Uremia: Difference between revisions

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***Loss of Vitamin D and erythropoietin
***Loss of Vitamin D and erythropoietin
**Regulatory failure
**Regulatory failure
***Uremic state produces excess free radicals -> atherosclerosis, amyloidosis
***Uremic state produces excess free radicals atherosclerosis, amyloidosis


==Clinical Features and Management==
==Clinical Features and Management==
===Neurologic===
===Neurologic===
*Uremic encephalopathy
*Uremic [[encephalopathy]]
**Diagnosis of exclusion
**Diagnosis of exclusion
**Cognitive defects, memory loss, decreased attentiveness, slurred speech
**Cognitive defects, memory loss, decreased attentiveness, [[dysarthria|slurred speech]]
**Asterixis, seizure, coma
**Asterixis, [[seizure]], [[coma]]
**Improves with dialysis
**Improves with [[dialysis]]
*Dialysis dementia
*Dialysis [[dementia]]
**Similar to uremic encephalopathy except progressive, no improvement with dialysis  
**Similar to uremic encephalopathy except progressive, no improvement with dialysis  
**EEG findings can differentiate uremic encephalopathy from dialysis dementia
**EEG findings can differentiate uremic encephalopathy from dialysis dementia
*[[CVA]]
*[[CVA]]
**Cerebrovascular disease, trauma, bleeding dyscrasias, anticoagulant, hypertension
**[[Stroke|Cerebrovascular disease]], trauma, [[coagulopathy|bleeding dyscrasias]], anticoagulant, hypertension
*[[Subdural hematoma]]
*[[Subdural hematoma]]
**10 times more likely than in general population
**10 times more likely than in general population
**Headache, focal neurologic deficits, seizure, coma
**Platelet dysfunction
**[[Headache]], [[focal neurologic deficits]], [[seizure]], [[coma]]
*Peripheral neuropathy
*Peripheral neuropathy
**Occurs in 60-100% of dialysis patients
**Occurs in 60-100% of dialysis patients
**Paresthesias, impaired proprioception, weakness
**[[Paresthesias]], impaired proprioception, [[weakness]]
**Autonomic neuropathy (postural dizziness, gastroparesis, bowel dysfunction)
**Autonomic neuropathy (postural [[dizziness]], [[gastroparesis]], bowel dysfunction)


===Cardiovascular===
===Cardiovascular===
*CK-MB and troponin are specific markers of MI even in patients undergoing regular dialysis
*CK-MB and [[troponin]] are specific markers of MI even in patients undergoing regular dialysis
*Mortality from CV disease is 10-30 times higher in dialysis patients than general population
*Mortality from cardiovascular disease is 10-30 times higher in dialysis patients than general population
*hypertension is common
*hypertension is common
*Uremic cardiomyopathy
*Uremic [[cardiomyopathy]]
**Diagnosis of exclusion
**Diagnosis of exclusion
**Circulating digitalis-like substances have been implicated
**Circulating digitalis-like substances have been implicated
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***Constitutional symptoms, such as fever, are more common  than in uremic pericarditis
***Constitutional symptoms, such as fever, are more common  than in uremic pericarditis
**Treatment
**Treatment
***Dialysis
***[[Dialysis]]
*[[Tamponade]]
*[[Tamponade]]
**Presents with altered mental status, hypotension, dyspnea
**Presents with [[altered mental status]], [[hypotension]], [[dyspnea]]
***Rarely present with classic signs of Beck's triad
***Rarely present with classic signs of Beck's triad
**Pericardiocentesis should only be attempted if hemodynamically unstable
**[[Pericardiocentesis]] should only be attempted if hemodynamically unstable
*[[Pulmonary Edema]]
*[[Pulmonary Edema]]
**Commonly ascribed to fluid overload; also consider MI
**Commonly ascribed to fluid overload; also consider MI
***Treat similar to non-ESRD patient
***Treat similar to non-ESRD patient
****Lasix 80mg IV may be effective even if minimal urine output (pulmonary vasodilation)
****[[Furosemide]] 80mg IV may be effective even if minimal urine output (pulmonary vasodilation)
***Preload reduction can be accomplished via:
***Preload reduction can be accomplished via:
****Induced diarrhea (sorbitol)
****Induced [[diarrhea]] (sorbitol)
****Phlebotomy - withdrawal of as little as 150 mL is safe and effective
****Phlebotomy - withdrawal of as little as 150 mL is safe and effective
*[[CHF]]
*[[CHF]]
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*Bleeding diathesis ([[Uremic bleeding syndrome]])
*Bleeding diathesis ([[Uremic bleeding syndrome]])
**Increased risk for of bleeding (GI, ICH, liver hematoma) due to impaired platelet function
**Increased risk for of bleeding (GI, ICH, liver hematoma) due to impaired platelet function
**Treatment = desmopressin, cryoprecipitate, conjugated estrogen, EPO, dialysis<ref>Hedges SJ et al. Evidence-based treatment recommendations for uremic bleeding. Nature Clinical Practice Nephrology (2007) 3, 138-153.</ref>
**Treatment = [[desmopressin]], [[cryoprecipitate]], conjugated estrogen, EPO, dialysis<ref>Hedges SJ et al. Evidence-based treatment recommendations for uremic bleeding. Nature Clinical Practice Nephrology (2007) 3, 138-153.</ref>


===GI===
===GI===
*Anorexia, [[nausea/vomiting]]
*Anorexia, [[nausea/vomiting]]
*Increased incidence of GI bleeding, diverticular disease, ascites
*Increased incidence of [[GI bleeding]], diverticular disease, [[ascites]]


===Dermatologic===
===Dermatologic===
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*Metastatic calcification ([[calciphylaxis]])
*Metastatic calcification ([[calciphylaxis]])
**When calcium-phosphate product (Ca x PO4) > 70-80, metastatic calcification can ensue
**When calcium-phosphate product (Ca x PO4) > 70-80, metastatic calcification can ensue
**Symptoms of pseudogout, skin/finger necrosis (small vessel involvement)
**Symptoms of [[pseudogout]], skin/finger necrosis (small vessel involvement)
**Life-threatening calcifications can occur in the cardiac and pulmonary systems
**Life-threatening calcifications can occur in the cardiac and pulmonary systems
**Treatment = use of low-calcium dialysate and phosphate-binding gels
**Treatment = use of low-calcium dialysate and phosphate-binding gels
*Hyperparathyroidism (osteitis fibrosa cystica)
*[[Hyperparathyroidism]] (osteitis fibrosa cystica)
**Calciphylaxis + vitamin D3 deficiency results in depressed Ca, stimulation of PTH
**Calciphylaxis + vitamin D3 deficiency results in depressed Ca, stimulation of PTH
**Leads to high bone turnover -> weakened bones -> increased fracture susceptibility
**Leads to high bone turnover weakened bones increased [[fracture]] susceptibility
**Treatment = phosphate binding gels, vitamin D3 replacement
**Treatment = phosphate binding gels, vitamin D3 replacement
*Vitamin D3 deficiency and aluminum intoxication (osteomalacia)
*[[Vitamin D deficiency|Vitamin D3 deficiency]] and [[aluminum toxicity|aluminum intoxication]] (osteomalacia)
**Leads to osteomalacia (defect in bone calcification)
**Leads to osteomalacia (defect in bone calcification)
**Symptoms similar to hyperparathyroidism (muscle weakness, bone pain)
**Symptoms similar to hyperparathyroidism (muscle weakness, bone pain)
**Treatment = desferrioxamine
**Treatment = desferrioxamine
*Amyloidosis
*[[Amyloidosis]]
**Common in patients >50yo who have received dialysis for >10yr
**Common in patients >50yo who have received dialysis for >10yr
**Complications: GI perforation, bone cysts with pathologic fracture, arthropathies
**Complications: GI perforation, bone cysts with pathologic fracture, arthropathies


===Anion Gap Metabolic Acidosis<ref>Angus S. Uremic Acidosis. University of Connecticut, 2006. http://fitsweb.uchc.edu/student/selectives/TimurGraham/Uremia.html</ref><ref>Nickson C. Renal Tubular Acidosis and Uraemic Acidosis. LITFL. http://lifeinthefastlane.com/ccc/renal-tubular-acidosis/.</ref>===
===[[Anion gap acidosis|Anion Gap Metabolic Acidosis]]<ref>Angus S. Uremic Acidosis. University of Connecticut, 2006. http://fitsweb.uchc.edu/student/selectives/TimurGraham/Uremia.html</ref><ref>Nickson C. Renal Tubular Acidosis and Uraemic Acidosis. LITFL. http://lifeinthefastlane.com/ccc/renal-tubular-acidosis/.</ref>===
*Early chronic kidney disease associated with hyperchloremic normal anion gap metabolic acidosis
*Early chronic kidney disease associated with hyperchloremic [[non anion gap acidosis|normal anion gap metabolic acidosis]]
*Late stage disease causes anion gap
*Late stage disease causes anion gap
**Failure to excrete acid anions, phosphate and sulfate
**Failure to excrete acid anions, phosphate and sulfate
**Bone demineralization - bone buffers H+, releasing calcium from bone, leads to osteopenia
**Bone demineralization - bone buffers H+, releasing calcium from bone, leads to osteopenia
*Treatment: PO sodium bicarbonate 1 mEq/kg/day
*Treatment: PO [[sodium bicarbonate]] 1 mEq/kg/day
 
==See Also==
*[[AKI]]


==References==
==References==
<references/>
<references/>
[[Category:Renal]]
[[Category:Renal]]

Latest revision as of 03:04, 21 February 2021

Background

  • Uremia = clinical syndrome associated with end-stage renal disease
    • Correlation exists between symptoms of uremia and low GFR (15-20% of nl)
    • BUN/creatinine are inaccurate markers of clinical syndrome of uremia
  • Contributing Factors:
    • Excretory failure
      • Leads to toxin accumulation
    • Biosynthetic failure
      • Loss of Vitamin D and erythropoietin
    • Regulatory failure
      • Uremic state produces excess free radicals → atherosclerosis, amyloidosis

Clinical Features and Management

Neurologic

Cardiovascular

  • CK-MB and troponin are specific markers of MI even in patients undergoing regular dialysis
  • Mortality from cardiovascular disease is 10-30 times higher in dialysis patients than general population
  • hypertension is common
  • Uremic cardiomyopathy
    • Diagnosis of exclusion
    • Circulating digitalis-like substances have been implicated
    • Dialysis rarely improves LV function
  • Pericarditis
    • Uremic pericarditis (75% of cases)
      • Most common when the other symptoms of uremia are most severe
      • BUN is nearly always >60
      • Loud friction rub that is often palpable
      • Typical pericarditis ECG changes are absent (inflammation does not involve myocardium)
        • If ECG does have typical changes consider infection
    • Dialysis-related (25% of cases)
      • Most common during increased catabolism (trauma, sepsis) or missed dialysis sessions
      • Constitutional symptoms, such as fever, are more common than in uremic pericarditis
    • Treatment
  • Tamponade
  • Pulmonary Edema
    • Commonly ascribed to fluid overload; also consider MI
      • Treat similar to non-ESRD patient
        • Furosemide 80mg IV may be effective even if minimal urine output (pulmonary vasodilation)
      • Preload reduction can be accomplished via:
        • Induced diarrhea (sorbitol)
        • Phlebotomy - withdrawal of as little as 150 mL is safe and effective
  • CHF
    • May be preexisting
    • May be caused by uremic cardiomyopathy, fluid overload, AV-related high-output failure

Hematologic

  • Anemia
    • Without treatment, the hematocrit in ESRD patients should stabilize at 15-20%
    • Treatment = erythropoietin
  • Immunodeficiency
  • Bleeding diathesis (Uremic bleeding syndrome)
    • Increased risk for of bleeding (GI, ICH, liver hematoma) due to impaired platelet function
    • Treatment = desmopressin, cryoprecipitate, conjugated estrogen, EPO, dialysis[1]

GI

Dermatologic

  • Uremic frost
  • Generated from crystallized nitrogenous waste from sweat
  • Typically in BUN > 200mg/dL
  • Treatment is lowering BUN

Renal bone disease

  • Metastatic calcification (calciphylaxis)
    • When calcium-phosphate product (Ca x PO4) > 70-80, metastatic calcification can ensue
    • Symptoms of pseudogout, skin/finger necrosis (small vessel involvement)
    • Life-threatening calcifications can occur in the cardiac and pulmonary systems
    • Treatment = use of low-calcium dialysate and phosphate-binding gels
  • Hyperparathyroidism (osteitis fibrosa cystica)
    • Calciphylaxis + vitamin D3 deficiency results in depressed Ca, stimulation of PTH
    • Leads to high bone turnover → weakened bones → increased fracture susceptibility
    • Treatment = phosphate binding gels, vitamin D3 replacement
  • Vitamin D3 deficiency and aluminum intoxication (osteomalacia)
    • Leads to osteomalacia (defect in bone calcification)
    • Symptoms similar to hyperparathyroidism (muscle weakness, bone pain)
    • Treatment = desferrioxamine
  • Amyloidosis
    • Common in patients >50yo who have received dialysis for >10yr
    • Complications: GI perforation, bone cysts with pathologic fracture, arthropathies

Anion Gap Metabolic Acidosis[2][3]

  • Early chronic kidney disease associated with hyperchloremic normal anion gap metabolic acidosis
  • Late stage disease causes anion gap
    • Failure to excrete acid anions, phosphate and sulfate
    • Bone demineralization - bone buffers H+, releasing calcium from bone, leads to osteopenia
  • Treatment: PO sodium bicarbonate 1 mEq/kg/day

See Also

References

  1. Hedges SJ et al. Evidence-based treatment recommendations for uremic bleeding. Nature Clinical Practice Nephrology (2007) 3, 138-153.
  2. Angus S. Uremic Acidosis. University of Connecticut, 2006. http://fitsweb.uchc.edu/student/selectives/TimurGraham/Uremia.html
  3. Nickson C. Renal Tubular Acidosis and Uraemic Acidosis. LITFL. http://lifeinthefastlane.com/ccc/renal-tubular-acidosis/.