Questions for Discussion:

1. Acute renal failure can be divided into prerenal, parenchymal and post-renal types.  These are differentiated by clinical findings and laboratory data, specifically renal ultrasound, urinalysis and urine lytes
2. 1. Prerenal acute renal failure can be distinguished from ATN by the fractional excretion of sodium.  A FENA of >1% is consistent with ATN. A fractional excretion of sodium <1% is seen in patients with prerenal causes of renal failure. The fractional excretion of sodium is calculated by (UNA/SNA)/(UcR/SCR) x 100.  In this case (35/138)/(56/10) x 100 = 4.5%.
   2. The fractional reabsorption of water can also be used to distinguish these to types of acute renal failure.  This is calculated by (100 – (100/UCR/SCR).  A value of <97.5 is consistent with acute tubular necrosis. In this case (100 – (100/5.6) = 82%.  
   3. Urine to serum creatinine ratio will be <20 in cases of ATN and >40 in patients with a prerenal cause of acute renal failure.  In this case 56/10 = 5.6.
3. This patient most likely has acute renal failure secondary to rhabdomyolysis.  The recent history of running in a marathon along with the presence of acute renal failure associated with 4+ blood on dipstick and 2-5 RBCs is consistent with the presence of myoglobinuria. 
4. Additional tests that would be useful are CPK and urine myoglobin.
5. A:
   1. Acidosis in a patient that is volume overloaded and unable to respond to diuretics.  These patients benefit from the ultrafiltration associated with dialysis as well as the high bicarbonate level in the dialysate.  If they are not volume overloaded the patient can be treated with bicarbonate supplementation. 
   2. Electrolyte disturbances such as hyperkalemia which is the most common indication to dialyze.
   3. Volume Overload not responding to medical management
   4. Intoxication with substances that are dialyzable.  In general, any drug which is not protein bound can be dialyzed.
   5. Uremia is another indication for acute dialysis and is diagnosed by the presence of pruritus, confusion, lethargy, inability to concentrate, nausea and emesis.  An elevated BUN in the absence of any of these clinical findings is not itself sufficient to require acute dialysis.
5. B: This patient exhibits signs of uremia and has EKG findings secondary to hyperkalemia.
6. EKG abnormalities seen with hyperkalemia range from peaked T waves with sinus rhythm to absence of the p wave with marked prolongation of the QRS complex which merges with the T wave forming the classic sine-wave pattern that is frequently misdiagnosed as ventricular tachycardia. The sine-wave pattern is seen with more severe elevations of the potassium level (K+ > 8meq/l). The electrocardiogram may further degenerate to ventricular fibrillation or asystole. In addition to this classic sequence of events outlined above, virtually any type of arrhythmia or conduction disturbance may occur.
7. Several options are available to treat hyperkalemia:
   1. The administration of 10-20 ml of 10% calcium gluconate .is recommended to stabilize the cardiac membranes and has an immediate onset of 1-3 minutes.  The effects of this infusion last for ~30-60 minutes.  If no response is seen in 5-10 minutes a second dose can be administered.  If the patient does not respond to the second dose it is unlikely that additional calcium will be of any benefit.
   2. Increasing the serum bicarbonate concentration will shift potassium into the cells.  However, the effect of this treatment is greatest when the patient has acidemia and a low pH.  Sodium bicarbonate is administered intravenously as a 50 meq bolus over 5 to 10 minutes, and the effect lasts for ~ 2 hours. 
   3. Intravenous insulin stimulates cellular potassium uptake.  This is due to the direct effect of insulin on the cell membrane. Glucose is administered to prevent hypoglycemia.  The usual dose is 10 units of insulin combined with 100 ml of 50% glucose solution.  The onset of the insulin effect is usually 30 minutes and lasts for up to 4 hours. 

   It should be kept in mind that these are at best only temporizing measures and the potassium must be removed from the patient by the kidneys or through the GI tract or dialysis. Loop and thiazide diuretics increase potassium excretion in the urine in patients with normal or mild to moderately impaired renal function, particularly when combined with saline hydration (in appropriate patients) to maintain distal sodium delivery and flow. Kayexalate works in the GI tract by promoting the exchange of potassium for sodium along the gastrointestinal tract.  Each gram of resin removes .5 to 1 meq of potassium in exchange for 2 to 3 meq of sodium.  Significant amounts of calcium and magnesium also may be removed. Two newer agents, Patiromer and Zirconium have been found to be effective alternatives for treatment of hyperkalemia. Only Patiromer has received FDA approval.  Patiromer is a nonabsorbable organic polymer that binds to potassium in the colon in exchange for calcium.

8. This ultrasound demonstrates a normal kidney by size and echogenicity.  This is consistent with the presence of acute renal failure and not chronic renal disease.  These patients tend to have a better chance of recovering normal renal function then a patient who has underlying renal disease, which would be manifested by increased echogenicity and small kidneys.  This ultrasound also rules out stone disease and the likelihood that obstruction is responsible for the acute renal failure.  It should be kept in mind that patients with renal obstruction might have low, normal or increased amounts of urine output due to a solute diuresis and for this reason one cannot make the diagnosis of obstruction on the basis of urine volume.  Occasionally early obstruction or ureteral obstruction secondary to infiltrating tumors may not be seen on an ultrasound because the ureters will not be dilated.  For this reason it is important to check the urine osmolality.  This will be very low in patients that have obstruction because of damage to the distal nephron.    

9. 1. The hyperkalemia in this patient is due to the extensive muscle damage, which has occurred and resulted in the release of potassium from the intracellular stores.  We have ~50 meq/kg body weight of potassium most of which is intracellular.
   2. The hypocalcemia is due to the muscle necrosis, which results in severe hyperphosphatemia.  This is due to the release of phosphate compounds from the muscle and facilitates the deposition of calcium and phosphate in soft tissues.  Widespread soft tissue calcification has been described shortly after the onset of renal failure in these patients.
      
      In addition, ARF itself will cause these abnormalities, though they are generally more severe in the setting of rhabdomyolysis.

Previous