Chronic Kidney Disease Flashcards
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Defined as a progressive, irreversible kidney injury & function does NOT recover
Chronic Kidney Disease
When kidney fxn becomes too poor to sustain life, it becomes end stage renal/kidney disease (ESRD or ESKD)
Described in 5 stages (stage 1 is @ risk & has normal kidney function as opposed to stage 2 where actual CKD begins & GFR is worse)
GFR
Kidney Failure: 0-15
Kidney Disease: 15-60
Normal: 60-120
Stage ?
<15 mL/min
- End-stage kidney disease (ESKD)
Implement RRT or kidney transplantation
Stage 5
Stage ?
30-59 mL/min
- Moderate CKD
Implement strategies to slow disease progression
Stage 3
Stage ?
60-89 mL/min
- Mild CKD; reduced kidney function; lab values and other findings (e.g., structural change) point to kidney disease
Focus on reduction of risk factors
Stage 2
Stage ?
15-29 mL/min
- Severe CKD
Manage complications
Discuss patient preferences & values
Educate about options & prepare for RRT
Stage 4
Stage ?
> 90 mL/min
- @ risk; normal kidney function but urine findings or structural abnormalities or genetic trait point to kidney disease
Screen for risk factors & manage care to reduce risk
> Uncontrolled HTN
> DM
> Chronic kidney or UTI
> Fhx of genetic kidney dz
> Exposure to nephrotoxic substances
Stage 1
CKD
- Up to 80% of GFR may be lost w/few changes in functioning of body
- Remaining nephrons hypertrophy to compensate
- End result is a systemic dz involving every organ
What are 2 of the leading causes of ESRD?
Diabetes (1/2 cases); HTN (1/3)
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Is azotemia w/clinical sx’s
- GFR </= to 10 mL/min
Uremia
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Is the buildup of nitrogen-based wastes in the blood
Azotemia
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Is a condition that incorporates all s/s seen in various systems throughout the body
Uremic syndrome
Urinary System
- Oliguria (occurs as CKD worsens)
? (urine output <40 mL over 24 hrs)
Anuria
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Results from inability of kidneys to concentrate urine
- Occurs most often at night
- SG fixed around 1.010
Polyuria
Metabolic Disturbances
- Waste product accumulation
As GFR ↓, BUN ↑ & serum creatinine lvls ↑
> BUN ↑
- Not only by kidney failure but by protein intake, fever, corticosteroids, & catabolism
- N/V, lethargy, fatigue, impaired thought processes, & headache may occur
- Altered carbohydrate metabolism
> Caused by impaired glucose use
> From cellular insensitivity to the normal action of insulin
- Defective carbohydrate metabolism
> Pts w/diabetes who become uremic may require less insulin than before onset of CKD
> Insulin dependent on kidneys for excretion
> HYPOglycemia becomes a concern
- Elevated triglycerides
> Hyperinsulinemia stimulates hepatic production of triglycerides
> Altered lipid metabolism
- ↓ lvls of enzyme lipoprotein lipase
- Important in breakdown of lipoproteins
! Most pts w/CKD die from cardiovascular disease
Acid-Base Imbalances
- Potassium
> Hyperkalemia - Most serious electrolyte disorder in kidney dz
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Fatal dysrhythmias = K levels 7-8 or >
! Tall, tented/peaked T waves
- Hyperkalemia d/t
> Dec excretion of K by kidneys
> Breakdown of cellular protein
> Bleeding
> Metabolic acidosis
Sodium
> May be normal or low
B/c of impaired excretion, sodium is retained = water is retained
Edema, HTN, CHF
! Sodium intake restricted indiv but ~2 g/day
- Calcium & phosphate alterations
- Mg alterations
> Absence of reflexes
> Dec mental status
> Cardiac dysrhythmias
> Hypotension
> Resp failure
- P is excreted by the kidneys; RF leads to retention
- Rx’s are given PO to combine w/P in GI tract for excretion through intestines
- aluminum hydroxide
- calcium carbonate (Tums)
- calcium acetate (Phos-Ex) [give w/food to promote P binding to rx]
- As P lvls inc, body tries to keep normal P:Ca ratio by taking Ca from bones
> bone demineralization & path fx’s - Hypocalcemia d/t inability of dz’d kidney to convert Vit D to active form
- Treatment: active forms of Vit D = calcitrol & DHT
Metabolic Acidosis
- From
> Inability of kidneys to excrete acid load (primary ammonia)
> Defective reabsorption/regeneration of bicarbonate
S&S
> Anorexia, weakness, lethargy, may become stuporus or comatose
> Kussmaul’s respirations, severe CNS depression causing shock, death
Treatment
- Promote output
- Maintain pulmonary function to allow some excretion (carbonic acid) via lungs (C&DB, avoid URI’s)
- Na bicarbonate given PO/IV to buffer acids
- Bistro (alkalinizing agent; chemicals in med convert to bicarbonate)
Hematologic System
- Anemia
> D/t ↓ production of erythropoietin (from ↓ in functioning of renal tubular cells)
- Bleeding tendencies
> Defect in platelet function (Factor III)
