CKD Flashcards
CKD: K+ status
Hyperkalemia:
• Due to difficulty excreting K+
• Not occur until GFR <10 ml/min because remaining nephrons increase K+ excretion (likely due to increased aldosterone)
• Multifactorial: CKD + increased intake + drug interactions
• Mechanisms that increase K+ in CKD:
• Increased intake: K+ supplements (pills, “no-salt”)
• Decreased excretion: ACE-I’s, ARB’s
• ECF shift: beta blockers, uncontrolled diabetes (lack of insulin), acidosis (K+/H+ exchange)
CKD: Acid base balance
o Metabolic acidosis due to impaired H+ handling
• Can be gapped or non-gapped
- As function declines = less able to make glutamine → NH3 for H+ excretion (normally, NH3 acts as H+ sink to rid body of H+)
- Free H+ diffuses back into body → non-anion gap acidosis
- As disease progresses = retain uremic toxins → gapped acidosis
- With acidosis: bone starts to act as buffer → bone disease
- Treat: NaHCO3 to keep serum HCO3 >20
CKD: Na+ and water status
o ECF Na+ and hypervolemia (peripheral and pulmonary edema)
• With CKD = loss of Na+ handling flexibility
• Ex: As decrease GFR:
• More predisposed to ECF sodium overload with ECF Na+ excess
• More predisposed to hypotension with ECF Na+ decrease
• With CKD = loss of water handling flexibility
• Ex: as decrease GFR
• More predisposed to hyponatremia with free water excess
• More predisposed to hypernatremai with free water deficit
CKD: cardiovascular effects
o Leading cause of death for CKD patients
o CKD associated with increased risk of LV hypertrophy, MI, arrhythmias, CHF, and over increased mortality
HT
• Both pressor and volume related
• Thus: respond to both vasodilators and diuretics/Na+ restriction
• As kidney function declines to ESRD = volume dependent HT becomes more important
• Often with dialysis = bring patients down to dry weight, able to remove anti-hypertensive agents
Increased coronary artery disease
• 30-50% ESRD patients have inflammation: increased CRP (primary marker for increased CV mortality on dialysis) & IL-6, decreased albumin
• Secondary hyperparathyroidism (due to hypocalcemia) → metastatic calcification of coronary arteries = increased risk CVD
o Decreased cardiac relaxation “diastolic dysfunction”
o Pericarditis = “uremic pericarditis”
CKD: endocrine effects
Secondary hyperparathyroidism
• Due to decreased Vit D & increased serum PO4 = leads to decreased serum Ca2+
• Results: Renal osteodystrophy (dynamic) or Osteitis fibrosa cystica (adynamic and low-turnover bone disease)
Sexual dysfunction
• Impotence
• Failure to conceive or carry to term
Decreased insulin requirements in diabetics (due to decreased metabolism by kidney) o Hyperlipidemia (type IVb = hypertriglyceridemia)
CKD: GI effects
o Nausea and vomiting = often due to gastritis
o Anorexia
o Increased incidence of pancreatitis
CKD: Hematologic effects
Anemia • HCT starts to decrease when GFR <60 ml/min (stage 3) • Primary cause: decreased erythropoietin production Other causes: Bone marrow resistance: o Iron deficiency o Infection or inflammation o Renal osteodystrophy o Aluminum toxicity o Folate deficiency o Malnutrition o Uremia Decreased RBC lifespan (from 120 → 60-90 days)
Platelet dysfunction → increased bleeding risk
• Likely from defect in GPIIb/IIIa protein (binds vWF and fibrinogen) → lack of adhesion
Cause in CKD may be due to:
• Retention of uremic toxins
• Anemia (rheologic factors)
• Increased NO
WBC dysfunction → increased risk of infections
• Granulocytes: defects in chemotaxis, adherence, phagocytosis, and ROS production
• Lymphocytes: decreased immunization responses, attenuation of autoimmune diseases, diminished delayed hypersensitivity
CKD: neurologic effects
Encephalopathy
• Confusion, lethargy, tremors, delirium, seizures
• Nonfocal neurlogic exam
• Asterixis: “flapping” of hands = loose ability to hold hands out
• Pathogenesis unknown (related to uremic toxin retention and increased PTH)
• Depends on severity AND speed of onset (so more common in AKI)
• Generally a late finding in uremia
• Treated with aggressive dialysis
Peripheral neuropathy
• Secondary to retention of uremic toxins
• Mixed sensory/motor neuropathy:
• Sensory: “burning foot”; difficult to distinguish from diabetic neuropathy
• “Restless legs” in 15-40% dialysis patients
• Motor: late, less common
• Treated with more aggressive dialysis and medications
CKD: Skin effects
Pruritis
• Calcium-phosphate deposition
• Uremia
o Porphyria cutanea tarda (bullous lesions in sun exposed areas)
o Nephrogenci systemic fibrosis (irreversible)
o Calciphylaxis (ulcers on skin from blood vessel calcification)
Describe the therapies for these abnormalities based on the pathophysiology of CKD
Acidosis:
o Oral sodium bicarbonate
Secondary hyperparathyroidism:
o Oral 1,25-dihyroxy Vit D, phosphate binders, low phosphorus diet
Anemia: o Adequate iron stores (oral iron) o Treat renal osteodystrophy o Good nutrition o Treat infections o Recombinant ESA’s (Erythrocyte stimulating agents like erythropoietin, darbepoetin)
Fluid overload:
o Diuretics, sodium restriction
HT:
o Antihypertensives (vasodilators, diuretics, ACE-I’s), sodium restriction
o Goal <130/80
Hyperkalemia:
o Removal of appropriate medications, K+ restriction
Hyperlipidemia:
o Anti-lipid medications (statins), diet control
Uremic platelet dysfunction: o DDAVP (synthetic vasopressin/ADH) = subcutaneous, intranasally • Before surgical procedures o Cryoprecipitate o Conjugated estrogens o Dialysis
WBC dysfunction:
o Need 4 (instead of 3) Hep B immunizations for proper immunity rates
o Predisposed to Staph aureus skin colonization
o Vaccines against Strep pneumoniae, influenza
List the indications for starting chronic dialysis therapy.
- Symptomatic uremia:(Fatigue, anorexia, nausea, vomiting, encephalopathy, pericarditis)
- Fluid overload NOT responsive to diuretics
- Hyperkalemia not controlled with diet or loop diuretics
- GFR < 10 ml/min; <15 if diabetic
