• 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



  • 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


  • 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]



  • 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


  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/.