Indication for dialysis

  1. decision is based on the presence of uremia-related signs and symptoms, eGFR, and the rate of decline of the eGFR
  2. eGFR>15 mL/min/1.73 = don’t initiate even with ESRD symptoms
  3. eGFR 5-15 mL/min/1.73 asymptomatic = Follow closely for emergence of ESRD-related s/s, but don’t initiate dialysis in the absence of signs or symptoms
  4. eGFR 5-15 mL/min/1.73 symptomatic = dialysis for patients who were refractory to medical treatment
  5. eGFR <5 ml/min/1.73 = initiate dialysis
  6. However, the decision varies by patients. Uremic symptoms are often not clear and loss of kidney function is variable and occur rapidly.
  7. Absolute indication: uremic pericarditis (inflammation of the pericardium) or pleuritis (lung tissue inflammation) and progressive uremic encephalopathy
  8. Common S/S for indication: declining nutritional status (<15 mL/min/1.73 m2 who have anorexia, weight loss, or poor caloric intake), persistent or difficult-to-treat volume overload, fatigue and malaise, mild cognitive impairment, and refractory laboratory abnormalities (acidosis, hyperkalemia, and hyperphosphatemia)

Comparison of glucocorticosteroid

  Equivalent doses*
Relative anti-inflammatory activity Relative mineralocorticoid activity Duration of action
Hydrocortisone (cortisol) 20 1 1 8 to 12
Cortisone acetate 25 0.8 0.8 8 to 12
Prednisone 5 4 0.8 12 to 36
Prednisolone 5 4 0.8 12 to 36
Methylprednisolone 4 5 0.5 12 to 36
Triamcinolone 4 5 0 12 to 36
Fludrocortisone Not used for an anti-inflammatory effect 10 125 12 to 36
Dexamethasone 0.75 30 0 36 to 72

AKI definition

  1. Increase in creatinine of >0.3 mg/dL
  2. A percentage increase in serum creatinine of >50%
  3. Reduction in urine output (documented oliguria of less than 0.5 mL/kg/hr for more than 6 hour)

Corticosteroid Withdrawal

  1. recurrent activity of the underlying disease
  2. possible cortisol deficiency resulting from hypothalamic-pituitary-adrenal axis (HPA) suppression during the period of steroid therapy which can cause symptoms of adrenal insufficiency.
  3. Presenting symptoms – The presenting symptoms and signs of bilateral adrenal hemorrhage (and the frequency with which they occurred in one report) include [14]:
    1. Hypotension or shock (>90 percent)
    2. Abdominal, flank, back, or lower chest pain (86 percent)
    3. Fever (66 percent, presumably a response to inflammation)
    4. Anorexia, nausea, or vomiting (47 percent)
    5. Neuropsychiatric symptoms such as confusion or disorientation (42 percent)
    6. Abdominal rigidity or rebound tenderness (22 percent)
  4. Treatment
    1. The goal of therapy is treatment of hypotension and reversal of electrolyte abnormalities and of cortisol deficiency. Large volumes (1 to 3 liters) of 0.9 percent saline solution or 5 percent dextrose in 0.9 percent saline should be infused intravenously (IV) to correct hypovolemia and hyponatremia associated with mineralocorticoid deficiency and/or syndrome of inappropriate antidiuretic hormone secretion (SIADH)
    2. In a patient without a previous diagnosis of adrenal insufficiency, dexamethasone, which is not measured in cortisol assays, should be used rather than hydrocortisone while biochemical testing is performed.
    3. For patients with a previously known diagnosis of adrenal insufficiency, IV hydrocortisone or any other glucocorticoid preparation may be used because diagnostic testing is not necessary.

AEIOU: indication for dialysis

  1. Acidosis
  2. Electrolyte ( K+,  Na+,  Ca++); Na is not excreted and build up fluid in body. Low calcium
  3. Intoxicants (methanol ethylene glycol, Lithium); toxins removed by dialysis
  4. Overload fluid
  5. Uremic symptoms (nausea, seizure, pericarditis, bleeding).

Hyperkalemia and action potential

  1. As the potassium in the extracellular space increases, the concentration gradient is reduced. The resting membrane potential decreases. Resting membrane potential moves closer to the threshold potential, making it easier to imitate an action potential. This change increases myocyte excitability initially, but as the value of membrane potential at the onset of an action potential determines the number of voltage-gated sodium channels activated during depolarization. As this value becomes less negative in hyperkalemia, the number of available sodium channels decreases, resulting in a slower influx of sodium and subsequently slower impulse conduction.


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