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Dr. Angelo Smith M.D
WHPL
NORMALARF CRF
Inability of kidney to maintain
homeostasis leading to a buildup
of nitrogenous wastes
Different to renal insufficiency
where kidney function is
deranged but can still support
life
 Occurs over hours/days
 Lab definition
 Increase in baseline creatinine of more than 50%
 Decrease in creatinine clearance of more than
50%
 Deterioration in renal function requiring dialysis
▪ Anuria – no urine output or less than 100mls/24 hours
▪ Oliguria - <500mls urine output/24 hours or <20mls/hour
▪ Polyuria - >2.5L/24 hours
Persons at Risks
 Major surgery
 Major trauma
 Receiving nephrotoxic medications
 Elderly
 Pre renal
(functional)
 Renal-intrinsic
(structural)
 Post renal
(obstruction)
Pathophysiology of ischemic and toxic ARF
Stages
 Onset – 1-3 days with ^ BUN and creatinine and
possible decreased UOP
 Oliguric – UOP < 400/d, ^BUN, Crest, Phos, K, may
last up to 14 d
 Diuretic – UOP ^ to as much as 4000 mL/d but no
waste products, at end of this stage may begin to see
improvement
 Recovery – things go back to normal or may remain
insufficient and become chronic
Subjective symptoms
Nausea
Loss of appetite
Headache
Lethargy
Tingling in extremities
 vomiting
 disorientation,
 edema,
 ^K+
 decrease Na
 ^ BUN and
creatinine
 Acidosis
 uremic breath
 CHF and pulmonary
edema
 hypertension caused
by hypovolemia,
anorexia
 sudden drop in UOP
 convulsions, coma
 changes in bowels
 Increased UOP
 Gradual decline in BUN and creatinine
 Hypokalemia
 Hyponaturmia
 Tachycardia
 Improved LOC
 Rising creatinine and urea
 Rising potassium
 Decreasing Hb
 Acidosis
 Hyponatraemia
 Hypocalcaemia
 Urinary sediment
 Urinary indices
 Urine volume
 Urine electrolytes
 Radiologic studies
 Immediate treatment of pulmonary edema and
hyperkalaemia
 Remove offending cause or treat offending cause
 Dialysis as needed to control hyperkalaemia,
pulmonary edema, metabolic acidosis, and uremic
symptoms
 Adjustment of drug regimen
 Usually restriction of water, Na, and K intake, but
provision of adequate protein
 Possibly phosphate binders and Na polystyrene
sulfonate
 Medical treatment
 Fluid and dietary restrictions
 Maintain E-lytes
 D/C or change cause
 May need dialysis to jump start renal function
 May need to stimulate production of urine with IV
fluids, Dopomine, diuretics, etc.
 Medical treatment
 Hemodialysis
▪ Subclavian approach
▪ Femoral approach
 Peritoneal dialysis
 Continous renal replacement therapy (CRRT)
▪ Can be done continuously
▪ Does not require dialysate
Involves progressive, irreversible loss of
kidney function
Defined as either presence of
 Kidney damage
▪ Pathological abnormalities
 Glomerular filtration rate (GFR)
▪ <60 ml/min for 3 months or longer
Glomerulonephritis – the most
common cause in the past
Diabetes mellitus
Hypertension
Tubulointerstitial nephritis
 are now the leading causes of CRF
 Subjective symptoms are relatively same as acute
 Renal
 Hyponaturmia
 Dry mouth
 Poor skin turgor
 Confusion, salt overload, accumulation of K with
muscle weakness
 Fluid overload and metabolic acidosis
 Proteinuria, glycosuria
 Urine = RBC’s, WBC’s, and casts
Cardiovascular
 Hypertension
 Arrythmias
 Pericardial
effusion
 CHF
 Peripheral edema
 Neurological
 Burning, pain, and itching,
parestnesia
 Motor nerve dysfunction
 Muscle cramping
 Shortened memory span
 Apathy
 Drowsy, confused,
seizures, coma, EEG
changes
GI
 Stomatitis
 Ulcers
 Pancreatitis
 Uremic fetor
 Vomiting
 consitpation
 Respiratory
 ^ chance of infection
 Pulmonary edema
 Pleural friction rub
and effusion
 Dyspnea
 Kussmaul’s
respirations from
acidosis
Endocrine
 Stunted growth in children
 Amenorrhea
 Male impotence
 ^ aldosterone secretion
 Impaired glucose levels
R/T impaired CHO
metabolism
 Thyroid and parathyroid
abnormalities
Hemopoietic
 Anemia
 Decrease in RBC survival
time
 Blood loss from dialysis
and GI bleed
 Platelet deficits
 Bleeding and clotting
disorders – purpura and
hemorrhage from body
orifices , ecchymoses
Skeletal
 Muscle and bone pain
 Bone demineralization
 Pathological fractures
 Blood vessel
calcifications in
myocardium, joints,
eyes, and brain
Skin
 Yellow-bronze skin
with pallor
 Puritus
 Purpura
 Uremic frost
 Thin, brittle nails
 Dry, brittle hair, and
may have color
changes and alopecia
• is clinical syndrome that results from profound loss
of renal function
• cause(s) of it remains unknown
• rerers generally to the constellation of signs and
symptoms associated with CRF, regardless of
cause
• presentations and severity of signs and symptoms
of uremia vary and depend on
• the magnitude of reduction in functioning renal
mass
• rapidity with which renal function is lost
 the most likely candidates as toxins in uremia are
the by–products of protein and amino acid
metabolism
 Urea – represents some 80% of the total nitrogen
excreted into the urine
 Guanidino compunds: guanidine, creatinine, creatin,
guanidin-succinic acid)
 Urates and other end products of nucleic acid
metabolism
 Aliphatic amines
 Peptides
 Derivates of the aromatic amino acids: tryptophan,
tyrosine, and phenylalanine
Metabolic acidosis of CRF is not due to
overproduction of endogenous acids
but is largely a reflection of the
reduction in renal mass, which limits
the amount of NH3 (and therefore
HCO3
-
) that can be generated
BUN – indicator of glomerular filtration rate and
is affected by the breakdown of protein. Normal is
10-20mg/dL. When reaches 70 = dialysis
 Serum creatinine – waste product of skeletal
muscle breakdown and is a better indicator of
kidney function. Normal is 0.5-1.5 mg/dL. When
reaches 10 x normal, it is time for dialysis
 Creatinine clearance is best determent of kidney
function. Must be a 12-24 hour urine collection.
Normal is > 100 ml/min
K+ -
 The kidneys are means which K+ is excreted.
Normal is 3.5-5.0 ,mEq/L. maintains muscle
contraction and is essential for cardiac function.
 Both elevated and decreased can cause problems
with cardiac rhythm
 Hyperkalemia is treated with IV glucose and Na
Bicarb which pushes K+ back into the cell.
Ca
 With disease in the kidney, the enzyme for
utilization of Vit D is absent
 Ca absorption depends upon Vit D
 Body moves Ca out of the bone to compensate
and with that Ca comes phosphate bound to it.
 Normal Ca level is 4.5-5.5 mEq/L
 Hypocalcemia = tetany
▪ Treat with calcium with Vit D and phosphate
▪ Avoid antacids with magnesium
Metabolic acidosis
Fluid imbalance
Insulin resistance
Anemia
Immunological problems
 Medical treatment
 IV glucose and insulin
 Na bicarb, Ca, Vit D, phosphate binders
 Fluid restriction, diuretics
 Iron supplements, blood, erythropoietin
 High carbs, low protein
 Dialysis - After all other methods have failed
Hemodialysis
 Vascular access
▪ Temporary – subclavian or femoral
▪ Permanent – shunt, in arm
▪ Care post insertion
 Can be done rapidly
 Takes about 4 hours
 Done 3 x a week
 Peritoneal dialysis
 Semipermeable
membrane
 Catheter inserted
through abdominal wall
into peritoneal cavity
 Cost less
 Fewer restrictions
 Can be done at home
 Risk of peritonitis
 3 phases – inflow, dwell
and outflow
 Automated peritoneal
dialysis
 Done at home at night
 Maybe 6-7 times /week
 CAPD
 Continuous ambulatory
peritoneal dialysis
 Done as outpatient
 Usually 4 X/d
Transplant
 Must find donor
 Waiting period long
 Good survival rate – 1 year 95-97%
 Must take immunosuppressant’s for life
 Decreased resistance to infections.
 Rejection
▪ Watch for fever, elevated B/P, and pain over
site of new kidney
• Potassium restriction
– 2 to 4 g
– High-potassium foods should be avoided
• Oranges
• Bananas
• Tomatoes
• Green vegetables
• Phosphate restriction
– 1000 mg/day
– Foods high in phosphate
• Dairy products
– Most foods high in phosphate are also high in
calcium
Renal failure   acute and chronic
Renal failure   acute and chronic

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Renal failure acute and chronic

  • 1. Dr. Angelo Smith M.D WHPL
  • 2.
  • 3.
  • 4.
  • 6.
  • 7. Inability of kidney to maintain homeostasis leading to a buildup of nitrogenous wastes Different to renal insufficiency where kidney function is deranged but can still support life
  • 8.  Occurs over hours/days  Lab definition  Increase in baseline creatinine of more than 50%  Decrease in creatinine clearance of more than 50%  Deterioration in renal function requiring dialysis ▪ Anuria – no urine output or less than 100mls/24 hours ▪ Oliguria - <500mls urine output/24 hours or <20mls/hour ▪ Polyuria - >2.5L/24 hours
  • 9. Persons at Risks  Major surgery  Major trauma  Receiving nephrotoxic medications  Elderly
  • 10.
  • 11.  Pre renal (functional)  Renal-intrinsic (structural)  Post renal (obstruction)
  • 12.
  • 13.
  • 14.
  • 15.
  • 16.
  • 18. Stages  Onset – 1-3 days with ^ BUN and creatinine and possible decreased UOP  Oliguric – UOP < 400/d, ^BUN, Crest, Phos, K, may last up to 14 d  Diuretic – UOP ^ to as much as 4000 mL/d but no waste products, at end of this stage may begin to see improvement  Recovery – things go back to normal or may remain insufficient and become chronic
  • 19. Subjective symptoms Nausea Loss of appetite Headache Lethargy Tingling in extremities
  • 20.  vomiting  disorientation,  edema,  ^K+  decrease Na  ^ BUN and creatinine  Acidosis  uremic breath  CHF and pulmonary edema  hypertension caused by hypovolemia, anorexia  sudden drop in UOP  convulsions, coma  changes in bowels
  • 21.  Increased UOP  Gradual decline in BUN and creatinine  Hypokalemia  Hyponaturmia  Tachycardia  Improved LOC
  • 22.  Rising creatinine and urea  Rising potassium  Decreasing Hb  Acidosis  Hyponatraemia  Hypocalcaemia
  • 23.  Urinary sediment  Urinary indices  Urine volume  Urine electrolytes  Radiologic studies
  • 24.
  • 25.
  • 26.
  • 27.  Immediate treatment of pulmonary edema and hyperkalaemia  Remove offending cause or treat offending cause  Dialysis as needed to control hyperkalaemia, pulmonary edema, metabolic acidosis, and uremic symptoms  Adjustment of drug regimen  Usually restriction of water, Na, and K intake, but provision of adequate protein  Possibly phosphate binders and Na polystyrene sulfonate
  • 28.  Medical treatment  Fluid and dietary restrictions  Maintain E-lytes  D/C or change cause  May need dialysis to jump start renal function  May need to stimulate production of urine with IV fluids, Dopomine, diuretics, etc.
  • 29.  Medical treatment  Hemodialysis ▪ Subclavian approach ▪ Femoral approach  Peritoneal dialysis  Continous renal replacement therapy (CRRT) ▪ Can be done continuously ▪ Does not require dialysate
  • 30.
  • 31. Involves progressive, irreversible loss of kidney function Defined as either presence of  Kidney damage ▪ Pathological abnormalities  Glomerular filtration rate (GFR) ▪ <60 ml/min for 3 months or longer
  • 32.
  • 33.
  • 34. Glomerulonephritis – the most common cause in the past Diabetes mellitus Hypertension Tubulointerstitial nephritis  are now the leading causes of CRF
  • 35.
  • 36.  Subjective symptoms are relatively same as acute  Renal  Hyponaturmia  Dry mouth  Poor skin turgor  Confusion, salt overload, accumulation of K with muscle weakness  Fluid overload and metabolic acidosis  Proteinuria, glycosuria  Urine = RBC’s, WBC’s, and casts
  • 37. Cardiovascular  Hypertension  Arrythmias  Pericardial effusion  CHF  Peripheral edema  Neurological  Burning, pain, and itching, parestnesia  Motor nerve dysfunction  Muscle cramping  Shortened memory span  Apathy  Drowsy, confused, seizures, coma, EEG changes
  • 38.
  • 39. GI  Stomatitis  Ulcers  Pancreatitis  Uremic fetor  Vomiting  consitpation  Respiratory  ^ chance of infection  Pulmonary edema  Pleural friction rub and effusion  Dyspnea  Kussmaul’s respirations from acidosis
  • 40. Endocrine  Stunted growth in children  Amenorrhea  Male impotence  ^ aldosterone secretion  Impaired glucose levels R/T impaired CHO metabolism  Thyroid and parathyroid abnormalities Hemopoietic  Anemia  Decrease in RBC survival time  Blood loss from dialysis and GI bleed  Platelet deficits  Bleeding and clotting disorders – purpura and hemorrhage from body orifices , ecchymoses
  • 41. Skeletal  Muscle and bone pain  Bone demineralization  Pathological fractures  Blood vessel calcifications in myocardium, joints, eyes, and brain Skin  Yellow-bronze skin with pallor  Puritus  Purpura  Uremic frost  Thin, brittle nails  Dry, brittle hair, and may have color changes and alopecia
  • 42.
  • 43. • is clinical syndrome that results from profound loss of renal function • cause(s) of it remains unknown • rerers generally to the constellation of signs and symptoms associated with CRF, regardless of cause • presentations and severity of signs and symptoms of uremia vary and depend on • the magnitude of reduction in functioning renal mass • rapidity with which renal function is lost
  • 44.  the most likely candidates as toxins in uremia are the by–products of protein and amino acid metabolism  Urea – represents some 80% of the total nitrogen excreted into the urine  Guanidino compunds: guanidine, creatinine, creatin, guanidin-succinic acid)  Urates and other end products of nucleic acid metabolism  Aliphatic amines  Peptides  Derivates of the aromatic amino acids: tryptophan, tyrosine, and phenylalanine
  • 45. Metabolic acidosis of CRF is not due to overproduction of endogenous acids but is largely a reflection of the reduction in renal mass, which limits the amount of NH3 (and therefore HCO3 - ) that can be generated
  • 46.
  • 47. BUN – indicator of glomerular filtration rate and is affected by the breakdown of protein. Normal is 10-20mg/dL. When reaches 70 = dialysis  Serum creatinine – waste product of skeletal muscle breakdown and is a better indicator of kidney function. Normal is 0.5-1.5 mg/dL. When reaches 10 x normal, it is time for dialysis  Creatinine clearance is best determent of kidney function. Must be a 12-24 hour urine collection. Normal is > 100 ml/min
  • 48. K+ -  The kidneys are means which K+ is excreted. Normal is 3.5-5.0 ,mEq/L. maintains muscle contraction and is essential for cardiac function.  Both elevated and decreased can cause problems with cardiac rhythm  Hyperkalemia is treated with IV glucose and Na Bicarb which pushes K+ back into the cell.
  • 49. Ca  With disease in the kidney, the enzyme for utilization of Vit D is absent  Ca absorption depends upon Vit D  Body moves Ca out of the bone to compensate and with that Ca comes phosphate bound to it.  Normal Ca level is 4.5-5.5 mEq/L  Hypocalcemia = tetany ▪ Treat with calcium with Vit D and phosphate ▪ Avoid antacids with magnesium
  • 50. Metabolic acidosis Fluid imbalance Insulin resistance Anemia Immunological problems
  • 51.  Medical treatment  IV glucose and insulin  Na bicarb, Ca, Vit D, phosphate binders  Fluid restriction, diuretics  Iron supplements, blood, erythropoietin  High carbs, low protein  Dialysis - After all other methods have failed
  • 52. Hemodialysis  Vascular access ▪ Temporary – subclavian or femoral ▪ Permanent – shunt, in arm ▪ Care post insertion  Can be done rapidly  Takes about 4 hours  Done 3 x a week
  • 53.  Peritoneal dialysis  Semipermeable membrane  Catheter inserted through abdominal wall into peritoneal cavity  Cost less  Fewer restrictions  Can be done at home  Risk of peritonitis  3 phases – inflow, dwell and outflow  Automated peritoneal dialysis  Done at home at night  Maybe 6-7 times /week  CAPD  Continuous ambulatory peritoneal dialysis  Done as outpatient  Usually 4 X/d
  • 54. Transplant  Must find donor  Waiting period long  Good survival rate – 1 year 95-97%  Must take immunosuppressant’s for life  Decreased resistance to infections.  Rejection ▪ Watch for fever, elevated B/P, and pain over site of new kidney
  • 55. • Potassium restriction – 2 to 4 g – High-potassium foods should be avoided • Oranges • Bananas • Tomatoes • Green vegetables • Phosphate restriction – 1000 mg/day – Foods high in phosphate • Dairy products – Most foods high in phosphate are also high in calcium