Search

Byline: A. Nobilis (1), I. Kocsis (2), P. Toth-Heyn (3), A. Treszl (2), A. Schuler (4), T. Tulassay (2), B. Vasarhelyi (2) Keywords: Keywords Acute renal failure; Very low birth weight infant; Angiotensin converting enzyme; Angiotensin II type 1 receptor; Genetic polymorphism Abstract: High neonatal activity of the renin-angiotensin system (RAS) is crucial for the maintenance of glomerular filtration of the newborn. The aim of the present study was to investigate whether genetic polymorphisms leading to lower angiotensin converting enzyme activity (ACE) or impaired functionality of angiotensin II (AII) type 1 receptor (AT1R) might predispose very low birth weight newborns (VLBWs) to the development of acute renal failure (ARF). The medical records of 110 VLBW infants were analyzed. ARF developed in 42 of them during the first postnatal week, while 68 neonates exhibited normal renal function. The ACE I/D polymorphism and the [A.sup.1166]C variants of AT1R were determined from dried blood samples. The frequency of the ACE I allele did not differ in ARF and non-ARF groups (0.307 and 0.284) the frequency of the AT1R C.sup.1166 variant was also the same in ARF and non-ARF groups (0.250 and 0.227). Although low activity of RAS has been implicated in the development of neonatal ARF and data indicated that the functionality of RAS is influenced by the I/D variants of the ACE gene and the [A.sup.1166]C variant of the AT1R gene, we could not demonstrate any effect of these polymorphisms on the development of ARF in VLBW infants. Author Affiliation: (1) Second Department of Obstetrics and Gynecology, Semmelweis University, Budapest, Hungary, HU (2) Joint Research Program of the First Department of Pediatrics and the Hungarian Academy of Sciences, Semmelweis University, Budapest, Hungary, HU (3) First Department of Pediatrics, Semmelweis University, Bokay u. 53, 1083 Budapest, Hungary. Vasbar@gyer1.sote.hu, HU (4) Budai Children's Hospital PKU Laboratory, Budapest, Hungary, HU Article note: Received: 7 March 2001 / Revised: 9 August 2001 / Accepted: 10 August 2001

Byline: G. Miltenyi (1), K. Tory (1), G. Stubnya (1), P. Toth-Heyn (1), B. Vasarhelyi (2), P. Sallay (1), A. Szabo (1), T. Tulassay (2), M. Dobos (1), G. S. Reusz (1) Keywords: KeywordsaCardiac output; Chronic renal failure; Endogenous digoxin-like factor; Impedance cardiography; Sodium pump Abstract: Hemodialysis (HD) causes rapid volume shifts and circulatory changes. In chronic renal failure (CRF) Na.sup.+/[K.sup.+]ATP-ase is depressed, whereas endogenous digoxin-like factor (EDLF) is elevated. Our aim was to characterize HD-induced cardiovascular adaptation and its possible links to Na.sup.+/[K.sup.+]ATP-ase and EDLF. Eleven children with CRF on HD (aged 14.7+-3.7 years) and 11 healthy children were investigated for basic circulatory parameters. Thoracic impedance (Zo) and circulatory parameters were monitored by impedance cardiography (ICG) during HD. Erythrocyte Na.sup.+/[K.sup.+]ATP-ase and EDLF were measured before and after HD. Up to the loss of 6% of total body weight, Zo rose linearly with fluid removal, above this no further increase occurred. Heart rate and mean arterial pressure (MAP) were inversely related (r=--0.97) MAP rose in the first and decreased in the second part of HD. Systemic vascular resistance paralleled MAP, whereas stroke volume rapidly decreased, but stabilized in the second part of HD. The ratio of preejection period/ventricular ejection time (PEP/VET) correlated positively with HD duration (r=0.92), suggesting diminished cardiac filling. Cardiac index (CI) remained stable. EDLF was high in uremia accompanied by depressed Na.sup.+/[K.sup.+]ATP-ase (P&lt 0.05 and P&lt 0.01, respectively). Following HD Na.sup.+/[K.sup.+]ATP-ase normalized. Correlation between Na.sup.+/[K.sup.+]ATP-ase activity and MAP was linear (r=0.85). In conclusion, ICG during HD provides detailed information concerning circulatory adaptation resulting in stable CI, suggesting that the dialysis-induced hypovolemia is compensated by the centralization of the blood volume. Changes of Na.sup.+/[K.sup.+]ATP-ase indicate that dialyzable blood pressure-regulating substance(s) inhibit(s) the pump. However, lack of further correlation between Na.sup.+/[K.sup.+]ATP-ase, EDLF, and cardiovascular parameters indicates the complexity of the regulatory processes. Author Affiliation: (1) Ist Department of Pediatrics, Semmelweis Medical University, Bokay u. 53, 1083 Budapest, Hungary, HU (2) Research Laboratory of the Hungarian Academy of Sciences, Bokay u. 53, 1083 Budapest, Hungary, HU (3) First Department of Pediatrics, Semmelweis Medical University, Bokay u. 53, 1083 Budapest, Hungary e-mail: reusz@gverl.sote.hu Fax: +36-1-3247795, HU Article note: Received: 12 May 2000 / Revised: 28 August 2000 / Accepted: 30 August 2000

Byline: B. Vasarhelyi (2), M. Dobos (2), G. S. Reusz (2), A. Szabo (2), T. Tulassay (1) Keywords: Key wordsaLow birth weight; Renal function; Natriuresis; Blood pressure; Na+/K+-ATPase activity Abstract: The aim of our study was to characterize renal function and its relationship to blood pressure in healthy young Caucasian men born with a birth weight under 2,500 g (LBW). Urinary protein patterns, N-acetylglucosamine and I3-glutamyltransferase activities, fractional sodium and potassium excretions, glomerular filtration rate, blood pressure, and erythrocyte Na.sup.+/K.sup.+-ATPase activities were determined in 65 subjects, of whom 49 were born with LBW. Signs of glomerular or tubular damage were not detected in the LBW population. However, the blood pressure and the renal sodium excretion were inversely correlated to the subjects' birth weight and were higher in LBW subjects than in controls. In contrast, the erythrocyte Na.sup.+/K.sup.+-ATPase activities were lower in LBW subjects. An inverse correlation was detected between the subjects' Na.sup.+/K.sup.+-ATPase activities and the renal sodium excretion or blood pressure. In summary, our results suggest that: (1) in young LBW Caucasian males signs of early glomerular and tubular impairment are not present (2) the elevated renal sodium excretion may be a result of higher blood pressure (3) the alteration of Na.sup.+/K.sup.+-ATPase activity might play a role either in the elevation of blood pressure and/or in the enhanced natriuresis of LBW subjects. Author Affiliation: (1) First Department of Pediatrics, Bokay u. 53, 1083 Budapest, Hungary e-mail: tulas@gyer1.sote.hu Tel.: +36-1-3142858, Fax: +36-1-3138212, HU (2) First Department of Pediatrics, Semmelweis Medical University, Budapest, Hungary, HU Article note: Received: 29 November 1999 / Revised: 20 March 2000 / Accepted: 22 March 2000

Byline: T. Tulassay (1), M. Dobos (1), A. Luczay (1), G. Stubnya (1), G. S. Reusz (1), B. Vasarhelyi (1), P. Sallay (1), A. Szabo (1) Keywords: Key wordsaNephrotic syndome; Sodium-lithium countertransport; Natrium-hydrogen exchanger; Edema sodium homeostasis Abstract: The mechanisms of sodium retention in edema-forming minimal change nephrotic syndrome (MCNS) have not been completely evaluated. The aim of this study was to characterize the transmembrane sodium transport in nephrotic syndrome by measuring the erythrocyte sodium-lithium countertransport (SLC) in vitro. Eighteen children with MCNS were studied in the edema-forming state, and subsequently at the beginning of remission. Nephrotic children with edema retained sodium (10+-12 umol/day) and had a higher SLC [426+-118 vs. 281+-60 Aumol/l red blood cells (RBC) per hour, P=0.003). The intracellular sodium concentration of nephrotics was 6.1+-2.1 mmol/l RBC, which did not differ from that of controls (6.42+-2.24, n=13). In remission sodium balance became negative (--30 +-21 mmol/day), and the SLC decreased but still differed significantly from control values (P=0.009). The intracellular sodium content decreased to 4.4+-0.9 mmol/l RBC (P=0.002). There was a negative correlation between erythrocyte SLC and plasma albumin concentration (r=0.48, P=0.003), and urinary sodium excretion rate (r=0.66, P=0.001). In conclusion, erythrocyte SLC is high in the edema-forming state of childhood nephrotic syndrome and decreases with the onset of remission. A role for the SLC in the altered sodium homeostasis of nephrotic syndrome is suggested. Author Affiliation: (1) 1st Department of Paediatrics, Semmelweis Medical University, Bokay utca 53, H-1083 Budapest, Hungary e-mail: tulas@gyer1.sote.hu Tel.: +36-1-31-42858, Fax: +36-1-30-36077, HU Article note: Received: 6 April 1998 / Revised: 5 October 1998 / Accepted: 4 November 1998