The document discusses renal failure and its relationship to cardiovascular disease. It provides statistics on the prevalence, incidence, and mortality rates of renal failure in the US and Australia. It then covers topics such as the structure and function of the kidneys, classification of renal failure, its effects on the cardiovascular system, and approaches to treatment including dialysis, transplantation, and their risks.

1. Renal Failure and Cardiovascular Disease Rey Tuando Renal Dialysis Unit

2. Introduction Refresh our knowledge Know more about the Kidney and RF Major Cardiovascular Changes in RF Review of Statistics Nursing implications

3. Prevelance statistics about Kidney failure: The following statistics relate to the prevalence of Kidney failure: 56,598 people with end-stage renal disease were waiting for kidney transplants in the US (United Network for Organ Sharing, 2003, NIDDK) 2,444 people with end-stage renal disease were waiting for kidney and pancreas transplants in the US (United Network for Organ Sharing, 2003, NIDDK)

4. Incidence statistics about Kidney failure: The following statistics relate to the incidence of Kidney failure : Kidney failure rates were approximately 5 times higher for the indigenous population in Australia 2000-02 (Australia’s Health 2004, AIHW) 93,327 people commenced treatment for end-stage renal disease annually in the US 2001 (United States Renal Data System, 2003, NIDDK)

5. Death statistics for Kidney failure: The following are statistics from various sources about deaths and Kidney failure: 76,584 people undergoing end-stage renal treatment died each year in the US 2001 (United States Renal Data System, 2003, NIDDK) 26.1% of deaths from kidney failure were also associated with coronary heart disease in Australia (Australia’s Health 2004, AIHW) 28.6% of deaths from kidney failure were also associated with heart failure in Australia (Australia’s Health 2004, AIHW) 1,006 women died from renal failure in Australia 2002 (AIHW National Morbidity Database, Australia’s Health 2004, AIHW) 919 men died from renal failure in Australia 2002 (AIHW National Morbidity Database, Australia’s Health 2004, AIHW) 1.3% of all male deaths was due to renal failure in Australia 2002 (AIHW National Morbidity Database, Australia’s Health 2004, AIHW) 1.6% of all female deaths was due to renal failure in Australia 2002 (AIHW National Morbidity Database, Australia’s Health 2004, AIHW) 15% of deaths from diabetes also had renal failure as an associated cause of death in Australia, 2002 (Australia’s Health 2004, AIHW)

6. Topics of Discussion Kidney and the Nephron. How is urine formed RF: Classification and Major Causes Effect on the CV System Approach to Treatment Dialysis and Transplantation

7. The Kidney Bean shaped; behind peritoneum; 12T-3L vertebra; right one a little lower; 10-15cm length; 120-170gm; 11x6x3cm size;<1% of body weight Blood supply 1-1.2M nephrons: 1. Bowman’s capsule 2. Proximal Convoluted Tubule 3. Loop Of Henle 4. Distal Convoluted Tubule 5. Collecting Ducts Cortex (outer) (pad of fat) (filtering and reabsorption components) Medulla (inner) (concentrating/diluting, collecting duct)

8. Kidney Functions Excretory Regulatory Metabolic

9. Mechanism of Renal Excretory Function Renal Blood/plasma flow 20% of CO Glomerular Ultrafiltration=protein-free ultrafiltrate Urine Volume = 1.5L/day (roughly 1ml/min) small residuum=2 opposing processes: Ultrafiltration (UF) of > 180L (125ml/min) Reclamation of 99% of ultrafiltrate Filtration < 10,000 molecular weight

10. Rate of Ultrafiltration (GFR) Glomerular Capillary Hydrosatic Pressure + Bowman’s space Oncotic Pressure = Glomerular Capillary Oncotic Pressure + Bowman’s Space Hydrostatic Pressure Rate of Plasma Flow Permeability and Total Surface Area Decrease in GFR: Glomerular Hydrostatic Pres. Tubule Hydrostatic Pres. Renal Blood/Plasma Flow Plasma Oncotic Pres. Permeability/Filtering Surface Area

11. Barrier to Protein filtration: 1.Glomerular Capillary Basement Membrane and Slitlike diaphragms 2. Eletrostatic Factors The Juxtaglomerular Apparatus a specialised structure: Tubular component Vascular component Interstitial component Erythropoietin production Acid Base Balance

15. Types of Renal Failure I. Acute RF ARF: i.e. Bi. Arterial Occlusion Bi. Acute Renal Vein Thrombosis ATN Acute Uric Acid Nephropathy Hypovolaemia CV Collapse RPRF: i.e. Idiopathic Rapidly Progressing GN Goodpasture’s Synd Acute Bacterial Endocarditis or Visceral Sepsis Microscopic Polyarteritis Nodosa Wegener’s Granulomatosis II. Chronic Several forms of GN HTN DM

16. Physiology of Ischaemic ARF INEFFECTIVE CIRCULATORY VOLUME-HYPOPERFUSION Activation of Central Baroreceptors Angiotensin II (+) Norepinephrine (+) Vasopressin (+) Endothelin (+) Preferrential Constriction Efferent Arteriole (-) Prostaglandin Synthesis (-) Renal Vasoconstriction Tubuloglomerular Mesangial Cell Contraction Feedback Autoregulation (-) Nitric Oxide (-) Epithelial Cell Ischaemic Injury Impaired NaCl (proximal tubule-pars recta Reabsorption medullary thick ascending limb) Tubule Obstruction Reduced Glomerular Filtration Pressure Tubular Backleak and Surface Area of Filtration Markers REDUCED GLOMERULAR FILTRATION RATE

17. Effect on Heart and Circulation Hypertension Volume Dependent (50%) Non-Volume Dependent (34% , 16%) Hyperlipidaemia Hypertriglyceridaemia (1/3) Abno Serum apolipoprotein concentrations Lipid peroxidation Hypercholesterolaemia Ischaemic Cardiac Disease Left Ventricular Dysfunction and Hypertrophy Heart Failure versus Fluid Overload

18. Pericardial Disease ( Pericarditis 3-4% of death) Uraemic Pericarditis Dialysis-associated Pericarditis (bact or viral infection, hypercatabolism, volume overload, HyperPTism, hyperuricaemia, malnutrition) Constrictive Pericarditis Purulent Pericarditis Endocarditis (from access site infection) Arrhythmias

19. Risk Factors for Atherogenesis in ESRD/F: Hypertension Cigarette Smoking DM Insulin Resistance Lipid Disorders Vascular Calcification ? Elevated plasma urate and oxalate ? Free oxygen radicals ? Polyamines

20. Risks of Dialysis Therapy in Patients with Pericarditis Bleeding Arrhythmia Hypotension and Cardiac Tamponade Dehydration Hypokalaemia and Hypophosphataemia Metabolic Alkalosis

21. Factors leading to Left Ventricular Dysfunction and/or Hypertrophy in Dialysis Patients Hypertension Fluid Overload Anaemia Ischaemic Heart Disease Arteriovenous Fistula Myocardial Calcification Systemic Disease ( e.g., amyloidosis, polyarteritis, scleroderma) Uraemia

22. BASELINE Comparison of Water gain versus Saline gain

23. + 4L WATER

24. BASELINE + 4L WATER

25. BASELINE

26. + 4L SALINE

27. BASELINE + 4L SALINE

28. Saline Overload is more important than Water Overload

29. CRP – thought to be an “idle” marker but is a nasty protagonist Present in damaged endothelium/vessel wall Attraction of monocytes via MCP-1 to vessel wall Attraction/adherence/migration of monocytes Opsonizes LDL and facilitates LDL uptake by macrophages Foam cell / atheroma propagation Activates C’ via classical pathway Promotes local inflammation Suppresses NO synthesis Endothelial dysfunction (vasoreaction)

30. Uraemia Characterized by: A chronic state of oxidant stress and disordered free radical chemistry A chronic state of activated inflammation Endothelial dysfunction and a highly proatherogenic state Excessive morbidity and mortality attributable to occlusive vascular disease

34. Dialysis Haemodialysis Peritoneal Dialysis Plasmapheresis (TPE) Transplantation