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Acute Renal Failure

 

Distinguishing Pre-renal Azotmeia from Acute Tubular Necrosis 

Value

Pre-Renal

Acute Tubular Necrosis

BUN/Creatinine ratio

>20/1

10-15/1

Urinary Na (U Na)

<20 meq/L

>40 meq/L

FeNa

<1 %

>1 %

Uosm

>500 mosm

<350

U/P Osm  urine/plasma

>1

<1


Some definitions before we start analyzing the above table:

Azotemia is a medical condition characterized by abnormal levels of urea, creatinine, various body waste compounds, and other nitrogen-rich compounds in the blood as a result of insufficient filtering of the blood by the kidneys.  Most commonly measured by an increase in BUN and creatinine.  Patients may be azotemic, but not at all uremic.

Uremic syndrome is azotemia with symptoms. Some of the early signs of uremia are lethargy, mental depression, loss of appetite, and edema; later symptoms include diarrhea, anemia, convulsions, coma, and a gray-brown coloration.  A patient with uremia will always be azotemic.

Explanations for values in the above table:

-          Distinguish pre-renal azotmeia from Acute Tubular Necrosis (intrinsic renal failure)

o        These factors are less valid clinically because IVs are usually started before the nephrologist sees the patient, which taints the values

o        Important: Pre-renal azotemia (Acute Renal Failure) shows higher BUN/Creatinine
 

 
§         In volume depleted states, there is enhanced reabsorption through the nephron because of slow flow of fluid through the nephron (because of low blood pressure) which increases the surface contact time between urea and the proximal tubule cells, so more urea is reabsorbed but (just to remind you) creatinine is not resorbed, which increases the BUN/creatinine ratio in pre-renal azotemia

o        patient will be holding on to sodium in volume depletion ŕ low sodium concentration in urine in pre-renal Acute Renal Failure; but in Acute Tubular Necrosis proximal tubules are destroyed, so ability to reabsorb sodium is diminished ŕ high sodium concentration in urine
 

o        Fractional excretion of Na – FeNa – this test is reliable for determining reabsorptive capacity of tubules (amount of Na that escapes in urine relative to amount that was filtered in first place).  The volume of anything that is found in the urine (UV of x) divided by the amount filtered (measured by Glomerular Filtration Rate multiplied by serum concentration of that substance) equals the fractional excretion of substance x.

§         Fractional excretion of x: UV/ (Glomerular Filtration Rate*serum concentration of x)

o        Urine osmolality – intact kidney that isn’t receiving enough blood will have concentrated urine ŕ urine osmolality will be high (ex. pre-renal Acute Renal Failure).  With Acute Tubular Necrosis, urine can’t be concentrated ŕosmolality will be low.  Another way to look at this is the U/P osm ratios.

 

Complications of Acute Renal Failure and Uremic Syndrome

-          metabolic complications

o        hyponatremia – low serum sodium concentration

§         usually mainly deals with water balance (not sodium); can mean patient is overhydrated or that the patient can’t excrete solute free water appropriately

o        hyperkalemia – high potassium concentration

§         potentially lethal complication because high potassium can cause cardiac arrhythmias that stop the heart and kill the patient

o        hypocalcemia and hyperphosphatemia

§         serum phosphate is high because it mainly involves a renal rate of excretion

§         calcium and phosphate are reciprocally related, as phosphorus goes up, calcium goes down

§         hypocalcemic tetany can be seen in untreated patients

·         Classic peripheral neurologic findings of hypocalcemia include Chvostek sign and Trousseau sign.

o        Chvostek sign: Tap over the facial nerve about 2 cm anterior to the tragus of the ear. Depending on the calcium level, a graded response will occur: twitching first at the angle of the mouth, then by the nose, the eye, and the facial muscles.

o        Trousseau sign: Inflation of a blood pressure cuff above the systolic pressure causes local ulnar and median nerve ischemia, resulting in carpal spasm.

o        hypermagnesemia

§         magnesium is excreted through the kidney

§         hypermagnesemia is iatrogenic most of the time because it is very effective in management of pre-eclampsia (hypertension in pregnancy or immediately after pregnancy accompanied by edema and proteinuria).  So, overly aggressive obstetricians can precipitate renal failure in their patients.

o        hyperuricemia – not lethal in short term

o        metabolic acidosis – will be talked about in the acid-base lecture

-          cardiovascular complications

o        Increase in total body sodium with expansion of ECF volume which makes the patients prone to pulmonary and peripheral edema, cardiac arrhythmias, and pericarditis

§         when there is a problem excreting Na+, there is an increase in ECV (extra cellular volume) and this can lead to congestive heart failure.  Don’t give renal failure patients saline because they have a problem secreting Na+ to begin with

§         pericarditis can occur, but is less common now because patients are dialyzed – pericarditis occurs when there is a fibrinous deposition of material between pericardial surfaces (visceral and parietal pericardium)

·         diagnosis of pericarditis is made clinically by the presence of a pericardial friction rub (you can mimic this sound by covering your ear with your hand and scratching the back of your hand with your index finger)

·         the danger of  pericarditis is that the two layers of the inflamed pericardium can separate (clinically, the rub can no longer be heard), and blood can accumulate in this space (cardiac tamponade).  This is more likely in patients with uremia (renal failure patients).

-          neurologic complications

o        metabolic encephalopathy

§         physical finding of ‘liver’ flap is seen in patients with this complication – asterixis – pathological neurologic sign which is elicited by having the patient extend their arms with their elbows straight and hyperextend the wrist, patient may move hand back and forth (flap) which is a positive ‘liver’ flap or flapping tremor

o        neuromuscular irritability – twitching that isn’t tetany

o        seizures

o        coma

-          hematologic complications

o        anemia – because of decreased secretion of erythropoietin

o        bleeding tendency secondary to defective platelet function

o        impaired white cell function and decreased immune response, subject to infections

-          gastrointestinal complications – GI tract is often first system affected

o        submucosal hemorrhages seen in kidney when viewed microscopically

o        uremic toxins (unidentified compounds that are not urea or creatinine) can cause uremic gastritis or enteritis

o        uremic gastritis, enteritis, and colitis with:

§         nausea

§         vomiting

§         diarrhea

§         bleeding

-          infectious complications

o        pneumonia

o        urinary tract infections

o        wound infections

o        line sepsis

o        bacteremia

-          multi-organ failure syndrome – renal failure developed due to profound sepsis or trauma, may be due in some cases to pure uremic syndrome

 

Management of Acute Renal Failure

-          accurate volume assessment at time of diagnosis is mandatory/necessary

-          fluid challenge and repletion if appropriate

-          fluid restriction and loop diuretic if appropriate

-          sodium and potassium restriction

-          maintain nutrition, transfuse if necessary

-          avoid nephrotoxins if possible – adjust dose of nephrotoxic medications if they are absolutely necessary

 

Renal replacement therapy (popular term for dialysis)

-          dialysis can be conventional or continuous

-          dialytic therapy may be necessary if medical therapy fails or is not feasible

o        uremic syndrdome

o        metabolic acidosis

o        CHF and fluid overload

o        refractory hyperkalemia

 

Prognosis of Acute Renal Failure

-          study comparing Korean war gunshot/trauma victims who did not have access to dialysis to Vietnam war injured veterans who did have access to dialysis shows that there was no difference in mortality

o        dialysis is important, but only permits you to get better if your underlying condition allows it

-          remember that Acute Renal Failure is a complication of many things, but ability to recover depends on your condition/health before renal failure sets in

o        prognosis is variable and depends on:

§         age

§         severity underlying conditions

§         degree of catabolism

§         number of co-morbid organ failure

§         control of sepsis

§         mortality may be as high as 70% in ICU – this is due to severity of underlying conditions

 

Summary of Acute Renal Failure

-          very common, particularly in ICU hospital patients who have a significant mortality

-          it is important to be aware of risk factors, to diagnose properly, to manage complications, and support the patient pending recovery of renal function

o        underlying conditions are very important in determining outcome of patients (an important risk factor to consider)


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