Uremia: Difference between revisions
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==Background== | ==Background== | ||
*Uremia = clinical syndrome | *Uremia = clinical syndrome associated with end-stage renal disease | ||
**Correlation exists between uremia | **Correlation exists between symptoms of uremia and low GFR (15-20% of nl) | ||
**BUN/ | **BUN/creatinine are inaccurate markers of clinical syndrome of uremia | ||
*Contributing Factors: | *Contributing Factors: | ||
**Excretory failure | **Excretory failure | ||
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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 | ***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 | **Improves with [[dialysis]] | ||
*Dialysis dementia | *Dialysis [[dementia]] | ||
**Similar to uremic encephalopathy except progressive, no improvement | **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, | **[[Stroke|Cerebrovascular disease]], trauma, [[coagulopathy|bleeding dyscrasias]], anticoagulant, hypertension | ||
*[[Subdural hematoma]] | *[[Subdural hematoma]] | ||
** | **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 | **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 | *CK-MB and [[troponin]] are specific markers of MI even in patients undergoing regular dialysis | ||
*Mortality from | *Mortality from cardiovascular disease is 10-30 times higher in dialysis patients than general population | ||
* | *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 | **Presents with [[altered mental status]], [[hypotension]], [[dyspnea]] | ||
***Rarely present | ***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 | ***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: | ***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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===Hematologic=== | ===Hematologic=== | ||
*[[Anemia]] | *[[Anemia]] | ||
**Without | **Without treatment, the hematocrit in ESRD patients should stabilize at 15-20% | ||
**Treatment = erythropoietin | **Treatment = erythropoietin | ||
*Immunodeficiency | *Immunodeficiency | ||
*Bleeding diathesis ([[Uremic bleeding syndrome]]) | *Bleeding diathesis ([[Uremic bleeding syndrome]]) | ||
**Increased risk for of bleeding (GI, ICH, liver hematoma) due to impaired | **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, [[ | *Anorexia, [[nausea/vomiting]] | ||
*Increased incidence of GI bleeding, diverticular disease, ascites | *Increased incidence of [[GI bleeding]], diverticular disease, [[ascites]] | ||
=== | ===Dermatologic=== | ||
*Uremic frost | *Uremic frost | ||
*Generated from crystallized nitrogenous waste from sweat | *Generated from crystallized nitrogenous waste from sweat | ||
*Typically in BUN > | *Typically in BUN > 200mg/dL | ||
* | *Treatment is lowering BUN | ||
===Renal bone disease=== | ===Renal bone disease=== | ||
*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 | ||
*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 | **Leads to high bone turnover → weakened bones → increased [[fracture]] susceptibility | ||
** | **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 | ||
*Amyloidosis | *[[Amyloidosis]] | ||
**Common in | **Common in patients >50yo who have received dialysis for >10yr | ||
**Complications: GI perforation, bone cysts | **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 | *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 | ||
==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
- Excretory failure
Clinical Features and Management
Neurologic
- Uremic encephalopathy
- Diagnosis of exclusion
- Cognitive defects, memory loss, decreased attentiveness, slurred speech
- Asterixis, seizure, coma
- Improves with dialysis
- Dialysis dementia
- Similar to uremic encephalopathy except progressive, no improvement with dialysis
- EEG findings can differentiate uremic encephalopathy from dialysis dementia
- CVA
- Cerebrovascular disease, trauma, bleeding dyscrasias, anticoagulant, hypertension
- Subdural hematoma
- 10 times more likely than in general population
- Platelet dysfunction
- Headache, focal neurologic deficits, seizure, coma
- Peripheral neuropathy
- Occurs in 60-100% of dialysis patients
- Paresthesias, impaired proprioception, weakness
- Autonomic neuropathy (postural dizziness, gastroparesis, bowel dysfunction)
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
- Uremic pericarditis (75% of cases)
- Tamponade
- Presents with altered mental status, hypotension, dyspnea
- Rarely present with classic signs of Beck's triad
- Pericardiocentesis should only be attempted if hemodynamically unstable
- Presents with altered mental status, hypotension, dyspnea
- 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
- Treat similar to non-ESRD patient
- Commonly ascribed to fluid overload; also consider MI
- 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
- Anorexia, nausea/vomiting
- Increased incidence of GI bleeding, diverticular disease, ascites
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
- ↑ Hedges SJ et al. Evidence-based treatment recommendations for uremic bleeding. Nature Clinical Practice Nephrology (2007) 3, 138-153.
- ↑ Angus S. Uremic Acidosis. University of Connecticut, 2006. http://fitsweb.uchc.edu/student/selectives/TimurGraham/Uremia.html
- ↑ Nickson C. Renal Tubular Acidosis and Uraemic Acidosis. LITFL. http://lifeinthefastlane.com/ccc/renal-tubular-acidosis/.