Is this patient hyponatremic? Why? Is he hyperkalemic? Does hyperkalemia need treatment? Why is the HCO₃ low? Will this patient’s urine be concentrated, dilute, or isosthenuric?

Is a hematocrit of 28 % normal for a patient like this? Should he be transfused prior to the procedure?

What is the GFR of a 16-year-old with a creatinine of 2.5?

Is the patient likely to have a low or high cardiac output? Is this patient hypertensive? Why? How will you assess this patient’s volume status?

Why is this patient on antibiotics? Is prophylaxis effective? Would infection make this problem worse? How so? Any particular implications for your anesthetic management?

The patient has a sodium level of less than 135 making him hyponatremic, most likely due to sodium wasting as part of his renal impairment. The patient’s potassium is elevated over 5.5 likely due in large part to impaired potassium elimination along with his acidosis that shifts K⁺ extracellularly. His total body potassium is not elevated. In addition, the use of renin-angiotensin converting enzyme inhibitors causes further elevation of K⁺ by decreasing aldosterone and thus diminishing the excretion of potassium. Acute hyperkalemia is dangerous because it lowers the resting membrane potential of myocardial cells. Renal failure patients tolerate chronic hyperkalemia relatively well because they are able to establish a stable, higher, resting membrane potential at their high K⁺ level (unlike those with acute hyperkalemia). If ECG does not show characteristic findings of hyperkalemia, treatment is not needed. If peaked T waves were present, treatment would be indicated. The plasma bicarbonate is low due to acidemia. Chronic renal failure results in a loss of renal tubular mass. When it reaches a critically low level, the kidney is unable to excrete adequate hydrogen ions in the distal tubule. The patient’s urine will be dilute because of failure of the tubules to concentrate the urine leading to both salt and water wasting.

The hematocrit is low for age due to reduction in erythropoietin production in the kidneys. Chronic low hemoglobin is compensated by an increase in 2-3DPG. As such transfusion is not needed for a procedure where copious blood loss is not expected.

A rough estimation of GFR can be calculated as GFR mL/ min /1.73M² = 0.55 × Length(cm)/plasma creatinine.

Due to the low hemoglobin, renal failure patients generally compensate with a high cardiac output. The patient is hypertensive. Patients with renal failure have an increased level of angiotensin II which is a potent vasoconstrictor. Its action is mediated through primary activation of renin-angiotensin-aldosterone system and/or depletion of the extracellular fluid due to salt and water wasting. Volume status is best estimated by evaluating clinical signs of dehydration – notably weight loss greater than 3 % of body weight, increased thirst, dry mouth and tongue, increased heart rate, fast breathing and cool extremities, sluggish capillary refill longer than 2 seconds, and impaired skin turgor.