12/13/09 Good morning! Prevalence Statistics of Renal 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 ) 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)
12/13/09 Death statistics for 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)
12/13/09 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
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12/13/09 Kidneys comprise <1% of total body weight but receives 20-25% of CO Blood supply starts from the Renal Artery, Interlobar Art, to the Arcuate arteries, to the Interllobular art, Afferent Arterioles, Glomerular Capillary tuft, Efferent Arteriole, Multiple parallel Vasa Recta, Medullary countercurrent Exchange System, Interlobular Veins, Arcuate Veins, Interlobar Veins, Renal Vein.
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12/13/09 Electrostatic factors retard filtration of plasma CHON; Ex. Albumin is a polyanion. It s passage is retarded by anionic glycoproteins in the glomerular wall. So that any disruption in this actor results to CHON in the urine Juxtaglomerualr Apparatus= Macula Densa monitor some aspect of Tubular fluid composition; Cytoplasmic Granules in the cells of walls of the Afferent and Efferent Arterioles contain RENIN and other components of the Renin-Angiotensin system. Precise role not clearly understood but involved in GLOMERULOTUBULAR FEEDBACK mechanism = wherein, an increase in the delivery of NaCl to the Macula densa causes a release of renin and angiotensin2 (present preformed in the granules), whereas a decrease inhibits their release. Angiotensin 2 acts on Afferent Art. Dec blood flow Dec GFR Dec amt of NaCl to Macula Densa, completing the feedback loop
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12/13/09 HTN is Major cause of morbidity and mortality Accelerates atherosclerosis and precipitates pressure-related complications such as heart failure, stroke, and dissecting aneurysm LVH= contributing factors: volume overload, abno hormone levels(plasma renin activity), PTH, and anaemia Ptho of HTN in RF(Dialysis pt): Volume dependent Non-volume dependent (altered autonomic-hormonal milieu) Guidelines for treatment includes: 1. Correction of the volume component = UF, but >50% normotension won’t be achieved by UF 2. Maintain Dry Weight= not gain >1.5-2.0L/day; Na intake <2g/day 3. Readjust Dry Weight= poor food intke or body wasting 4. Oral Antihypertensives Hypertriglyceridaemia - predominant underlying cause is deficiency of lipoprotein lipase resulting in reduced lipolysis of triglyceride-rich lipoproteins (VLDL). Exaggerated by beta-adrenergic blockers, high CHO, Gluco seabsorption from PD, use of acetate dialysate, heparin use, decreased hepatic blood flow from cardiac insufficiency
12/13/09 Ischemic Heart Dis= control plasma Phos rigidly; consider parathyroidectomy early when Calcitriol fails to control progressive biochemical evidence of hyperparathyroidism Coronary Artery Dis is commonly unmasked when Hb falls to critical level Dialysis Aso. Pericarditis= inadequate dialysis; dx established by friction rub in pt with CP; tx= smalll asymptomatic pericardial effusion (<100ml) are not uncommon in dialysis pts but shld be intervened if impending cardiac tamponade present; Surgical drainage by subxiphoid pricardiostomy if effusion size by echocardiography estimates >250ml even when haemodynamic compromise is absent Arrhythmias= cause: LVH or IHD; Serum levels of ions affecting cardia conduction= K, Ca, Mg, and H, are often abno and may undergo rapid fluctuations during HD; Hypoxaemia; Calcific cardiomyopathy; hypophosphataemia; drugs such as Digitalisprep
12/13/09 Ischemic Heart Dis= control plasma Phos rigidly; consider parathyroidectomy early when Calcitriol fails to control progressive biochemical evidence of hyperparathyroidism Coronary Artery Dis is commonly unmasked when Hb falls to critical level Dialysis Aso. Pericarditis= inadequate dialysis; dx established by friction rub in pt with CP; tx= smalll asymptomatic pericardial effusion (<100ml) are not uncommon in dialysis pts but shld be intervened if impending cardiac tamponade present; Surgical drainage by subxiphoid pricardiostomy if effusion size by echocardiography estimates >250ml even when haemodynamic compromise is absent Arrhythmias= cause: LVH or IHD; Serum levels of ions affecting cardia conduction= K, Ca, Mg, and H, are often abno and may undergo rapid fluctuations during HD; Hypoxaemia; Calcific cardiomyopathy; hypophosphataemia; drugs such as Digitalisprep
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12/13/09 +4L H2O = 0.9l Increase in EV vol = 0.6L increase in Blood vol = 3L increase in ICF vol
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12/13/09 +4L H2O = 0.9l Increase in EV vol = 0.6L increase in Blood vol = 3L increase in ICF vol +4L Saline = 2.9L increase in EV = 1.1L increase in Blood vol = 0 increase in ICF
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12/13/09 Diseases responsive to TPE: as first line therapy Cryoglobulinaemia Anti-GBM disease Guillain-Barre Hyperviscousity Syndrome TTP/HUS as adjunctive treatment: Rapidly progressing GN Systemic Vasculitis, asso w/ANCA Multiple Myeloma with renal involvement SLE
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