Uremia
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/.