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Biomedical subjects

M Litwin

Publications and source records attributed to M Litwin.

At least 19 recordsLinked to original sources

Folate, vitamin B12, and sulfur amino acid levels in patients with renal failure.

We examined the plasma profile of sulfur amino acids (SAA) in patients with chronic renal failure (CRF) and looked for any correlation with serum folate (FA) and/or vitamin B12. Group 1 comprised 9 patients with CRF and glomerular filtration rate (GFR) >20 ml/min per 1.73 m2, 9 patients with GFR<20 ml/min per 1.73 m2 comprised group 2, and 14 patients on hemodialysis group 3. The control group comprised 16 healthy children. Homocysteine (Hcy), methionine (Met), cysteine (Cys), and serine (Ser) were measured with gas chromatography. FA and vitamin B12 were measured using enzymatic immunoassay. Median SAA concentrations were significantly lower in controls than in the three groups of patients. Hcy concentrations were 0.8 micromol/l in controls versus 5 micromol/(group 1), 9 micromol/l (group 2), and 20 micromol/l (group 3). Met concentrations were 26 micromol/l in controls versus 26 micromol/l (group 1), 66 micromol/l (group 2), and 281 micromol/l (group 3). Cys concentrations were 10 micromol/ in controls versus 98 micromol/l (group 1), 54 micromol/l (group 2), and 122 micromol/l (group 3). Ser concentrations were 88 micromol/ in controls versus 153 micromol/l (group 1), 239 micromol/l (group 2), and 240 micromol/l (group 3). The median concentrations of FA were lower in controls than in groups 2 and 3: 5.5 ng/ml versus 8 ng/ml and 15 ng/ml, respectively. Vitamin B12 concentrations did not differ between groups. Vitamin levels did not correlate with SAA. The only difference between patients with Hcy levels in the lower and upper quartile was in Met concentration (38 vs. 263 micromol/l, P<0.02) and GFR (P<0.01). In conclusion, patients with CRF had higher SAA concentrations than healthy children. FA concentrations are higher in CRF patients than in healthy children but did not correlate with concentrations of SAA.

Adolescent↗

Patient survival and causes of death on hemodialysis and peritoneal dialysis--single-center study.

Survival and causes of death in children dialyzed in a single center were analyzed. During the last 12 years a chronic dialysis program was introduced in 146 children in our center and 125 of them, eligible for observation, were included in this analysis; 58 patients were on hemodialysis (HD) and 67 on peritoneal dialysis [continuous ambulatory peritoneal dialysis/automated peritoneal dialysis (CAPD/APD)]. Mean age at the start of dialysis was 13.1 years in HD and 9.8 years in CAPD/APD patients. Overall, 16 patients died (12.5%); 6 (10.3%) on HD and 10 (14.9%) on CAPD/APD; 4 HD patients died of hemorrhagic stroke and 2 were killed in road traffic accidents. Of 10 CAPD/APD patients, 7 died of heart failure, ischemic stroke, and/or disseminated thromboembolic disease. Another was killed in a road traffic accident and 2 died during the course of severe infections. The 1-year patient survival rate was 96.6% in HD patients and 95% in CAPD/APD patients, 2-year survival 94% and 93% and 5-year survival 91% and 78%, respectively (P=0.2, NS). In conclusion, the survival rate for HD and CAPD patients is similar, although after 2 years of therapy, it is lower in CAPD patients. The main causes of death are cardiovascular. However, in CAPD/APD patients, heart failure with low cardiac output and thromboembolic complications are major causes of death, and in HD patients the main cause is hemorrhagic stroke.

Adolescent↗

[Tubulointerstitial nephritis related to immunotherapy and immunostimulation: a report of two cases].

Two cases of tubulointerstitial nephritis (TIN) with renal failure related to immunotherapy (case 1) and immunostimulation (case 2) have been described. Case 1: 18 years old male patient with hay fever was admitted because of rapid increase of serum creatinine from 1.1 mg/dl to 5.5 mg/dl, fever, weight loss and anemia which developed during 6 months after second course of immunotherapy. Case 2: 12 years old boy was admitted because of fever, weight loss and rapid progression to renal failure after treatment of pharyngitis with antibiotics and immunostimulant drug. In both patients renal biopsy was performed and TIN with huge lymphocytes T infiltrates was diagnosed. After 6 months treatment with corticosteroids renal function turned back to previous levels in both patients. Pathogenesis and treatment of TIN is discussed.

Adjuvants, Immunologic↗

[Sulphur amino acids, vitamin B12 and folic acid in children with chronic renal failure].

UNLABELLED: Aim of the study was to: 1) estimate plasma profile of sulphur AA in children with chronic renal failure (CRF) and in children on hemodialysis (HD), and 2) to evaluate any correlation with serum folic acid (FA) and vitamin B12. PATIENTS: 32 pts with CRF: 9 with GFR > 20 ml/min/1.73 m2 (group 1), 9 with GFR < 20 ml/min/1.73 m2 (group 2), and 14 pts on HD (group 3). METHODS: plasma homocysteine (Hcys), methionine (Met), cysteine (Cys), serine (Ser) were measured with gas chromatography. Serum FA and vit. B12 were measured using MEIA method. RESULTS: median Hcys concentrations were the lowest in group 1: 5 mumol/l vs 9 mumol/l (group 2) and 20 mumol/l (group 3) (p = 0.03). Similarly, the lowest Met levels were observed in group 1--26 mumol/l, vs 66 mumol/l (group 2) and 281 mumol/l (group 3) (p = 0.001). Median Cys level in group 1 was 98 mumol/l vs 54 mumol/l (group 2), and 122 mumol/l (group 3) (p = 0.02). No differences were found in median Ser levels: 153 mumol/l (group 1) vs 239 mumol/l (group 2) and 240 mumol/l (group 3). The median concentrations of FA were 6.3 ng/ml (group 1) vs 8 ng/ml (group 2) and 15 ng/ml (group 3) (NS). Median concentrations of vit. B12 were 256 pg/ml (group 1) vs 379 pg/ml (group 2) and 322 pg/ml (group 3) (NS). There were no correlation between sulphur AA and FA and vit. B12 levels. The only difference between pts with Hcys levels remaining in lower and upper quartile concerned Met concentration (38 vs 263 mumol/l, p < 0.02) and GFR (p < 0.01). CONCLUSIONS: Hyperhomocysteinemia develops already in moderate CRF. In pts on HD levels of Met and Cys are also raised. FA and vit. B12 concentrations are normal and do not correlate with plasma concentrations of sulphur AA.

Adolescent↗

[Analysis of causes of death in children and adolescents on chronic peritoneal dialysis and hemodialysis in 10 year period: single center experience].

Causes of death in children and adolescents treated with chronic peritoneal dialysis or hemodialysis in 1990-1999 in single centre were analysed. Overall 131 patients were treated, including 55 on peritoneal dialysis (PD) and 76 on hemodialysis (HD). Overall mortality in a 10-year period was 12% (16 patients). 10 patients in PD (18%) and 6 patients in HD group (7.8%) died. The main causes of death in PD patients were cardiac insufficiency, sudden cardiac arrest, ischemic stroke and atherothrombotic disease. In HD patients the main cause of death was hemorrhagic stroke.

Adolescent↗

[Familial, recurring plasma infusion dependent thrombotic thrombocytopenic purpura/hemolytic uremic syndrome].

Two siblings with chronic relapsing TTP/HUS from early childhood are presented. An onset of the disease was probably neonatal period and it did not involved the organ until puberty. During puberty the course of the disease aggravated with renal involvement and became fulminant in a girl who died disseminated TTP. Her older brother had episode of severe atypical HUS responding to plasma therapy. Now, his renal function is normal but the symptoms are depend an regular, prophylactic plasma infusions.

Adolescent↗

[Different effect of angiotensin convertase inhibitors and AT1 receptor blockers on renal function in patients with chronic renal failure: report of two cases].

In two patients with chronic renal failure (CRF) different effects of angiotensin convertase inhibitors (ACEI) and angiotensin receptor 1 blockers (AT1B) were observed. In patient 1 with CRF due to hemolytic-uremic syndrome (HUS), with arterial hypertension (HT) and proteinuria, a switch from AT1B to ACEI led to significant deterioration of renal function. After restitution of AT1B, renal function returned to previous range. The 2nd patient with CRF and severe HT, without proteinuria, due to atypical HUS, was on CAPD. Because of severe HT he received 3-4 hypertensives and ACEI in full dose was the main medication. Despite relatively low urea and creatinine values while on dialysis and high residual diuresis several attempts an end of CAPD was unsuccessful because of hyperkalemia and unacceptable increase of urea and creatinine concentrations after few days. Conversion from ACEI to AT1B enabled withholding CAPD, stabilisation of renal function and good control of HT. It seems that in patients with CRF without hyperfiltration syndrome and sensitive to changes in glomerular hemodynamics, in whom blockade of angiotensin action is needed AT1B may be a better option than ACEI. When using ACEI in patients with CRF, it is important to adjust the dose to renal function.

Adolescent↗

[Mechanism of progression of chronic renal failure and new treatment strategies].

Chronic renal failure is a self-perpetuating, progressive disease leading to end-stage renal failure, even if primary insult to the kidneys was removed. Progressive course of disease is caused by chronic interstitial inflammation leading to fibrosis, tubular atrophy, and glomerular sclerosis. Main predictive risk factors of the disease progression include: proteinuria, systemic and glomerular hypertension. It is presumed that in most cases progressive course of the disease is related to genetic predisposition to greater activity of renin-angiotensin system. Among attempts to slow progressive course of the disease effective are interventions acting on renin-angiotensin system, endothelin 1 and on profibrotic cytokines. Role of dietary factors and potential treatment modalities are discussed.

Angiotensin-Converting Enzyme Inhibitors↗

Novel cytokine-independent induction of endothelial adhesion molecules regulated by platelet/endothelial cell adhesion molecule (CD31).

Tumor necrosis factor-alpha, interleukin-1, and endotoxin stimulate the expression of vascular endothelial cell (EC) adhesion molecules. Here we describe a novel pathway of adhesion molecule induction that is independent of exogenous factors, but which is dependent on integrin signaling and cell-cell interactions. Cells plated onto gelatin, fibronectin, collagen or fibrinogen, or anti-integrin antibodies, expressed increased amounts of E-selectin, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1. In contrast, ECs failed to express E-selectin when plated on poly-L-lysine or when plated on fibrinogen in the presence of attachment-inhibiting, cyclic Arg-Gly-Asp peptides. The duration and magnitude of adhesion molecule expression was dependent on EC density. Induction of E-selectin on ECs plated at confluent density was transient and returned to basal levels by 15 h after plating when only 7 +/- 2% (n = 5) of cells were positive. In contrast, cells plated at low density displayed a 17-fold greater expression of E-selectin than did high density ECs with 57 +/- 4% (n = 5) positive for E-selectin expression 15 h after plating, and significant expression still evident 72 h after plating. The confluency-dependent inhibition of expression of E-selectin was at least partly mediated through the cell junctional protein, platelet/endothelial cell adhesion molecule-1 (PECAM-1). Antibodies against PECAM-1, but not against VE-cadherin, increased E-selectin expression on confluent ECs. Co- culture of subconfluent ECs with PECAM-1- coated beads or with L cells transfected with full-length PECAM-1 or with a cytoplasmic truncation PECAM-1 mutant, inhibited E-selectin expression. In contrast, untransfected L cells or L cells transfected with an adhesion-defective domain 2 deletion PECAM-1 mutant failed to regulate E-selectin expression. In an in vitro model of wounding the wound front displayed an increase in the number of E-selectin-expressing cells, and also an increase in the intensity of expression of E-selectin positive cells compared to the nonwounded monolayer. Thus we propose that the EC junction, and in particular, the junctional molecule PECAM-1, is a powerful regulator of endothelial adhesiveness.

Blood Platelets↗