Lecture 15 - Renal Failure Flashcards
What are the 2 types of dialyses? Is one better?
- Hemodialysis: dialysis machine hook up to a surgically made fistula between an artery and a vein in the arm, 3 x /week for 4 hours (to remove 2 days of fluid intake) => uses hydrostatic pressure, clearance is due to passive diffusion from plasma to dialysate
- Peritoneal dialysis: underused, more life independence => uses oncotic pressure
About the same outcomes
Purpose of dialysis?
- Control volume via ultrafiltration
- Clearance
- Acid base balance to correct acidosis, hyperkalemia, and low Ca++
What issue cannot be corrected via dialysis?
Phosphate accumulate
Dietary management of renal failure?
- Limit dietary salt to limit volume accumulation and regulate BP
- Limit dietary K+, since excess in ECF can cause depolarization of muscles and death
- Limit dietary phosphate with drugs that bind phosphate in the gut to inhibit it from being absorbed
- Vitamin D supplement needed since kidneys can no longer product the active form, which causes issues with Ca++ absorption and PTH regulation
Can failed kidneys still secrete renin/stimulate the SNS?
YUP
Why do patients with renal disease have anemia? Treatment?
Because the kidneys make erythropoietin
Treatment: erythropoietic agents, iron as needed
Describe the physiologic response of acute renal failure.
Loss of HALF THE RENAL FUNCTION:
- GFR is suddenly cut in half, since of the kidneys is no longer working
- Serum creatinine doubles over a certain period of time (increases exponentially) => positive balance until new steady state is reached
Normal production creatinine rate?
10-20 mg/kg/day
List the concentration changes due to renal failure (from highest to lowest)
INCREASES:
- Non protein nitrogen
- K+
- H2O
- Na+
- H+
- Phenols
- HPO4–/SO4–
DECREASES:
1. HCO3-
What are the 3 types of acute renal failure?
- Block perfusion = pre-renal
- Damage/kill nephrons = intrarenal
- Block urinary drainage = post-renal (or intra-renal in all collecting ducts, still considered post though)
Examples of causes of damaged/dead nephrons?
- Sepsis with inflammatory mediators
- Nephrotoxic injury
- Inflammation due to allergies => interstitial nephritis
- Ischemic tubular necrosis
- Transplant rejection
4 clinical examples of pre-renal acute renal failure?
- Volume depletion
- Hemorrhage
- Decompensated CHF
- Arterial-arteriolar occlusion
Physiology of pre-renal acute renal failure?
Decreased afferent perfusion/pressure => Ang II-dependent effort to maintain GFR via efferent vasoconstriction + afferent vasodilation with opposing effects of NO and prostaglandins
=> high filtration fraction
Consequence of increase filtration fraction?
Increased peritubular oncotic pressure => increased proximal and distal tubular reabsorption => salt-avid kidneys
Describe plasma urea and creatinine in pre-renal acute renal failure.
Decrease in urea clearance exceeds the decrease in creatinine clearance (so higher plasma urea) because urea can be reabsorbed but not secreted and creatinine can be secreted but not reabsorbed => high plasma BUN/creatinine ratio (>20)
Describe urine concentration and solute avidity in pre-renal acute renal failure.
- Urine concentration > 500 mOsm/L
- Increase in urine creatinine
- Decrease in fractional excretion of Na+ (<1%)
- Decrease in fractional excretion of urea (<35%)
Normal BUN/creatinine plasma ratio?
10:1
Describe plasma urea and creatinine in intra-renal acute renal failure.
Normal BUN/creatinine (unless production changed)
Describe urine concentration and solute avidity in intra-renal acute renal failure.
Impaired tubular function, which varies with the predominant site of damage
- Acidemia
- Impaired urine concentration/dilution => isosthenuria (same osmolarity of plasma)
- Low urine creatinine
- Salt wasting, with an increase in excretion fraction of Na+ (>2%)
Consequence of post-renal acute renal failure?
Transmission of pressures back along the nephron leading to a stop in filtration
Where is tubular dysfunction more severe in post-renal acute renal failure?
Distal nephron
Describe plasma urea and creatinine in post-renal acute renal failure.
High BUN/creatinine due to stasis in tubule causing increase urea reabsorption
Describe urine concentration and solute avidity in post-renal acute renal failure.
- Decrease in fractional excretion of Na+ (<1%)
- Hyperkalemia
- Acidosis
What is the intact nephron hypothesis?
No matter where you injure the nephron, the entire nephron will be injured
What happens during the shift from acute renal failure to chronic kidney disease?
Decrease in number of nephrons => hypertrophy and vasodilation of surviving nephrons + increase in arterial pressure => increase in glomerular pressure and filtration => glomerular sclerosis => further decrease in number of nephrons
Why is the sensitivity of plasma creatinine low to detect GFR decrease?
Because plasma creatinine is low and because there is tubular secretion
Which happens first during renal failure: high plasma creatinine or phosphate accumulation/acidosis?
Phosphate accumulation/acidosis
How is plasma osmoregulation (and K+, Na+, and Cl-) affected by renal failure?
Preserved into advanced CKD because they are mostly being reabsorbed by the kidneys normally so low GFR doesn’t affect the plasma levels much, PLUS thirst still works even when dilution/concentration by the kidney fails
What is the staging of CKD dependent on?
Estimated GFR normalized to body surface area
Describe the 5 stages of CKD and their necessary action.
- Normal GFR but indication of renal failure (e.g. albuminuria) => manage CVD risks and avoid nephrotoxic drugs
- Mild GFR decrease = 60-89
- Moderate GFR decrease = 30-59
- Severe GFR decrease = 15-29
- Kidney failure: GFR < 15 => replacement if uremia present
At what CKD stage is it noticeable? Why?
Stage 3 because of lab values
At what CKD stage is there an ABSOLUTE need for replacement therapy (transplant or dialysis) in an otherwise healthy person? What does this mean?
GFR = 4-5 mL/min
With artful medical management, the first 95% of kidney function is the safety margin
Why does the specific gravity of urine decrease as number of nephrons decrease? What to note?
Hypertrophy and vasodilation of surviving nephrons => flow through residual nephrons increases => inability to maintain medullary concentration or to reabsorb water => ability to maximally concentrate/dilute urine falls => isosthenuria => make more urine to excrete the same amount of waste => bladder capacity exceeds overnight
Prevalence of HT in patients with CKD?
80-100%
What is HT with CKD due to?
- Primarily to increased volume
2. Also due to vasoconstriction due to SNS and RAAS
2 consequences of HT with CKD?
- Accelerates loss of renal function
2. Worsens proteinuria
What do most patients with CKD die of?
CVD more than end stage renal disease
What vessels are use to create a fistula in the arm for hemodialysis? Purpose?
Radial or brachial vessels => loop of of high flow/low resistance causing vein to arteriolize
How does hemodialysis work?
Pump before hemodialyzer pushing blood into the hemodialyzer (artificial glomerulus), in which it is pressurized => water and waste products leave and blood is pressured back out => back into vein
How does peritoneal dialysis work?
Catheter inserted into peritoneal cavity and patient learns sterile technique to hook it up to sterile dialysis fluid (2L) => ultrafilter into the fluid (contains glucose as an osmotic agent) => drain 3 L out
Clearance of hemodialysis? What does this mean? Average urea clearance?
200 mL/min => 156 hours/week w/o clearance
Average urea clearance = 14mL/min
Clearance in peritoneal dialysis? How does this compare to HD?
5.5 mL/min (lower than HD)
Which dialysis method has better volume control?
PD
What is uremia?
Syndrome due to retention of toxic wastes in the blood: multiple toxins but urea is used as a marker
Does a low BUN dialytic clearance in patient with renal failure a good sign?
Could be, but could also mean that the dialysis is inadequate leading to uremia
Symptoms of uremia?
Decreased appetite, overlap with anemia symptoms, malnutrition
What is uremic acidosis?
Nephron loss => impaired renal ammoniagenesis => sulfate/phosphate retention => mild bicarbonate wasting + mild increase in anion gap
How to control acidosis of renal failure patients? What to note?
- Oral Na+HCO3- (or citrate) => problem with increased volume caused
- HCO3- in HD (but engineering issue because substances can bubble away)
- Lactate in PD
Describe K+ excretion in renal failure?
Without a tubular defect, normal until ESRD
Describe the removal of K+ in patients in renal failure.
Either dialysis or GIT removal
What is K+ removal limited by?
Redistristribution to intracellular compartment, which happens fast
When does low vitamin D and increasing PTH occur in CKD? Consequence?
Very early on => renal metabolic bone disease => increased osteoclastic bone reabsorption due to calcium insufficiency + calcium mobilization from bone due to acidosis
Phosphate concentration during dialysis? Implication?
Falls rapidly during but rebounds within hours because of redistribution => inefficient => instead we use phosphate binds in GIT
When does metabolic bone disease start?
Stage 2
Why do you have to be careful with VD supplement?
Too much can cause a different bone disease
Prevalence of dialysis patients?
1/2 M
Incidence of ESRD patients?
115 K
Number of kidney transplants/year?
17 K
