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  • Lethargy, anorexia, nausea, pruritus, reflux nephropathy, hypertension, peripheral vascular disease, ischaemic heart disease, hypercolesterolaemia and gout.
    • Not coping
  • Nonspecific - could be depression
    • ASADFACES
    • Neurotic vs major vs biological. Biological depression can also have precipitating event
      • Symptoms to tease them out - sleep deprivation. Classic/biological depression = early waking and inability to get back to sleep. Other = difficulty getting to sleep. Hypersomnolence in day, harder to sleep at night
  • Expiratory wheeze, smoker
    • But we also think fluid overload/increased intravascular volume in end stage renal disease
  • Malnutrition? ask about dietary history
  • Pain - loin to groin? e.g. output obstruction
  • Urine - quantity and haematuria, dysuria, frequency, nocturia
    • UTIs - pyelonephritis? she has reflux. Precipitant for acute-on-chronic renal impairment
  • Medications - aminoglycasides, other antibiotics, NSAIDS: aspirin, paracetamol (people take it and don't tell you), ACE inhibitors - shutting down ACE/blocking receptors - then bilateral renal artery stenosis - low renal artery perfusion - less perfusion of JG apparatus - renin release, efferent arteriolar constriction --> increases filtration at glomerulus
    • If you block this --> no filtration, infamous cause of acute renal failure
    • Both renal artery stenosis and ACEI use are common, so actually this complication is very uncommon
  • Hypertension - control? hypertensive nephrosclerosis is possible, could be ischaemic nephrosclerosis
  • ?Diabetes
  • ?Gouty nephropathy - rare
  • Aminoglycasides are given IV, so she might not know she's on them
  • Other drug causes of nephrotoxicity - assume any drug can cause interstitial nephritis
    • Cyclosporin
    • Heavy metals e.g. lead
    • APCs - compound analgesics e.g. Bex; aspirin and phenacetin and caffeine
      • caffeine withdrawal headache, treated by bex. Highly addictive due to the caffeine
      • ischaemic necrosis in the medulla of the kidney; also transitional carcinoma in lower urinary tract
      • Major cause of dialysis back in the day
    • Radiocontrast agents
  • Cause of her symptoms: uraemia - buildup of nitrogenous wastes
    • 1 Pigmentation of skin
    • 2 Uraemic flap - asterixis
    • 3 Uraemic fetor - ammonia/uriniphorus
    • 4 Pericarditis - pericardial rub
    • Uraemic frost - lips, forehead, need extreme uraemia for this, not a big deal
  • Cachexia
    • Chronic inflammation causing cachexia - vascular disease and advanced kidney disease; both proinflammatory
    • Proteinuria causing protein catabolism
  • Tachypneic - acidosis, and fluid overload - pulmonary oedema
  • Hypertensive
  • Euvolemic - normal fluid status in vascular compartment
    • But some people mean total body fluid
  • Upper limb pulses
    • Looking to create an A-V fistula. Sometimes use a vein graft, sometimes connected directly
    • Checking to make sure collateral supply to the hand is OK so that you don't get an ischaemic hand
  • High K - because she's acidotic. Acidosis due to H+ - K+ exchange pump (because inside cells K+ is high, can be shunted between inside and outside cells)
  • Bicarbonate low - consumed by acidosis, kidney can't create it due to failure
    • Need ECG
  • Creatinine ridiculously high
  • Calcium bound to albumin sometimes. So with the albumin she has at the moment, her calcium is normal
    • For every 10g that the albumin falls below the normal (40), should expect to see the calcium drop by 0.25 mmol/L
    • Calcium number = free calcium
  • Phosphate very high - failure of excretion
    • Precipitates out the free calcium
    • Low free calcium - secondary hyperparathyroidism
    • This produces more PTH, and the osteoclasts in the bone digest bone
    • Causes renal osteodystrophy
    • Also accelerates atherosclerosis
    • NB: this excess phosphate is not going to go away, so this cycle continues - continually stripping the free calcium --> terrible secondary hyperparathyroidism
      • Reversible if you can control the phosphate
  • Can become uncontrolled: tertiary hyperparathyroidism - secondary hyperparathyroidism (where parathyroids are still responsive to free calcium) has evolved to the parathyroid has become unresponsive to free calcium: severe metastatic calcification, accelerated vascular disease, terrible osteodystrophy
    • Treatment: parathyroidectomy
  • Vitamin D: renal disease = less 1-hydroxylation of vitamin D in the kidney. Low vitamin D = low calcium absorption (osteomalacia). So also affects bone that way
    • Therefore renal osteodystrophy also includes a component of osteomalacia
    • Vitamin D supplementation and phosphate binding to eliminate phosphate
  • Anaemia: low EPO, anaemia of chronic disease, malnourishment, bleeding (coagulopathy in proteinuria, GI bleed - poor platelet function due to uraemia)

ECG

  • Indication: IHD, electrolyte imbalance
  • Look for: peaked T waves (first change due to hyperkalemia), then next is longer PR interval (first degree heart block), then QRS widens
  • High potassium
    • Highest he's seen = 8.9. This = death.
  • Management
    • Insulin + Dextrose. Because potassium and glucose go into cells together
    • Bicarbonate IV - to fix the acidosis. So you're no longer pushing H+ into the cell, so you draw the H+ out of the cell, which drives K+ into the cell. Takes 20-30 mins. This is an adjunct
    • Salbutamol - causes K+ to go into cells
    • {Protect the heart} Give CaGlucanate or CaCl to stabilise cardiomyocytes
    • Risonium - Reduces absorption of K+. Can draw K+ out into the gut from the circulation
      • Good because it's not sending more into cells. It actually reduces total body K
      • The other mechanisms we mentioned can reverse later - only work acutely
    • Better treatment = dialysis. But vascath has a high risk of infection etc. But not a great option when there is forethought and planning for dialysis
  • See wikipedia:Hyperkalemia#Treatment
  • Indications for dialysis:
    • Hyperkalemia
    • Uraemic symptoms
    • Acidosis
    • GFR - not waiting for metabolic consequences. But not available, very costly
  • Types of dialysis
    • Haemodialysis: hospital, home - can do it more frequently at home, must be competent, must have someone around - e.g. hypotension, LOC, seizures (due to rapid electrolyte shifts). Compliance problems. Cost: $80k/year for hospital haemodialysis (cost of staffing). Home haemodialysis: $40-60
      • Cardiovascular implications - need strong heart to pump the blood out into the dialysis machine. Need cardiac reserve
    • Peritoneal dialysis. Use peritoneal membrane for exchange. Can run it at night. Risk = peritonitis (everyone gets it, can be fatal). Over time with repeated episodes of peritonitis, the peritoneal membrane becomes less effective due to scarring
      • Peritoneal dialysis - put dialysis fluid in the peritoneum and the blood in the mesenteries will be filtered into the dialysis fluid in the peritoneum
  • Stop passing urine when on dialysis
  • Do we dialyse this person
    • Comorbidities may be too difficult
    • lives at home alone
    • equivocal as to whether she wants it or not
    • she will die if she doesn't get dialysis (acutely even if there's a reversible cause e.g. UTI)
    • dialysis actually causes poor quality of life
    • incredibly difficult decision, need patient's involvement and benefits and risks discussion


  • Causes of death
    • Arrhythmia
    • Encephalopathy/coma - uraemia
  • NB: pericarditis not usually severe enough to be fatal
  • There are worse ways to die than these two above
  • Back in the day, if someone >65 years, they don't get dialysis