ANATOMY OF THE KIDNEY

http://www.venofer.com/VenoferHCP/Venofer_kidneyFunction.html
 NEPHRON

http://www.venofer.com/VenoferHCP/Venofer_kidneyFunction.html
CHRONIC RENAL
FAILURE
ESRF
 DEFINITION

• ALSO KNOWN AS END-STAGE RENAL FAILURE (ESRF),

IS A PROGRESSIVE DETERIORATION IN RENAL
FUNCTION IN WHICH THE BODY’S ABILITY TO
MAINTAIN METABOLIC AND FLUID AND
ELECTROLYTE BALANCE FAILS, RESULTING IN
UREMIA (RETENTION OF UREA AND OTHER
NITROGENOUS WASTES IN THE BLOOD).
• DECREASED KIDNEY GLOMERULAR FILTRATION RATE
(GFR) OF <60 ML/MIN/1.73 M2 FOR 3 OR MORE MONTHS
 PATHOPHYSIOLOGY

• AS RENAL FUNCTION DECLINES, THE END PRODUCTS OF PROTEIN

METABOLISM (WHICH ARE NORMALLY EXCRETED IN THE URINE),
ACCUMULATE IN THE BLOOD. UREMIA DEVELOPS AND ADVERSELY EFFECTS
EVERY SYSTEM IN THE BODY.
• THE GREATER THE BUILDUP OF WASTE PRODUCTS, THE MORE SEVERE THE
SYMPTOMS.
• APPROXIMATELY 1 MILLION NEPHRONS ARE PRESENT IN EACH KIDNEY, EACH
CONTRIBUTING TO THE TOTAL GFR. REGARDLESS OF THE ETIOLOGY OF
RENAL INJURY, WITH PROGRESSIVE DESTRUCTION OF NEPHRONS, THE
KIDNEY HAS AN INNATE ABILITY TO MAINTAIN GFR BY HYPERFILTRATION
AND COMPENSATORY HYPERTROPHY OF THE REMAINING HEALTHY
NEPHRONS.
• THIS NEPHRON ADAPTABILITY ALLOWS FOR CONTINUED NORMAL
CLEARANCE OF PLASMA SOLUTES SUCH THAT SUBSTANCES SUCH AS UREA
AND CREATININE START TO SHOW SIGNIFICANT INCREASES IN PLASMA
LEVELS ONLY AFTER TOTAL GFR HAS DECREASED TO 50%, WHEN THE RENAL
RESERVE HAS BEEN EXHAUSTED. THE PLASMA CREATININE VALUE WILL
DOUBLE WITH A 50% REDUCTION IN GFR.
 STAGES OF CHRONIC RENAL
DISEASE
• 3 STAGES IN NEPHRON FUNCTION

• STAGE 1: REDUCED RENAL RESERVE

CHARACTERIZED BY A 40%-75% LOSS OF
NEPHRON FUNTION. THE PATIENT IS USUALLY
ASYMPTOMATIC BECAUSE THE REMAINING
NEPHRONS ARE ABLE TO CARRY OUT NORMAL
FUNCTION OF THE KIDNEY
 STAGE 2 OF RENAL DISEASE

• STAGE 2: RENAL INSUFFICIENCY

OCCURS WHEN 75%-90% OF NEPHRON

FUNCTION IS LOST. AT THIS POINT, THE
SERUM CREATININE AND BUN RISE, THE
KIDNEY LOSES ITS ABILITY TO CONCENTRATE
URINE AND ANEMIA DEVELOPS. THE PATIENT
MAY REPORT POLYURIA AND NOCTURIA
 STAGE 3 OF RENAL DISEASE

• STAGE 3: END-STAGE RENAL DISEASE

THE FINAL STAGE, OCCURS WHEN THERE IS LESS

THAN 10% OF NEPHRON FUNCTION REMAINING. ALL
NORMAL REGULATORY, EXCRETORY, AND
HORMONAL FUNCTIONS OF THE KIDNEYS ARE
SEVERELY IMPAIRED. ESRD IS EVIDENCED BY
ELEVATED CREATININE AND BUN LEVELS AS WELL
AS ELECTROLYTE IMBALANCES.
DIALYSIS IS USUALLY INDICATED AT THIS POINT.
 GLOMULAR FILTRATION RATE

• GFR: A KIDNEY FUNCTION

TEST IN WHICH RESULTS
CAN BE DETERMINED FROM
AMOUNT OF
ULTRAFILTRATE FORMED BY
PLASMA FLOWING
THROUGH THE GLOMERULI
OF THE KIDNEY.
• AS GLOMULAR FILTRATION
DECREASES, THE SERUM
CREATININE AND BUN
LEVELS INCREASE.
 CAUSES
 TYPE 1 AND TYPE 2 DIABETES
MELLITUS CAUSE A CONDITION
CALLED DIABETIC NEPHROPATHY,
WHICH IS THE LEADING CAUSE OF
KIDNEY DISEASE IN THE UNITED
STATES.  

 HIGH BLOOD PRESSURE

(HYPERTENSION), IF NOT
CONTROLLED, CAN DAMAGE THE
KIDNEYS OVER TIME.

 GLOMERULONEPHRITIS IS THE
INFLAMMATION AND DAMAGE OF
THE FILTRATION SYSTEM OF THE
KIDNEY AND CAN CAUSE KIDNEY
FAILURE.
POSTINFECTIOUS CONDITIONS
AND LUPUS ARE AMONG THE
MANY CAUSES OF
GLOMERULONEPHRITIS.
 MORE CAUSES
 POLYCYSTIC KIDNEY DISEASE IS AN EXAMPLE OF A HEREDITARY CAUSE
OF CHRONIC KIDNEY DISEASE WHEREIN BOTH KIDNEYS HAVE
MULTIPLE CYSTS 

 USE OF ANALGESICS SUCH AS ACETAMINOPHEN (TYLENOL) AND

IBUPROPHEN REGULARLY OVER LONG DURATIONS OF TIME CAN CAUSE
ANALGESIC NEPHROPATHY, ANOTHER CAUSE OF KIDNEY DISEASE.
CERTAIN OTHER MEDICATIONS CAN ALSO DAMAGE THE KIDNEYS.

 CLOGGING AND HARDENING OF THE ARTERIES (ATHEROSCLEROSIS)

LEADING TO THE KIDNEYS CAUSES A CONDITION CALLED ISCHEMIC
NEPHROPATHY, WHICH IS ANOTHER CAUSE  OF PROGRESSIVE KIDNEY
DAMAGE.

 OBSTRUCTION OF THE FLOW OF URINE SUCH AS BY STONES, AN

ENLARGED PROSTATE, STRICTURES (NARROWINGS), OR CANCERS MAY
ALSO CAUSE KIDNEY DISEASE
 CLINICAL MANIFESTATION

• PATIENTS WITH CRF STAGE 3 OR LOWER (GFR >30

ML/MIN) GENERALLY ARE ASYMPTOMATIC AND DO
NOT EXPERIENCE CLINICALLY EVIDENT
DISTURBANCES IN WATER OR ELECTROLYTE
BALANCE OR ENDOCRINE/METABOLIC
DISTURBANCES.
• GENERALLY, THESE DISTURBANCES CLINICALLY
MANIFEST WITH CRF STAGES 4 AND 5 (GFR <30
ML/MIN).
 CLINICAL MANIFESTATIONS

• HYPERKALEMIA USUALLY DEVELOPS WHEN GFR FALLS TO

LESS THAN 20-25 ML/MIN BECAUSE OF THE DECREASED
ABILITY OF THE KIDNEYS TO EXCRETE POTASSIUM.

• METABOLIC ACIDOSIS BECAUSE THE KIDNEY CANNOT

EXCRETE INCREASED LOADS OF ACID.
 CLINICAL MANIFESTATIONS

• EXTRACELLULAR VOLUME EXPANSION AND TOTAL-

BODY VOLUME OVERLOAD RESULTS FROM FAILURE
OF SODIUM AND FREE WATER EXCRETION.
• ANEMIA PRINCIPALLY DEVELOPS FROM DECREASED
RENAL SYNTHESIS OF ERYTHROPOIETIN, THE
HORMONE RESPONSIBLE FOR BONE MARROW
STIMULATION FOR RED BLOOD CELL (RBC).
• CALCIUM AND PHOSPHORUS IMBALANCE OCCURS
BECAUSE OF A DISORDER IN METABOLISM. THEY
HAVE A RECIPROCAL RELATIONSHIP IN THE BODY;
AS ONE RISES, THE OTHER DECREASES.
 SIGNS AND SYMPTOMS
• NEUROLOGIC
WEAKNESS, FATIGUE, CONFUSION,
DISORIENTATION, TREMORS,
SEIZURES, RESTLESSNESS OF LEGS,
BURNING OF SOLES OF FEET,
BEHAVIORAL CHANGES.
• INTEGUMENTARY
GRAY-BRONZE SKIN COLOUR, DRY,
FLAKY SKIN, PRURITUS,
ECCHYMOSIS, THIN BRITTLE NAILS,
COARSE, THINNING HAIR
• PULMONARY
CRACKLES, THICK TENACIOUS
SPUTUM, DEPRESSED COUGH
REFLEX, PLEURITIC PAIN,
SHORTNESS OF BREATH, ENGORGED
NECK VEINS, TACHYPNEA, UREMIC
PNEUMONITIS, “UREMIC LUNG”
• GASTROINTESTINAL
AMMONIA ODOUR TO BREATH,
METALLIC TASTE, MOUTH
ULCERATIONS AND BLEEDING,
ANOREXIA, N&V, HICCUPS,
CONSTIPATION OR DIARRHEA,
BLEEDING FROM GI TRACT.
• HEMATOLOGIC
ANEMIA, THROMBOCYTOPENIA
• MUSCULOSKELETAL
MUSCLE CRAMPS, LOSS OF
MUSCLE STRENGTH, RENAL
OSTEODYSTROPHY, BONE
PAIN, BONE FRACTURES, FOOT
DROP
 NURSING CARE PLAN
 EXCESS FLUID VOLUME R/T
DECREASED URINE OUTPUT, AND
RETENTION OF SODIUM AND
WATER
GOAL IS MAINTENANCE OF IDEAL
BODY WEIGHT WITHOUT ACCESS
FLUID
• NURSING INTERVENTIONS
 ASSESS FLUID STATUS
 DAILY WEIGHT
I&O
 SKIN TURGOUR & EDEMA
 DISTENTION OF NECK VEINS
 BP, P, R
 LIMIT FLUID INTAKE TO
PRESCRIBED VOLUME
 EXPLAIN TO PT AND FAMILY
RATIONALE FOR RESTRICTION OF
FOOD
 PROVIDE OR ENCOURAGE
FREQUENT ORAL CARE
 RATIONALE
 ASSESSMENT PROVIDES BASELINE
AND ONGOING DATABASE FOR
MONITORING CHANGES AND
EVALUATING INTERVENTIONS
 FLUID RESTRICTION WILL DETERMINE
ON THE BASIS OF WEIGHT, URINE
OUTPUT, AND RESPONSE OF THERAPY
 UNDERSTANDING PROMOTES PT AND
FAMILY COOPERATION WITH FLUID
RESTRICTIONS
 ORAL HYGIENE MINIMIZES DRYNESS
OF ORAL MUCOUS MEMBRANES
 EXPECTED OUTCOMES
 DEMONSTRATES NO RAPID WEIGHT
CHANGES
 MAINTAINS DIETARY AND FLUID
RESTRICTIONS
 EXHIBITS NORMAL SKIN TURGOUR
WITHOUT EDEMA
 NORMAL VITALS
 REPORTS NO DIFFICULTY BREATHING
OR SHORTNESS OF BREATH
 REPORTS DECREASE DRYNESS OF
ORAL MUCOUS MEMBRANES.
 NURSING CARE PLAN

 HYPERKALEMIA, • RATIONALE
PERICARDITIS, PERICARDIAL  HYPERKALEMIA CAUSES
EFFUSION AND TEMPONADE, POTENTIALLY LIFE-
HYPERTENSION, ANEMIA, THREATENING CHANGES TO THE
BONE DISEASE BODY
• GOAL: PATIENT EXPERIENCES  CARDIOVASCULAR S & S ARE
AND ABSENCE OF CHARACTERISTIC OF
COMPLICATIONS HYPERKALEMIA
 NURSING INTERVENTIONS  EXPECTED OUTCOMES
 HYPERKALEMIA  PT HAS NORMAL K LEVEL
 MONITOR SERUM K LEVELS  EXPERIENCES NO MUSCLE
AND NOTIFY PHYSICIAN IF WEAKNESS OR DIARRHEA,
GREATER THAN 5.5 MEQ/L.
 ASSESS PATIENT FOR MUSCLE  EXHIBITS NORMAL ECG
WEAKNESS, DIARRHEA, ECG PATTERN
CHANGES( TALL TENTED  VITAL SIGNS ARE WITHIN
TWAVES, WIDENED QRS). NORMAL LIMITS
 • RATIONALE
• PERICARDITIS,  ABOUT 30-50% OF CRF PTS
PERICARDIAL DEVELOP PERICARDITIS DUE TO
EFFUSION, UREMIA; FEVER ,CHEST PAIN, AND
PERICARDIAL FRICTION RUB ARE
TAMPONADE CLASSIC SIGNS
ASSESS FOR FEVER,  PERICARDIAL EFFUSION IS
CHILLS, CHEST PAIN COMMON FOLLOWING
AND PERICARDIAL PERICARDITIS. SIGNS OF
EFFSUSION: PARADOXICAL PULSE
FRICTION RUB (SIGNS (> 10 MM DROP IN BPDURING
OF PERICARDITIS). INSPIRATION) AND SIGNS OF
SHOCK D/T COMPRESSION OF THE
IF PT HAS PERICARDITIS, HEART BY A LG EFFUSION.
AX Q 4 HRS  CARDIAC TAMPONADE EXISTS
• EXTREME WHEN THE PT IS SEVERELY
COMPROMISED
HYPOTENSION HEMODYNAMICALLY
• WEAK OF ABSENT  OUTCOMES
PERIPHERAL PULSES,  HAS STRONG AND EQUAL
ALTERED LEVEL OF PERIPHERAL PULSE
CONSCIOUSNESS,  ABSENCE OF PARADOXICAL PULSE
BULGING NECK VEINS.
 ABSENCE OF PERICARDIAL
EFFUSION, OR TAMPONADE
 • RATIONALE
• HYPERTENSION  ANTIHYPERTENSIVES PLAY A
 MONITOR AND RECORD KEY ROLE IN TX OF
HYPERTENSION ASSOCIATED
BLOOD PRESSURE WITH CRF.
 ADMINISTER  ADHERENCE TO DIET AND
ANTIHYPERTENSIVES AS FLUID RESTRICTIONS
PRESCRIBES PREVENTS EXCESS FLUID AND
SODIUM ACCUMULATION
 ENCOURAGE COMPLIANCE  THESE ARE INDICATIONS OF
WITH DIETARY AND FLUID INADEQUATE CONTROL OF
RESTRICTION THERAPY HYPERTENSION, AND NEED TO
ALTER THERAPY
 TEACH PT REPORT SIGNS OF  OUTCOMES
FLUID OVERLOAD, VISION  BP IS WITHIN NORMAL LIMITS
CHANGES, HEADACHES,
EDEMA, SEIZURES  NO HEADACHES, VISUAL
PROBLEMS OR SEIZURES
 NO EDEMA
 DEMONSTRATES COMPLIANCE
WITH DIETARY AND FLUID
RESTRICTIONS
 • RATIONALE
• ANEMIA  PROVIDES AX OF DEGREE OF
ANEMIA
 MONITOR RBC COUNT, HG,
AND HCT LEVELS  RBCS NEED IRON AND FOLIC
ACID TO BE PRODUCED.
 ADMINISTER PRESCRIBES  ANEMIA IS WORSENED BY
MEDS: IRON AND FOLIC DRAWING NUMEROUS
ACID SPECIMENS
 AVOID DRAWING  BLOOD COMPONENT
UNNECESSARY BLOOD THERAPY MAY BE NEEDED IF
PT HAS SYMPTOMS
SPECIMENS
 OUTCOMES
 TEACH PT TO PREVENT
 PT HAS NORMAL COLOUR
BLEEDING; AVOID WITHOUT PALLOR
VIGOROUS NOSE BLOWING
 HEMATOLOGY VALUES ARE
 ADMINISTER BLOOD WITHIN ACCEPTABLE LIMITS
COMPONENT THERAPY  EXPERIENCES NOT
BLEEDING FORM ANY SITE.
• BONE DISEASE  RATIONALE
 CRF CAUSES NUMEROUS
ADMINISTER THE PHYSIOLOGIC CHANGES
AFFECTING CALCIUM,
FOLLOWING MEDS AS PHOSPHORUS AND VIT D
PRESCRIBED: METABOLISM.
 HYPERPHOPHATEMIA,
PHOSPHATE BINDERS, HYPOCALCEMIA, AND EXCESS
CALCIUM ALUMINUM ACCUMULATION ARE
COMMON
SUPPLEMENTS, VIT D  BONE DEMINERALIZTION
SUPPLEMENTS DECREASES WITH IMMOBILITY.
MONITOR SERUM LAB  OUTCOMES
VALUES ( CALCIUM,  SERUM CALCIUM, PHOSPHORUS,
AND ALUMINUM LEVELS ARE
PHOSPHORUS, WITHIN ACCEPTABLE RANGES.
ALUMINUM)  HAS NO BONE
DEMINERALIZATION
ASSIST PT WITH  DISCUSS IMPORTANCE OF
EXERCISE PROGRAM MAINTAINING ACTIVITY LEVEL
AND EXERCISE PROGRAM.
 DIET
• PROTEIN RESTRICTION B/C UREA, URIC ACID AND
ORGANIC ACIDS- THE BREAKDOWN PRODUCT OF
DIETARY AND TISSUE PROTEINS- ACCUMULATE RAPIDLY
IN THE BLOOD WHEN THERE IS IMPAIRED RENAL
CLEARANCE.
• THE ALLOWED PROTEIN MUST BE OF HIGH BIOLOGIC
VALUE (DIARY PRODUCTS, EGGS, MEATS). THESE
PROTEINS ARE THOSE THAT ARE COMPLETE PROTEINS
AND SUPPLY THE ESSENTIAL AMINO ACIDS NECESSARY
FOR CELL GROWTH AND REPAIR; ALSO MAINTENANCE OF
FLUID BALANCE, HEALING AND SKIN INTEGRITY, AND
MAINTENANCE OF IMMUNE FUNCTION.
• FLUID RESTRICTIONS: FLUID ALLOWANCE IS USUALLY
500-600 ML MORE THAN THE PREVIOUS DAY’S 24 HR
OUTPUT.
• CALORIES ARE SUPPLIED BY CARBS AND FATS TO
PREVENT WASTING AND MALNUTRITION
• VITAMIN SUPPLEMENTATION BECAUSE A PROTEIN
RESTRICTED DIET DOES PROVIDE THE NECESSARY
AMOUNTS OF VITAMINS AND THE PT ON DIALYSIS MAY
LOSE WATER SOLUBLE VITAMINS FROM THE BLOOD
DURING TREATMENT.
CHRONIC RENAL FAILURE

LAB VALUES
 MEDICATIONS FOR CRF
• DIURETICS
• FUROSEMIDE (LASIX) ONLY GIVEN WITH
SEVERE FLUID OVERLOAD
• INCREASES EXCRETION OF WATER BY INTERFERING
WITH CHLORIDE-BINDING COTRANSPORT SYSTEM,
WHICH, IN TURN, INHIBITS SODIUM AND CHLORIDE
REABSORPTION IN THE THICK ASCENDING LOOP OF
HENLE AND THE DISTAL RENAL TUBULE
• ADULT DOSE: 20-80 MG PO/IV ONCE; REPEAT 6-8H PRN OR DOSE
MAY BE INCREASED BY 20-40 MG NO SOONER THAN 6-8H
AFTER PREVIOUS DOSE UNTIL DESIRED EFFECT
• NURSING ASSESSMENTS: WATCH FOR HYPOKALEMIA, ASSESS
BP BEFORE AND DURING THERAPY CAN CAUSE HYPOTENSION
 MEDICATIONS FOR CRF
CONTINUED
• PHOSPHATE-LOWERING AGENTS
• CALCIUM ACETATE (CALPHRON, PHOSLO)
• COMBINES WITH DIETARY PHOSPHORUS TO FORM
INSOLUBLE CALCIUM PHOSPHATE, WHICH IS EXCRETED IN
FECES.
• ADULT DOSE: 1-2 G PO BID-TID WITH EACH MEAL;
INCREASE TO BRING SERUM PHOSPHATE VALUE TO 6
MG/DL AS LONG AS HYPERCALCEMIA DOES NOT
DEVELOP;
• CALCIUM CARBONATE (CALTRATE, APO-CAL, TUMS)
• SUCCESSFULLY NORMALIZES PHOSPHATE
CONCENTRATIONS
• NEUTRALIZES GASTRIC ACIDITY, INCREASE SERUM CA
• ADULT DOSE: 1-2 G PO DIVIDED BID-TID; WITH MEALS
AS A PHOSPHOROUS BINDER; BETWEEN MEALS AS A
CALCIUM SUPPLEMENT
PHOSPHATE-LOWERING AGENTS
• CALCITRIOL (ROCALTROL, CALCIJEX)
• INCREASES INTESTINAL ABSORPTION OF CALCIUM
FOR TREATMENT OF HYPOCALCEMIA AND
INCREASES RENAL TUBULAR RESORPTION OF
PHOSPHATE
• ADULT DOSE FOR HYPOCALCEMIA DURING
CHRONIC DIALYSIS:
• 0.25 MCG/DAY OR EVERY OTHER DAY, MAY
REQUIRE 0.5-1 MCG/DAY PO
• SEVELAMER (RENAGEL)
• INDICATED FOR THE REDUCTION OF SERUM
PHOSPHOROUS IN PATIENTS WITH ESRD.
• ADULT DOSE: INITIAL: 800-1600 MG PO TID
WITH MEALS
MAINTENANCE: INCREASE OR DECREASE BY
400-800 MG PER MEAL Q2WK TO MAINTAIN
SERUM PHOSPHOROUS AT 6 MG/DL OR LESS
PHOSPHATE-LOWERING AGENTS
• LANTHANUM
CARBONATE
(FOSRENAL)
• FOR REDUCTION OF
HIGH PHOSPHORUS
LEVELS IN PATIENTS
WITH ESRD
• ADULT DOSE: INITIAL:
250-500 MG PO TID PC
(CHEWABLE TABS);
ADJUST DOSE Q2-3WK
TO TARGET SERUM
PHOSPHORUS LEVEL
MAINTENANCE: 500-
1000 MG PO TID PC
PHOSPHATE-LOWERING AGENTS
• DOXERCALCIFEROL (HECTOROL)
• TO LOWER PARATHYROID HORMONE LEVELS IN
PATIENTS UNDERGOING CHRONIC KIDNEY DIALYSIS.
INCREASES SERUM CA
• ADULT DOSE: 10 MCG PO 3 TIMES/WK AT
DIALYSIS; INCREASE DOSE BY 2.5 MCG/8 WK IF
IPTH IS NOT LOWERED BY 50% AND FAILS TO
REACH THE TARGET RANGE; NOT TO EXCEED 20
MCG/3 TIMES/WK
ALTERNATIVELY, 4 MCG IV 3 TIMES/WK; MAY
ADJUST DOSE BY 1-2 MCG/8 WK TO MAINTAIN
IPTH LEVELS
• NURSING ASSESSMENT FOR ALL PHOSPHATE
LOWERING AGENTS: MONITOR BUN, CREATININE,
CHLORIDE, ELECTROLYTES, URINE PH, URINARY
CALCIUM, MG, PHOSPHATE, URINALYSIS URINARY
CA SHOULD BE 9-10MG/DL, ASSESS FOR
HYPOCALCEMIA: HEADACHE, N/V, CONFUSION
 MEDICATIONS FOR CRF
CONTINUED
• ANEMIA
• EPOETIN ALFA (EPOGEN, PROCRIT)
• STIMULATES RBC PRODUCTION

• ADULT DOSE: 50 -150 U/KG IV/SC 3 TIMES PER

WEEK, THEN ADJUST DOSE BY 25 U/KG/DOSE TO
MAINTAIN APPROPRIATE HCT; MAINTENANCE
12.5-25 U/KG, TITRATE TO TARGET HCT,
• NURSING ASSESSMENT: MONITOR RENAL
STUDIES: URINALYSIS, PROTEIN, BLOOD, BUN,
CREATININE; I&O. MONITOR BLOOD STUDIES,
HGB, HCT, RBC, WBC, INR, PTT
 MEDICATIONS FOR CRF
CONTINUED
• DARBEPOETIN (ARANESP)
• STIMULATES ERYTHROPOIESIS
• ADULT DOSE: 0.45 UG/KG IV/SC AS A SINGLE INJECTION,
TITRATE NOT TO EXCEED A TARGET HGB OF 12 G/DL
• HAS A LONGER HALF-LIFE THAN EPOETIN ALFA
• NURSING ASSESSMENTS: ASSESS BLOOD STUDIES, RENAL
STUDIES; ASSESS BP, CHECK FOR RISING BP AS HCT RISES
 MEDICATIONS FOR CRF
• IRON SALTS
CONTINUED
• TO TREAT ANEMIA
• FERROUS SULFATE (FEOSOL, FERATAB, SLOW
FE)
• REPLACES IRON STORES NEED FOR RBC DEVELOPMENT
• ADULT DOSE: 100-200MG TID
• IRON SUCROSE (VENOFER)
• USED TO TREAT IRON DEFICIENCY DUTE TO CHRONIC
HEMODIALYSIS
• ADULT DOSE: IV 5ML (100MG OF ELEMENTAL
IRON) GIVEN DURING DIALYSIS, MOST WILL NEED
1000MG OF ELEMENTAL IRON OVER 10 DIALYSIS
• NURSING ASSESSMENTS: MONITOR BLOOD
STUDIES, HCT, HGB, TOTAL FE, MONTHLY.
ASSESS BOWEL ELIMINATION FOR
CONSTIPATION
DIALYSIS
 WHAT IS DIALYSIS?

• DIALYSIS IS A TYPE OF RENAL REPLACEMENT THERAPY WHICH IS USED TO PROVIDE

ARTIFICIAL REPLACEMENT FOR LOST KIDNEY FUNCTION DUE TO ACUTE OR CHRONIC
KIDNEY FAILURE
• IT IS A LIFE SUPPORT TREATMENT, IT DOES NOT CURE ACUTE OR CHRONIC RENAL FAILURE
• MAY BE USED FOR VERY SICK CLIENTS WHO HAVE SUDDENLY LOST KIDNEY FUNCTION
• MAY BE USED FOR STABLE CLIENTS WHO HAVE PERMANENTLY LOST KIDNEY FUNCTION
• HEALTHY KIDNEYS REMOVE WASTE PRODUCTS (POTASSIUM, ACID, UREA) FROM THE
BLOOD AND THEY ALSO REMOVE EXCESS FLUID IN THE FORM OF URINE
• DIALYSIS HAS TO DUPLICATE BOTH OF THESE FUNCTIONS
 DIALYSIS – WASTE REMOVAL
 ULTRAFILTRATION – FLUID REMOVAL
 PRINCIPLE OF DIALYSIS

• DIALYSIS WORKS ON THE PRINCIPLE OF

DIFFUSION OF SOLUTES ALONG A
CONCENTRATION GRADIENT ACROSS A
SEMIPERMIABLE MEMBRANE
• BLOOD PASSES ON ONE SIDE OF THE
SEMIPERMEABLE MEMBRANE, AND A DIALYSIS
FLUID IS PASSED ON THE OTHER SIDE
• BY ALTERING THE COMPOSITION OF THE
DIALYSIS FLUID, THE CONCENTRATIONS OF
THE UNDESIRED SOLUTES (POTASSIUM, UREA)
IN THE FLUID ARE LOW, BUT THE DESIRED
SOLUTES (SODIUM) ARE AT THEIR NATURAL
CONCENTRATION FOUND IN HEALTHY BLOOD
 PRESCRIPTION FOR DIALYSIS

• A PRESCRIPTION FOR DIALYSIS IS GIVEN BY A PHYSICIAN

WHO SPECIALIZES IN THE KIDNEY (NEPHROLOGIST)
• THE MD WILL SET VARIOUS PARAMETERS FOR THE
TREATMENT
 TIME AND DURATION OF THE DIALYSIS SESSIONS
 SIZE OF THE DIALYZER
 RATE OF BLOOD FLOW
 2 MAIN TYPES OF DIALYSIS

• HEMODIALYSIS
• PERITONEAL DIALYSIS
 HEMODIALYSIS

Adapted from National Institute of Diabetes and Digestive and Kidney Diseases.

National Institute of Diabetes and Digestive and Kidney Diseases. End-stage renal disease: choosing a treatment that's right for
you. Available at: http://www.niddk.nih.gov/health/kidney/pubs/esrd/esrd.htm. Accessed May 10, 2000.
 WHAT IS HEMODIALYSIS (HD)?

• CLIENT’S BLOOD IS PASSED THROUGH A SYSTEM OF

TUBING (DIALYSIS CIRCUIT) VIA A MACHINE TO A
SEMIPERMEABLE MEMBRANE (DIALYZER) WHICH HAS
THE DIALYSIS FLUID RUNNING ON THE OTHER SIDE
• THE CLEANSED BLOOD IS THEN RETURNED VIA THE
CIRCUIT BACK TO THE BODY
• THE DIALYSIS PROCESS IS VERY EFFICIENT (MUCH
HIGHER THAN IN THE NATURAL KIDNEYS), WHICH
ALLOWS TREATMENTS TO TAKE PLACE
INTERMITTENTLY (USUALLY 3 TIMES A WEEK), BUT
FAIRLY LARGE VOLUMES OF FLUID MUST BE
REMOVED IN A SINGLE TREATMENT WHICH CAN BE
VERY DEMANDING ON A CLIENT
 SIDE EFFECTS OF HD

• THE SIDE EFFECTS ARE PROPORTIONATE TO THE AMOUNT

OF FLUID BEING REMOVED
• DECREASED BLOOD PRESSURE
• FATIGUE
• CHEST PAINS
• LEG CRAMPS
• HEADACHES
• ELECTROLYTE IMBALANCE
• N&V
• REACTION TO THE DIALYZER
• AIR EMBOLISM
 COMPLICATIONS OF HD

• BECAUSE HD REQUIRES ACCESS TO THE CIRCULATORY

SYSTEM, CLIENTS HAVE A PORTAL OF ENTRY FOR
MICROBES, WHICH COULD LEAD TO INFECTION
 THE RISK OF INFECTION DEPENDS ON THE TYPE OF ACCESS USED
• BLEEDING MAY ALSO OCCUR AT THE ACCESS SITE
• BLOOD CLOTTING WAS A SERIOUS PROBLEM IN THE PAST,
BUT THE INCIDENCE OF THIS HAS DECREASED WITH THE
ROUTINE USE OF ANTICOAGULANTS (HEPARIN IS THE MOST
COMMON)
 ANTICOAGULANTS ALSO COME WITH THEIR OWN RISK OF SIDE
EFFECTS AND COMPLICATIONS
 RARE COMPLICATION OF HD

• ON THE RARE OCCASION, A CLIENT MAY HAVE

A SEVERE ANAPHYLACTIC REACTION
SNEEZING
WHEEZING
SOB
BACK PAIN
CHEST PAIN
SUDDEN DEATH
• THIS CAN BE CAUSED BY THE STERILANT IN
THE DIALYZER OR THE MATERIAL IN THE
MEMBRANE ITSELF
 THREE TYPES OF ACCESS FOR HD

• IV CATHETER
• ARTERIOVENOUS (AV) FISTULA
• SYNTHETIC GRAFT
• THE TYPE OF ACCESS IS INFLUENCED BY
FACTORS SUCH AS EXPECTED TIME COURSE OF
THE CLIENTS RENAL FAILURE AND THE
CONDITION OF THE CLIENTS VASCULATURE
• SOME CLIENTS MAY HAVE MULTIPLE ACCESSES,
USUALLY BECAUSE AN AV FISTULA OR A GRAFT IS
MATURING AND AN IV CATHETER IS STILL BEING
USED
 IV CATHETER
(CENTRAL VENOUS CATHETER)
• CONSISTS OF A PLASTIC CATHETER WITH TWO LUMENS WHICH
IS INSERTED INTO A LARGE VEIN (VENA CAVA VIA THE
INTERNAL JUGULAR VEIN) TO ALLOW LARGE FLOWS OF BLOOD
TO BE WITHDRAWN FROM THE FIRST LUMEN
• THE BLOOD GOES INTO THE DIALYSIS CIRCUIT, AND IS
RETURNED TO THE BODY VIA THE SECOND LUMEN
 NON-TUNNELED
 TUNNELED
• THIS TYPE OF ACCESS IS USED FOR CLIENTS WHO NEED RAPID
ACCESS FOR IMMEDIATE DIALYSIS
 CLIENTS WHO ARE LIKELY TO RECOVER FROM ARF
 CLIENT WITH END-STAGE RENAL FAILURE
 CLIENTS WAITING FOR OTHER SITES TO MATURE
• THIS TYPE OF ACCESS IS VERY POPULAR FOR CLIENTS BECAUSE
IT DOESN’T INVOLVE NEEDLES FOR EACH TREATMENT
 COMPLICATIONS OF AN IV
CATHETER
• VENOUS STENOSIS
 THIS IS THE ABNORMAL NARROWING OF THE BLOOD VESSEL
 BECAUSE THE CATHETER IS A FOREIGN BODY IN THE VESSEL,
IT OFTEN PROVOKES AN INFLAMMATORY REACTION IN THE
VEIN WALL
 THIS RESULTS IN SCARRING AND NARROWING OF THE VEIN,
OFTEN TO THE POINT WHERE THE VEIN OCCLUDES
 AV FISTULA

• THIS ACCESS IS RECOGNIZED AS THE PREFERRED ACCESS METHOD

• TO CREATE A FISTULA A VASCULAR SURGEON JOINS AN ARTERY
AND A VEIN TOGETHER
• SINCE THIS BYPASSES THE CAPILLARIES, BLOOD FLOWS AT A VERY
HIGH RATE THROUGH THE FISTULA
 THIS CAN BE FELT BY PLACING A FINGER OVER A MATURE FISTULA
(THRILL)
• USUALLY CREATED IN THE NON-DOMINANT HAND
• IT CAN BE SITUATED ON THE HAND, FOREARM OR THE ELBOW
• IT WILL TAKE APPROXIMATELY 4-6 WEEKS TO MATURE
• DURING TREATMENT, 2 NEEDLES ARE INSERTED, ONE TO DRAW
BLOOD OUT OF THE BODY AND THE OTHER TO RETURN BLOOD TO
THE BODY
 ADVANTAGES OF AN AV FISTULA

• DECREASED INFECTION RATE

• INCREASED BLOOD FLOW RATES, THEREFORE A MORE
EFFECTIVE DIALYSIS TREATMENT
• DECREASED INCIDENCE OF THROMBOSIS
 COMPLICATIONS OF AN AV
FISTULA
• IF AN AV FISTULA HAS A VERY HIGH FLOW RATE AND THE
VASCULATURE THAT SUPPLIES THE REST OF THE LIMB IS
POOR, THAN A ‘STEAL SYNDROME’ CAN OCCUR
 BLOOD THAT ENTERS THE LIMB IS DRAWN INTO THE FISTULA
AND RETURNED TO THE GENERAL CIRCULATION WITHOUT
ENTERING THE CAPILLARIES OF THE LIMB
 THIS RESULTS IN COOL EXTREMITIES OF THE LIMB, CRAMPING
PAINS AND POSSIBLE TISSUE DAMAGE
• LONG TERM COMPLICATIONS CAN BE THE DEVELOPMENT
OF A BULGING IN THE WALL OF THE VEIN (ANEURYSM)
 THE VESSEL WALL IS WEAKENED BY THE REPEATED INSERTION
OF NEEDLES OVER TIME
 CAN BE REDUCED BY CAREFUL NEEDLING TECHNIQUE
 AV GRAFT

• THIS IS MUCH LIKE A FISTULA, EXCEPT AN ARTIFICIAL

VESSEL IS USED TO JOIN THE ARTERY AND THE VEIN
• GRAFTS ARE USED WHEN CLIENT’S OWN VASCULATURE
DOES NOT PERMIT A FISTULA
• AN AV GRAFT WILL MATURE MUCH FASTER THAN AN AV
FISTULA, AND IT COULD BE READY TO USE WITHIN DAYS
AFTER FORMATION
COMPLICATIONS OF AN AV GRAFT

• AV GRAFTS ARE AT HIGH RISK FOR NARROWING WHERE

THE GRAFT IS SEWN TO THE VEIN
 AS A RESULT CLOTTING OR THROMBOSIS MAY OCCUR

• AS A FOREIGN MATERIAL IS BEING PLACED IN THE BODY,

THERE IS A GREATER RISK OF INFECTION
 EQUIPMENT NEEDED FOR HD

• THE HD MACHINE PERFORMS THE FUNCTION OF

PUMPING THE PATIENT'S BLOOD AND THE DIALYSATE
THROUGH THE DIALYZER.
• THE NEWEST DIALYSIS MACHINES ON THE MARKET
ARE HIGHLY COMPUTERIZED AND CONTINUOUSLY
MONITOR AN ARRAY OF SAFETY-CRITICAL
PARAMETERS, INCLUDING BLOOD AND DIALYSATE
FLOW RATES, BLOOD PRESSURE, HEART RATE,
CONDUCTIVITY, PH, ETC.
• IF ANY READING IS OUT OF NORMAL RANGE, AN
AUDIBLE ALARM WILL SOUND TO ALERT THE
PATIENT-CARE TECHNICIAN WHO IS MONITORING THE
PATIENT.
 EQUIPMENT – WATER SYSTEM

• AN EXTENSIVE WATER PURIFICATION SYSTEM IS

ABSOLUTELY CRITICAL FOR HD
• SINCE DIALYSIS PATIENTS ARE EXPOSED TO VAST
QUANTITIES OF WATER, WHICH IS MIXED WITH THE
ACID BATH TO FORM THE DIALYSATE, EVEN TRACE
MINERAL CONTAMINANTS OR BACTERIAL
ENDOTOXINS CAN FILTER INTO THE PATIENT'S BLOOD.
• BECAUSE THE DAMAGED KIDNEYS ARE NOT ABLE TO
PERFORM THEIR INTENDED FUNCTION OF REMOVING
IMPURITIES, IONS THAT ARE INTRODUCED INTO THE
BLOOD STREAM VIA WATER CAN BUILD UP TO
HAZARDOUS LEVELS, CAUSING NUMEROUS
SYMPTOMS INCLUDING DEATH
• FOR THIS REASON, WATER USED IN HD IS PURIFIED
 EQUIPMENT – THE DIALYZER

• THE DIALYZER, OR ARTIFICIAL KIDNEY, IS THE PIECE OF

EQUIPMENT THAT ACTUALLY FILTERS THE BLOOD
• THE BLOOD IS RUN THROUGH A BUNDLE OF VERY THIN
CAPILLARY-LIKE TUBES, AND THE DIALYSATE IS PUMPED IN A
CHAMBER BATHING THE FIBERS
• THE PROCESS MIMICS THE PHYSIOLOGY OF THE GLOMERULUS
AND THE REST OF THE NEPHRON
• DIALYZERS COME IN MANY DIFFERENT SIZES. A LARGER
DIALYZER WILL USUALLY TRANSLATE TO AN INCREASED
MEMBRANE AREA, AND AN INCREASE IN THE AMOUNT OF
UNDESIRED SOLUTES REMOVED FROM THE PATIENT'S BLOOD.
• THE NEPHROLOGIST WILL PRESCRIBE THE DIALYZER TO BE
USED DEPENDING ON THE PATIENT
• DIALYZERS ARE NOT SHARED BETWEEN PATIENTS IN THE
PRACTICE OF REUSE.
PERITONEAL DIALYSIS
 WHAT IS PERITONEAL
DIALYSIS (PD)?
• PERITONEAL DIALYSIS WORKS BY USING THE BODY'S
PERITONEAL MEMBRANE, WHICH IS INSIDE THE ABDOMEN, AS A
SEMI-PERMEABLE MEMBRANE.
• A SPECIALLY FORMULATED DIALYSIS FLUID IS INSTILLED
AROUND THE MEMBRANE, USING AN INDWELLING CATHETER,
THEN DIALYSIS CAN OCCUR, BY DIFFUSION
• EXCESS FLUID CAN ALSO BE REMOVED BY OSMOSIS, BY
ALTERING THE CONCENTRATION OF GLUCOSE IN THE FLUID.
• DIALYSIS FLUID IS INSTILLED VIA A PERITONEAL DIALYSIS
CATHETER, WHICH IS PLACED IN THE PATIENT'S ABDOMEN,
RUNNING FROM THE PERITONEUM OUT TO THE SURFACE, NEAR
THE NAVEL
• PERITONEAL DIALYSIS IS TYPICALLY DONE IN THE PATIENT'S
HOME AND WORKPLACE, BUT CAN BE DONE ALMOST ANYWHERE
 ADVANTAGES OF PD

• CAN BE DONE AT HOME

• RELATIVELY EASY FOR THE CLIENT TO LEARN
• EASY TO TRAVEL WITH, BAGS OF SOLUTION ARE EASY TO
TAKE ON HOLIDAY
• FLUID BALANCE IS USUALLY EASIER WHEN THE CLIENT IS
ON PD THAN IF THE CLIENT IS ON HD
 DISADVANTAGE OF PD

• REQUIRES A DEGREE OF MOTIVATION AND ATTENTION TO

CLEANLINESS WHILE PERFORMING PD
• THERE ARE A NUMBER OF COMPLICATIONS
 COMPLICATIONS OF PD

• PERITONEAL DIALYSIS REQUIRES ACCESS TO THE

PERITONEUM. AS THIS ACCESS BREAKS NORMAL SKIN
BARRIERS, AND AS PEOPLE WITH RENAL FAILURE GENERALLY
HAVE A SLIGHTLY SUPPRESSED IMMUNE SYSTEM, INFECTION IS
A RELATIVELY COMMON PROBLEM
• LONG TERM PERITONEAL DIALYSIS CAN CAUSE CHANGES IN
THE PERITONEAL MEMBRANE, CAUSING IT TO NO LONGER ACT
AS A DIALYSIS MEMBRANE AS WELL AS IT USED TO.
• THIS LOSS OF FUNCTION CAN MANIFEST AS A LOSS OF
DIALYSIS ADEQUACY, OR POORER FLUID EXCHANGE (ALSO
KNOWN AS ULTRAFILTRATION FAILURE)
• FLUID MAY LEAK INTO SURROUNDING SOFT TISSUE, OFTEN
THE SCROTUM IN MALES
• HERNIAS ARE ANOTHER PROBLEM THAT CAN OCCUR DUE TO
THE ABDOMINAL FLUID LOAD
 NURSING ASSESSMENTS

• BEFORE CLIENT IS IN THE UNIT, LOOK AT THE NURSES NOTES

FROM THE TREATMENT BEFORE
 ANY PROBLEMS, WILL HELP NURSE PLAN FOR THE UPCOMING
TREATMENT
• LOOK AT THE CLIENT
 STRENGTH
 GAIT
 WHETHER CLIENT NEEDS ASSISTANCE
 COLOR
 PUFFINESS
 COULD BE CAUSED BY EXCESS FLUID, TOO MUCH TO DRINK, MORE FLUID
SHOULD BE TAKEN OFF WITH EACH TREATMENT, CHANGES IN VOIDING
PATTERN (ARE THEY VOIDING LESS THAN THEY DID LAST MONTH)
 ASSESSMENTS CON’T

• SHORTNESS OF BREATH
 COULD INDICATE FLUID AROUND THE LUNGS
 ASK ABOUT SOB AT NIGHT (DOES CLIENT HAVE TO SLEEP IN A
SITTING POSITION?)
• ASK THE CLIENT HOW THEY ARE FEELING
 THE CLIENT IS USUALLY THE BEST SOURCE OF INFORMATION
 CLIENTS ARE IN 3 TIMES A WEEK, DIALYSIS NURSES REALLY
GET TO KNOW THEIR CLIENTS
• EVALUATE ACCESS
 BRUISING, SWOLLEN, TENDER
 BRUIT – LISTEN WITH THE STETHOSCOPE FOR A SWISHING
SOUND OF THE BLOOD, LISTEN ALL THE WAY UP THE ARM
 THRILL – FELT WITH THE FINGERS, TELLS THE NURSE IF THE
BLOOD IS FLOWING IN THE FISTULA (CLIENT’S ARE TOLD TO
FEEL FOR THIS AT HOME WHEN A FISTULA IS FIRST INITIATED)
 ASSESSMENTS DURING
TREATMENT
• ASK CLIENT HOW HE/SHE FEELS
 DIZZINESS, DIAPHORETIC,
• THE MACHINES AUTOMATICALLY TAKE BP AND HR EVERY 30
MINUTES
 CAN PROGRAM THE MACHINES TO TAKE IT AT WHATEVER
INTERVAL IS NECESSARY (EVERY MIN, 10 MIN, 15 MIN)
• TRY TO RECOGNIZE A PROBLEM BEFORE IT STARTS (EX.
HYPOVOLEMIC SHOCK)
• ASSESS ACCESS SITE
 WATCH TREND OF BP
 IT USUALLY GRADUALLY DECREASES THROUGHOUT THE
COURSE OF THE TREATMENT, BUT LOOK FOR SUDDEN OR
DRASTIC DROPS
• ASSESS ACCESS SITE
 BLEEDING, SWELLING, TENDERNESS
 NURSING INTERVENTIONS

• IF CLIENT COMES IN WITH SHORTNESS OF

BREATH, OFFER O2 WHICH CAN BE KEPT ON FOR
THE FULL TREATMENT IF NECESSARY
• COMFORT
 CLIENT’S ARE SITTING IN THE SAME CHAIR FOR UP TO
FOUR HOURS
 OFFER EXTRA PILLOWS, SOME CLIENTS HAVE SPECIAL
BACK PILLOW THEY LEAVE IN THE UNIT
 ENSURE TV AND AUDIO IS WORKING PROPERLY
 NURSING INTERVENTIONS CON’T

• IF THE BLOOD PRESSURE IS DROPPING TOO QUICKLY:

SLOW OR STOP FLUID REMOVAL FOR A TIME PERIOD
THE MACHINES ARE CONSTANTLY BEING ADJUSTED
THROUGHOUT THE COURSE OF THE TREATMENT
DEPENDING ON THE BP
IF THE BP DROPS SUDDENLY 200-300CC OF NORMAL
SALINE CAN BE GIVEN TO BALANCE FLUID LEVELS
• USUALLY, MORE FLUID WILL BE TAKEN OFF AT THE
BEGINNING OF THE TREATMENT, THIS WILL ALLOW
THE CLIENT TO FEEL BETTER AT THE END
• IF THE CLIENT IS ELDERLY, FLUID REMOVAL STARTS
SLOWLY TO EASE THEM INTO THE TREATMENT
 RESPONSIBILITIES OF NURSING
STAFF
PRIOR TO DIALYSIS
• ENSURE CLIENT IS READY TO SIT FOR UP TO FOUR HOURS
 ENCOURAGE CLIENT TO USE WASHROOM BEFORE ARRIVING
TO THE UNIT
 TRY TO AVOID LAXATIVES IF POSSIBLE BEFORE TREATMENT

• ENSURE CLIENT HAS EATEN MEAL PRIOR TO TREATMENT

 RESPONSIBILITIES OF NURSING
STAFF
AFTER DIALYSIS
• A DIALYSIS NURSE WILL GIVE UNIT LEADER OR PRIMARY
NURSE A VERBAL REPORT OF TREATMENT
 ANY COMPLICATIONS DURING TREATMENT
 CHECK BP STANDING AND SITTING
 ASSESS ACCESS SITE
• ENCOURAGE CLIENT TO REST
 AVOID TREATMENTS OR PHYSIO FOR A COUPLE OF HOURS IF
POSSIBLE
• WATCH FLUID INTAKE
 BE AWARE IF CLIENT IS ON FLUID RESTRICTION
• CHECK THRILL AND BRUIT
• DO NOT TAKE A BP ON ACCESS ARM
• DO NOT TAKE BLOOD FROM ACCESS ARM
 Questions?
Thank you for listening.