 70 normal individuals using a biochemical autoanalyzer. Urinary triglycerides (TGs) ranging from 10 to 1955 mg/dl were detected in 13 individuals with a history of chyluria, including 3 with TG levels ranging from 233 to 1955 mg/dl and cholesterol levels of 6–35 mg/dl. Three patients who had a filarial history but without chyluria were also found to have urinary TGs (1315 mg/dl) without detectable cholesterol. Neither TGs nor cholesterol were detected in the urine of normal individuals. Fluctuations in postprandial urine lipid contents were measured by time course determinations of urinary TG and cholesterol in 17 patients with filariasis and a history of chyluria, 16 patients with filariasis and hydrocele and 16 normal individuals. The level of urine lipid excretion was found to increase within 1–4 h postprandially, with urinary TG levels ranging between 7.8 and 1284 mg/h in eight patients and urinary cholesterol levels between 1.2 and 138 mg/h in seven patients with a history of chyluria. To evaluate the origin of the urine lipids in hematochyluria, fish oil containing 360 mg eicosapentaenoic acid (EPA) and 240 mg docosahexaenoic acid (DHA) was prescribed to a patient with hematochyluria. The excretion of EPA and DHA in urine was increased postprandially in the patient, similar to the elevation of urinary TG and cholesterol. The profile of fatty acids from urine samples showed it was of dietary origin. Our results suggest that postprandial urine lipids, especially TG, might be used as markers for the clinical evaluation of chyluria.     

Effects of glutamine supplements and radiochemotherapy on systemic immune and gut barrier function in patients with advanced esophageal cancer.

OBJECTIVE: The objective of this study was to determine whether oral glutamine supplements can protect lymphocyte and gut barrier function in patients with advanced esophageal cancer undergoing radiochemotherapy. SUMMARY BACKGROUND DATA: Glutamine supplements improved protein metabolism in tumor bearing rats who underwent chemotherapy and reduced the toxicity of chemotherapy through an enhancement of glutathione production in rats. METHODS: Thirteen patients with esophageal cancer were randomly placed in either a control or a glutamine group. Glutamine was administered orally (30 g/day) at the start of radiochemotherapy and for the subsequent 28 days. All patients underwent mediastinal irradiation and chemotherapy consisting of 5-fluorouracil and cisplatin. The lymphocyte count was determined, and blast formation was assessed after stimulation with phytohemagglutinin and concanavalin A. Gut barrier function was assessed by measuring the total amount of phenolsulfonphthalein excreted in the urine after the oral administration of phenolsulfonphthalein. RESULTS: Glutamine supplements prevented a reduction in the lymphocyte count (control: 567 +/- 96/mm3 vs. glutamine: 1007 +/- 151, p < 0.05), and blast formation of lymphocyte (phytohemagglutinin, control: 19478 +/- 2121 dpm vs. glutamine: 33860 +/- 1433, p < 0.01, concanavalin A, control: 19177 +/- 1897 dpm vs. glutamine: 29473 +/- 2302, p < 0.01), and amount of phenolsulfonphthalein excretion in the urine was greater with control than with glutamine group (control: 15.4 +/- 2.4% vs. glutamine: 7.4 +/- 1.2, p < 0.05) 7 days after the initiation of radiochemotherapy. CONCLUSIONS: Oral glutamine supplementation protects lymphocytes and attenuates gut permeability in patients with esophageal cancer during radiochemotherapy.     

Incidence of acquired renal cysts in biopsy specimens

AIMS: This study investigated whether or not acquired renal cysts develop in patients with mild chronic renal failure. METHODS: A retrospective study was carried out using renal biopsy specimens from 720 patients. A renal cyst was defined as a tubule dilated >200 microm. RESULTS: Renal cysts were found in 21 of 720 renal biopsy specimens. Serum creatinine of 21 patients with renal cysts was significantly higher than that of 699 patients without cysts (2.59 +/- 2.64 vs. 1.09 +/- 0.79 mg/dl) (p < 0.0001). Poor renal function (serum creatinine >1.6 mg/dl) reveals more cyst formation on biopsy specimens than good renal function (serum creatinine <1.5 mg/dl). Cysts were observed in 11 of 607 (1.8%) patients less than 50 years of age and in 10 of 113 (8.8%) patients over 51 years. To exclude simple cysts which are commonly observed in older subjects, 11 patients under 50 years of age were extensively examined. Mean serum creatinine was 2.98 +/- 3.06 mg/dl (0.7-10.4 mg/dl). These 11 patients revealed low creatinine clearance of 47.5 +/- 25.6 ml/min (5-71 ml/min). Creatinine clearances in 7 patients were 52-71 ml/min (serum creatinine 0.7-2.0 mg/ dl). One of 11 biopsy specimens with cysts was examined by immunohistochemistry on lectin. This specimen was positive for tetragonolobus lectin and negative for peanut lectin, suggesting that the epithelial cells lining the cyst were derived from proximal tubules, unlike those of simple cysts. CONCLUSION: These results suggest that low normal renal function such as creatinine clearances 52-71 ml/min due to nephron loss is sufficient to induce acquired cyst development in various renal diseases.     

The "low TBG syndrome" in patients on chronic hemodialysis: evolution after renal transplantation

Patients on chronic hemodialysis may have a spuriously low TBG level, tentatively ascribed to uremia-induced changes in TBG immunoreactivity. In order to test this hypothesis, the effect of restoration of a normal renal function on TBG immunoreactivity was evaluated. TBG concentration was measured in 20 patients both by radioimmunoassay and by a T4-binding capacity assay, before, 4 and 10 months after a successful renal transplantation. Mean pretransplant TBG value measured by RIA was in the low normal range (1.60 +/- 0.14 mg/dl; normal limits 1.6-2.4 mg/dl). Twelve patients (60%) had TBG levels below 1.6 mg/dl (group I), while T4-binding capacity of TBG (TBC) measured in 7 of them was normal, so that the TBG/TBC ratio was characteristically reduced. The 8 remaining patients (group II) had TBG levels within or slightly above the normal range (mean value 2.26 +/- 0.17 mg/dl) and in the 5 tested patients, TBC and TBG/TBC ratio were normal. Four months after transplantation, mean TBG increased significantly in group I from 1.15 +/- 0.03 mg/dl before transplantation to 1.54 +/- 0.12 mg/dl (p less than 0.01). TBC increased also from 269 +/- 37.5 to 335 +/- 24 nmol/l (p less than 0.01) but to a significantly lesser extent than TBG (24% vs 48%, p less than 0.05). As a result, the TBG/TBC ratio returned to normal values, rising from 0.79 +/- 0.07 to 0.95 +/- 0.07 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Calcium,phosphate, and PTH levels in the hemodialysis population: a multicenter study

BACKGROUND: Hyperphosphatemia is one of the main factors in the pathogenesis of secondary hyperparathyroidism. In addition, in dialysis patients elevated levels of phosphate and calcium times phosphate (Ca x P) ion product are associated with extraskeletal calcifications, as well as an increased risk of death. Cardiovascular calcifications may possibly be related to the high cardiovascular mortality seen in dialysis patients. In the USA the prevalence of hyperphosphatemia among dialysis patients is very high, over 60% of patients having serum P levels > 5.5 mg/dl, but no data are available for the Italian population, which follows different diet and dialysis schedules. METHODS: We looked at a random sample of 638 patients enrolled in 29 outpatient dialysis units in Southern Italy (Campania and Sicily). Data were centrally analyzed after extraction from a computerized database. In each patient the average of two or more values obtained in the six-month observation period (from Jan. 99 to June 99) was calculated. Mean age was 61.2 years (95% CI 59.9-62.5) years, dialytic age 72.2 months (95% CI 67.4-77.0). RESULTS: Mean +/- SD (95% CI) levels of phosphate were 5.74 +/- 1.57 (5.62-5.86) mg/dl; total calcium 9.06 +/- 0.98 (8.98-9.14) mg/dl; Ca x P 51.4 +/- 14.4 (50.3-52.5) mg2/dl2; alkaline phosphatase was 167 +/- 119 (157-177) IU/L; intact parathyroid hormone (PTH) levels, available in a subset of 239 patients, were 318 +/- 413 (265-370) pg/ml. Among these patients 51.6% had serum P > 5.5 mg/dl, 36% > 6 mg/dl; Ca x P levels were > 55 mg2/dl2 in 35.5% of the population, 24% > 60 mg2/dl2; iPTH levels were < 100 pg/ml in 43%; 25.4% had hyperparathyroidism (defined as iPTH > 400 pg/ml), and only 19.5% of patients had PTH in the desired interval of 100 to 250 pg/ml. CONCLUSIONS: Compared to data reported from the USA, mean levels of phosphate, Ca x P, and PTH seem better controlled in this Italian hemodialysis population. However, in a significant number of patients these parameters were still outside the normal range. Both over-suppression of PTH levels and hyperparathyroidism are present, although surprisingly the former was more frequent. Treatment of hyperphosphatemia should be more aggressive in hemodialysis patients; PTH levels are difficult to maintain in the desired range of 100-250 pg/ml.     

Reversal of protein-energy malnutrition in children during treatment of advanced neoplastic disease.

The effectiveness of enteral and parenteral feeding in supporting a satisfactory nutritional status and/or reversing protein-energy malnutrition was evaluated in 28 children, ages 1-19 (14 female) with advanced malignant disease (21 solid tumors, 7 leukemia-lymphoma). At the onset of treatment, 21 patients received intensive nutritional counseling (INC) and oral supplementation while seven received total parenteral nutrition (TPN). Sixteen of 21 patients who received INC had a decreased intake (x 48 +/- 24%) Recommended Dietary Allowances (RDA) for kilocalories and dramatic weight loss (x 16.4 +/- 12.4%). A total of 18 patients received TPN for a mean of 24 days (7-60); kcal averaged 90 +/- 26% RDA during weight gain. At onset of TPN, the mean serum albumin, transferrin and total lymphocyte counts were 3.06 +/- 0.38 g/dl, 175 +/- 62 mg/dl, and 1102 +/- 966/mm3 respectively, 15/18 children had subnormal anthropometric measurements and 17/18 patients were anergic to recall skin test antigens. TPN for less than 9-14 days neither repleted weight, skinfold reserves, nor serum albumin concentrations (greater than 3.2 g/dl) although an early increase (p less than .02) in transferrin concentration was observed. However, TPN for 28 days supported weight gain (3.27 kg, 16 +/- 6%), increased serum albumin (0.62 +/- 0.43 g/dl, p less than .001) and transferrin (62 +/- 42, p less than .002) to normal concentrations and reversed anergy in 7/11 patients retested. This study documents the severity of protein energy malnutrition which accompanies intense treatment of children with cancer and the nutritional and immunological benefits of a 28 day course of TPN.     

Sarpogrelate reduces mechanical hemolysis in patients with heart valve prostheses.

OBJECTIVE: We evaluate the clinical efficacy of sarpogrelate, an antiplatelet drug that improves red blood cell deformability, to reduce the intravascular hemolysis problems suffered frequently by patients implanted with heart valve prostheses. SUBJECTS: Subjects were 34 patients undergoing mechanical heart valve replacement and having serum lactate dehydrogenase concentrations 20% above the maximum normal range. METHOD: Sarpogrelate was given daily, 100 mg orally for the first 6 months and 200 mg thereafter. RESULTS: Average serum lactate dehydrogenase decreased significantly from 423 +/- 108 IU/l, to 391 +/- 83 IU/l with the 100 mg dose, and to 361 +/- 86 IU/l with the 200 mg dose. The percentage of reticulocytes decreased from 15.5 +/- 5.3/1000 to 15.3 +/- 5.7/1000 at the 100 mg dose and 13.1 +/- 4.0/1000 at the 200 mg dose. Serum iron concentrations increased significantly from 63.2 +/- 24.8 micrograms/dl to 76.2 +/- 16.2 micrograms/dl at the 100 mg dose, and to 70.9 +/- 26.2 micrograms/dl with the 200 mg dose. CONCLUSION: Sarpogrelate is a useful drug for patients with implanted heart valve prostheses and subsequent high serum lactate dehydrogenase because it works as an antiplatelet drug and reduces mechanical hemolysis.     

Examining chronic kidney disease management in a single center

AIMS: The management of patients with chronic kidney disease in outpatient clinics was assessed for the ability to achieve targets of care advocated in clinical practice guidelines. METHODS: 272 records of outpatients with increased serum creatinine (> or = 1.5 mg/dl for women, > or = 2.0 mg/dl for men) were reviewed for details of their assessment and management. Prevailing data on blood pressure, anemia, bone disease and lipid status as well as therapeutic changes were evaluated. RESULTS: The subjects were aged 64 +/- 18 years, serum creatinine 2.6 +/- 1.1 mg/dl, and calculated GFR (MDRD formula) 19.2 +/- 9.9 ml/min. Median UproV was 1.0 (0.024 - 12.4) g/day. Causes of CKD were diabetes (33.5%), HTN (8.8%), GN (19.5%), and adult PKD (3.3%). Treatment targets were BP < 130/85 mmHg, Hct > or = 36%, serum Ca++ > or = 8.5 mg/dl, serum Po4 < 4.5 mg/dl and cholesterol < 200 mg/dl. Of the patients with abnormal findings, mean values for SBP were 153 +/- 17 mmHg, DBP 93 +/- 6 mmHg, Hct 31.7 +/- 2.9%, Ca++ 8.0 +/- 0.7 mg/dl, PO4 5.6 +/- 1.0 mg/dl, and cholesterol 236 +/- 37 mg/dl. Only a minority of patients with abnormal values had their treatment altered. Furthermore, only 54% of patients with hypertension were treated with either ACEi or ARB therapy. Finally, only 6% of patients with hypercholesterolemia had fasting lipid levels measured. CONCLUSION: This data suggests that treatment of patients with CKD has improved, but that many opportunities exist to optimize their care.     

Renal allograft rejection with normal renal function in simultaneous kidney/pancreas recipients: does dissynchronous rejection really exist?

BACKGROUND: Between July 1, 1994 and December 1, 1998, 147 simultaneous kidney/pancreas transplantations were performed at our center. Of 95 patients who experienced at least one acute renal allograft rejection episode after transplantation, 7 (7.4%) developed rejection in the presence of stable and normal or near-normal renal function. METHODS: The indication for renal allograft biopsy was a rising serum lipase, i.e., suspected pancreatic rejection. All seven patients were treated with steroids and augmentation of the tacrolimus dose, with a fall in the serum lipase and no change in the serum creatinine. RESULTS: The serum creatinine levels just before, at the time of, 1 week after the biopsy, and at most recent follow-up were 1.4+/-0.4, 1.3+/-0.3, 1.2+/-0.2, and 1.2+/-0.2 mg/dl. The serum lipase levels just before, at the time of, 1 week after the biopsy, and at most recent follow-up were 1022+/-1157 mg/dl, 874+/-996 mg/dl, 243+/-260 mg/dl, and 94+/-75 mg/dl. The tacrolimus dosages and levels at the time of the biopsy and 1 week later were 14.9+/-5.0 mg/day and 15.0+/-4.0 ng/ml, and 16.4+/-6.3 mg/day and 15.1+/-6.8 ng/ml. CONCLUSIONS: These findings suggest that, in patients undergoing simultaneous kidney/pancreas transplantation, the entity of dissynchronous pancreatic allograft rejection without renal allograft rejection may not really exist. These data also make an additional fundamental point that acute rejection may occur in patients with normal and stable renal function.     

A long-term, multicenter study of the efficacy and safety of paricalcitol in end-stage renal disease.

BACKGROUND: Paricalcitol is a vitamin D analog approved for the prevention and treatment of secondary hyperparathyroidism associated with chronic renal failure. This study was designed to evaluate the long-term efficacy and safety of paricalcitol. Additional analysis evaluated the effects of paricalcitol in hypocalcemic and hyperphosphatemic subpopulations. PATIENTS AND METHODS: One hundred sixty-four end-stage renal disease (ESRD) patiesnts on hemodialysis were treated in an open-label, multicenter study lasting up to 13 months in duration. After a baseline or washout period, an initial starting dose of 0.04-0.393 microg/kg was given 2-3 times per week. This dose was adjusted at the discretion of the investigator according to the patient's intact parathyroid hormone level (iPTH), calcium level, and calcium-phosphorus (Ca x P) product. The therapy was intended to reproduce expected clinical use of paricalcitol. Patients represented a wide cross-section of the ESRD population, and were not excluded from the study based on age or underlying disease. RESULTS: The mean paricalcitol dose level throughout the study was 0.10 microg/kg. The mean iPTH levels (baseline mean 628.3 +/- 27.65 pg/ml) decreased rapidly during the first 4 months of therapy, and reached the designated target range (100-300 pg/ml) by month 5 (mean 295.3 +/- 25.69 pg/ml). A maximum mean decrease in iPTH level of 409 +/- 35.01 pg/ml was seen at month 13. Throughout the course of the study, the mean normalized calcium level was maintained well within the normal range (9.44-9.94 mg/dl). The mean phosphorus level was maintained in an acceptable range throughout the study (5.92-6.53 mg/dl). Mean Ca x P product was maintained between 52 and 65. Mean alkaline phosphatase levels decreased significantly from baseline with a maximum mean decrease of 62 +/- 17.3 U/l observed at month 9. In 34 initially hypocalcemic patients (mean of 7.7 mg/dl) iPTH levels decreased from baseline, on average, by 443 +/- 81.86 pg/ml while mean calcium levels rose by 1.2 +/- 0.23 mg/dl to reach the normal range. In 35 initially hyperphosphatemic patients (mean of 8.0 mg/dl) iPTH levels decreased, on average, by 515 +/- 103.31 pg/ml with an associated mean decrease in phosphorus of 0.57 +/- 0.52 mg/dl. Adverse events that were considered by the investigator to have a possible. probable, or definite relationship to study drug occurred in 26% of patients. Other than expected temporary effects of hypercalcemia and hyperphosphatemia. the only possible trends for causally-related adverse events were for nausea/vomiting and metallic taste. CONCLUSIONS: This long-term study of paricalcitol demonstrates that it rapidly and effectively suppresses iPTH levels in a wide spectrum of ESRD patients and caused no unexpected adverse events.     

初治骨关节结核患者外周血T细胞亚群特点及临床意义

目的 探讨初治骨关节结核患者外周血T细胞亚群特点、与临床观测指标的关系及抗结核治疗对患者细胞免疫状况的影响。方法 采用单平台流式细胞术检测骨关节结核患者治疗前和治疗后1-2个月T细胞亚群的绝对数及百分比，并与恶性骨肿瘤患者和健康人比较。结果 初治骨关节结核组CD4及CD8T细胞绝对数较健康对照组低（P〈0．01）。骨关节结核患者在治疗1-2个月后CD4T细胞百分比升高（P〈0．05）。青年组CD8T细胞绝对数和百分比显著高于中年组和老年组（P〈0．05，P〈0．01），CD4／CD8显著低于中年组及老年组（P〈0.01）。T细胞亚群各参数与PPD反应直径、红细胞沉降率和C反应蛋白之间无显著相关性（P〉0．05）。脊柱结核合并脓肿组CD4／CD8较低，CD8T细胞百分比较高（P〈0．01）。结论 初治骨关节结核患者存在细胞免疫缺陷，以中老年组更明显。脊柱结核是否形成脓肿与CD8T细胞有关。初治骨关节结核患者经1～2个月化疗后，细胞免疫状况改善，是病灶清除术的有利时机．     

Calcium carbonate is an effective phosphate binder when dialysate calcium concentration is adjusted to control hypercalcemia

The efficacy of calcium carbonate (CaCO3) as a phosphate binder has been limited by its tendency to cause hypercalcemia. Since standard dialysate calcium concentrations (3.0-3.5 mEq/l) increase the risk of developing hypercalcemia with large doses of CaCO3 by inducing positive calcium balance during hemodialysis (HD), we compared control of hyperphosphatemia in 41 HD patients during 4 months each of aluminum hydroxide (Al(OH)3) and CaCO3 when the dialysate calcium concentration was lowered, as required, to maintain the predialysis serum calcium concentration within the normal range. Mean predialysis serum phosphorus and calcium concentrations were 5.0 +/- 0.2 mg/dl and 9.3 +/- 0.1 mg/dl, respectively, during 4 months CaCO3 (9.2 +/- 0.3 g/day) and 4.9 +/- 0.2 g/dl and 9.1 +/- 0.1 mg/dl during the previous 4 months Al(OH)3 therapy (2.9 +/- 0.2 g/day). Reducing the dialysate calcium concentration to below 3.0 mEq/l (mean 2.1 +/- 0.04) in the 11 patients who developed hypercalcemia on CaCO3 decreased serum calcium (-1.1 +/- 0.15 mg/dl) and ionized calcium (-0.3 +/- 0.04 mEq/l) during HD, enabled CaCO3 (8.8 +/- 0.4 g/day) to be continued, and maintained predialysis serum calcium and phosphorus at 10.4 +/- 0.1 mg/dl and 5.2 +/- 0.3 mg/dl, respectively. No improvement in acidosis or biochemical hyperparathyroidism was observed during CaCO3 therapy but serum aluminum was significantly decreased after CaCO3 (p less than 0.005). We conclude that CaCO3 prevents interdialytic hyperphosphatemia as effectively as Al(OH)3 without increasing the predialysis serum calcium x phosphorus product, provided serum calcium is maintained within the normal range by adjusting the dialysate calcium concentration.     

Immunological state of patients with carcinoma of the bronchus before and after radiotherapy.

The immunological state of 30 patients with carcinoma of the bronchus was assessed before and after radiotherapy by lymphocyte response to PHA and E and EAC rosette formation. The results were compared with those from age-matched patients with benign chest disease and a group of healthy control subjects. Differences were found between the three groups and decreased immunological responses were found to correlate with shorter survival times for patients with cancer of the bronchus. These differences were not associated with the extent of the disease, or with the smoking habits of the patients. Significant differences in percentage EAC cell rosetting were demonstrated between lymphocytes from patients with malignant disease (31.3 +/- 2.0) and those for control groups (21.5 +/- 1.9 and 24.0 +/- 2.2). Cancer patients and benign chest disease patients both had significantly decreased mean E rosetting values (59.3% and 55.6%) compared with healthy control subjects (69.7%). The group of cancer patients with a normal percentage of T lymphocytes and total number of lymphocytes after radiotherapy, or those with low percentage EAC cell rosettes, had a greater than 80% survival after seven months compared with less than 50% for the rest of the patients with carcinoma of the bronchus.     

Bone histology in patients with nephrotic syndrome and normal renal function

BACKGROUND: The prevalence of metabolic bone disease in patients with nephrotic syndrome (NS) at normal level of renal function remains uncertain. METHODS: To address this issue, we studied 30 patients (20 men and 10 women, mean age 27.3 +/- 11.7 years) with NS who had normal renal function (mean creatinine clearance 103 +/- 4 ml/min). We evaluated their serum calcium, phosphorus, alkaline phosphatase, immunoreactive parathyroid hormone (iPTH), vitamin D metabolites, urinary calcium, and skeletal survey. The extent of bone mineralization was analyzed by histomorphometric analysis of iliac crest bone biopsy specimens in all patients. The findings on bone histology were correlated with biochemical parameters. RESULTS: The mean duration of NS was 35.5 +/- 26.9 months, with a protein excretion of 7.3 +/- 3.2 g/24 hr and a serum albumin of 2.2 +/- 0.8 g/dl. Total serum calcium was 7.8 +/- 0.8 mg/dl, whereas ionized calcium was 5.7 +/- 0.7 mg/dl, phosphorus 3.2 +/- 1.2 mg/dl, and alkaline phosphatase 149 +/- 48.6 U/liter. Serum iPTH levels were normal in all except two patients. The mean serum 25-hydroxyvitamin D [25(OH)D] level was 3.9 +/- 1.2 ng/ml (normal 15 to 30 ng/ml), whereas 1,25-dihydroxyvitamin D was 24 +/- 4.7 pg/ml (normal 16 to 65). There was an inverse correlation between serum levels of 25(OH)D and the magnitude of proteinuria (r = -0.42, P < 0.05). The mean 24-hour urinary calcium excretion was 82 +/- 21 mg/day. The skeletal survey was normal in all patients. Bone histology was normal in 33.3% of the patients, whereas 56.7% had isolated osteomalacia (OSM), and 10% had an increased bone resorption in association with defective mineralization. The severity of OSM measured by mineralization lag time correlated linearly with the duration (r = 0.94, P < 0.0001) and the amount (r = 0.97, P < 0.0001) of proteinuria. All patients with NS for more than three years had histological changes. Patients with OSM had lower 25(OH)D and serum albumin as compared with those with normal histology (P < 0.005). Bone mineralization had no significant correlation with serum iPTH, divalent ions, or vitamin D levels. CONCLUSIONS: OSM is a frequent finding in adult patients with NS, even at a normal level of renal function. Its severity correlates with the amount and duration of proteinuria.     

Intraperitoneal fibrin-formation and its inhibition in CAPD

The intraperitoneal fibrin formation and its inhibition by intraperitoneal heparin (5000 U) was investigated in six patients on CAPD. The intraperitoneal heparin concentration decreased linearily from 1.78 U/ml to 1.13 U/ml during a 4-hour dwell time. The antithrombin III-concentration increased to 0.56 +/- 0.1 mg/dl, reaching 1.87% of normal plasma values. The antithrombin III-portion of total protein was 0.62% in plasma and 0.79% in dialysate. The fibrinopeptide A-concentration, a specific product of thrombin action on fibrinogen was 37.1 +/- 11.8 ng/ml in plasma (normal range: less than 2.5 ng/ml) and 153.4 +/- 16.8 ng/ml in dialysate during regular CAPD. After the addition of 5000 U heparin the fibrinopeptide A-concentration in dialysate decreased to 11.6 +/- 2.6 ng/ml during a 4-hour dwell time. In vitro experiments showed no remarkable inhibition of fibrin formation by heparin without antithrombin III in dialysate. We suggest that the fibrinopeptide A is produced intraperitoneally and the antithrombin III-concentration in dialysate is sufficient to inhibit the fibrin formation after acceleration by heparin.     

Apoptosis of circulating lymphocyte in rats with unilateral ureteral obstruction: role of angiotensin II

BACKGROUND: Unilateral ureteral obstruction (UUO) could induce increased renal angiotensin II (ANG II), which enhances apoptosis of renal tubular cells and renal tissue loss. Systemic ANG II is also increased in UUO. There are no data available about whether UUO can induce apoptosis of circulating lymphocytes or not. METHODS: UUO or sham-operated male Wistar rats (n = 8 in each group) were fed a drinking solution containing water, angiotensin II receptor type 1 antagonist (ARA; losartan, 500 mg/L) or angiotensin-converting enzyme inhibitor (ACEI; enalapril: 200 mg/L) for 1 day or 7 days. Blood samples were collected and circulating lymphocyte cells were separated. The apoptotic cells were detected by in situ terminal deoxynucleotidyl transferase (TdT assay)-mediated digoxigenin/antidigoxigenin conjugated fluorescein method and counted under a fluorescence microscope. The apoptotic index was calculated. RESULTS: UUO caused marked increases in the apoptotic index of circulating lymphocytes in UUO rats at both 1 day and 7 days when compared with the respective sham groups (P < 0.001). Neither ARA nor ACEI treatment had an effect on the apoptotic index values in the UUO rats at 1 day. In the UUO rats at 7 days, the apoptosis of circulating lymphocytes was markedly decreased from 29.2 +/- 2.7% to 11.9 +/- 2.7% (P < 0.01) in the ARA-treated rats and to 7.6 +/- 2.7% (P < 0.001) in the ACEI-treated rats. CONCLUSION: UUO, via stimulation of ANG II, could promptly enhance apoptosis of circulating lymphocytes. The apoptosis persisted throughout the 7 days of the study. Prolonged UUO would impair lymphocyte cell immunity and the host defense mechanism. Continuous treatment with either ARA or ACEI could abrogate ANG II-stimulated circulating lymphocyte apoptosis.     

Etomidate inhibits adrenocortical function in surgical patients

Postoperative adrenocortical function was compared in 23 out-patients receiving either thiopental, 4 mg/kg, for induction and a thiopental infusion, 0.26 mg . kg-1 . min-1, in combination with nitrous oxide 70% for maintenance of anesthesia (control); etomidate, 0.4 mg/kg, for induction followed by an etomidate infusion, 0.02 mg . kg-1 . min-1, and nitrous oxide 70% for maintenance (etomidate I); or etomidate, 0.4 mg/kg, for induction and a thiopental infusion, 0.22 mg . kg-1 . min-1, in combination with nitrous oxide 70% for maintenance (etomidate II). The norepinephrine response to anesthesia and surgery did not differ significantly between the three groups. The postoperative cortisol response to ACTH stimulation was normal in the control group (maximum rise in plasma cortisol was 20.1 +/- 2.9 micrograms/dl [mean +/- SEM] ), however, it was decreased in all patients receiving etomidate, whether by a short infusion (mean change in plasma cortisol was -3.8 +/- 1.9 micrograms/dl) or as a single induction dose (mean change in plasma cortisol was -4.0 +/- 2.0 micrograms/dl). Similarly, the postoperative aldosterone levels in the control group increased normally in response to ACTH (+ 10.2 +/- 3.0 ng/dl) but decreased in both the etomidate I and etomidate II groups (-3.0 +/- 0.7 ng/dl and -3.3 +/- 1.0 ng/dl, respectively). Because ACTH was administered exogenously, etomidate-induced suppression of adrenocortical response appeared to be a direct effect on the adrenal gland, which was present at a time when the serum etomidate levels were in the subhypnotic range.(ABSTRACT TRUNCATED AT 250 WORDS)     

Treatment of azotemic, nonoliguric, anemic patients with human recombinant erythropoietin raises whole-blood viscosity proportional to hematocrit.

It has been reported that patients with azotemia have reduced red blood cell (RBC) deformability. Since this is a major determinant of whole-blood viscosity (WBV) and rigid RBCs increase WBV disproportionately relative to the level of hematocrit, it is conceivable that sustained improvement of hematocrit with recombinant human erythropoietin (rhEPO) therapy in azotemic patients might result in abnormally raised WBV. To address this concern, WBV and plasma viscosity (PV) were measured in 9 adult patients (4 men, 5 women) with anemia (mean hematocrit 29.2 +/- 2.7%) and azotemia [mean serum creatinine concentration 339.85 +/- 102.44 mumol/l (3.8 +/- 1.1 mg/dl)] before and after 6 months of treatment with rhEPO (50-175 U/kg given intravenously thrice weekly). Baseline and post-treatment hematocrit, WBV and PV were compared to values derived in 50 normal adult subjects with normal renal function [25 women, 25 men; mean serum creatinine concentration 79.56 +/- 8.84 mumol/l (0.9 +/- 0.1 mg/dl), mean hematocrit 42.4 +/- 3.7%]. To compare rheologic factors at subnormal hematocrits, blood from subjects with normal renal function was diluted with autologous plasma to achieve a range of hematocrits from 20 to 50%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Association of morbidity with markers of nutrition and inflammation in chronic hemodialysis patients: a prospective study

BACKGROUND: Numerous studies suggest a strong association between nutrition and clinical outcome in chronic hemodialysis (CHD) patients. Nevertheless, the pathophysiological link between malnutrition and morbidity remains to be clarified. In addition, recent evidence suggests that nutritional indices may reflect an inflammatory response, as well as protein-calorie malnutrition. In this study, we prospectively assessed the relative importance of markers of nutritional status and inflammatory response as determinants of hospitalization in CHD patients. METHODS: The study consisted of serial measurements of concentrations of serum albumin, creatinine, transferrin, prealbumin, C-reactive protein (CRP), and reactance values by bio-electrical impedance analysis (BIA) as an indirect measure of lean body mass every 3 months over a period of 15 months in 73 CHD patients. Outcome was determined by hospitalizations over the subsequent three months following each collection of data. RESULTS: Patients who required hospitalization in the three months following each of the measurement sets had significantly different values for all parameters than patients who were not hospitalized. Thus, serum albumin (3.93 +/- 0.39 vs. 3.74 +/- 0.39 g/dl), serum creatinine (11.0 +/- 3.7 vs. 9.1 +/- 3.5 mg/dl), serum transferrin (181 +/- 35 vs. 170 +/- 34 mg/dl), serum prealbumin (33.6 +/- 9.2 vs. 30.0 +/- 10.1 mg/dl), and reactance (50.4 +/- 15.6 vs. 43.0 +/- 13.0 ohms) were higher for patients not hospitalized, whereas CRP (0.78 +/- 0.89 vs. 2.25 +/- 2.72 mg/dl) was lower in patients who were not hospitalized. All differences were statistically significant (P < 0.05 for all parameters). When multivariate analysis was performed, serum CRP and reactance values were the only statistically significant predictors of hospitalization (P < 0.05 for both). When a serum CRP concentration of 0.12 mg/dl was considered as a reference range (relative risk 1.0), the relative risk for hospitalization was 7% higher (relative risk = 1.07) for a CRP concentration of 0.92 mg/dl and was 30% (relative risk = 1.30) higher for a CRP concentration of 3.4 mg/dl. When a reactance value of 70 ohms was considered as a reference range with a relative risk of 1.0, the relative risk of hospitalization increased to 1.09 for a reactance value of 43 ohms and further increased to 1.14 for a reactance value of 31 ohms. CONCLUSIONS: The results of this study strongly indicate that both nutritional status and inflammatory response are independent predictors of hospitalization in CHD patients. CRP and reactance values by BIA are reliable indicators of hospitalization. Visceral proteins such as serum albumin, prealbumin, and transferrin are influenced by inflammation when predicting hospitalization. When short-term clinical outcomes such as hospitalizations are considered, markers of both inflammation and nutrition should be evaluated.     

Efficiency of 1-year treatment with fluvastatin in hyperlipidemic patients with nephrotic syndrome.

The influence of fluvastatin, a liver-selective, competitive inhibitor of the 3-hydroxymethyl-glutaryl-coenzyme A reductase, on the lipoprotein metabolism was investigated in 9 patients with nephrotic syndrome. All patients had biopsy-proven renal disease as cause of their nephrotic syndrome and exhibited severe hyperlipidemia [baseline: serum cholesterol 358 +/- 46 mg/dl (9.3 mmol/l), low-density lipoprotein cholesterol 236 +/- 18 mg/dl (6.1 mmol/l), triglycerides 333 +/- 28 mg/dl (3.8 mmol/l), and lipoprotein Lp(a) 46 +/- 11 mg/dl]. After 1 year of 40 mg of fluvastatin, significant reductions of total cholesterol by 31% to 242 +/- 26 mg/dl (6.3 mmol/l) and low-density lipoprotein cholesterol by 29% to 162 +/- 12 mg/dl (4.2 mmol/l) were observed. Furthermore, triglyceride values were also lowered significantly by 19% to 268 +/- 21 mg/dl (3.1 mmol/l). Lipoprotein Lp(a) and high-density lipoprotein-cholesterol remained unchanged by fluvastatin. These improvements in lipid profile were maintained during the entire follow-up period of 1 year. There were no adverse events, and the slight increase in serum creatinine observed during the study was considered to be due to the primary renal disease. In conclusion, long- term administration of fluvastatin in patients with nephrotic syndrome appears to be an effective and safe treatment of the hyperlipidemia associated with this disorder.