RenalDialysis

Question 1

Explain acute renal disease characteristics?

Answer 1

AKI. Onset is hours to days. 50-95% nephron loss. Duration is 2-4 weeks, less than or under 3 months. Prognosis is good with supportive care, treat the underlying problem and preserve the nephrons.

Question 2

Explain chronic renal disease characteristics?

Answer 2

CKD, ESKD. Onset is gradual, from greater than 3 months to years. Nephron involvement varies by age but symptomatic at 75%. 90-95% nephron loss they needs dialysis. Duration is permanent. Prognosis is fatal without dialysis or transplant.

Question 3

AKI involving conditions that decrease systemic blood flow to the kidney.

Answer 3

Prerenal AKI.
Etiology includes dehydration, hypotension, HF (not getting enough blood to kidneys), hypovolemia, anaphylaxis, renal stenosis, decreased CO, severe sepsis, shock

Question 4

AKI involving tissue damage to the kidney.

Answer 4

Intrarenal (intrinsic) AKI.
Acute tubular necrosis (ATN) is the most common etiology, but includes acute glomerulonephritis, diabetes, toxins, drugs (contrast, ahminoglycosides), blood transfusion reactions, pyelonephritis, infections.

Question 5

AKI involving obstruction of the urine collecting system.

Answer 5

Postrenal AKI.
Etiology includes renal calculi, obstruction (strictures, clots), BPH in elderly men, inflammation, atony of the bladder, anything that causes backup into kidney.

Question 6

Creatinine increases >25% within 3 days of intravascular exposure to contrast from cardiac catheterization, CT scan, MRI, surgical procedures.

Answer 6

Contrast-induced nephropathy. Treated with a combo of N-acetylcysteine (Mucomyst) + IV saline, combo of statins + Mucomyst + saline. Increase PO and IV fluids before/after contrast test (want urine OP of 150mL/hr?).

Question 7

Begins with the precipitating event and ends when oliguria develops, lasts hours to days. Gradual accumulation of nitrogenous wastes, azotemia. Increased serum Cr/BUN from baseline happens very quickly. Renal damage may or not be present.

Answer 7

Initiation period of AKI, can reverse and prevent here.
Interventions to re-establish function: fluid challenges (IV bolus) for pre-renal/intra-renal to attempt to get the kidneys to flush through. Also helps to differentiate between pre/intra vs obstructive AKI. Diuretics to ensure diuresis and avoid fluid overload.

Question 8

AKI in which fluid challenge is completed but oliguria still. Urine OP is less than 100-400 mL/24 hrs. Nephron damage is likely. Increased nitrogenous waste. Metabolic acidosis (bicarb deficit).

Answer 8

Oliguric period.
Increased creatinine, BUN, K, mag. Decreased Ca, increased Ph (kidney not excreting Ph, not retaining Ca). Fluid retention s/s, circulatory overload may be seen. Non-oliguric patients may have high urine output but decreased renal function continues.

Question 9

Interventions for the oliguric period of AKI?

Answer 9

Identify underlying cause. Fluid challenges or diuretics may need to be stopped if they were already tried in initiation phase. Monitor for circulatory overload (may need to treat w/ diuretics), metabolic acidosis. Frequent I/O, daily weights. Constant nursing supervision. Labs, ABGs. Ca channel blockers used for nephrotic HTN. They increase the renal blood flow and GFR.

Question 10

Laboratory findings in AKI (oliguria)?

Answer 10

Increased BUN/Cr, K, Mg, Ph. Decreased Ca (the bones then begin to release Ca in response). Metabolic acidosis, decreased pH, decreased CO2, decreased HCO3. Decreased Hgb, decreased erythropoietin or fluid overload (dilutional). Decreased Cr clearance (test, waste first void, then collect all urine for 24 hours). Increased protein in urine (large molecules escaping, serum protein decreases). Urine may be dilute or concentrated.

Question 11

AKI in which kidneys are beginning to regain function. Gradual increase in urine OP, up 10 10L/day of dilute urine. If this stage is not reached then dialysis is required.

Answer 11

Diuresis period. Stabilization of lab values, fluid loss and electrolyte changes, decreasing Cr/BUN. Monitor for fluid and electrolyte deficits, if they need replacement. I+O’s.

Question 12

AKI in which kidneys are returning to normal levels of activity. Complete recovery may take up to 12 months. Renal insufficiency may be noted on routine monitoring.

Answer 12

Recovery period and post-hospital. Function may never return to pre-illness state. Follow-up care with HCP, frequent appointments, labs. Diet modifications. Watch function tests, Cr/BUN will remain high with renal insufficiency. Special care taken not to injure kidneys further.

Question 13

Protein in diet for AKI and CKD?

Answer 13

Normal: 0.8 g/kg/day
AKI (no dialysis): 0.6 g/kg/day
Acute renal failure or ESKD: Dialysis. 1-1.5 g/kg/day

Question 14

Non-protein diet recommendations for AKI and CKD?

Answer 14

Increased carbs for calories. Decreased Na when fluid overloaded, depends on pt. Decreased K and Ph.
Fluid intake restriction = urine output + 500 mL (oliguric/anuric).

Question 15

Teaching for fluid restriction for those pts with AKI and CKD?

Answer 15

Urine output + 500 mL (oliguric/anuric).
Fluid restriction includes PO and IV. Signs on room and pitcher. Pt/family education. Ice chips (1/2 times the fluid oz). Tell cafeteria no fluids.

Question 16

Progressive, irreversible kidney damage with azotemia that will progressively worsen with each stage. Goal is to preserve kidney function for as long as possible

Answer 16

Chronic kidney disease (CKD), End stage kidney disease (ESKD). In ESKD the kidneys are unable to sustain life. The three leading causes are HTN, DM (esp type 1), and glomerulonephritis.
Uremia/uremic syndrome: azotemia with clinical manifestations, happens as they approach stage 4.

Question 17

Morphologic (structural) causes of CKD?

Answer 17

Glomerular. Tubular.
Vascular: renal nephrosclerosis and artery stenosis.
Urinary tract: calculi.
Inherited/genetic: polycystic kidney disease, renal tubular acidosis.

Question 18

Etiologic casues of CKD?

Answer 18

Infection: glomerulonephritis, chronic pyelonephritis, TB.
Systemic vascular: HTN
Connective tissue: systemic lupus erythematous, progressive systemic sclerosis

Question 19

What are the five stages of CKD and their GFR’s?

Answer 19

1, at risk: > or equal to 90 mL/min
2, mild CKD: 60-89 mL/min
3, moderate CKD: 30-59 mL/min
4, severe CKD: 15-29 mL/min
5, ESKD: <15 mL/min

Question 20

Stage in CKD with decreased function/GFR but no waste accumulation. Normal BUN/Cr with no s/s. Healthy renal cells are able to compensate for diseased cells. Diminished renal reserve. Avoid shocks to the kidney.

Answer 20

Stage 1, at risk, GFR>=90. Healthy renal cells are under stress, decreased function may be apparent but no other clinical manifestations. Focus on the CVD risk reduction to slow progression, avoid nephrotoxic drugs. Control BP, glucose, CHF. Assess meds, make sure none are nephrotoxic.

Question 21

Stage in CKD that involves renal insufficiency alone. Decreased ability to concentrate urine and renal reserve. Some waste accumulation. Decreased Cr clearance with slight increase in BUN/Cr possible.

Answer 21

Stage 2, mild, GFR60-89. Nocturia, polyuria possible because of decreased ability to concentrate urine. Increased BP means more nephron damage. Microalbuminuria maybe. No other s/s.
Focus on CVD risk reduction to slow progression still.

Question 22

Stage of CKD at which renal damage has progressed past renal insufficiency. Metabolic wastes accumulate, are apparent. Microalbuminuria, polyuria. Initial electrolyte imbalances. S/s may appear, fatigue, sluggishness, electrolyte imbalance s/s.

Answer 22

Stage 3, moderate, GFR30-59. Increased BUN/Cr, K, Ph, Mg, slightly low Ca. Increase or decrease in Na, depends. Control co-morbidities strictly, esp. BP (ACE inhibitor, Ca channel blocker) and glucose.

Question 23

Interventions for stage 3 of CKD?

Answer 23

Control co-morbidities strictly. Treat with fluid. No excessive protein and no restricting either. Na restriction depends. Monitor/ manage electrolytes, K and Ph diet reduction because they can’t excrete it. Encourage vitamin and iron supplementation.

Question 24

Stage of CKD in which there is more metabolic waste with s/s present (although they vary depending on the urea level, uremic syndrome possible). Electrolytes more severely abnormal.

Answer 24

Stage 4, severe, GFR15-29. Higher BUN/Cr. Decreased urine OP possible. Follow closely w/ specialist. Refer to vascular access surgeon for dialysis. Both stage 4 (severe) and stage 5 (ESKD) require regular dialysis.

Question 25

What are the neuro and cardiac systemic changes due to CKD and s/s due to uremia?

Answer 25

Neuro: Uremic encephalopathy. LOC change, weak, confused, lethargy, seizures, paresthesias.
Cardiac: Fatigue, HTN, hyperlipidemias, HF, uremic pericarditis

Question 26

Respiratory, integumentary, and musculoskeletal systemic changes due to CKD and s/s due to uremia?

Answer 26

Resp: dyspnea due to acidosis
Integ: Itching (crystals, phosphate salts settle in the skin). Pigment changes.
Muscle: Cramping (from electrolyte imbalance), hiccuping

Question 27

GI and hematologic systemic changes due to CKD and s/s due to uremia?

Answer 27

GI: uremic stomatitis, PUD, diarrhea (uremic colitis), uremic halitosis (ammonia breath), N/V, anorexia, metallic taste, gastritis, diarrhea. Normal flora changes
Heme: Decreased erythropoietin which leads to decrease RBC production

Question 28

Explain metabolic acidosis in relation to CKD

Answer 28

Unable to excrete excess H+, related to deceased bicarb production, increased ammonium. Decreased reabsorption of bicarb. Increased azotemia waste. Respiratory compensation via Kussmaul. Sodium bicarb replacement for deficient base.

Question 29

Explain hypokalemia and hyperphosphatemia in relation to CKD?

Answer 29

Influenced by vit D. Kidneys produce calcitriol needed for the intestinal reabsorption of Ca. Ca is release from bone storage because there isn’t enough. Osteodystrophy leads to bone density loss (fractures). Metastatic calcifications from hyperphosphatemia.

Question 30

Phosphate-lowering agents?

Answer 30

Binders.
Calcium acetate (PhosLo) and calcium carbonate (Caltrate, Os-Cal) both increase CA and lower Ph. Contraindications for Ca carbonate include hypercalcemia or urolithiasis.
Sevelamer (Renagel) deceases Ph only with no effect on Ca, best for when Ca is normal but Ph is high (dialysis). Active vit D to increase absorption of Ca.

Question 31

Meds that aren’t phosphate-binding for CKD?

Answer 31

Ferrous sulfate (Feosol): iron for anemia, general wellness.
Folic acid, multivitamins.
Kayexalate to decrease K (not needed with dialysis).
Epoetin alfa (Epogne, Procrit) to stimulate RBC production. Given 3x/week after dialysis (post-dialysis stage 5) or in non-dialysis pts (stage 4). Get Hgb back up to 11

Question 32

Stage of CKD in which there’s less than 15% function. Metabolic wastes/fluid must be removed. High BP, cardiac dysrhythmias. Treat w/ RRT.

Answer 32

Stage 5. Fluid restriction 500 mL + previous day’s 24hr output (for fluid overload). Increased Na (2gm) and protein allowance on dialysis. Psychosocial support. Renal transplant option.

Question 33

Oliguric injury vs. oliguric failure?

Answer 33

Oliguria: less than 400mLs OP in 24hrs, less than 30mL/hr, less than 0.5mL/kg/hr.
Injury: oliguria for more than 12 but less than 24 hrs w/ GFR decrease >=50%.
Failure: oliguria for 24hrs or anuria for 12hrs with further rise in Cr and worsening GFR in accordance with urine OP changes

Question 34

What are the two parts of stage 3 of CKD?

Answer 34

3A: 45-59
3B: 30-44. The closer the pt. is to 3B, the more apparent the changes and s/s are. Here they start meds for renal support.

Question 35

Interventions for stage 4 of CKD?

Answer 35

Increase protein restriction for sure, but increase carbs, fats. Diet is similar to AKI not on dialysis, based on trying not to build up more nitrogenous wastes. Na, fluid restriction. Electrolyte abnormalities. When K+ is high from acidosis use insulin. Continue meds from stage 3.

Question 36

Removes excess fluid and waste products, does whatfior the kidney is supposed to be doing. Improves electrolyte balance. Adjusts acid/base balance. 3 types?

Answer 36

Dialysis. Continuous renal replacement therapy, hemodialysis, peritoneal dialysis. All require sterile technique because high r/f infection! Does not compensate for loss of endocrine or metabolic function of kidneys.

Question 37

Dialyzable and vasoactive meds to hold before dialysis?

Answer 37

Aminoglycosides, antibiotics, antiviral agents, anticonvulsants, cephalosporins, anti-TB agents, water-soluble vitamins, anti-dysrhythmias, narcotics, sedatives, vasodilators, aspirin. Mostly give BP meds when pt. is back

Question 38

Temporary measure for pts. who are too unstable for other dialysis, circulatory/fluid overload, uremia, kidneys cannot handle acutely high metabolic/nutritional needs. Around-the-clock.
Requires an actual dialysis catheter, not a fistula. Needs to be able to use heparin to keep blood thinner.

Answer 38

Continuous renal replacement therapy (CRRT), a type of hemodialysis that’s slower. Advantages: better tolerated for critically ill pts, avoids rapid shift of fluid/electrolytes seen with hemodialysis. Requires ICU care. Possible r/f bleeding if heparin is used. Once pt. is stabilized, routine long-term dialysis (daily or 3x/week) or kidney function returns

Question 39

Dialysis that occurs 3-5hrs, either 3ish times per week or daily, but not continuously. Extracts toxic nitrogenous substances from the blood, removes excess fluid. Can be done in hospital or outpatient.

Answer 39

Hemodialysis. Uses dialysate, an ideal mix of electrolytes and water that surrounds the pt.’s blood. Inside the dialyzer, a synthetic membrane through which blood is filtered to remove toxins and a certain amount of fluid. K+/Na move from plasma to dialysate, bicarb/Ca move rom dialysate to plasma.

Question 40

How does the dialyzer work in hemodialysis?

Answer 40

Toxins/wastes removed by diffusion, moving from area of higher concentration in blood to lower in dialysate. Semipermeable membrane impedes diffusion of large molecules, RBCs, proteins. Excess fluid is removed from blood by osmosis, water moving from low concentration potential (blood) to high concentration potential (dialysate). In ultrafiltration, fluid moves from high pressure to lower pressure.

Question 41

Temporary vascular access for hemodialysis in the subclavian, internal jugular, or femoral vein?

Answer 41

Double-lumen or triple lumen for both. Noncuffed for more acute, immediate access. More temporary.
Cuffed into the internal jugular. Insertion site heals, sealing wound, reducing r/f infection. Safer for long-term use. But watch for sepsis in both.

Question 42

Fistula permanent vascular access for hemodialysis?

Answer 42

AV fistula: Anastomosis of artery & vein, usually cephalic vein, AV artery. Arterial segment is used for arterial flow to the dialyzer, venous segment for reinfusion of dialyzed blood. Will need 2-3 months to “mature” before it’s used, needs to dilate be to able to accommodate needles for treatment. Longest useful life and best for chronic pt.

Question 43

Graft permanent vascular access for hemodialysis?

Answer 43

Usually used when artery/vein aren’t strong enough on their own to make a connection so tubing is used instead. More complex surgery but it can be used in 1-2 weeks, whereas a fistula can take up to 3 months to heal.

Question 44

Complications of permanent access for hemodialysis?

Answer 44

Thrombosis or clotting of AV access. High Risk for Disequilibrium Syndrome (Rare). Infection. Stenosis in graft. Bleeding from anti-coagulation, heparin.

Question 45

Disequilibrium syndrome?

Answer 45

Can occur during or after dialysis due rapid shift in fluid level, causing ICP. Rare but more likely if pt. has AKI or high BUN.
S/s: LOC, n/v, seizure, coma, restlessness, headache, seizures.

Question 46

Nursing care of AV access?

Answer 46

No BP, IVs or venipuncture on access arm, may even restrict all phlebotomy because no tourniquets. Infection risk near the site. Assess bruit (audible swishing), thrill (palpable vibrating pulsation). Distal circulation on that side, make sure pulses/cap refill are intact, compare sides of pt. Monitor cannulation site for bleeding. Report if not scant and dry but still bleeding. No compression on access limb, no carrying objects, sleeping on it for a long time

Question 47

Nursing care for inpatient dialysis?

Answer 47

Pre-dialysis: Ensure current labs drawn, reviewed, on chart for access for dialysis nurse. Weight/VS both before/ after. At risk for hypotension after.
Assess site for s/s infection or bleeding. Hold dialyzable medications, antihypertensives. ADLs prior to treatment
Post dialysis: Monitor v/s, subjective complaints, assess site bleeding. Avoid invasive procedures for 4-6 hours.

Question 48

Selection of patients for peritoneal dialysis (PD)?

Answer 48

Pt.’s are: Hemodynamically unstable, if in hospital VS are good, they can be sterile/compliant. Can’t have a fistula or a graft, vascular access problems. Cannot tolerate anticoagulation (PD doesn’t need heparin). Used until fistula matures. Treatment of choice for those who need flexibility w/ frequent status change. Can’t do kidney transplant.
Contraindications: Peritoneal adhesions or membrane fibrosis, extensive abdominal surgeries, abdominal scarring. Obese, DM, elderly, long term steroid clients may have problems with PD in general.

Question 49

How does peritoneal dialysis work?

Answer 49

Catheter inserted into peritoneal cavity. Sterile dextrose dialysate fluid. Fill 1-2L dialysate from a bag infused by gravity over 10-20 min. Diffusion/osmosis occurs as waste products move from higher concentration (bloodstream) to lesser (dialysate fluid) through smei-permeable membrane (peritoneum).

Question 50

Peritonitis and pain associated with PD?

Answer 50

Peritonitis: Fever, ab tenderness/pain, malaise, N/V. Cloudy dialysate effluent (early sign). Prevention: meticulous sterile technique, high risk if not sterile. These pt.’s can have renal dialysis but not a great candidate for it
Pain upon inflow is normal for first 1-2 weeks during initial treatments. After they get used to expansion of volume, shouldn’t feel pain. If they have pain after that they need to see PCP.

Question 51

Exit site and tunnel infection w/ PD? Poor outflow?

Answer 51

Teach s/s of infection, culture wound. Treatment may be difficult, may need internal antibiotics in cavity.
Poor outflow after dwelling: should be more fluid coming out of pt. than was put in! Inflow should be less than outflow.
Constipation, bowels aren’t allowing outflow, kinked or clamped catheter, catheter displacement, clot formation

Question 52

Dialysate leakage with PD? Blood return?

Answer 52

Dialysate leakage: too much then report it. Clear fluid around catheter site. Use smaller volumes at start, takes about 2 weeks to get used to it and allow the cavity to expand.
Blood tinged return with initial treatments in the first week or two but shouldn’t be seen after that. In dialysis in general, blood cells shouldn’t be leaving (they don’t leave in the normal kidney nephron do they?).

Question 53

Nursing care of PD?

Answer 53

Usually allowed protein, K, Na, fluids like most dialysis pts. Not so worried about fluid volume cause they’re getting filtration. Weight, assess before/after PD.
VS before, q15-30min during, after. Assess for signs of resp. distress, pain, discomfort, site dressing for wetness, leaking too much then report.

Question 54

More nursing care of PD?

Answer 54

Monitor glucose levels. Peritoneal dialysate has a lot of glucose. Some pts w/ diabetes can’t be on it, or they add insulin to it. Ensure outflow > inflow, record I&O. Infection is going to be be a big deal because it’s hard to treat! 
Warm dialysate (in all types of dialysis!) to make sure the pt. doesn’t get hypothermia during the process, dilate blood vessels to increase clearance in PD

Question 55

Renal transplant candidate selection criteria?

Answer 55

Free of medical problems that would complicate procedure. Age 2-70.
Exclusions, things that complicate procedure: Advanced, uncorrectable heart disease or metastatic cancer because they’ll be on steroids. (Implying life expectancy is less too.) Severe psychological issues, more so people with substance abuse. Need to manage it for an extended period of time before they’ll be considered.
Donors usually 18-65 years of age, in good health, adequate function in both kidney donated/one left behind

Question 56

Pre-operative care of kidney transplant pt.’s?

Answer 56

Compatibility Studies: Tissue typing, human leukocyte antigens (HLA, blood typing
Preop teaching: explaining what’s going to happen post-op, esp. post-op pulmonary hygiene, pain, diet, lines, tubes, ambulation, medications.
Dialysis 24 hours prior to procedure for the pt. receiving the kidney to get them as healthy as possible to receive the kidney, not the donor.
Blood transfusion from the donor’s blood given ahead of time.

Question 57

2 types of kidney donors?

Answer 57

Living: usually a family member, someone who’s matched well. Best viable, long-term success. Kidney can be transplanted quickly, esp. w/ willing participant.
Cadaveric: experienced brain death, being kept alive on vent. Legally dead, confirmed true brain death. Because they have specific meds, donation is being decided on, some of the organs aren’t in the best state. Longer they’re artificially supported, less great the organs are going to be. Might be put into preserving solution outside body for several hours, ice less preferred. Non-heart beating

Question 58

Post-op urologic management after kidney transplant?

Answer 58

Large indwelling foley catheter: a lot of fluids to make sure the kidney is being perfused, to help make sure there’s no backflow and nothing building up in the bladder. Hourly urine OP, really watched for 48 hrs. Daily urinalysis to make sure it’s working well. Diuretics PRN.
May have diuresis → ↓K+ and Na++, ↓BP. Low perfusion will threaten graft survival

Question 59

Renal transplant rejection w/in 48hrs. Requires immediate removal of organ. Severe pain, elevated BP, temp. Immediate reaction from donor’s antibodies that were part of the new kidney’s blood are being rejected by the recipient

Answer 59

Glomerular capillary thrombosis. Renal tissue can become obstructed with a clot, causing ischemia, kidney death.

Question 60

Renal transplant rejection w/in 7 days or longer, a few days to weeks after surgery. Requires early recognition, treatment w/ immunosuppressive therapy.

Answer 60

Acute. Immunosuppressants in hopes they can get through this period. BUN and creating may start to rise, oliguria might start.

Question 61

Renal transplant rejection that occurs around months to years after surgery.The corticosteroid is decreased after being put on maintenance to prevent chronic rejection

Answer 61

Chronic. Kidney may not need to be taken out until stuff becomes really bad.

Question 62

Occurs with a delay in transplanting kidney, can result from cadaveric or non-heart beating donor. Ischemia injured kidney, not working right away.

Answer 62

Acute tubular necrosis. Might take about a week to happen. Need dialysis until UO ↑ and ↓ BUN and ↓ creatinine

Question 63

Non-Rejection complications of renal transplant surgery?

Answer 63

Thrombosis of renal vessel needs emergent surgery. First 48-72 hours post op. Impaired perfusion → sudden ↓ UO
Infection: Immunosuppressive drugs means higher risk, but they have to be taken for life
S/S of infection may be lessened. If a dose is missed call the PCP.
Transplant related Renal artery stenosis: Elevated BP can cause it , HTN, fluid retention. Doppler flow study

Question 64

Types of immunosuppressants for renal transplants?

Answer 64

Corticosteroids, higher in beginning, lower with maintenance. Anti-lymphocyte preparations: Stop the T cells from attacking and flagging the kidney as foreign, stops them from overacting. Monoclonal antibodies

Question 65

Issues w/ immunosuppressants for renal transplant?

Answer 65

High risk for opportunistic infections. Death from cardiac disease is most common: Steroids increase cortisol and glucose, promoting fatty acids and worsening cardiac issues. Caution when they have a pre-existing cardiac issue.

Question 66

Home care management for renal transplant post-op?

Answer 66

Importance of immunosuppressive therapy. Monitor for graft rejection: increased pain, elevated BP and fever, rejection from failure to take med. Monitor for complications: early vs late complications. Renal diet per provider orders. Avoid unpasteurized or raw food.
Activity level, only light activity for about 6 weeks but then normal after that with permission. No heavy lifting, watch BP for life, may be on meds for BP for life.