Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Centers have reported superior growth in children on peritoneal dialysis (PD) as compared to hemodialysis (HD). Many factors may influence this outcome including diet, adequacy of dialysis, and control of metabolic acidosis. The role of insulin-like growth factor-1 (IGF-1) and its bioactivity in patients with end-stage renal disease (ESRD) have been recently examined. Insulin-like growth factor binding protein-3 (IGFBP-3) has been shown to be elevated in ESRD, possibly resulting in inhibition of the bioactivity of IGF-1. Potentially, the removal of IGFBP-3 may improve the bioactivity of IGF-1, with resulting improvement in growth. The molecular weight of IGFBP-3 (30.5 kDa) is in the range of other proteins cleared by PD (e.g., albumin-69 kDa). Therefore, we have analyzed 10 samples of IGFBP-3 in the dialysis effluent of 9 children on peritoneal dialysis, and have found that the mean level +/- SEM was 0.21 +/- 0.03 mg/L, while the 3 analyses of children on standard HD was 0.02 +/- 0.01 mg/L. In addition, the effluent of 2 children on a high-efficiency dialyzer had an IGFBP-3 level of 0.45 +/- 0.25 mg/L. Even though quite preliminary, these data may suggest another reason for improved growth in children on PD and a potential advantage to high-efficiency HD. Further analysis in a larger population of ESRD patients will be needed in order to confirm these preliminary findings.
Adv Perit Dial 1994
PMID:Dialysis modality comparison of insulin-like growth factor binding protein-3 removal in children: could this have a potential growth benefit? 752 57

Because adhesion properties of leukocytes are important for the influx and localization of leukocytes in sites of inflammation, we studied, the expression of intercellular adhesion molecule 1 (ICAM-1), lymphocyte-function-associated antigen 1 (LFA-1), vascular cell adhesion molecule- 1 (VCAM-1) and CD 11b in 14 kidney biopsies of PSGN patients, arbitrarily divided into early biopsies (less than 15 days after onset of PSGN) and late biopsies (17-90 days). In PSGN, intraglomerular ICAM-1 expression was increased in early biopsies (score 3.1 +/- SEM 0.2; P < 0.005) and decreased with time; in late biopsies the score (2.0 +/- 0.2) was similar to that of normal kidney (1.3 +/- 0.3). In the interstitium ICAM-1 was increased (early PSGN = 836 +/- 56 positive cells/mm2, late = 552 +/- 60.0; versus normal = 364 +/- 12.4; P < 0.05). LFA-1 expressing cells in glomeruli were also increased in early biopsies (10.0 +/- 2.1 positive cells per glomerular cross-section (gcs), versus normal 2.9 +/- 1.4; P < 0.05). In the interstitium, LFA-1 positive cells were increased (early PSGN = 221 +/- 79.6 cells/mm2, late PSGN = 134.5 +/- 45.1, normal = 21 +/- 8.7; P < 0.05). VCAM-1 in glomeruli and interstitium was not increased in PSGN. Our studies demonstrate increased expression of adhesion molecules ICAM-1 and LFA-1 in the kidney of PSGN patients, and these findings were more pronounced in early biopsies; adhesion molecules are probably involved in the inflammatory infiltration of this disease.
Nephrol Dial Transplant 1994
PMID:Expression of adhesion molecules in poststreptococcal glomerulonephritis. 752 80

Patients on cyclosporin A (CsA) often develop hyperuricaemia and gout. In transplant patients the use of uricosuric drugs for treating hyperuricaemia may be preferable to allopurinol because of the known interaction of the latter with azathioprine. We therefore prospectively studied the uricosuric efficacy of 100 mg benzbromarone (Bbr;Desuric) daily in 25 CsA-treated renal transplant patients with stable graft function and hyperuricaemia (> 359 mumol/l for females, > 491 mumol/l for males). Benzbromarone decreased plasma uric acid from 579 + 18 mumol/l to 313 +/- 24 mumol/l (mean +/- SEM; P < 0.0001) and thereby normalized plasma uric acid in 21 of 25 patients. The remaining four patients had creatinine clearances between 21 and 25 ml/min, the lowest of the entire study group. Mean fractional clearance of uric acid increased from 5.4 +/- 0.4% to 17.2 +/- 1.0% (P < 0.001). The relative decrease of plasma uric acid closely correlated with baseline creatinine clearance (r = 0.67; P < 0.001). CsA trough values were not influenced. None of the patients experienced any significant side-effects. As an unexpected find-ing, urinary uric acid excretion increased from 2082 +/- 175 mumol/24 h to 3233 +/- 232 mumol/24 h after 4 weeks' treatment with benzbromarone. In conclusion, benzbromarone normalized plasma uric acid in all CsA-treated renal transplant recipients with a creatinine clearance > 25 ml/min. Due to its excellent efficacy and lack of significant side-effects, benzbromarone appears to be preferable to allopurinol in CsA-treated renal transplant recipients with a creatinine clearance over 25 ml/min.
Nephrol Dial Transplant 1994
PMID:Excellent uricosuric efficacy of benzbromarone in cyclosporin-A-treated renal transplant patients: a prospective study. 809 Mar 36

Loss of net ultrafiltration capacity is an important complication in long-term continuous ambulatory peritoneal dialysis (CAPD). It has been reported in animal studies that the drained volumes after a dwell period were larger when amphotericin B had been given intraperitoneally. In this study the effect of intraperitoneally administered amphotericin B on fluid kinetics was evaluated in 3 CAPD patients. The first patient lost 2.5 kg body weight during the first 4 days of treatment, whereas the net ultrafiltration in the second patient was higher in the treatment period compared with the nontreatment period (750 +/- 38 mL/day vs 438 +/- 34 mL/day (mean +/- SEM), p < 0.0001). In the last patient it can be demonstrated that the increase in the net ultrafiltration was caused by an increase in the transcapillary ultrafiltration (570 vs 454 mL/4 hours), but that lymphatic absorption was not different (251 vs 265 mL/4 hours). The higher transcapillary ultrafiltration capacity is probably caused by an increase in the hydraulic permeability. It is likely that this phenomenon is governed by the interaction of amphotericin B with membrane-bound cholesterol leading to the formation of transcellular pores. However, the administration of amphotericin B caused a chemical peritonitis, probably due to its solvent, sodium desoxycholate. Therefore, before amphotericin B can be used for the treatment of CAPD patients with ultrafiltration failure, further investigations are necessary to obtain a solvent for amphotericin B that is nontoxic and causes no chemical peritonitis.
Adv Perit Dial 1993
PMID:The effect of amphotericin B on fluid kinetics and solute transport in CAPD patients. 810 4

Renal patients are prone to malnutrition. This is of particular concern in patients undergoing peritoneal dialysis because of the loss of protein in the dialysate. Data comparing the adequacy of continuous cycling peritoneal dialysis (CCPD) and continuous ambulatory peritoneal dialysis (CAPD) are few. To compare nutritional status and dialysis adequacy, 32 patients were studied (19 CAPD, 13 CCPD). Weight change, dietary intake, degree of edema, and laboratory parameters (hemoglobin, albumin, urea, creatinine) were assessed. Dialysis efficiency was compared using urea and creatinine kinetics [KT/V(urea), normalized protein catabolic rate (PCRN), efficacy number, weekly creatinine clearance]. Age was similar in each group [CAPD 56.5 years (34-75 years); CCPD 53.5 years (14-76 years)]. There were no significant differences in hemoglobin, albumin [29 +/- 1.3 g/L CAPD; 32 +/- 1.5 g/L CCPD (mean +/- SEM)], urea, or creatinine between groups, nor in KT/V (1.72 +/- 0.15 CAPD; 1.93 +/- 0.17 CCPD) and PCRN (0.79 +/- 0.05 CAPD; 0.97 +/- 0.08 CCPD). The efficacy number was significantly higher in the CCPD patients (6.95 +/- 0.66 CAPD; 9.93 +/- 1.3 CCPD; p = 0.03). This study indicates that the nutritional status of CCPD patients at our center was similar to that of CAPD patients. Adequacy of dialysis was also similar in CCPD patients as compared with CAPD patients.
Adv Perit Dial 1993
PMID:Nutritional status and efficiency of dialysis in CAPD and CCPD patients. 810 68

Cytosolic free sodium concentration ([Na+]i) and sodium transport systems were measured in intact platelets from 19 patients with early-stage chronic renal failure and 33 healthy control subjects using the novel fluorescent dye sodium-binding-benzofuran-isophthalate. Resting [Na+]i was significantly greater in patients with chronic renal failure compared to control subjects (40.8 +/- 3.1 mmol/l versus 32.2 +/- 2.0 mmol/l, mean +/- SEM, P < 0.05). After inhibition of Na-K-ATPase by 1 mmol/l ouabain a higher net sodium influx was observed in platelets from patients with chronic renal failure compared to control subjects (49.8 +/- 8.7 mmol/l versus 28.5 +/- 5.2 mmol/l, P < 0.05). The platelet Na-H exchanger was similar in the two groups. Cytosolic free calcium concentration ([Ca2+]i) was measured using fura2 and did not show significant differences between the two groups. To evaluate whether a circulating factor may be associated with elevated [Na+]i, a linked-enzyme Na-K-ATPase assay was included. Compared to control subjects plasma from patients with chronic renal failure produced a significant inhibition of steady-state Na-K-ATPase activity by 11.2 +/- 3.0% (P < 0.01). It is concluded that early-stage renal failure is associated with significant impairment of platelet sodium metabolism.
Nephrol Dial Transplant 1994
PMID:Increased cytosolic free sodium in platelets from patients with early-stage chronic renal failure. 817 73

We studied 38 patients (9 haemodialysis, 18 peritoneal dialysis, 11 advanced renal failure) over the first 12 weeks of erythropoietin therapy. In 14 iron-overloaded patients (ferritin > 500 micrograms/l the haemoglobin (+/- SEM) increased from 6.74 +/- 0.27 to 9.85 +/- 0.36 g/dl (P < 0.0001) entirely by mobilizing iron reserves (reduced from 1,220 +/- 73 to 739 +/- 111 mg, P < 0.0001). In the 24 non-overloaded patients (ferritin < 500 micrograms/l) the haemoglobin rose similarly from 7.04 +/- 0.18 to 10.70 +/- 0.36 g/dl (P < 0.0001), partly from iron reserves (depleted from 200 +/- 74 to -44 +/- 77 mg, P = 0.016) and partly from oral iron supplements (305 +/- 110 mg). In the overloaded patients the ferritin declined from 1057 micrograms/l (geometric mean, range 504-3699) to 317 micrograms/l (42-1505, P < 0.0001). In the non-overloaded patients it declined from 82 micrograms/l (8-461) to 45 micrograms/l (5-379, P = 0.016). The transferrin saturation (TS) in the overloaded patients appeared to decline from 38.3 +/- 7.2% to 24.0 +/- 3.7% but this was not statistically significant. In the non-overloaded the TS was unchanged (23.3 +/- 2.4 before and 28.1 +/- 3.6% after treatment). Considering all 38 patients together, the haemoglobin correlated negatively with the ferritin (r = 0.3731, P < 0.001) but not with the TS. The TS correlated with the serum ferritin initially (r = 0.75, P < 0.001) but not after the first 4 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephrol Dial Transplant 1993
PMID:Monitoring of iron requirements in renal patients on erythropoietin. 797 Jan 8

The effects of nifedipine retard and captopril on renal haemodynamic parameters have been examined in a double blind randomised cross-over trial in 10 insulin-dependent diabetic males with hypertension (systolic pressure > 150 mmHg or diastolic pressure > 90 mmHg). The acute renal haemodynamic response to nifedipine retard 20 mg and captopril 25 mg was monitored at the start of therapy and again after 8 weeks treatment with nifedipine retard 20 mg b.d. and captopril 25 mg b.d. Blood pressure fell from 148/97 +/- 4/2 (SEM) during the run-in phase to 135/87 +/- 4/1.5 on nifedipine retard and to 131/83 +/- 5/1 on captopril. There was no difference between the initial renal response to the two agents; an increase in renal plasma flow and a non-significant decline in glomerular filtration rate resulted in similar decreases in filtration fraction. After 8 weeks therapy, neither drug had a significant effect on urinary albumin excretion. Baseline renal function did not differ and no acute changes in renal haemodynamics were seen after nifedipine. Following captopril there was no acute change in systemic blood pressure but RPF rose from 572 +/- 41 to 638 +/- 42 ml/min per 1.73 m2 (P < 0.05) and filtration fraction fell from 0.21 to 0.16 (P < 0.02). This sustained acute response of the renal circulation to angiotensin-converting enzyme (ACE) inhibition after chronic therapy may be relevant to the apparent renal protection afforded by ACE inhibitors in experimental nephropathies.
Nephrol Dial Transplant 1993
PMID:Renal responses to nifedipine and captopril in hypertensive insulin-dependent diabetic men: a randomized cross-over study. 838 84

Twenty-seven patients with renal failure (16 on CAPD and 11 predialysis) were treated with erythropoietin. At 12 weeks, the mean haemoglobin concentration (+/- SEM) in the CAPD patients had increased from 7.07 +/- 0.20 to 10.88 +/- 0.45 g/dl (two-tailed paired t test, P < 0.0001) and in the predialysis patients from 6.90 +/- 0.35 to 10.05 +/- 0.47 g/dl (P < 0.0001). Predialysis patients were taking more antihypertensive medication at baseline. No increase was required in either group after erythropoietin; there was no change in blood pressure in the CAPD patients, though in the predialysis patients the systolic blood pressure rose slightly from 132 to 146 mmHg (P = 0.029) and the mean blood pressure from 95 to 103 mmHg (P = 0.028). In 12 patients (6 on CAPD and 6 predialysis) the red cell volume, plasma volume, and total blood volume were measured before and after treatment. In the CAPD patients there was a marked expansion of the red cell volume from 912 +/- 127 to 1471 +/- 222 ml (P = 0.004) and a concomitant contraction of the plasma volume from 3932 +/- 250 to 3178 +/- 326 ml (P = 0.005), leaving the blood volume unchanged from 4843 +/- 352 to 4649 +/- 503 ml. Predialysis patients had a similar expansion of the red cell volume from 733 +/- 59 to 1304 +/- 161 ml (P = 0.017) but no contraction of the plasma volume (from 3417 +/- 354 to 3314 +/- 260 ml), so that the blood volume tended to expand from 4149 +/- 347 to 4618 +/- 414 ml (P = 0.053).(ABSTRACT TRUNCATED AT 250 WORDS)
Nephrol Dial Transplant 1993
PMID:Influence of blood volume on the blood pressure of predialysis and peritoneal dialysis patients treated with erythropoietin. 839 46

We conducted a single, blinded cross-over placebo versus lovastatin study on 10 continuous ambulatory peritoneal dialysis (CAPD) patients with dyslipoproteinemia who failed to respond to diet control. They were given 8 weeks of lovastatin (20-40 mg) and placebo, respectively. After 8 weeks of lovastatin treatment, total cholesterol was significantly reduced by 28.6% (6.68 +/- 0.26 mmol/L, mean +/- SEM, to 4.77 +/- 0.12, p < 0.01); low-density lipoprotein cholesterol by 40.5% (4.57 +/- 0.27 mmol/L to 2.72 +/- 0.09, p < 0.01); apolipoprotein B by 32.4% (115.9 +/- 6.99 mg/dL to 78.3 +/- 2.9 mg/dL, p < 0.01); and triglyceride by 17.8% (1.92 +/- 0.38 mmol/L to 1.58 +/- 0.32, p < 0.05). Simultaneously high-density lipoprotein cholesterol increased by 7.6% from 1.24 +/- 0.13 mmol/L to 1.34 +/- 0.16, p < 0.05. There were no significant changes in other lipid profiles between placebo and drug treatment. No significant adverse effects were observed with lovastatin treatment. Lovastatin appears to be effective in treating dyslipoproteinemia in CAPD patients.
Perit Dial Int 1993
PMID:Lovastatin treatment of dyslipoproteinemia in patients on continuous ambulatory peritoneal dialysis. 839 31


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