Continuous Renal Replacement Therapy (CRRT) Workshop Cyrus Custodio, CNC King Faisal Specialist Hospital & RC Riyadh, Saudi Arabia. CRRT: Important Points to Remember During This Workshop Maintaining expertise with a rarely-performed procedure can be difficult.
History of CRRT 1987 – Uldall introduces CVVHD 1990s – Transition to VV therapies from AV therapies 1996 – R. Terminology Hemodialysis transport process by which a solute passively diffuses down its concentration gradient from one fluid compartment (either blood or dialysate) into the other Hemofiltrattiion use of a hydrostatic pressure gradient to induce the filtration (or convection) of plasma water across the membrane of the hemofilter.
Modality: SCUF Slow Continuous Ultrafiltration PRINCIPLE Ultrafiltration PROCESS Usual blood circuit, synthetic membrane and anticoagulation. Modality: CVVH Continuous Veno-Venous Hemofiltration PRINCIPLE Hemofiltrattiion Ultrafiltration & Convection. Modality: CVVHD Continuous Veno-Venous Hemodialysis PRINCIPLE Diffusion and Ultrafiltration PROCESS Blood circuit, filter and anticoagulation.
Modality: CVVHDF Continuous Veno-Venous Hemodiafiltration HEMODIAFILTRATION Hemodialysis and Hemofiltration PRINCIPLE Diffusion, Convection and Ultrafiltration. CRRT Education Plan DialysisICU History of CRRT Definition of Acronyms and Terms The Pediatric Ideal Concepts related to fluid removal Concepts related to solute removal Formulas related to CRRT Components of a CRRT System CRRT Procedures Procedures related to initiation of therapy Procedures related to monitoring therapy Procedures related to terminating therapy Potential problems encountered during CRRT Indications for CRRT in the critical care setting CRRT outcomes research 12 th Annual International Conference on Continuous Renal Replacement Therapy, San Diego, CA, USA. Department of Internal Medicine, Diabetes and Vascular Centre, Sint Franciscus Gasthuis, Rotterdam, P.O. The hallmark of dyslipidemia in obesity is hypertriglyceridemia in part due to increased free fatty acid (FFA) fluxes to the liver, which leads to hepatic accumulation of triglycerides (TG).
Free fatty acid (FFA) uptake and its related triglyceride (TG) synthesis in adipocytes are highly depended of C3adesArg or acylation-stimulation protein (ASP). Continuous therapies closely mimic the native kidney in treating ARF and fluid overload Slow, gentle and well tolerated by hypotensive patients Remove large amounts of fluid and waste products over time Tolerated well by the hemodynamically unstable patient Slower solute & fluid removal - IHD removes fluid & solutes more rapidly than CRRT does. In every single country in the world, the incidence of obesity is rising continuously and therefore, the associated morbidity, mortality and both medical and economical costs are expected to increase as well.
This leads to an increased hepatic synthesis of large very low density lipoproteins (VLDL) 1, which hampers the lipolysis of chylomicrons due to competition mainly at the level of lipoprotein lipase (LPL) with increased remnant TG being transported to the liver.
Several investigators have demonstrated an association between TG-rich lipoproteins and remnant cholesterol levels with the presence of coronary [34,35,36,38,39,40,41,42,68], cerebral [37], and peripheral atherosclerosis [69]. Chylomicrons and VLDL undergo lipolysis by lipoprotein lipase (LPL) with subsequent release of FFA into the circulation.
Lifestyle Interventions for Dyslipidemia in ObesityTreatment of obesity-associated dyslipidemia should be focused on lifestyle changes including weight loss, physical exercise and a healthy diet.
If the patient has a life-threatening condition hemodialysis may be used initially to correct and stabilize …… then CRRT used to further correct the condition. Patients with hospital-acquired ARF are more likely than those with community-acquired ARF to be admitted to the ICU. The majority of these complications are related to co-morbid conditions that include coronary artery disease, hypertension, type 2 diabetes mellitus, respiratory disorders and dyslipidemia.
Lipolysis is further impaired in obesity by reduced mRNA expression levels of LPL in adipose tissue and reduced LPL activity in skeletal muscle. In addition to a direct detrimental effect by chylomicron remnants on vessels [59], impaired endothelial function after an oral fat load [70] and after infusion of artificial TG-rich lipoproteins have been described [71].
The FFA are then transported into the subendothelial space by the scavenger receptor CD36 and other transporters where C3adesArg plays an important role in the subsequent TG synthesis for storage of lipids in the adipocytes. Obesity increases cardiovascular risk through risk factors such as increased fasting plasma triglycerides, high LDL cholesterol, low HDL cholesterol, elevated blood glucose and insulin levels and high blood pressure. It is especially alarming that in recent years the increase was most pronounced in children and that it occurs both in developed, but perhaps even more, in developing countries [1]. Hypertriglyceridemia further induces an increased exchange of cholesterolesters (CE) and TG between VLDL and HDL and low density lipoproteins (LDL) by cholesterylester-transfer-protein (CETP).
This phenomenon may take place by elevated levels of FFA [72], which are generated by the action of LPL mediated lipolysis.
C3adesArg is the most potent molecule known, which induces transmembrane transport of FFA and its intracellular esterification into TG within adipocytes.
The amount of ingested fat and total calories are the most important dietary factors to induce obesity and its related postprandial lipemia [109]. Novel lipid dependent, metabolic risk factors associated to obesity are the presence of the small dense LDL phenotype, postprandial hyperlipidemia with accumulation of atherogenic remnants and hepatic overproduction of apoB containing lipoproteins.


Visceral obesity leads to insulin resistance in part mediated by adipokines and free fatty acids (FFA). Other mechanisms of remnant-mediated atherogenesis which may play a role in obesity comprise the postprandial activation of leukocytes, generation of oxidative stress and production of cytokines [55,73,74].Postprandial hyperlipidemia with accumulation of atherogenic remnants is especially linked to visceral obesity [75,76].
C3adesArg is metabolized from complement component (C) 3a by carboxypeptidase N and C3a is again the splice product from C3, which is formed in case of complement activation. All these lipid abnormalities are typical features of the metabolic syndrome and may be associated to a pro-inflammatory gradient which in part may originate in the adipose tissue itself and directly affect the endothelium.
Adipokines such as resistin and retinol-binding protein 4 decrease insulin sensitivity, whereas leptin and adiponectin have the opposite effect. In addition, hepatic lipase (HL) removes TG and phospholipids from LDL for the final formation of TG-depleted small dense LDL.
Postprandial lipid metabolism has been investigated in metabolic ward studies using non-physiological high amounts of fat [77]. Weight loss has been demonstrated to markedly reduce fasting and non-fasting TG concentrations, which can be attributed to an increase in LPL activity with a concomitant reduction in apo C-III levels [111], a decrease in CETP activity [112,113] and an increased catabolism of TG-rich lipoproteins [114]. An important link between obesity, the metabolic syndrome and dyslipidemia, seems to be the development of insulin resistance in peripheral tissues leading to an enhanced hepatic flux of fatty acids from dietary sources, intravascular lipolysis and from adipose tissue resistant to the antilipolytic effects of insulin. In addition, cytokines like TNF-? and IL-6, which originate from macrophages in adipose tissue, are involved [2]. The intense yellow color represents cholesterol, whereas the light yellow color represents the TG content within the different lipoproteins. A more physiological method to study postprandial lipemia has been developed in our laboratory, namely the measurement of daytime capillary TG profiles using repeated capillary self-measurements in an out of hospital situation [78,79]. For example, adipocytes secrete C3 when incubated with TG-rich lipoproteins like chylomicrons or very low density lipoproteins (VLDL), but also Factor B and Factor D, thereby causing activation of the complement cascade.
Besides reductions in fasting and non-fasting TG concentrations, a small reduction in LDL-C can be expected upon weight loss, which may be attributed to increased LDL receptor activity. The current review will focus on these aspects of lipid metabolism in obesity and potential interventions to treat the obesity related dyslipidemia. Obesity, especially central obesity, is probably the main cause of the metabolic syndrome (MetS), which includes insulin resistance, type 2 diabetes mellitus, hypertension, the obstructive sleep apnea syndrome, non-alcoholic fatty liver disease (NAFLD) and dyslipidemia, all risk factors for cardiovascular disease [3,4].
Obesity induced increases in metabolic processes are marked with green arrows, whereas reductions are marked with red arrows.
It has been shown that diurnal triglyceridemia in obese subjects correlates better to waist circumference than to body mass index [78,80], which is in agreement with the hypothesis that the distribution of adipose tissue modulates postprandial lipemia [81]. A weight loss of 4–10 kg in obese subjects resulted in a 12% reduction in LDL-C and a 27% increase in LDL receptor mRNA levels [111,115].The type of dietary fat also affects postprandial lipemia [109]. Although doubts have arisen about the significance of the term metabolic syndrome in relation to cardiovascular complications, it has been suggested that identifying the condition will stimulate the physician to search also for the other risk factors clustering in the MetS [5].The typical dyslipidemia of obesity consists of increased triglycerides (TG) and FFA, decreased HDL-C with HDL dysfunction and normal or slightly increased LDL-C with increased small dense LDL. All these mechanisms have been related to the higher incidence of cardiovascular disease seen in obesity [82].HDL metabolism is also strongly affected by obesity because of the increased number of remnants of chylomicrons and VLDL together with impaired lipolysis. A study in rats showed that a diet high in saturated fats reduced LPL protein levels and LPL activity in skeletal muscle, whereas LPL activity was increased in adipose tissue favoring shunting of lipids from skeletal muscle to adipose tissue [116]. The concentrations of plasma apolipoprotein (apo) B are also often increased, partly due to the hepatic overproduction of apo B containing lipoproteins [6,7]. The increased number of TG-rich lipoproteins results in increased CETP activity, which exchanges cholesterolesters from HDL for TG from VLDL and LDL [60]. Moderate weight loss (approximately 10%) in obese, but otherwise healthy men, which was induced by a diet low on carbohydrates and SFA and high on mono-unsaturated fatty acids (MUFA) resulted in a 27%–46% reduction in postprandial TG levels [117]. The current review will focus on general lipid metabolism, the pathophysiological changes in lipid metabolism seen in obesity with the focus on postprandial lipemia and free fatty acid (FFA) dynamics and the potential pharmacological and non-pharmacological interventions. Moreover, lipolysis of these TG-rich HDL occurs by hepatic lipase resulting in small HDL with a reduced affinity for apo A-I, which leads to dissociation of apo A-I from HDL. Long term intervention with MUFA resulted in a reduction in postprandial inflammation when compared to a diet rich in SFA in patients with the MetS [118].
This will ultimately lead to lower levels of HDL-C and a reduction in circulating HDL particles with impairment of reversed cholesterol transport [83]. Recent genome wide association studies have found more than 95 loci associated with lipid levels, but together they explain less than 10% of the variation in lipids.
Interactions between genes, obesity and lipid levels but also with the type of dietary fat consumed have recently been described [119,120,121,122].


In a Spanish population with a relatively high MUFA intake, carriers of the minor C allele of the APOA5 ?1131T > C polymorphism, which is associated with increased plasma TG, appear to be more resistant to weight gain by fat consumption and showed an inverse relationship between fat intake and plasma TG [122].
However, high PUFA consumption was associated with increased plasma TG and decreased LDL particle size in carriers of the C allele in a U.S. These results suggest the potential usefulness of a nutrigenomic approach for dietary interventions to prevent or treat obesity and its related dyslipidemia.Physical exercise has been shown to increase LPL and hepatic lipase activity, which stimulates TG lipolysis [123,124]. The mechanism of exercise-induced LPL activity remains unclear, but it was hypothesized that exercise stimulates especially muscular LPL activity, although this could not be confirmed in a recent study [125]. A 12-week walking program supplemented with fish oil (1000 mg eicosepantenoic acid and 700 mg docosahexaenoic acid daily) in subjects with the MetS resulted in lower fasting TG and decreased the postprandial response of TG and apoB48 [126].
Exercise training for 16 weeks in obese subjects with NAFLD resulted in a small reduction in intra-hepatic TG content, although no changes in VLDL-TG or apoB100 secretion were observed [127].
Exercise induced reductions in intra-hepatic TG content have also been reported even in the absence of weight loss [128]. Moreover, intra-hepatic TG content was reduced in overweight men after a low fat diet for three weeks, whereas a high fat diet increased intra-hepatic TG [129].
The plasma TG lowering effect of exercise and weight loss is the most consistent finding in studies concerning blood lipids [130], whereas increasing HDL-C levels by exercise remains controversial, especially in those subjects with high TG and low HDL-C levels [131].Other dietary factors besides calorie restriction and the type of dietary fat have also been shown to have beneficial effects on dyslipidemia.
Dietary intake of resistant starch, a dietary fiber, has been shown to improve nutrient absorption and has also been linked to insulin metabolism. Resistant starch ingestion resulted in lower fasting FFA concentrations, increased TG lipolysis by enhanced expression of related genes like LPL together with increased FFA uptake by skeletal muscle [133]. However, no effect from resistant starch supplementation was observed on TG and cholesterol concentrations [132,133].Unfortunately, lifestyle modifications are often insufficient to achieve weight loss and improvement of the dyslipidemia. A recent meta-analysis concerning anti-obesity drugs reported a mean weight loss of 3.13 kg, but marked improvements in dyslipidemia were absent [134].
Finally, bariatric surgery-induced weight loss has been associated with decreased TG and increased HDL-C levels [135]. Obesity Induced Changes in Lipoprotein Metabolism and Atherogenic EffectsThe hallmark of dyslipidemia in obesity is elevated fasting and postprandial TG in combination with the preponderance of small dense LDL and low HDL-C (Figure 1). Hypertriglyceridemia may be the major cause of the other lipid abnormalities since it will lead to delayed clearance of the TG-rich lipoproteins [34,35,36,37,38,39,40,41,42,43,44,45,46,47,48] and formation of small dense LDL [48,49].Lipolysis of TG-rich lipoproteins is impaired in obesity by reduced mRNA expression levels of LPL in adipose tissue [50], reductions in LPL activity in skeletal muscle and competition for lipolysis between VLDL and chylomicrons [11].
Increased postprandial lipemia leads to elevated levels of FFA, resulting in detachment of LPL from its endothelial surface [51,52]. The exchange of TG from these remnants for cholesterol-esters from HDL by CETP with the concerted action of hepatic lipase, ultimately leads to the formation of small dense LDL [48,49]. In the presence of hypertriglyceridemia, the cholesterol-ester content of LDL decreases, whereas the TG content of LDL increases by the activity of CETP. However, the increased TG content within the LDL is hydrolyzed by hepatic lipase, which leads to the formation of small, dense LDL particles.
The development of small dense LDL in obesity is mainly due to increased TG concentrations and does not depend on total body fat mass [53].
Small dense LDL have an increased affinity for arterial proteoglycans resulting in enhanced subendothelial lipoprotein retention [58]. However, subendothelial remnants of chylomicrons and VLDL do not need to become modified to allow uptake by scavenger receptors of macrophages in contrast to native LDL [59]. It has been described that small dense LDL are more susceptible for oxidation, in part due to less free cholesterol and anti-oxidative content [60]. It should be noted that the lipoprotein size is a limiting factor for migration through the endothelium and that LDL particles migrate more easily than chylomicron remnants, but the number of migrated particles does not necessarily translate into more cholesterol deposition since chylomicron remnants contain approximately 40 times more cholesterol per particle than LDL [57]. Alternatively, LPL-enriched remnants of chylomicrons and VLDL may be transported to the tissues where interaction with proteoglycans and lipoprotein receptors lead to particle removal. Taskinen and co-workers showed that the defective clearance of remnant lipoproteins can be explained by elevated concentrations of apo C-III in the situation of obesity [64]. Elevated levels of apo C-III in obesity can be explained by glucose-stimulated transcription of apo C-III and it has been described that plasma apo C-III levels correlate with fasting glucose and glucose excursion after an oral glucose test in obese humans [65].



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Comments

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