Chronic Kidney Disease

Chronic Kidney Disease
CKD Dialysis Renal Transplant

Bones can break, muscles can atrophy, glands can loaf, even the brain can go to sleep without immediate danger to survival. But -- should kidneys fail.... neither bone, muscle, nor brain could carry on. Homer Smith, Ph.D.

Functions of the Kidney
Primary function _________________________ Other functions ______________________ Primary function Regulate volume and composition of ECF (extracellular fluid) Excrete waste products Other functions Regulate acid-base balance Control BP Produce Erthyropoietin Activate Vitamin D

Review What are nephrons?
Why would a person with kidney disease have anemia? What happens to the serum calcium? Why? How does the kidney control blood pressure? What are nephrons? Functional unit of the kidney millions in each kidney Why would a person with kidney disease have anemia? Impaired Erythropoietin production What happens to the serum calcium? Why? Decreases due to lack of activated vitamin D How does the kidney control blood pressure? RAAS

Biopsy Ultrasound X-Rays Labs Anything else?

Diagnostic studies Blood Tests BUN Creatinine K+ PO4 Ca Urinalysis
Specific gravity Protein Creatinine clearance BUN and creatinine up K+ up Phosphorus up Magnesium up Calcium down

BUN and Creatinine BUN- Normal 6-20 mg/dl
Nitrogenous waste product of protein metabolism By itself: Unreliable in measurement of renal function Creatinine- Normal mg/dl A waste product of muscle metabolism 2 times normal = 50% damage 8 times normal = 75% damage 10 times normal = 90% damage Exception -_______________________ severe muscular disease can greatly  Creatinine levels

Glomerular Filtration Rate
GFR- Cannot be directly measured Uses Serum creatinine Gender Ethnicity Age Weight Why would you need to estimate GFR?

Glomerular Filtration Rate
Creatinine Clearance 24 hour urine for creatinine clearance Most accurate indicator of Renal Function Reflects GFR Formula: urine creatinine X urine volume serum creatinine What is a normal GFR? 125ml/min

Chronic Kidney Disease (CKD)
Slow and progressive, irreversible loss of kidney function occurring over months to years National Kidney Foundation- Presence of kidney damage or decreased GFR < 60 mL/min for longer than 3 months End Stage Renal Disease -GFR<15 mL/min Renal transplant/dialysis

Chronic Kidney Disease (CKD)
Cause & onset often unknown Loss of function _________ lab abnormalities Lab abnormalities ________ symptoms Symptoms (usually) evolve in orderly sequence Renal size is usually decreased Loss of function precedes lab abnormalities Lab abnormalities precede symptoms

Chronic Kidney Disease Causes
_________________ Cystic disorders Developmental /Congenital Infectious Disease Diabetes Hypertension Glomerulonephritis

Chronic Kidney Disease Causes
Neoplasms Obstructive disorders Autoimmune diseases Hepatorenal failure Scleroderma Amyloidosis Drug toxicity

Stages of CKD Stage 1: GFR >/= 90 ml/min despite kidney damage
Mild reduction -GFR 60 – 89 ml/min 1. GFR of 60 may represent 50% loss in function 2. Parathyroid hormones starts to increase As stage increases so does the mortality rate. Stage 5 rate is 19-24% or about 90,000 people /year

CKD During Stage 1& 2 No symptoms Serum creatinine doubles
Up to 50% nephron loss Why does PTH increase? (2 reasons) Low serum calcium inability kidneys to activate vit D  hypocalcemia  parathyroid gland  secretes PTH  stimulates bone demineralization  release calcium from bones Elevatated Phosphorus PTH  controls reabsorption of phos  (phos excreted through kidneys)  CKD  inc. PTH

Stages of CKD Stage 3: Moderate reduction -GFR 30-59 ml/min
1. Calcium absorption decreases 2. Malnutrition onset 3. Anemia 4. Left ventricular hypertrophy Why? Ca ---- inc in phos & dec in vit d metabolism Nutrition  anorexia, N&V, uremia, hormone imbalance, acidosis starting Anemia --- erythopoeitin reduction LVH arterial HTN  rapid atheroscleorsis  LVH

Stages of CKD Stage 4: Severe reduction -GFR 15-29 ml/min Why?
1. Serum triglycerides increase 2. Hyperphosphatemia 3. Metabolic acidosis 4. Hyperkalemia Why? Inc glucose levels  inc. insulin prod  inc. plasma insulin level  inc hepatic production of triclycerides Others kidney not excreting them

Stages of CKD During Stage 3-4
Signs and symptoms worsen if kidneys are stressed Decreased ability to maintain homeostasis 75% nephron loss

Stages of CKD During Stage 3 &4
Decreased: __________ Symptoms: elevated BUN & Creatinine mild azotemia anemia glomerular filtration rate solute clearance ability to concentrate urine hormone secretion

Stages of CKD Stage 5: Kidney failure -GFR < 15 ml/min Azotemia
Residual function < 15% of normal Excretory, regulatory and hormonal functions severely impaired. Metabolic acidosis Azotemia Inc nitrogenous waste BUN is hallmark ---- urea, creatinine, metabolic wastes, Symptoms Neuro confusion, dec LOC, fatigue CV inc HR, swelling, orthostatic hypotension Related to comorbities, cause of failure, age, compliance with POC

Marked increase in: Marked decrease in: Fluid overload ___________
BUN Creatinine Phosphorus Marked decrease in: Hemoglobin Hematocrit Calcium (possibly) Fluid overload

CKD Stage 5 Uremic syndrome develops affecting all body systems
can be diminished with early diagnosis & treatment Last stage of progressive CKD Fatal if no treatment Uremia- Same as azotemia inc K, anemia, acidosis, in BP, dec Ca with symptoms of each

Loss of renal function impacts every body system.
Retention of urea, creatinine, phenols, hormones, electrolytes, water Uremia- kidney function so low that multiple body systems develop symptoms, GFR usually <10 mL/min

CKD Manifestations Urinary Early may be no change in urine output
May see polyuria (not related to kidney disease) why? Later- Fluid retention, edema Dialysis- may develop anuria Polyuria due to Diabetes. Diabetes is a cause of CKD. Diabetes can cause polyuria.

CKD Manifestations Metabolic Waste Products Accumulate
Altered carbohydrate Metabolism Insulin resistance Elevated triglycerides BUN/serum Creatinine rise BUN also increased by protein intake, fever, corticosteroids and catabolism As BUN rises- N, V, fatigue, HA, lethargy, confusion Carbohydrate metabolism caused by impaired glucose use due to cellular insensitivity to insulin hyperglycemia inc glucose  inc insulin  inc. plasma insulin insulin dep on kidneys for excretion- inc hepatic release of tryglycerides to serum

CKD Manifestations Electrolyte and acid Base Potassium Sodium
Calcium and Phosphorus Magnesium Metabolic Acidosis Volume expansion and fluid overload Change in urine specific gravity Fixed specific gravity , morning & night no matter the fluid intake. Normal – 1.025 K+- Most serious, fatal arrythmias. Decreased K+ excretion by kidneys also breakdown of cellular protein, bleeding, meatbolic acidosis, food, drugs, IV No P No K Nausea, fatigue, tingling, muscle weakness, tall peaked t waves, fatal arrythmias Calcium/Phosphorus- later Sodium - low or normal, add too much water creates dilutional hyponatremia, edema, hypertension HF Mag- not usually an issue unless MOM, Mag Citrate, Antacids given , sedative effect

CKD Manifestations Endocrine Hyperparathyroidism Hypothyroidism
Erythropoietin production decreased Parathyroid hormone and Vitamin D3 Reproductive Amennorrhea Erectile dysfunction Gonadal dysfunction

CKD Manifestations Anemia
Hematologic Anemia Bleeding tendencies Platelet dysfunction Infection Impaired platelet function - r/t inc K & Ca Anemia Erythropoietin, nutrition, GI bleed, hemodialysis Iron, folic acid Bleeding tendencies Platelet dysfunction Infection altered immune response

CKD Manifestations Cardiovascular Hypertension
Congestive heart failure Pericarditis Atherosclerotic vascular disease Cardiac dysrhythmias Respiratory Pulmonary edema Pleural effusions HTN volume & na retention CHF LVH atherosclerosis Pericarditis uremic issues  pericardial effusions  tampanode Atherosclerosis ---- inc tri  inc MI inc glucose  inc insulin  inc. plasma insulin  inc hepatic release of tryglycerides to serum Dysrhythmias inc K, dec. Ca, dec perfusion Pulm edema  volume ---- fluid in air sacs Pleural effusion  volume fluid in layers of tissues

CKD Manifestations GI tract Uremic fetor Anorexia, nausea, vomiting
GI bleeding Musculoskeletal Muscle cramps Soft tissue calcifications Weakness Renal Osteodystrophy GI- Uremic fetor - ammonia on breath GI bleed- irritation, platelet dysfunction, diarrhea d/t increase K Musculoskeletal- Related to calcium phosphorous imbalances

CKD Manifestations Psychologic Anxiety Depression Neurologic
Mood swings Impaired judgment Inability to concentrate and perform simple math functions Tremors, twitching, convulsions Peripheral Neuropathy Increase nitrogenous wastes Lyte imbalances Metabolic acidosis

CKD Manifestations Skin Pale, grayish-bronze color Dry scaly
Severe itching Bruise easily Uremic frost Calcium/Phos deposits Eyes Visual blurring Blindness Skin- Pale --- anemia Bronze – urinary pigments Brusing platelet abnormalities ca involved Uremic frost --- urea cystals on skin ---neuropathies here diluted vinegar & lanolin Eyes- Related to phos & glucose deposits

Treatment Options Conservative Therapy Hemodialysis
Peritoneal Dialysis Transplant Nothing

Conservative Treatment
GOALS: Detect & treat potentially reversible causes of renal failure Preserve existing renal function Treat manifestations Prevent complications Provide for comfort Heart failure, dehydration, infection, nephrotoxins, urinary tract obstructions, glomerulonephritis, renal artery stenosis

Conservative Treatment
Control Hyperkalemia Hypertension Hyperphosphatemia Hyperparthryoidism Anemia Hyperglycemia Dyslipidemia Hypothyroidism Nutrition : Describe a renal diet

Control Hyperkalemia – limit ex: citrus, meats, fish, avocado, beans, spinach Hypertension -- weight loss, dec. etoh, smoking, DASH diet, meds, fluids Hyperphosphatemia – meds, low phos diet – ex: milks & cheese Hyperparthryoidism -- deal with Calcium/Phos issue Anemia – procrit/epogen (could take 2-3 weeks to see a change in HH) Why don’t we transfuse these patients? Hyperglycemia – oral anti-diabetic meds, insulin, diet Dyslipidemia -- statins, keep LDL <100 & triglycerides <200 Hypothyroidism – hormone replacement Nutrition : NOW, describe a renal diet?

Renal Diet Fluids ? Avoid high protein diet Restrict:
sodium potassium phosphorous Consume enough calories, to maintain weight esp. if losing weight Fluids not usually restricted until on hemodialysis --- or if causes complications. All proteins are high in phosphorus – what to do? What about protein & phosphorus?

Patient Teaching

Dialysis Removal of soluble substances and water from the blood by diffusion through a semi-permeable membrane. Peritoneal Dialysis Hemodyalisis

Dialysis Osmosis Diffusion Ultrafiltration
What GFR value indicates need for hemodialysis? <15ml/min Uncontolled symptoms encephalopathies, inc K, neuropathies, pericarditis, HTN Osmosis- movement of particles through a semi-permeable membrane into a region of higher concentration in an attempt to reach equilibrium Diffusion movement of molecules across membrane from high  low Ultrafiltration separation of particles from suspension through a filter

Peritoneal Dialysis(PD)
12% dialysis in US is PD Types APD: Automated Peritoneal Dialysis (CCPD: Continuous cycling peritoneal dialysis) CAPD: Continuous ambulatory peritoneal dialysis IPD: Intermittent peritoneal dialysis

Phases of A Peritoneal Dialysis Exchange
Fill: fluid infused into peritoneal cavity Dwell: time fluid remains in peritoneal cavity Drain: time fluid drains from peritoneal cavity Fill minutes Dwell hours Drain – minutes Candidate? diligent in care, able to manipulate bag -- organized

PD Warm, sterile dialysate infused into peritoneal cavity through catheter. ml High concentration of glucose in dialysate Wastes & lytes diffuse into dialysate until equilibrium achieved Bag lowered, gravity drain Solution should be clear/straw colored Warm to prevent vasoconstriction Sterile to prevent infection If cramping, slow infusion Creates hypertonic solution, draws wastes in through osmosis and diffusion. Concentrations available: 1.5%, 2.5%, 4.25% If less out than in, check for kinks, change position, roll side to side If cloudy assume infection

CAPD Catheter into peritoneal cavity Exchanges 4 - 5 times per day
Treatment 24 hours; 7 days a week Solution remains in peritoneal cavity except during drain time Independent treatment May be done times/day if hospitalized

PD Teaching Asepsis Empty bladder first Monitor urine output
Monitor s/s of infection Monitor s/s of FVO Asepsis Empty bladder first Why? Monitor urine output Monitor s/s of infection What are they? Monitor s/s of FVO

Complications of Peritoneal Dialysis
Exit site infection Peritonitis Hernias Low Back problems Bleeding Pulmonary Complications Protein Loss Peritonitis -cloudy dialysate drainage , pain, tenderness, Infection catheter exit site Can turn into tunnel infections and abscess Hernias and Lower back problems due to increased intra-abdominal pressure Bleeding-blood in drainage may mean intraperitoneal bleed, may also be seen with menstuation, check H&H, BP Pulmomary- diaphragm displaced, pushes up on lungs, atalectasis, pneumonia, bronchitis. Elevate HOB, change position Protein – can lose large amts of protein esp with peritonitis (causes membrane to become more permeable). Can lead to malnutrition

Nursing considerations
Fluid & electrolyte balance must be maintained to prevent dehydration and/or fluid overload. Assess: Daily weights. Lung sounds. Presence of edema. Total I & O (including + and – PD fluid balances). Blood pressure. Other S&S of dehydration or fluid overload Assess the patient for fluid volume status and obtain orders from the MD to adjust dextrose in dialysate if needed

Nursing considerations
Assess for alterations in blood glucose levels in diabetics from the use of dextrose-based dialysate. Check visually for changes in the appearance of the effluent with each exchange. Reinforce exit site dressing for newly inserted PD catheters. Do not remove original dressing unless trained to do so. Be alert to tubing getting kinked or caught under patient, which will prevent infusion or draining of dialysate. If effluent is cloudy, Notify Nephrologist & initiate peritonitis protocol. Document clarity of each exchange on PD flow sheet.

Advantages of CAPD Independence for patient No needle sticks
Better blood pressure control Some diabetics add insulin to solution Fewer dietary restrictions protein loses in dialysate generally need increased potassium less fluid restrictions

Hemodialysis (HD) Dialysis Survival Rates (probability of survival)
approx: 1 year 80% 2 years 68% 5 years 35.8% 10 years 11% 5 year survival rate for transplant: 85.5%

History of HD Early animal experiments began 1913
1st human dialysis 1940’s by Dutch physician Willem Kolff Considered experimental through 1950’s, No intermittent blood access; for acute renal kidney injury only. 1940’s -1960’s Dr. Scribner developed Scribner Shunt 1960’s machines expensive, scarce, no funding “Death Panels” panels within community decided now who got to dialyze Using 50 feet of sausage casing wrapped around a wooden drum that rotated in a tank of water and salts, Kolff invented the first dialysis machine. In 1962, with help from a $100,000 foundation grant, Seattle's King County Medical Society opened an artificial kidney clinic at Swedish Hospital and established two committees that, together, would decide who received treatment. The first was a panel of kidney specialists that examined potential patients. Anyone older than 45 was excluded; so were teenagers and children; people with hypertension, vascular complications or diabetes; and those who were judged to be emotionally unprepared for the demanding regimen. Patients who passed this first vetting moved on to another panel, which decided their fate. It soon gained a nickname -- the "God committee." Born of an effort to be fair, the anonymous committee included a pastor, a lawyer, a union leader, a homemaker, two doctors and a businessman and based its selection on applicants' "social worth." Of the first 17 patients it saw, 10 were selected for dialysis. The remaining seven died. In the fall of 1962, Life magazine published a story about the "life and death committee." In Washington, D.C., the deputy surgeon general fired off a memo to the secretary of health, education and welfare, warning that "strong pressure for some federal action" from the public might ensue.

Hemodialysis Process Blood removed from patient into the extracorporeal circuit. Diffusion and ultrafiltration take place in the dialyzer. Cleaned blood returned to patient Diffusion movement of molecules across membrane from high  low Ultrafiltration separation of particles from suspension through a filter

Vascular Access Arterio-Venous shunt Arterio-venous fistula (AVF)
Arterio-venous Graft (AVG) Temporary Catheters

Arterio-Venous (AV) Fistula Primary Fistula
Patients artery and vein surgically anastomosed. Advantages patients own vein longevity low infection and thrombosis rates Disadvantages long time to mature, months “steal” syndrome requires needle sticks Who not a candidate? Drug abusers, HTN, PVD, DM uncontrolled NEED GOOD VEINS – pressure Steal syndrome – results from poorly constructed AV fistula --- pallor, pain, dec pulses (distal the site), necrosis

PTFE (Polytetrafluoroethylene) Graft
Synthetic “vessel” anastomosed into an artery and vein. Advantages for people with inadequate vessels can be used in 1-4 weeks prominent vessels Disadvantages clots easily “steal” syndrome more frequent requires needle sticks infection may necessitate removal of graft

Scribner Shunt External Advantage Disadvantages One end into artery
One end into vein Advantage Place at bedside Use immediately Disadvantages Infection Skin erosion Accidental separation Limits use of extremity

Vascular Access Complications
AV fistula with aneursym Steal syndrome

Temporary Catheters Dual lumen catheter placed into a central vein- subclavian, jugular or femoral. Advantages immediate use no needle sticks Disadvantages high incidence of infection subclavian vein stenosis poor flow-inadequate dialysis clotting restricts movement Subclavian should be last resort Good for 1-3 weeks subclavian & juglar 1 week femoral

Cuffed Tunneled Catheters
Dual lumen catheter with Dacron cuff surgically tunneled into subclavian, jugular or femoral vein. Advantages immediate use can be used for patients that can have no other permanent access no needle sticks Disadvantages high incidence of infection poor flows result in inadequate dialysis clotting Weeks  months

Care of Vascular Access (PTFE Graft or AV Fistula)
NO BP’s, needle sticks to arm with vascular access. This includes finger sticks. Place ID bands on other arm whenever possible. Palpate thrill and listen for bruit. Teach patient nothing constrictive. Listen bruit Feel thrill Circulation Constricting bands

Potential Complications of HD During dialysis
Fluid and electrolyte related Hypotension Cardiovascular Arrythmias Associated with the extracorporeal circuit exsanguination

Potential Complications of HD During dialysis
Neurologic Disequilibrium Syndrome & seizures Musculoskeletal Cramping Other fever & sepsis blood born diseases Disequilibrium syndrome: extracellular fluid changes, removed too fast from blood and not as fast from CSF INCREASED cerebral edema Nausea, Vomiting, Restlessness, Seizures Hep B, Hep C, CMV, HIV

Potential Complications of HD Between treatments
Hypertension/Hypotension Edema Pulmonary edema Hyperkalemia Bleeding Clotting of access

Potential Complications of HD Long term
Metabolic Hyperparathyroidism Diabetic complications Cardiovascular CHF AV access failure Cardiovascular disease Respiratory Pulmonary edema

Neuromuscular neuropathy Hematologic Anemia GI Bleeding Dermatologic calcium phosphorous deposits

Rheumatologic amyloid deposits Genitourinary infection sexual dysfunction Psychiatric depression *Infection blood borne pathogens What is most common cause of death among hemodialysis patients? CV --- MI & Stroke Infections

Continuous Renal Replacement Therapy (CRRT)
Used on hemodynamically unstable patients Slower blood flow rates than HD Uses double lumen catheter CVVHD-Continuous venovenous hemodialysis Solute loss via convection/diffusion CVVH-Continuous venovenous hemofiltration Solute loss via convection (more like mammalian filtration) Replacement fluid via hemodilution

CVVH/CVVHD When is it indicated? AKI
patient usually has low blood pressure or other contraindications to hemodialysis Not a treatment for acute hyperkalemia slow continuous process sessions usually last between 12 to 24hrs usually performed daily in the ICU

Dietary Restrictions on Hemodialysis
Fluid restrictions Phosphorous restrictions Potassium restrictions Sodium restrictions Protein to maintain nitrogen balance too high - waste products too low - decreased albumin, increased mortality Calories to maintain or reach ideal weight 1000cc ---- or hr urine output High K foods citris OJ, tomatoes, bananas, greens

Medications Vitamins - water soluble
Phosphate binder ---- Give with_____ Phoslo (calcium acetate) Renagel (sevelamere hydrochloride) Caltrate (calcium carbonate) Amphojel (aluminum hydroxide) Iron Supplements – don’t give with phosphate binder or calcium Anti-hypertensives When do we give these? Give with FOOD! Calcium may inhibit absorption of iron

Medications Erythropoietin Calcium Supplements Activated Vitamin D3
Between meals, not with ______ Activated Vitamin D3 Antibiotics hold dose prior to dialysis Why? Iron Hold antibiotic- will be dialyzed out

Medications Many drugs or their metabolites are excreted by the kidney
Dosages many change when used in kidney failure patients Why? Dialyzability many removed by dialysis varies between HD and PD NSAIDS – not metabolized by kidney, but through liver…. However NSAIDS inhibit an enzyme that regulates renal blood flow – These drugs reduce renal blood blow – worsen renal function Insulin –metabolized through kidney – may need lower dose to prevent hypoglycemia

Patient Education Alleviate fear Dialysis process
Fistula/catheter care Diet and fluid restrictions Medication Diabetic teaching Ethics-time runs out

Transplantation Treatment not cure

Transplantation Only 4% ESRD get transplant 75,000 on list in 2010
17,500 received kidney Most die while on wait list 1 year survival rate 90% for deceased donor 95% for live donor

Advantages Disadvantages
Restoration of “normal” renal function Freedom from dialysis Return to “normal” life Reverses pathophysiological changes related to Renal Failure Less expensive than dialysis after 1st year Life long medications Multiple side effects from medication Increased risk of tumor Increased risk of infection Major surgery

Exclusion for Transplant
Morbidly obese or Current smoker CV disease and DM considered high risk Malignancies that have metastasized untreated cardiac disease chronic respiratory failure extensive vascular disease chronic infection unresolved psych disorder (non-compliance with prescribed medications, alcoholism, drug addiction) HIV used to be is not anymore, same survival rate and non-HIV, Hep B or C not contraindication

Criteria for Living Donors
Psychiatric evaluation Anesthesia evaluation Medical Evaluation Free from diseases listed under deceased donor criteria Kidney function Cross-matches done at time of evaluation and 1 week prior to procedure Radiological evaluation ethics and organ transplant

Criteria for Deceased Donors
Usually irreversible brain injury MVA, gunshot wounds, hemorrhage, anoxic brain injury from MI Must have effective cardiac function Must be supported by ventilator to preserve organs Age 2-70 No IV drug use, HTN, DM, Malignancies, Sepsis, disease Permission from legal next of kin & pronouncement of death made by MD

Nurses Role in Event of Potential Donation
Notify TOSA of possible organ donation Identify possible donors Make referral in timely manner Do not discuss organ donation with family Offer support to families after referral is made & donation coordinator has met with family TOSA- Texas Organ Sharing Alliance

Care of the Recipient Major surgery with general anesthesia
Assessment of renal function Assessment of fluid and electrolyte balance Prevention of infection Prevention and management of rejection

Monitoring Transplant Function
ATN? (acute tubular necrosis) Urine output >100 <500 ml/hr (initially) Labs Fluid Balance Ultrasound Renal scans Renal biopsy Hospital stay days ATN --- may resolve --- may need dialysis until it resolves death of tubule cells Labs: BUN, creatinine, creatinine clearance

Fluid & Electrolyte Balance
Accurate I & O CRITICAL TO AVOID DEHYDRATION Output normal - >100 <500 ml/hr, could be 1-2 L/hr Potential for volume overload/deficit Daily weights Postassium (K+)___________ Sodium (Na) _____________ Blood sugar _____________ Hyper/hyponkaemia Hyponatremia Hyperglycemia

Prevention of Infection
Major complication of transplantation due to immunosuppression What do you teach? HANDWASHING Limit Crowds, Kids, and visitors

Rejection Hyperacute preformed antibodies to donor antigen
function ceases within 24 hours Rx = removal Accelerated same as hyperacute but slower, 1st week to month

Rejection Acute – First 6 months 50% experience
must differentiate between rejection and cyclosporine toxicity Rx= Usually reversible with additional immunosuppressants- put at higher risk for infection Weight gain Tenderness at the site Fever Decreased urine output HTN

Rejection Chronic gradual process over months or years Irreversible
Repeated rejection episodes that have not been completely resolved with treatment Rx = return to dialysis or re-transplantation Regular lab work is very important to follow the health of the new transplant as clinical symptoms often do not occur with early transplant rejection. For example, kidney transplant patients are asked to undergo percutaneous ultrasound-guided kidney biopsies at both three months and one year to evaluate the status of their kidney transplant. At these same time points, blood is drawn to monitor for the development of harmful antibodies against the transplant, which can affect the long-term survival of the transplanted kidney. When found early, the transplant team is better able to successfully make plans to prevent irreversible injury to the transplanted kidney. Source: Transplant Recovery With an Easier Pill to Swallow | University of Maryland Medical Center University of Maryland Medical Center Follow on Twitter | MedCenter on Facebook

Immunosuppressant Drugs
Need to balance suppression with maintenance of adequate defense Side effects- Infection Malignancies Toxicity Require frequent monitoring Lowest dose to get response will least side effects

2 categories: Induction agents Powerful antirejection medications used at the time of transplant Maintenance agents Antirejection medications used for the long term. Broadly, the immunosuppressants can be classified into 2 categories: Induction agents: Powerful antirejection medications used at the time of transplant Maintenance agents: Antirejection medications used for the long term.

Maintenance agents -4 classes 1. Calcineurin Inhibitors: Tacrolimus,Cyclosporine 2. Antiproliferative agents:Mycophenolate Mofetil 3. mTOR inhibitor: Sirolimus 4. Steroids: Prednisone Used in combination Triple therapy Wean off steroids or avoid use The maintenance agents are generally 4 classes of drugs Calcineurin Inhibitors: Tacrolimus and Cyclosporine Antiproliferative agents: Mycophenolate Mofetil, Mycophenolate Sodium and Azathioprine mTOR inhibitor: Sirolimus Steroids: Prednisone Although there are multiple methods of mixing and matching the above drugs, the most common combination employed by the transplant centers is Tacrolimus, Mycophenolate Mofetil and Prednisone

Cyclosporine Azathioprine (Imuran) Prednisone OKT3 Atgam Cytoxan - in place of Imuran less toxic FK x more potent than Cyclosporine Prograf CellCept

many medications and food and supplements can alter blood levels Grapefruit juice St. John's Wort Erythromycin anti TB medications antiseizure medications common blood pressure medications (cardizem or diltiazem, and Verapamil

Patient Education Signs of infection Prevention of infection
Signs of rejection ____________ Medications _____________ Signs of infection Prevention of infection Signs of rejection decreased urine output increased weight gain --- 2lbs in 24 hrs tenderness over kidney fever > 100 degrees F Medications time, dose, side effects

Monitor the site of the shunt for infection
The client with chronic renal failure returns to the nursing unit following a hemodialysis treatment. On assessment the nurse notes that the client’s temperature is Which of the following is the most appropriate nursing action? Encourage fluids Notify the physician Monitor the site of the shunt for infection Continue to monitor vital signs The client may have an elevated temperature following dialysis because the dialysis machine warms the blood slightly. If the temperature is elevated excessively and remains elevated, sepsis would be suspected and a blood sample would be obtained as prescribed for culture and sensitivity purposes

Follow a high potassium diet Strictly follow the hemodialysis schedule
A client is diagnosed with chronic renal failure and told she must start hemodialysis. Client teaching would include which of the following instructions? Follow a high potassium diet Strictly follow the hemodialysis schedule There will be a few changes in your lifestyle. Use alcohol on the skin and clean it due to integumentary changes. To prevent life-threatening complications, the client must follow the dialysis schedule. Alcohol would further dry the client’s skin more than it already is. The client should follow a low-potassium diet because potassium levels increase in chronic renal failure. The client should know hemodialysis is time-consuming and will definitely cause a change in current lifestyle

Change the client’s position. Call the physician.
A client is undergoing peritoneal dialysis. The dialysate dwell time is completed, and the dwell clamp is opened to allow the dialysate to drain. The nurse notes that the drainage has stopped and only 500 ml has drained; the amount the dialysate instilled was 1,500 ml. Which of the following interventions would be done first? Change the client’s position. Call the physician. Check the catheter for kinks or obstruction. Clamp the catheter and instill more dialysate at the next exchange time. The first intervention should be to check for kinks and obstructions because that could be preventing drainage. After checking for kinks, have the client change position to promote drainage. Don’t give the next scheduled exchange until the dialysate is drained because abdominal distention will occur, unless the output is within parameters set by the physician. If unable to get more output despite checking for kinks and changing the client’s position, the nurse should then call the physician to determine the proper intervention.

Elevate the foot of the bed Restrict the client’s fluids
A client receiving hemodialysis treatment arrives at the hospital with a blood pressure of 200/100, a heart rate of 110, and a respiratory rate of 36. Oxygen saturation on room air is 89%. He complains of shortness of breath, and +2 pedal edema is noted. His last hemodialysis treatment was yesterday. Which of the following interventions should be done first? Administer oxygen Elevate the foot of the bed Restrict the client’s fluids Prepare the client for hemodialysis. 1. Airway and oxygenation are always the first priority. Because the client is complaining of shortness of breath and his oxygen saturation is only 89%, the nurse needs to try to increase his levels by administering oxygen. The client is in pulmonary edema from fluid overload and will need to be dialyzed and have his fluids restricted, but the first interventions should be aimed at the immediate treatment of hypoxia. The foot of the bed may be elevated to reduce edema, but this isn’t the priority.

Chronic Kidney Disease

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