Week 11: Acute Kidney Injury and Chronic Kidney Failure/Dialysis

Guidelines for collecting 24-hour urine specimen:

-test begins at the time of first void, discard first void

-void prior to defecating

-avoid placing toilet paper into collection container

-collect all urine voided over the next 24 hrs that is kept on ice or refrigerated

-test must be restarted if any urine is missed

Function of kidneys:

-regulate fluid, acid-base, and electrolyte balance

-eliminate wastes from the body

Kidney failure:

diagnosed as acute kidney injury or chronic kidney disease

Acute kidney injury:

a SUDDEN loss of kidney function that occurs over hours or days

-occurs w/ or w/out kidney damage

-s/s occur ABRUPTLY

-potentially reversible

Phases of acute kidney injury:

Onset

Oliguria

Diuretic

Recovery

Onset phase of acute kidney injury:

Begins with the onset of the event, ends when oliguria develops, and lasts for hours to days

Oliguria phase of acute kidney injury:

Begins with the kidney insult; urine output is 100 to 400 mL/24 hr with or without diuretics; and lasts for 1 to 3 weeks

Diuresis phase of acute kidney injury:

Begins when the kidneys start to recover; diuresis of a large amount of fluid occurs; and can last for 2 to 6 weeks

Recovery phase of acute kidney injury:

Continues until kidney function is fully restored and can take up to 12 months

Acute kidney injury stage 1 class:

Risk stage:

Blood creatinine 1.5 to 1.9 times baseline and urine output less than 0.5 mL/kg/hr for 6 hr or more

Acute kidney injury stage 2 class:

Injury stage:

Blood creatinine 2 to 2.9 times baseline and urine output less than 0.5 mL/kg/hr for 12 hr or more

Acute kidney injury stage 3 class:

Failure stage:

Blood creatinine 3 times baseline and urine output less than 0.3 mL/kg/hr for 12 hr or more

Prerenal type of acute kidney injury:

-caused by conditions that impair blood flow to the kidneys

-Early intervention: restoring fluid volume deficit can reverse injury and prevent chronic kidney disease (CKD)

Intrarenal type of acute kidney injury:

caused by conditions that cause actual damage to the glomeruli or the tubules

-prolonged obstruction leads to hydronephrosis (kidney ischemia and inflammation)

-within the kidney

Postrenal type of acute kidney injury:

caused by conditions that cause mechanical obstruction to the outflow or urine

-after the kidney

Disease prevention for acute kidney injury:

-drink at least 2L water per day

-stop smoking

-healthy weight

-use NSAIDS cautiously

-complete antibiotics track in full

Risk factors for acute kidney injury:

-diabetes, longstanding HTN, heart failure, CKD

-over 60 yrs of age

-w/recent history of sustained v. low BP

-receiving more than one nephrotoxic drug

How does prerenal AKI occur?

reduction in renal blood flow

-hypovolemia

-dehydration/GI losses/hemorrhage

-decreased cardiac output

renal artery obstruction

S/s of prerenal AKI:

-sudden oliguria

-azotemia (build up of nitrogenous waste products in blood)

-fall in glomerular filtration rate

-fall in amount of sodium in urine

Oliguria guidelines:

-output less than 0.5 mL/kg/hr

-output less than 30 mL/hr

-output less than 400 mL/day

BUN guidelines:

10-20 mg/dL

-urea is a waste product of protein metabolism and tissue protein turnover

Creatinine guidelines:

M: 0.6-1.2 mg/dL

F: 0.5-1.1 mg/dL

-waste product that comes from the metabolism of creatine in skeletal muscle

-more reliable than BUN

Nursing considerations for prerenal AKI:

-closely monitor I&O

-quickly restore circulating volume

-increase cardiac output

--maintain MAP>60

S/s of intrenal AKI:

-flank or groin pain

-hematuria

-sudden oliguria or anuria (no urine)

-azotemia

-sodium wasting

How does intrarenal AKI occur?

direct damage to kidney tissue (glomerulonephritis/necrosis)

-nephrotoxic injury (drug or chemical exposure)

-interstitial nephritis (allergic reaction, infections)

-prolonged prerenal ischemia

Ischemia

a condition where there is an inadequate blood supply to a specific part of the body

Nursing considerations for IV radiographic contrast-induced AKI:

-screen all patients for pre existing impairment of kidney function

-hold metformin before and for 48 hrs after contrast dye

S/s of fluid volume excess:

-distended neck veins and hand veins

-bounding pulses

-hypertension

-dyspnea, crackles, pulmonary edema

-weight gain

-peripheral edema

How to treat hypermagnesemia:

-eliminate magnesium containing medications (antacids, laxatives)

-administer fluids and loop diuretics

-dialysis

How to treat hyperkalemia:

-restrict K. hold K supplements

-administer loop diuretics

-administer Kayexalate, Veltassa, Lokelma

Sodium Plystyrene Sulfate (Kayexalate)

-exchanges potassium in the GI tract (poops K out)

-onset is fast (1-24 hrs)

-can cause bowel necrosis

Sodium zirconium cyclosilicate (Lokelma)

-binds and removes K from the GI tract

-onset is 1 hr

Patiromer (Veltassa)

-binds and removes K from GI tract

-onset is medium (6-8 hrs)

-hold all other meds for 3 hrs before and after adminstration

Emergency measures for hyperkalemia:

remember weird K values=cardiac conditions

-place patient on cardiac monitor

-administer calcium gluconate

-loop diuretics

Relationship between acidosis and K levels:

acidosis increases serum potassium levels

-treated by sodium bicarbonate

Relationship between insulin and K levels:

insulin lowers serum potassium levels

Foods high in phosphorus:

-dairy foods

-nuts and seeds

-dried beans and lentils

-meats

-bran cereal

-beer and cola

-chocolate

Relationship between Calcium and Phosphorus:

INVERSE

-when serum phosphorus levels rise calcium levels fall

Azotemia

elevated blood urea nitrogen (BUN) and creatine (CR) levels in the blood

Uremia

the clinical syndrome associated w/the toxic effects of azotemia and other waste products in the blood

S/s of Diuretic phase of AKI:

-high urine output

-hypovolemia, hypokalemia, hypomagnesemia

-improved mental alertness

-resolved azotemia

Nursing considerations for diuretic phase of AKI:

-monitor I&O and daily weights

-monitor serum electrolytes

--replace as needed

1 kg = how many mL

1 kg=1000 mL

2.2lb=1 kg

Chronic kidney disease (CKD):

slow and progressive destruction of nephrons and glomeruli over years

-results in kidney failure

-irreversible

Tests used to screen for CKD:

-estimated glomerular filtration rate

-albuminuria: (greater than 30 indicates kidney damage)

Markers for CKD:

1 or more of the following:

-albumin to creatine ratio >30

-urine sediment abnormalities (hematuria)

-abnormalities detected by imahing

-GFR less than 60 mL for greater than 3 months

Stage 1 of CKD:

kidney damage w/NORMAL GFR

-diagnosis and treatment

Stage 2 of CKD:

kidney damage w/mild decreased GFR

-diagnosis and treatment

Stage 3 of CKD:

moderate decrease GFR

-GFR<60 = kidney failure

Stage 4 of CKD:

severe decrease GFR

-GFR 15-29

-prepare for RRT (dialysis)

Stage 5 of CKD:

kidney failure, end stage kidney disease

-GFR<15

-renal replacement theory

GFR guidelines:

GFR<60 = kidney failure

GFR< 15 = renal replacement therapy

Nursing considerations for CKD:

-lifestyle interventions (diet, activity, tobacco, weight)

-manage blood sugar

-avoid NSAIDs, contrast dye

-control protein intake

-limit Na,K,P, calories, vit/minerals

S/s of CKD:

-hematological disturbances (anemia, bleeding, infection)

-cardiovascular risk factors (dyslipidemia, HTN)

-psychological disturbances

Formula for BUN/Creatinine ratio:

Divide BUN by creatinine

Pre and Intra lab values:

PRE:

na= LOW

BUN/creatinine ratio= HIGH (20<)

INTRA:

na=HIGH

ratio= LOW (10>)

Indications for dialysis:

-fluid volume excess

-hyperkalemia

-uncompensated metabolic acidosis

-uremic complications

-chronic renal failure (GFR < 15)

Osmosis and dialysis:

excess water is removed by OSMOSIS

Diffusion and dialysis:

excess solutes are removed by DIFFUSION

Ultrafiltration and dialysis:

excess water and solute are also removed by ULTRAFILTRATION

-more efficient than osmosis and diffusion

In center hemodialysis:

-trained staff perform treatment

-friendship and camaraderie develop

-must travel to center at least 3x per week

-no family during treatment

Home hemodialysis:

-no need to travel to center

-dialysis parter must be present

-no medical professionals at home to monitor treatment

-studies show better outcomes

Peritoneal dialysis:

-more mobility and flexibility

-no machine/needle required

-done everyday

-potential weight gain

-potential for infection in catheter

Types of vascular accesses:

internal access

-AV fistula, AV graft

external access

-central lines (short and long term)

What is AV fistula:

combining of radial artery and vein

-takes 3 months to mature

AV graft:

A surgical connection is made between an artery and a vein to allow hemodialysis access.

-2 to 6 weeks to heal (QUICKER)

-not as effective

Nursing considerations for AV fistula or graft:

-assess for patency

-palpate for a thrill

-monitor for infection

-NEVER take BP, draw blood, or use a wrist restraint on an extremity w/graft or fistula

Potential complications of hemodialysis:

-hypotension

-muscle cramps

-bleeding/loss of blood

-blood borne infectious disease

-disequilibrium syndrome

Disequilibrium syndrome

neurologic condition believed to be caused by cerebral edema; the shift in cerebral fluid volume occurs when the concentrations of solutes within the blood are lowered rapidly during dialysis