Chapter 22 - Managing fluid and electrolyte disorders in renal failure

Question 1

In what pressure range, healthy kidney can autoregulate renal blood flow?

Answer 1

80-180 mmHg (but renal perfusion may be more linear in damaged kidneys)

Question 2

What’s the definition of absolute oliguria, relative oliguria, and polyuria respectively?

Answer 2

Absolute oliguria: in a hydrated, well-perfused patient, less than 1.0 ml/kg/hr

Relative oliguria: 1-2 ml/kg/hr UOP in a patient on fluid therapy.

Polyuria: 2 ml/kg/hr

Question 3

What are proposed advantages of using Mannitol in the renal oliguric patient?

Answer 3

1. inhibit renin (expand extracellular volume)- improve GFR, inhibit sodium reabsorption
2. increase tubular flow, which may relieve intratubular obstruction from case and debris
3. decrease vascular resistance and cellular swelling
4. increases renal blood flow, GFR, and solute excretion
5. scavenge free radicals
6. induces intrarenal prostaglandin production and vasodilation
7. induced atrial natriuretic peptide release
8. blunt the influx of calcium into mitochondria in sublethally injured renal cells, thus decreasing the risk of sublethal injury progressing to lethal damage

Despite the advantages, no rRCT have shown a better clinical response with the use of mannitol.

Question 4

What’s the suggested dosage of mannitol for oliguric patient?

Answer 4

0.25-1.0 g/kg, if urine production increases, CRI 1-2 mg/kg/min IV or 0.25-0.6 g/kg q4-6h. Doses in excess of 2-4 g/kg/day may cause ARF

Question 5

Why mannitol should not be given to patients that are dehydrated?

Answer 5

It will further exacerbate intracellular dehydration

Question 6

What are potential advantages of furosemide in oliguric patient?

Answer 6

1. increase urine flow without increasing the GFR
2. inhibit Na-K-2Cl pump in the luminal cell membrane of the Loop of Henle, decreasing trancellular sodium transport. Basal Na-K-ATPase activity becomes un-necessary and the medullary oxygen consumption decreases, which is hypothesized to protect the kidney from further injury
3. renal vasodilatory effects

Question 7

What are potential reasons for detrimental effect of the furosemide?

Answer 7

1. delay in recognizing the severity of renal failure with a subsequent delay in starting dialysis
2. preferential use of loop diuretics in patients with a more severe course of the disease.

Question 8

What are the indications of use of furosemide for oliguric patient in veterinary medicine?

Answer 8

1. treatment of overhydration

2. hyperkalemia

Question 9

How long it takes to see the increase in UOP after an IV furosemide 2-6 mg/kg?

Answer 9

20-60 minutes

Question 10

What is potential advantage of CRI furosemide or intermittent IV?

Answer 10

more sustained diuresis with a lower cumulative dose compared with bolus infusion.

Question 11

What’s the recommended dosage of furosemide for dogs and cats with naturally occuring renal failure?

Answer 11

0.25-1 mg/kg/hr

Question 12

What’s MOA of femoldopam?

Answer 12

Selective DA-1 receptor agonist, increases cortical and medullary blood flow, sodium excretion, and urine output while maintaining GFR in people. It does NOT have DA-2 or alpha or beta activity, so it does not cause vasoconstriction, tachycardia, or arrhythmias as seen with dopamine.

Question 13

What are potential advantages of CCB in oliguric patient?

Answer 13

1. presumptively reverse renal vasoconstriction by causing predominantly preglomerular vasodilation
2. inhibit vasoconstriction induced by tubuloglomerular feedback mechanism
3. cause natriuresis independent of the GFR

Question 14

What are potential advantages of ANP (atrial natriuretic peptide) in oliguric patient?

Answer 14

1. increases tubular excretion of salt and water
2. stimulates afferent arteriolar dilation and effect arteriolar constriction
3. increase GFR

It has not been effective in clinical trials thus far.

Question 15

When do we decide to wean AKI patients off of IV fluid?

Answer 15

1. plateau azotemia (or resolved)

2. plateau urine output

Question 16

What are the characters of renal diet?

Answer 16

restricted phosphorus and restricted quantities of high quality protein

Question 17

T/F: Dibartola suggests to replace initial fluid deficit with isonatremic solution, and use lower sodium fluid after the initial rehydration phase

Answer 17

True

Question 18

What are mechanisms of the development of hypokalemia in renal failure?

Answer 18

1. excessive renal wasting associted with polyuria
2. alkalemia worsens hypokalemia as potassium shifts intracellularly in response to translocation of hydrogen ions out of the cells
3. vomiting
4. loop diuretics
5. prolonged anorexia
6. diuretic phase of recovery from AKI

Question 19

What is the changes on ECG associated with hypokalemia?

Answer 19

1. U wave
2. ventricular arrhythmias
3. supraventricular arrhythmias

Question 20

What can we measure to distinguish renal potassium loss from non-renal loss?

Answer 20

evaluation of the fractional excretion of potassium
if > 4%, renal loss
if < 4%, nonrenal loss

Question 21

Describe how to bolus KCL for life-threatening hypokalemic emergency

Answer 21

1. calculate potassium deficit (patient K - desired K;3 mEq/L)
2. estimate plasma volume
3. multiply plasma volume by the difference (potassium deficit) to determine the number of mEq of KCl to administer
4. IV bolus over 1-5 minutes through central vein
5. Can give 2nd bolus

Question 22

What are other options of potassium administration other than IV KCL?

Answer 22

1. potassium gluconate PO (5-10 mEq/day divided into 2-3 doses to replenish K, followed by 2-4 mEq/day for maintenance)
2. potassium citrate (40-60 mEq/kg/day divided into 2-3 doses)
3. KCL SQ up to a concentration of 35 mEq/L