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M Polenakovic

Publications and source records attributed to M Polenakovic.

48 records · Page 3Linked to original sources
PubMed1996

Is erythropoietin a survival factor for red blood cells?

Recombinant human erythropoietin (rhuEPO) therapy has been reported to maintain corrected hematocrit values by increasing the length of red blood cell (RBC) survival. This article presents a controlled study that assessed the RBC survival before, during, and after termination of prolonged rhuEPO treatment of chronic hemodialysis patients. Two groups of 20 patients were studied. The hematocrit value of each patient was below 28 vol%. One group (Group A) was treated with rhuEPO for 1 yr and then treatment was stopped because of the unavailability of the drug. The second group (Group B) was treated for 2 yr. Epoetin beta was administered subcutaneously. The initial dose was 20 U per kg body weight three times weekly. Upon reaching the target hematocrit value of 30 to 35 vol%, the dose was individualized for each patient, to maintain target range. RBC survival was determined by the chromium-51 technique. In Group A, RBC survival was determined: (1) before, (2) at 12 months, and (3) 1 yr after cessation of rhuEPO treatment. In Group B, RBC survival was determined: (1) at 24 months of therapy, and (2) 1 yr after cessation of rhuEPO treatment. RBC survival increased significantly in both patient groups under rhuEPO treatment. After cessation of therapy, the RBC survival decreased to pretreatment values. During the correction period, reticulocyte counts increased significantly in both groups. Over the maintenance period, they slightly decreased, and after termination of rhuEPO therapy, they decreased to the pretreatment values. The results of this study could suggest the possibility that RBC survival was prolonged by the action of EPO on the erythroid progenitors, resulting in the production of RBC with improved viability.

Adult↗
PubMed1995

Crescentic glomerulonephritis as renal cause of acute renal failure.

Over a period of 5 years, we observed 28 patients with biopsy-proven crescentic glomerulonephritis. Four of these patients were ANCA associated (pauci immune), 1 had anti-glomerular basement membrane antibodies (anti-GBM), and the other 23 cases had immune complex form (22 poststreptococcal and 1 poststaphylococcal). Acute renal failure as a main clinical feature was found in 11/28 (35.7%), all with more than 80% crescents, including all ANCA-associated cases, anti-GBM form, and the patient with poststaphylococcal form. Using "pulse" therapy with methylprednisolone, cyclophosphamide, and plasmapheresis, renal function was improved in 5/11 (45.4%), diuresis started, and end-stage renal disease was delayed. The therapy was continued orally with steroids and cyclophosphamide. The second attach of oligoanuria developed after a period of 6-12 months without improvement after the therapy used previously (during the first attack), and it was necessary to begin chronic hemodialysis treatment.

Acute Kidney Injury↗
PubMed1994

Tubular basement membrane changes during induction and regression of drug-induced polycystic kidney disease.

Defective cell-extracellular matrix (ECM) biophysiology is considered a factor in the development of polycystic kidney disease (PKD). Altered biosynthesis of various ECM components may result in tubular dysmorphogenesis and uncontrolled tubular cystic expansion. In this study, expression of certain ECM components was investigated in a diphenylthiazole (DPT)-induced rat model of PKD. DPT induces cystic change in all the collecting tubules, most severe in the outer medulla and inner cortex, and following withdrawal of DPT, cystic tubules return to normal with persistence of focal interstitial fibrosis. SDS-PAGE analyses of isolated tubular basement membranes (TBMs) of control and PKD kidneys revealed overall similar electrophoretic migratory bands. However, in PKD, there were relative increases in components with M(r) approximately 380,000, 250,000 and 145,000, and a decrease in the component with M(r) approximately 55,000. Immunoblot analyses revealed that the major components of TBM (type-IV collagen, laminin beta 1 and beta 2 chains and entactin) were present in the same relative concentrations in control and PKD. The expression of tubulointerstitial (TIN) antigen was decreased. Also, the relative concentrations of type-I collagen and fibronectin were increased in the PKD group. Following recovery, the expressions of TIN and fibronectin returned to normal, whereas type-I collagen remained elevated. ELISA determinations revealed increased expression of interstitial collagens type-I, -V and -VI in PKD vs control and they remained elevated following recovery, while that of type-III was unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Analysis of heart morphology and function following erythropoietin treatment of anemic dialysis patients.

In a two-way study, we treated renal anemia in chronic hemodialysis patients with recombinant human erythropoietin (rh-EPO) and followed heart morphology and function dynamics by echocardiography. Thirty-eight patients were randomly divided in two equal groups: the therapy group, treated with rh-EPO for 24 months, and the control group, not treated during the first 12 months and treated with rh-EPO during the second 12 months. Anemia was corrected, and hematocrit was maintained between 30 and 35 vol% by subcutaneous rh-EPO administration. Echocardiographic assessment was performed at the end of the untreated control phase and was repeated after 12 months of rh-EPO treatment in the control group and after 12 and 24 months of treatment in the therapy group. The results revealed significant morphologic, hemodynamic, and eventually functional changes. After 12 months of rh-EPO treatment, the end-diastolic volume (EDV) decreased from 135.8 +/- 23.7 to 109.8 +/- 25.3 ml, p < 0.001; stroke volume (SV) from 91.9 +/- 17.6 to 71.3 +/- 12.4 ml, p < 0.001; left ventricular mass-Devereux (LVMD) from 297.2 +/- 57.8 to 218.0 +/- 50.4 g, p < 0.01; cardiac output (CO) from 7,279 +/- 1,932 to 5,711 +/- 1,276 ml/min, p < 0.002; total peripheral resistance (TPR) rose from 1,330 +/- 390 to 1,707 +/- 373 dynes x s/cm5, p < 0.007. After 24 months, LVMD decreased further from 224.6 +/- 43.1 to 195.7 +/- 46.3 g, p < 0.004. The relaxation time index (RTI) decreased from 64.7 +/- 20.4 to 52.4 +/- 18.0 ms, p < 0.045, suggesting improved diastolic function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Autonomic nervous system dysfunction and volume nonresponsive hypotension in hemodialysis patients.

Studies were conducted in 9 dialysis patients with volume-nonresponsive hypotension, 6 dialysis patients with volume-responsive hypotension and in 10 normal subjects in an effort to evaluate the role of dysfunction of the autonomic nervous system (ANS) in the genesis of volume-nonresponsive hypotension. ANS function was evaluated by the Valsalva maneuver, handgrip exercise, and by the response of heart rate and blood pressure to change of posture from a supine to a standing position. Patients with volume-nonresponsive hypotension displayed significant derangements in the function of ANS as compared to normal subjects and to patients with volume-responsive hypotension. Data show that dysfunction of ANS plays an important role in the genesis of volume-nonresponsive hypotension in dialysis patients.

Autonomic Nervous System Diseases↗
PubMed1985

Unilateral renal vein occlusion in rats.

To study the relationship of renal vein thrombosis to membranous glomerulonephritis with the nephrotic syndrome, we attempted to simulate the former by occluding to 0.5 mm one renal vein in rats. Although increased proteinuria did occur during the first 3 days after such occlusion, there was little difference from control animals in the amount of proteinuria thereafter, up to 46 days, and no evidence of membranous glomerulonephritis by light, immunofluorescent, or electron microscopy.

Animals↗