Metabolic complications in patients ongoing pd
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Metabolic complications in patients ongoing pd

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ภาวะแทรกซ้อนทางเมตะบอลิกในผู้ป่วยล้างไตทางช่องท้อง

ภาวะแทรกซ้อนทางเมตะบอลิกในผู้ป่วยล้างไตทางช่องท้อง

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    Metabolic complications in patients ongoing pd Metabolic complications in patients ongoing pd Presentation Transcript

    • Metabolic Complications in Patients Ongoing Peritoneal dialysis Piti Niyomsirivanich, MD.
    • Outlines• Metabolic syndrome• Hyperglycemia• Dyslipidemia• Protein loss• Na• K• Mg and vascular calcification• PO4• Ca
    • Metabolic Syndrome• Central obesity• High blood pressure• High triglyceride• Low HDL-cholesterol• Insulin resistance
    • Metabolic Syndrome
    • WHR = Waist hip ratio
    • ระบาดวิทยาของโรคอ้วนและภาวะ ไตเสื่อม• Ejerblad et al. – BMI > 25 kg/m2  CKD 2-3 X – BMI > 35 kgm2 c diabetes  17.7 X• Hsu et al. – BMI 25-29.9 kg/m2  1.87 X – BMI 30-34.9 kg/m2  3.57 X – BMI 35-39.9 kg/m2  6.12 X – BMI > 40 kg/m2  7 X• Central adiposity Versus Peripheral adiposity
    • Metabolic syndrome & kidney disease• Chen et al. – Metabolic syndrome increase risks of kidney disease 2.6 X – 3 risk factors 3.38 X – 4 risk factors 4.23 X – 5 risk factor 5.85 X• Palaniappan et al. – Metabolic syndrome increased risk albuminurea
    • Mechanism of CKD in obesity with metabolic syndrome• Inflammation• Renin angiotensin system• Lipotoxicity• Hemodynamic factors
    • Cytokine
    • Cytokine from adipose tissue
    • Cytokines• 1. Leptin – 167 amino acid – Adipocyte-derived hormone – More fat more leptin – Pass Blood brain barrier – Inhibit neuropeptide Y  decrease appetide
    • Leptin and Energy balance
    • Mechanism of leptin Leptin secrete via kidney
    • IL-6 and CRP• Produced from visceral , peripheral tissue• decrease cytokine signal and leptin• Adiponectin• Increase TGF-b1  kidney fibrosis• Increased CRP from hepatocyte  metabolic syndrome visceral adiposity and atherosclerosis
    • TNF-a• 26-kDa• Macrophage• Increased in metabolic syndrome• Adipogenesis & lipogenesis
    • MCP-1• Pro-inflammatory cytokines  macrophage – Increased glucose uptake  insulin induced insulin receptor tyrosine phosphorylation insulin resistance
    • Adiponectin• 30 kDa• Produced from subcutaneous fat > visceral fat• Insulin sensitizing , anti inflammatory , anti- artherogenic• Increased in thinner person• Decreased in obesed person
    • RAS• Obesity  increase renin , angiotensinogen , ACE , Angiotensin II , aldosterone• Angiotensinogen , angiotensin II increase adipocyte growth –  lipogenesis , hepatic gluconeogenesis ,glycogenolysis – Inh. Lipolysis , insulin dependent glucose uptake•  metabolic syndrome
    • Conclusion
    • Metabolic syndrome in PD patient• Cardiovascular death • LANDMARK STUDY (Longtitudinal Assessment of Numerous Discrete Modification of Atherosclerosis Risk in Kidney Disease)
    • FBM & CD-163 (pro-inflammatory marker) Axelsson et al.
    • Treatment of metabolic syndrome• Low glucose in dialysate  icodextrin• Control blood sugar• Reduced peritonitis  inflammation• RAS blockage• PPAR agonists (thiazolidinedione)  insulin sensitizer• HMG-CoA reductase• Cardiovascular risks
    • Hyperglycemia
    • Insulin resistance in CAPD• 1/3 of insulin renal excretion• CKD  insulin resistance – increased insulin – Hyperparathyroidism – Animia – Malnutrition• Osmitic agent (glucose) absorption• Insulin resistance  decrease function of lipoprotein lipase
    • Glucose absorption• Osmotic agent – Glucose : cheap , stable , non toxic • Absorp across membrane • 60-80% of dialysate absorbed • Glucose absorption APD < CAPD (shorter duration) • Glucose 100-150 g per day absorbed – 500-800 kcal/day significant weight gain 5-10% – Increase insulin secretion  insulin resistance atherosclerosis – Required increase hypoglycemic drug – Amino acids – Polyglucose solution
    • Minimized glucose absorbtion• Appropriate salt and water management – Decrease need for hypertonic solutions• Non-glucose based solutions
    • Target of glucose control• FBS < 140 mg/dl• 1 hr post prandial glucose < 200 mg/dl• HbA1C 7-8 mg/dl• Uremia  increased measure HbA1C (Carbymylated hemoglobin) – Differentiate • borate-agarose affinity chromatography • Thiobarbituric acid
    • Hypoglycemia agent• Not recommend oral hypoglycemic drugs• May use Thiazolidinediones – Except CHF• Subcutaneous insulin
    • Subcutaneous insulin• No guidelines• Icodextrin – CPG  glucose dehydrogenase- pyrroloquinolinequinone , glucose dye oxidoreductase enzyme  over estimate due to maltose in blood • Accu-check , FreeStyle – Recommend  glucose dehydrogenase-nicotinamide adenine dinucleotide , glucose dehydrogenase flavin adenine dinucleotide ,glucose oxidase instead
    • IP insulin• adventage – Absorbed via lymphatic system  constant delivery 1 ml/min – Less variation among administration – Lower dosage than other route – Lesser Atheroscleosis risk• Disadventage – More expensive – Decrease HDL in some small studies – Infection – Subcapsular liver steatonecrosis  insulin induced triglyceride accumulation in liver – Malignant omentum syndrome  require more insulin
    • Insulin dosage• Mutiple subcutaneous injection• Total insulin per day• Divided – 10% at night time – 85-90% at day time /3• Added 1 ,2 ,3 unit/l for 1.5%D 2.5%D 4.25%D• FBS < 140 mg/dl , CBG tid pc 1 hr < 200 mg/dl• CCPD , NIPD for high transporter (rapid glucose absorption)•
    • • IP insulin – Stability – Peak concentration 90-120 min – 60% dose absorbed• Direct Via tenckhoff catheter – Peak concentration 15 min
    • TZDs• Insulin sensitizer – Troglitazone  withdrawed – Rosiglitazone – Pioglitazone – Ciglitazone  animal study – Englitazone  animal study• Excretedliver
    • Dyslipidemia
    • Lipoprotein
    • Lipoprotein• Chylomicrons – largest – GI lymphatic – A-I , A-II , A-IV , B-48 , C-I , C-II , C-III , E• Very low density lipoprotein – Liver  circulation – B-100 , C-I , C-II , C-III , E• IDL – VLDL Lipoprotein lipase  triglyceride >> IDL – B-100 , C-III , E• LDL – IDL Hepatic triglyceride lipase LDL – B-100 , C• HDL – A-I , A-II , C-I , C-II , C-III , D , E – return
    • Lipid metabolism : endogenous PW
    • Atherogenicity of lipoprotein• Esp. LDL , LP(a)• Small LDL > large LDL• Lipoprotein (a) increased in patients with proteinuria• HDL – Uremia  acute phase response (IL-6, CRP)  decreased HDL
    • Glomerular response to lipid• Nephron loss  renal adaptation (ขยายขนาด)•  increase single nephron GFR –  glomerulosclerosis and interstitial fibrosis in long term• Leakage of lipoprotein – Increase mesangial cell cytokine , increased macrophage – Macrophage  ROS – ECM  increased matrix glomerulosclerosis – Endothelial  NO + endothelin , thromboxane A2 – PTC  endocytosis , endothelin-1  cell death • Endothelin -1  peritubular capillary vasoconstriction , fibroblast ,monocyte – JG apparatus  renin  increase BP
    • Lipid metabolism abnormality due to kidney disease• Increase carbohydrate intake due to protein restriction• Lipoprotein lipase abnormality – Insulin resistance , – High PTH , uremic toxin – Low Erythopoietin (unknown mechanism)
    • Hypertriglyceridemia in patient w CKD w/wo dialysis
    • Treatment• Diet – Fat < 30% of total calories – Poly:mono:sat = <0.7 : 1 : 1-1.5 (Nephrotic Syndrome , post KT) – decreased calories , simple sugar (CKD) – High fiber – 35 kcal/kg/day in < 60 yo – 30-35 kcal/kg/day in > 60 yo• Exercise• Medication
    • HMG-CoA reductase inhibitor• Inhibit HMG-CoA reductase• Decreased cholesterol by 20-30%• CYP3A4 and CYP 2C9• Atorvastatin & pravastatin  decrease dose• Rosuvastatin90% excreted from kidney  avoid• Rhabdomyositis , hepatitis
    • Ezethimibe• Inhibit dietary & biliary cholesterol absorption• Decrease LDL 20% – Total cholesterol 15%
    • Bile acid binding resins• Not recommend in patients with uremia (increased VLDL)• Others – Fish oilhigh dose , expensive – ACTH  short term study long term?? – Sevalemer decrease P ,LDL, increase HDL – L-carnitine cofactor FA into mitochondria • Not recommend due to adverse effect to muscle ,blood – Heparin HD decreased TG , cholesterol – Dialysis membrane
    • Treatment for dyslipidemia in PD• LDL/apoB protein – The lower the better – Statins – No equivalent studies have been done in PD – NKF (National kidney foundation) ,KDOQI ,International Society for Peritoneal dialysis • Elevated LDL-c w/wo CAD • PD with dyslipidemia Rx as nonuremic pt. c CAD
    • Elevated triglycerides• Always found in association with other lipid and lipoprotein abnormalities• Carbohydrate loading from the dialysis solution  hypertriglyceridemia• Na and water Mx  minimize the use of hypertonic solutions• Alcohol increase triglycerides• Triglyceride > 350 mg/ml Rx• Fibrate – (benzofibrate ,fenofibrate ,gemfibrozil)dose reduced by 25% – Muscle enzyme
    • Low HDL-c• Fibrate class  raises HDL• Reducing cardiac morbidity and mortality has not been established
    • AntioxidantsVit E not proven to reduce CV eventsNo trials both PD and HD
    • Protein loss• Protein 0.5 g/L of dialysate drainage – May 10-20 g/day• Amino acid loss 2-3 g/day• Albumin• IgG 15%• Protein loss greatest in high and high-average transporters• Peritonitis• Nephrotic syndrome
    • Hyponatremia/hypernatremia• Hyponatremias –  excessive water drinker – Hyperglycemia  translocational hyponatremia – 1.3 mmol/L : 100 mg/dl of Na• Hypernatremia – Rapid UF more water than salt convects across membrane – Short dwell PD more likely hypernatremia – Esp. low transporters
    • Hypokalemia / Hyperkalemia• Hypokalemia  10%-30% of CAPD patients – Associate poor potassium intake – Diet – K < 3 mmol/L  K supplement• Hyperkalemia  non compliance , excessive K intake
    • Hypercalcemia / hypocalcemia• Ca 2.5 ,3.5 mEq/L• 3.5 mEq/L  positive calcium balance• 2.5 mEq/L  slightly negative balance of calcium• Concerns about vascular calcification  lower 2.5 mEqL• Hypercalcemia – Large doses of calcium based phosphate binders – Rx • Non-cacium based phosphate binder • Stop Vit-D • Ca 2.5mEq/L solution of dialysate• Hypocalcemia – Not common due to use of calcium base phosphate binder & Vit D – Rx • Cacium & vitamin D • Ca 3.5 mEq/L dialysate solution
    • Magnesium and vascular calcification• Mg depletion  increased risk of atherosclerosis and cardioevents• Excess > deficiency• Higher dialysate solution Mg  suppress PTH  adynamic bone disease• Optimum Mg in dialysate remain unknown
    • Hypophosphatemia/hyperphosphatemia• Calcium based Phosphate binder , Sevalemer –  fall in serum bicarbonate• Amino acid based dialysis solution has been reported to lower the serum bicarbonate level in some patients