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Increased VLDL in nephrotic patients results from a decreased catabolism while increased LDL results from increased synthesis.
Kidney Int. 1998 Apr; 53(4):994-1001.KI

Abstract

Increased very low density lipoprotein (VLDL) in nephrotic patients results from a decreased catabolism while increased low density lipoprotein (LDL) results from increased synthesis. Hyperlipidemia is a hallmark of nephrotic syndrome that has been associated with increased risk for ischemic heart disease as well as a loss of renal function in these patients. The hyperlipidemia usually is characterized by increased cholesterol levels, although hypertriglyceridemia may be present as well. The factors that determine the phenotype of nephrotic dyslipidemia are not understood, nor has the primary stimulus for nephrotic hyperlipidemia been identified. One hypothesis is that nephrotic hyperlipidemia is the result of a coordinate increase in synthesis of proteins by the liver. To address these issues we simultaneously measured the in vivo rate of VLDL apolipoprotein B100 (apo B100) secretion, LDL apo B100 synthesis and albumin synthesis in patients with a nephrotic syndrome (N = 8) and compared them with a control group (N = 7) using a primed/continuous infusion of the stable isotope L-[1-13C] valine for six hours. Kinetic data were analyzed by multicompartmental analysis. Patients studied had combined hyperlipidemia as reflected by an significant increase in both VLDL and LDL apo B100 pool sizes. In contrast, the albumin pool size was significantly decreased. VLDL apo B100 levels were primarily increased as a consequence of a decrease in fractional catabolic rate (FCR) rather than from an increase in the absolute synthesis rate (ASR). Both VLDL apo B100 and triglycerides were inversely related to the fractional catabolism (FCR) of VLDL apo B100 (r2 = 0.708; P = 0.0088) while neither had any relationship to the ASR of VLDL apo B100. In contrast to VLDL, increased LDL apo B100 was not a consequence of decreased catabolism. The LDL apo B100 ASR was significantly increased (P = 0.001) in the nephrotic patients compared to controls. Low density lipoprotein apo B100 ASR was greater than that of VLDL apo B100 in some patients, suggesting that LDL in these patients was not only derived from VLDL delipidation, but also by an alternative secretory pathway. There was no clear relationship between the ASR of VLDL apo B100 and the ASR of albumin within the current study population. Our data indicate that increased VLDL in nephrotic patients results from a decreased catabolism, while increased LDL results from increased synthesis.

Authors+Show Affiliations

Department of Nephrology, University Hospital Utrecht, The Netherlands.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

9551409

Citation

de Sain-van der Velden, M G., et al. "Increased VLDL in Nephrotic Patients Results From a Decreased Catabolism While Increased LDL Results From Increased Synthesis." Kidney International, vol. 53, no. 4, 1998, pp. 994-1001.
de Sain-van der Velden MG, Kaysen GA, Barrett HA, et al. Increased VLDL in nephrotic patients results from a decreased catabolism while increased LDL results from increased synthesis. Kidney Int. 1998;53(4):994-1001.
de Sain-van der Velden, M. G., Kaysen, G. A., Barrett, H. A., Stellaard, F., Gadellaa, M. M., Voorbij, H. A., Reijngoud, D. J., & Rabelink, T. J. (1998). Increased VLDL in nephrotic patients results from a decreased catabolism while increased LDL results from increased synthesis. Kidney International, 53(4), 994-1001.
de Sain-van der Velden MG, et al. Increased VLDL in Nephrotic Patients Results From a Decreased Catabolism While Increased LDL Results From Increased Synthesis. Kidney Int. 1998;53(4):994-1001. PubMed PMID: 9551409.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Increased VLDL in nephrotic patients results from a decreased catabolism while increased LDL results from increased synthesis. AU - de Sain-van der Velden,M G, AU - Kaysen,G A, AU - Barrett,H A, AU - Stellaard,F, AU - Gadellaa,M M, AU - Voorbij,H A, AU - Reijngoud,D J, AU - Rabelink,T J, PY - 1998/4/29/pubmed PY - 1998/4/29/medline PY - 1998/4/29/entrez SP - 994 EP - 1001 JF - Kidney international JO - Kidney Int. VL - 53 IS - 4 N2 - Increased very low density lipoprotein (VLDL) in nephrotic patients results from a decreased catabolism while increased low density lipoprotein (LDL) results from increased synthesis. Hyperlipidemia is a hallmark of nephrotic syndrome that has been associated with increased risk for ischemic heart disease as well as a loss of renal function in these patients. The hyperlipidemia usually is characterized by increased cholesterol levels, although hypertriglyceridemia may be present as well. The factors that determine the phenotype of nephrotic dyslipidemia are not understood, nor has the primary stimulus for nephrotic hyperlipidemia been identified. One hypothesis is that nephrotic hyperlipidemia is the result of a coordinate increase in synthesis of proteins by the liver. To address these issues we simultaneously measured the in vivo rate of VLDL apolipoprotein B100 (apo B100) secretion, LDL apo B100 synthesis and albumin synthesis in patients with a nephrotic syndrome (N = 8) and compared them with a control group (N = 7) using a primed/continuous infusion of the stable isotope L-[1-13C] valine for six hours. Kinetic data were analyzed by multicompartmental analysis. Patients studied had combined hyperlipidemia as reflected by an significant increase in both VLDL and LDL apo B100 pool sizes. In contrast, the albumin pool size was significantly decreased. VLDL apo B100 levels were primarily increased as a consequence of a decrease in fractional catabolic rate (FCR) rather than from an increase in the absolute synthesis rate (ASR). Both VLDL apo B100 and triglycerides were inversely related to the fractional catabolism (FCR) of VLDL apo B100 (r2 = 0.708; P = 0.0088) while neither had any relationship to the ASR of VLDL apo B100. In contrast to VLDL, increased LDL apo B100 was not a consequence of decreased catabolism. The LDL apo B100 ASR was significantly increased (P = 0.001) in the nephrotic patients compared to controls. Low density lipoprotein apo B100 ASR was greater than that of VLDL apo B100 in some patients, suggesting that LDL in these patients was not only derived from VLDL delipidation, but also by an alternative secretory pathway. There was no clear relationship between the ASR of VLDL apo B100 and the ASR of albumin within the current study population. Our data indicate that increased VLDL in nephrotic patients results from a decreased catabolism, while increased LDL results from increased synthesis. SN - 0085-2538 UR - https://www.unboundmedicine.com/medline/citation/9551409/Increased_VLDL_in_nephrotic_patients_results_from_a_decreased_catabolism_while_increased_LDL_results_from_increased_synthesis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0085-2538(15)30501-9 DB - PRIME DP - Unbound Medicine ER -