CKD Flashcards
3 Primary Kidney Functions
- Filtration of blood
- Regulation of fluid and electrolytes & acid base balance
- Excretion of metabolic waste products
3 Secondary Kidney Functions
To regulate:
1. BP (RAAS system)
2. Bone density
3. Erythropoiesis (RBC production)
What does the RAAS system stand for? What 3 factors regulate BP from the RAAS system?
Renin-angiotensin-aldosterone system
Regulates BP by increasing salt reabsorption, water reabsorption, and vascular tone
How does the RAAS system work?
Renin splits angiotensinogen into angiotensin I which is split by ACE (angiotensin-converting enzymes) in the lungs and kidney into angiotensin II which causes vasoconstriction and the release of aldosterone and ADH in the adrenal gland which causes salt retention (more water in body increases BV and BP) and K+ excretion in urine
CKD is defined by the presence of:
either kidney damage or GFR < 60 mL/min/1.73 m2 for 3 months or longer
Description of stage 5 CKD
End-stage Renal Disease (ESRD)
Kidney failure, GFR <15 (or dialysis), action is renal replacement therapy (if uremia present and Pt desires treatment)
Normal GFR
125 mL/min
Leading causes of ESRD
DM (38%), Renal vascular disease (50%)
2 ESRD tx options
Renal Replacement Therapy (either HD or PD)
Transplant
2 General Clinical manifestation of CKD
- Retained Urea, creatinine, phenols, hormones, electrolytes, and water
- Uremia (when GFR<10, syndrome that incorporates all S&S seen in various systems throughout body due to waste product retention and excess fluid)
Psychological S&S of CKD
anxiety, depression (changes in body image with devices)
CV S&S of CKD!!
HTN (fluid retention)
HF
L ventricular hypertrophy (has to work harder)
Peripheral edema
Dysrhythmias
Uremic pericarditis
CAD
Peripheral artery disease
GI S&S of CKD
Anorexia
NV (increased urea circulating)
GI bleeding
Gastritis
Inflammation of GI mucosa (increased urea circulating)
Uremic fetor (urine breath odor)
Constipation (limited fluid intake)
Endocrine/Reproductive S&S of CKD
Hyperparathyroidism
Thyroid abnormalities
Amenorrhea
Erectile dysfunction
Infertility
Decreased libido
Low sperm counts
Metabolic S&S of CKD
Carbohydrate intolerance: Insulin resistance d/t insulin antagonists (ex. urea, a waste product) circulating = hyperglycemia and a need for less insulin because it’s already circulating but the waste prevents it from acting. Insulin is dependent on kidneys for excretion.
Hyperlipidemia: hyperinsulinemia stimulates triglyceride production in liver
Waste product accumulation - Kidney can’t filter out wastes, GFR ↓ and BUN ↑ and serum creatinine levels ↑
Hematological S&S of CKD
Anemia: decreased erythropoietin production (what stimulates RBC production in bone marrow), causes fatigue and SOB (increased O2 demand). Angina is secondary to anemia in a predisposed Pt (like a smoker).
Bleeding: defect platelet function, usually corrected with PD or HD
Infection: changed leukocyte function, diminished inflammatory response
Neurological S&S of CKD
fatigue, headache, sleep disturbances, encephalopathy, restless legs syndrome, muscle twitching, apathy, decreased ability to concentrate, peripheral neuropathy
Because of increased nitrogenous waste, electrolyte imbalance, metabolic acidosis, axonal atrophy, and demyelination of nerve fibers. Most change once on dialysis
Ocular S&S of CKD
HTN retinopathy
Respiratory S&S of CKD
Kussmaul’s resps
Dyspnea
Pulmonary edema (fluid overload)
Uremic pleuritis
Uremic pneumonitis
Pleural effusion
Predisposition to respiratory infection
Integumentary S&S of CKD
Pruritus (most common - d/t increased serum urea)
Ecchymosis
Dry, scaly skin
Uremic frost
Musculo-skeletal S&S of CKD
Osteomalacia (bone demineralization)
Osteitis fibrosa (↑ PTH)
CKD-MBD (CKD mineral and bone disorder)
Vascular and soft tissue calcification (↑ serum Ca, ↑ serum phosphate)
Decreased kidney function → less conversion of activated Vit D which is essential for Ca absorption in GI → Hypocalcemia → causes PTH excretion → stimulates bone demineralization → releases phosphate → hyperphosphatemia decreases Ca serum → causes PTH excretion → parathyroid gland hypertrophy
Peripheral neuropathy S&S of CKD
paresthesia, restless legs syndrome
GU S&S of CKD
Polyuria - in early stages due to inability of kidneys to concentrate urine. Often nocturia. 1.010 specific gravity.
Oliguria - in worsening stages. < 400-500 mL/day
Anuria - urine output < 40mL/day
Electrolyte/Acid-Base imbalances
K: Hyperkalemia - most serious electrolyte disorder in kidney disease, can cause fatal dysrhythmias when K+ > 7-8 mmol/L in blood. Kidneys not able to excrete K+ into urine.
Na+ : Dilutional hyponatremia - retained longer with water causing edema, HTN, CHF
Ca and phosphate (PO₄³⁻) alterations
Mg alterations
Metabolic acidosis: HCO3 can’t be reabsorbed (plasma bicarb falls to 16-20 mmol/L), makes body less basic and more acidic, as well acidic ammonia can not be excreted
When to treat K+ imbalance
When K+ > 3.5 mmol/L
What can become deficient in HD?
Folic acid - related to RBC maturation, removed by dialysis so replaced supplementally
Why morbidity and mortality from CVD high in Pts with CKD
Worsened by sodium retention, increased extracellular volume, vascular changes from long standing HTN and accelerated atherosclerosis from elevated triglyceride levels are responsible for many of the CV complications that end up ensuing pts with CKD
Diagnostic studies for CKD
Urinalysis dipstick evaluation
Albumin-creatinine ratio (1st AM void)
Renal ultrasound
Xray KUB (kidneys, ureters, bladder)
CT KUB
Renal biops
What is the earliest marker of kidney damage
Proteinuria (albumin)
What patients are at high risk of CKD that should be routinely screened for proteinuria?
DM
HTN
Vascular diseases
Autoimmune diseases
GFRs
Edema
Normal urinalysis
clear, light yellow/amber
1.005-1.03 specific gravity (concentration of solutes)
pH - 4.6-8
No protein, RBC, glucose, ketones, nitrites, leukocyte esterase, casts, and bilirubin (product of RBC breakdown removed by liver into bile)
May see RBCs in pts menstruating, kidney stones, and UTI
What is BUN
Measures urea levels in the blood, elevated if excretion is insufficient
Creatinine
nitrogenous waste produce from muscle metabolism, elevated if excretion is insufficient
Creatinine clearance
- commonly used to assess GFR, determines how efficiently kidneys clear creatinine from blood
GFR
how fast blood is filtered through the glomerulus
CP7
Channel of 7 blood tests
1. Na
2. K+
3. Creatinine
4. BUN
5. eGFR
6. Glucose
7. Cl-
Management of CKD
Correcting ECF volume overload
Nutrition
Erythropoietin therapy
Ca supplementation, phosphate binders, HTN meds, lowering K+
Adjusting drug dosages to degree of renal function
Hyperkalemia drug therapy
C BIG K+ D(rop)
C - Ca gluconate - stabilize myocardium
B - B2-adrenergic agonists (shift K+ into cells)
I - IV insulin (shift K+ into cells)
G - ^ with IV Glucose to manage hypoglycemia
K - Kayexalate (commonly used in stage 4, laxative action to exchange K and Na in bowel)
D - diuretics or dialysis
HTN drug therapy
Thiazide or loop diuretics, CCB,
Non-DM: ACE inhibitors, ARB (angiotensin II receptor blocker) agents
Target BP in CKD pts should be < 140/90 and 130/80 in DM pts
CKD-MBD drug therapy
Phosphate restriction < 1000mg/day
Phosphate binders (Ca carbonate binds phosphate in bowel and excretes in stool, Sevelamer hydrochloride lowers cholesterol and LDLs)
Vit D supplements
If med intervention does not help bone breakdown, parathyroidectomy may occur
Anemia therapy
Erythropoiesis-stimulating agents (ESA) IV or SC
Iron supplements
Folic acid supplements (needed for RBC formation)
Avoid blood transfusions
Drug toxicity is commonly produced by:
digoxin, PO glycemic agents, antibiotics, opioids, NSAIDs
