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Proteinuria, Not Altered Albumin Metabolism, Affects Hyperlipidemia in the Nephrotic Rat

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Proteinuria, Not Altered Albumin Metabolism, Affects Hyperlipidemia in the Nephrotic Rat Proteinuria, not altered albumin metabolism, affects hyperlipidemia in the nephrotic rat. R W Davies, … , F N Hutchison, G A Kaysen J Clin Invest. 1990;86(2):600-605. https://doi.org/10.1172/JCI114750. Research Article It has been established previously that nephrotic hyperlipidemia is characterized by both an increase in lipid synthesis and a defect in removal of lipoproteins. The relationship between these defects and altered albumin metabolism is uncertain. One hypothesis is that hepatic lipogenesis increases in parallel with albumin synthesis. To test this hypothesis, albumin synthesis was increased in nephrotic rats fed an 8.5% protein diet (LPN) by increasing dietary protein to 40% (HPN). Proteinuria was modulated in half of the rats fed 40% protein by enalapril (HPE). Albumin synthesis was the same in both HPN and HPE, but proteinuria was reduced in HPE compared to HPN, and so were serum cholesterol and triglycerides (TG). To examine the effect of serum albumin on lipid clearance in the absence of proteinuria, plasma clearance of chylomicrons (CM) and VLDL was measured in Nagase analbuminemic rats (NAR) and found to be no different than in normal SD rats. When proteinuria was induced in NAR and in SD rats, a severe and identical defect in both CM and VLDL clearance was acquired in both groups and blood lipid levels were increased to a similar degree in both groups. Neither hyperlipidemia nor defective removal of lipoproteins from the circulation are linked to albumin synthesis or serum albumin concentration but result, at least in part, from proteinuria. Postheparin lipoprotein […] Find the latest version: https://jci.me/114750/pdf Proteinuria, Not Altered Albumin Metabolism, Affects Hyperlipidemia in the Nephrotic Rat R. William Davies, ilona Staprans,* Florence N. Hutchison, and George A. Kaysen Renal Biochemistry Laboratory, Division ofNephrology Department ofMedicine, Veteran's Administration Medical Center, Martinez, California 94553, Department ofMedicine, University of California Davis School ofMedicine at Davis, California, 94110; *Department ofSurgery, Veteran's Administration Medical Center, San Francisco, California 94121; and University of California at San Francisco, San Francisco, California 94143 Abstract ance of circulating lipids, specifically chylomicrons (CM)' (1, 2) and VLDL is reduced (3) and hepatic synthesis of lipids and It has been established previously that nephrotic hyperlipid- lipoproteins is increased (4, 5). The nephrotic syndrome re- emia is characterized by both an increase in lipid synthesis and sults from altered glomerular permselectivity resulting in the a defect in removal of lipoproteins. The relationship between urinary loss of macromolecules. As a consequence, serum al- these defects and altered albumin metabolism is uncertain. bumin concentration and oncotic pressure (Xr) are reduced. One hypothesis is that hepatic lipogenesis increases in parallel The relationship between disordered lipid metabolism and with albumin synthesis. To test this hypothesis, albumin syn- these other manifestations of the nephrotic syndrome has been thesis was increased in nephrotic rats fed an 8.5% protein diet a subject of controversy. (LPN) by increasing dietary protein to 40% (HPN). Protein- Two separate hypotheses have been proposed to establish a uria was modulated in half of the rats fed 40% protein by relationship between proteinuria and altered lipid metabolism. enalapril (HPE). Albumin synthesis was the same in both One postulate is that proteinuria causes reduced serum 7r, HPN and HPE, but proteinuria was reduced in HPE compared which in turn directly stimulates albumin synthesis. The rate to HPN, and so were serum cholesterol and triglycerides (TG). of synthesis of all other liver-derived exported proteins, in- To examine the effect of serum albumin on lipid clearance in cluding lipoproteins, is proposed to be increased coordinately the absence of proteinuria, plasma clearance of chylomicrons with that of albumin since all share a common secretory path- (CM) and VLDL was measured in Nagase analbuminemic rats way (6-8). This model provides a mechanism for increased (NAR) and found to be no different than in normal SD rats. lipogenesis in nephrosis, but does not account for deranged When proteinuria was induced in NAR and in SD rats, a severe lipid removal. and identical defect in both CM and VLDLL clearance was A second hypothesis, proposed by Staprans and Felts was acquired in both groups and blood lipid levels were increased to that the urinary loss of a liporegulatory substance caused de- a similar degree in both groups. Neither hyperlipidemia nor fective removal of lipids from the circulation. They identified a defective removal of lipoproteins from the circulation are lipoprotein lipase (LPL) cofactor, heparan sulfate, lost in the linked to albumin synthesis or serum albumin concentration urine in the nephrotic syndrome (1, 2). but result, at least in part, from proteinuria. Postheparin lipo- The Nagase analbuminemic rat (NAR) is a strain of protein lipase (LPL) activity was reduced slightly in nephrotic Sprague Dawley (SD) rat incapable of synthesizing albumin animals compared to nonnephrotic controls, but the most (9). Albumin is replaced by several larger liver-derived macro- striking finding was a highly significant decrease in posthepa- globulins (10, 11). Serum protein concentration is normal rin LPL activity in normal NAR compared to SD rats (P (12), but serum ir is reduced. Although no urinary protein loss < 0.001), suggesting that reduced LPL activity is not responsi- occurs in normal NAR, serum cholesterol and TG are in- ble for reduced clearance of CM and VLDL in nephrotic rats. creased (13-15). The NAR provides an opportunity to study (J. Clin. Invest. 1990. 86:500-505.) Key words: analbumin- lipoprotein clearance in animals that have no albumin yet emia * nephrosis * chylomicrons * VLDL * lipoprotein lipase have no defect in glomerular permselectivity. It is also possible to alter glomerular permselectivity in these animals and deter- mine the effect of nonalbumin urinary protein loss on lipid Introduction metabolism. Dietary protein augmentation increases both the rate of Hyperlipidemia and hypoproteinemia are hallmarks of the ne- albumin synthesis (16) and impairs glomerular permselectivity phrotic syndrome. There is general agreement that the clear- (17) in SD rats with Heymann nephritis. Treatment with ena- lapril blunts the proteinuric effect of dietary protein augmen- tation, but not the stimulation of albumin synthesis (18). Thus A portion of this work has been published in abstract form in 1989. it is possible to independently modulate albumin synthesis and (Kidney Int. 35: 425a.) Address reprint requests to Dr. Kaysen, Associate Chief of Staff of for Education 1 l/E, VA Medical Center, 150 Muir Road, Martinez, 1. Abbreviations used in this paper: CM, chylomicrons; HPC, 40% CA 94553. protein diet control; HPCE, 40% protein control + enalapril; HPNE, Received for publication 27 June 1989 and in revised form 28 high protein diet with enalapril; LPC, 8.5% protein diet control; LPCE, March 1990. 8.5% protein control + enalapril; LPN, 8.5% protein diet nephrotic; LPNE, 8.5% protein nephrotic + enalapril; LPL, lipoprotein lipase; The Journal of Clinical Investigation, Inc. NAR, Nagase analbuminemic rat; SD, Sprague-Dawley; TG, triglyc- Volume 86, August 1990, 600-605 erides. 600 R. W. Davies, I. Staprans, F. N. Hutchison, and G. A. Kaysen glomerular permselectivity in nephrotic SD rats and determine cycle. Two groups of rats (five SD and four NAR) were rendered whether an enhanced rate of albumin synthesis would increase nephrotic as in protocol I while the remaining rats (four SD and five blood lipid levels independent of changes in proteinuria. NAR) served as controls. We report here the relationship between albumin synthesis Measurement ofplasma VLDL clearance. Labeled VLDL was pre- and blood lipid levels in both nephrotic and normal SD rats as pared by the method of Bar-on et al. (21) using [3H]glycerol. VLDL well as the metabolic was isolated by the method of Havel et. al. (22). 0.6 1ACi of VLDL was clearance of both CM and VLDL in injected into a tail vein of each experimental animal without anesthe- normal and nephrotic NAR and SD rats. sia for measurement of VLDL removal from whole blood. Samples and calculations were treated the same as for CM clearance described Methods above. Measurement ofpostheparin LPL activity. At the end of measure- Four separate experimental protocols were performed. In the first pro- ment of VLDL clearance, animals were allowed free access to food and tocol CM clearance was compared in normal NAR and SD rats to water for 48 h. They were then anesthetized with sodium pentobarbi- determine whether the clearance of CM was altered by the absence of tal, the abdomen was incised and heparin (10 U/kg) was injected into serum albumin. Proteinuria was then produced in both SD and NAR the right femoral vein. Rats were exsanguinated 5 min later from the rats to determine whether CM clearance became abnormal after an abdominal aorta for measurement of postheparin LPL. LPL activity alteration in glomerular permselectivity. was then assayed by measurement of hydrolysis of intralipid (23). In protocol 2, VLDL clearance was measured in nephrotic and 1 ml reaction mixtures consisted of: 0.1 ml of 1.3 M Tris-HCI, pH normal NAR and SD rats as in protocol 1. Postheparin LPL activity 8.6; 0.1 ml of 0.025 M NH40H, pH 8.6; 0.3 ml of 15% (wt/vol) was then measured in the same animals. crystalline bovine serum albumin (Sigma Chemical Co., St. Louis, In the third and fourth protocols the relationship between blood MO), 0.1 ml of 10% Intralipid (Vitrum, Stockholm, Sweden), 0.2 ml lipids and albumin synthesis was evaluated utilizing SD rats with ex- normal rat serum, and 0.2 ml of postheparin plasma. Duplicate sam- perimental nephrotic syndrome (passive Heymann nephritis) (proto- ples were incubated for 60 min at 370C. Free fatty acids (FFA) were col 3) and normal SD rats (protocol 4).
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