renal Flashcards
risk factors associated with kidney disorders
Low birth weight which can lead to reduced nephron endowment and lower renal volume Chemical or environmental toxin exposure Contact sports/trauma Diabetes mellitus Family history of renal disease Frequent urinary tract infections Heart failure High-sodium diet Hypertension Medications Race, ethnicity
aging and kidneys
amount of kidney tissue decreases and kidney function diminishes
number of nephrons decrease
blood vessels supplying the kidneys can become hardened causing the kidneys to filter blood more slowly
aging and bladder
bladder wall changes = elastic tissue becomes stiffer and the bladder becomes less stretchy, bladder cannot hold as much urine as before
the bladder muscles weaken
the urethra can become partially or totally blocked
chronic kidney disease (CKD)
The progressive loss and ongoing deterioration in kidney function
Characterized by a glomerular filtration rate (GFR) of less than 60 mL/minute for a period of 3 months or longer
Progression based on degree of proteinuria
It is irreversible and results in uremia or end-stage kidney disease (ESKD)
CKD requires dialysis or kidney transplantation to maintain life
ckd associated labs and clinical manifestations
Creatinine and Urea
As glomerular filtration rate (GFR) declines, the plasma creatinine increases by a reciprocal amount to maintain a constant rate of excretion.
GFR goes down and creatinine and urea go up
Fluid and electrolyte balance
When the GFR decreases to 25% there is an obligatory loss of 20 to 40 mEq of sodium per day with osmotic loss of water.
Ultimately the kidney loses its ability to regulate sodium and water balance causing retention of sodium and water = edema and hypertension.
Total body potassium can increase to life-threatening levels and must be controlled by dialysis
Calcium, Phosphate, and Bone
Changes begin when the GFR decreases to 25% or less
Hypocalcemia is accelerated by impaired renal synthesis
Renal phosphate excretion decreased and the increased serum phosphate binds calcium, further contributing to hypocalcemia.
Acidosis contributes to a negative calcium balance
Decreased serum calcium levels stimulate parathyroid hormone secretion to mobilize calcium from bone.
Ultimately increases risk of fractures
Protein and Albumin
Monitor protein and albumin excretion in patients with chronic renal failure
Repeated measurement of the urine protein- or albumin- to-creatinine ratio every few months, using a first-morning void whenever feasible
ckd neurological manifestations
Asterixis (tremor of the hand when the wrist is extended)
Ataxia (alteration in gait)
Coma
Inability to concentrate or decreased attention span
Myoclonus (involuntary twitching of a muscle or a group of muscles)
Paresthesias (sensation of tingling, tickling, burning)
Seizures
Slurred speech
ckd cardiovascular manifestations
Cardiac tamponade (cardiac filling is impeded by an external force) Cardiomyopathy Heart failure Stroke Pericarditis Hypertension Pericardial effusion Peripheral edema Dyslipidemia Ischemic Heart Disease Sudden cardiac death
ckd respiratory manifestations
Crackles because of pulmonary edema
Deep sighing, yawning
Depressed cough reflex
Kussmaul’s respirations in response to Metabolic Acidosis
Pulmonary hypertension due to LV dysfunction or uremic-associated vascular changes
Pleural effusion (result of extra volume, tissues become leaky)
Shortness of breath in response to pulmonary edema, pulm HTN
Tachypnea- required to improve gas exchange
Unpleasant “uremic” breath odour
ckd GI manifestations
Anorexia Changes in taste acuity and sensation Constipation Uremic gastroenteritis Nausea Vomiting GI bleeding Diarrhea
ckd hematologic manifestations
Noromochromic-normocytic anemia Impaired platelet function Decreased platelet numbers and altered vascular endothelium promote increased bleeding Hypercoagulability Alterations in thrombin and other clotting factors contribute to hypercoagulability what conditions are these patients at risk for if they are hypercoagulable??? Lethargy Dizziness Low hematocrit
ckd immune system
Suppressed immune system: Chemotaxis Phagocytosis Antibody production Cell-mediated immune responses Malnutrition Metabolic acidosis Hyperglycemia ^ increase immunosuppression Deficient responses to vaccinations Increased risk for infection Virus associated cancers (EBV, HPV, Hep B and C)
ckd integumentary manifestations
Uremic frost Decreased skin turgor Dry skin Ecchymosis Pruritus Purpura Yellow-gray pallor
ckd urinary manifestations
Diluted, straw-colored appearance Hematuria Oliguria (later) Polyuria (early) Proteinuria
ckd msk manifestations
Bone pain
Muscle weakness and cramping
Pathological fractures
ckd reproductive manifestations
Decreased fertility
Decreased libido
Impotence
Infrequent or absent menses
function of hemodialysis
Cleanses the blood of accumulated waste products
Removes the by-products of protein metabolism such as ammonia, urea, creatinine, uric acid from the blood
Removes excess body fluids
Corrects electrolyte levels in the body
Cannot replace hormones
peritoneal dialysis
Diffusion of fluid and solutes from the bloodstream through the peritoneum into the dialysate solution – peritoneum acts as natural filter
The peritoneal cavity is rich in capillaries –provides easy access to blood supply
complications during hemodialysis
Disequilibrium syndrome–removal of urea from blood resulting in greater concentration in brain reverse osmosis occurs and water moves into brain cells cerebral edema possible headache, nausea, vomiting, confusion, decreased level of consciousness, and convulsions
Hypotension- related to rate and amount of fluid removed or antihypertensive medications
Intradialytic hypertension- Increase in SBP during or immediately following dialysis
Transfusion reactions
Dysrhythmias—due to hypotension, fluid overload, or rapid removal of potassium
Sepsis
Shock
Psychological problems
complications during peritoneal dialysis
Peritonitis -- infection Abdominal pain Bladder or bowel perforation Insufficient outflow (full colon) Leakage around the catheter site Blockage of catheter
kidney transplants
A human kidney from a compatible donor is placed into the iliac fossa of a recipient and the anastomosis of its ureter to the bladder of the recipient.
Is performed for irreversible kidney failure; specific criteria are established for eligibility for a transplant.
kidney transplant living donor
Most desirable source of kidneys for transplantation
Extensive screening process
Must have 2 working kidneys
Emotional well-being of the donor is determined.
Complete understanding of the donation process and outcome
kidney transplant cadaver donor
Must meet the institution’s criteria of brain death
Usually need to be younger than 70 years
Have normal renal function
No malignant disease outside the CNS can be present
No generalized infection or communicable disease can be present
No renal trauma can be present
acute rejection of kidney transplant
Most common type
Within 6 weeks postoperatively
Potentially reversible with increased immunosuppression and if treated early; high doses of corticosteriods
Fever, anuria, oliguria, graft swelling and tenderness, increased serum creatinine, hypertension, weight gain, graft swelling, tenderness
Appearance of protein, lymphocytes, and renal tubular cells in urine sediment
chronic rejection of kidney transplant
Occurs slowly months to years after transplant and mimics CKD
Interventions-immunosuppressive medications and re-transplantation if necessary.
Proteinuria with or without hypertension, nephrotic syndrome
clinical signs of kidney transplant rejection
Temperature > 37.7 °C
Pain or tenderness over the grafted kidney
2-3 lb weight gain in 24 hours
Edema
Hypertension
Malaise
Elevated blood urea nitrogen and serum creatinine levels
Decreased creatinine clearance
Elevated white blood cell count
Rejection indicated by ultrasound or biopsy
