Critical Care: Acute & Chronic Renal Failure. HELP!

  1. 0
    First off thank you to everyone who I've been emailing back and forth - I haven't had the chance to personally thank you. My EKG skills are slowly improving, Thanks.

    We are currently studying Acute & Chronic Renal failure. I am having the hardest time grasping how lab values will manifest.

    Acute Renal Failure may be caused by 3 methods:
    • Prerenal
    • Intrarenal
    • Postrenal

    Prerenal - basically factors outside the kidney itself. These factors (Hemorrhage, Hypovolemia, Decreased cardiac output) can all contribute to decreased renal blood flow. Eventually this will lead to renal ischemia

    Intrarenal - Direct damage eventually causing the nephron dysfunction. The damage may be caused by (ABX like aminoglycosides, contrast media, etc.) The point is the damage (insult) is direct.

    Postrenal - I will automatically think some form of mechanical obstruction. Reflux of urine into the renal pelvis eventually causes kidney dysfunction. Examples are (BPH, tumors, etc.)

    Renal Failure is further divided into phases.
    • Oliguric
    • Diuretic
    • Recovery

    Oliguric Phase: This is the phase I am confused and need HELP on.

    MY BOOK SAYS: That damaged tubules can't conserve Na+ and therefore urinary excretion of Na+ will INCREASE and thusly the Laboratory data will show a Normal to decreased level of Na+. My book lastly warns against high sodium consumption as it can cause fluid expansion and CHF.

    However; if the insult is due to decreased renal perfusion as in CHF or blood loss (as in Prerenal); wouldn't it make sense that the body would detect the decrease in blood pressure and initiate Angiotensin I > Angiotensin II (which help of ACE). Angiotensin II will then cause release of aldosterone from the adrenal cortex; consequently water and sodium retention will occur.

    SO is the elevated SODIUM in the urine ALWAYS true? Wouldn't NOT be applicable to Prerenal etiology? (Unless prolonged ischemia occurred? So perhaps initially we would see normal Na+ levels in urine then as it progresses increased levels?)

    It sounds like high Na+ in the urine would be more for Intrarenal. (Where the nephrotoxic agents can damage the tubules).

    IN both cases we would see the fluid ret (JVD+, Edema, Bounding pulse, Tachycardic, CVP of 8 or greater, increased BP... correct?). We would see Hyperkalemia and it could be expressed in the EKG as a tall peaked T wave (treatment for hyperkalemia could be kayexalate which will rid the K+ via the stool).

    I don't know if I'm along the right lines in regard to sodium in water. I was always taught that where sodium goes; water goes. So that concept is also conflicting with me.



    NOTE: Is there a way I could post this in the critical care section and the nursing student assistance section for more answers?
    Last edit by Joe V on Jul 24, '13 : Reason: spacing
  2. 2,594 Visits
    Find Similar Topics
  3. 3 Comments so far...

  4. 0
    I moved to critical care for best response....I am on the run and will be back...and get more response here.



    http://emedicine.medscape.com/articl...ew#aw2aab6b2b2

    My favorite resource is medscape you have to register but it is FREE!!!!!!!!!
    http://emedicine.medscape.com/article/983156-overview


    Last edit by Esme12 on Jul 22, '13
  5. 0
    When it comes to the renal system, it always breaks down to compensation. The kidneys will always be the last line of defense in trying to correct what is ever wrong in the disease process (take a look at DKA or HHNS).

    High levels of Na+ in the urine would automatically indicate that the body is trying to excrete as much as possible to correct some other underlying problem. When it comes to laboratory data, they are almost ALWAYS refering to blood samples. The higher the concentration of urine Na+, the lower venous Na+. Physicians will typically order a 24-hour urine after a collection of both...the typical first test is a Renal Failure Profile which will require a blood and urine sample at the same time. The 24-hour collection will usually consume of a Na+, Creatinine, Protein and Filtration Rate.

    In a instance of Septic Shock, the body will begin to retain sodium, bicarb, potassium, etc. and decrease urine output to retain all necessary electrolytes to sustain normal bodily function. The part that is tricky, hypotension will occur. Due to the fact that retention of electrolytes is happening, the circulatory system will dilate to have enough room for all of these elements. Hence, renal failure begins in the intrarenal phase. This is due in part because the kidneys begin to process excretion, however, they are told to shunt all of its filtration back to systemic circulation to sustain life.

    Most renal functions/dysfunctions are happening due to some underlying cause (ie sepsis, MSOD, CHF, etc.). However, diuresis is not the key treatment. It is extremely important to find out what the underlying cause is and HYDRATE, HYDRATE, HYDRATE the patient (examine their H&H, Creatinine). Fluid challenges and renal replacement therapy lead to the best outcomes for your patient. Yes, even in CHF. If your patient is mechanically ventillated, a CVP > 12 is acceptable. WHEN IN DOUBT, PUT A CALL OUT...to your attending. If you feel that your patient is not having adequate or too much output, let the doc know.
  6. 0
    I just saw this... Wow thanks!


Top