CKD And Renal Replacement Therapies Flashcards
In development of CKD, _____ is an initially appropriate adaptation but ultimately becomes maladaptive as it leads to sclerosis and decrease in number of nephrons d/t distortion of renal architecture, abnormal podocyte function, and disruption of filtration barrier
____ is also involved in initial protective increase in filtration, but worsens hypertrophy and sclerosis over time
Hyperfiltration
RAAS
Most common diseases associated with CKD
Diabetes and HTN = most common
Others: glomerulonephritis, ADPKD, other cystic and tubulointerstitial nephropathies
What parameter is used to define and stage CKD?
GFR
[contrast to AKI which is defined and staged by rate of rise in serum creatinine]
Normal GFR is ~100
Define GFR changes in stages of CKD
Stage 2: GFR 60-89
Stage 3: GFR 30-59
Stage 4: GFR 30-44
Stage 5: GFR <15 (renal failure)
Progressive lab changes/clinical features in worsening stages of CKD
Stage 2, or GFR ~80 = HTN
Stage 3, or GFR ~30-60 = elevated PTH, anemia, hyperphosphatemia, hyperkalemia, possible mild uremic syndrome
Stages 4-5, or GFR <30 = all of the above changes + acidosis + uremic syndrome
How does sodium change in CKD?
ECV increases as Na excretion decreases (so lab levels may appear normal)
This worsens HTN and often requires diuretic therapy
Potassium is typically unaffected in CKD except under what circumstances?
Dietary changes!
If there is an increase in dietary intake, consider potassium wasting diuretics like loop diuretics
Potassium sparing diuretics are also used (triamterene); other meds that interfere with RAAS include spironolactone, ACE, ARB, etc. may need adjusing
How does acid/base status change in CKD?
Initially (GFR ~40), a NAGMA/hyperchloremic metabolic acidosis — related to reduced ammonia production
As renal function worsens (GFR ~15-20), becomes HAGMA d/t retained organic acids/failure to excrete anions
Presence of acidosis can induce protein catabolic state
______ is a syndrome caused by accumulation of multiple toxins in CKD as well as loss of fluid/electrolyte homeostasis, hormone regulation, and progressive increase in systemic inflammation affecting bone, blood, skin, heart, nervous system, GI system, etc.
Uremia
Characteristic changes with CKD include:
_____phosphatemia
_____calcemia
______vitaminosis D
The above 3 result in secondary _____parathyroidism
Hyperphosphatemia
Hypocalcemia
Hypovitaminosis D
Hyperparathyroidism
[hyperparathyroid symptoms include fatigue, malaise, muscle weakness]
Changes in bone metabolism (due to hyperparathyroidism induced by hyperphosphatemia, hypocalcemia, and hypovitaminosis D) with CKD lead to what abnormalities?
Osteitis fibrosa cystica (high turn-over bone disease causing cysts to form in bones)
Osteomalacia (defective mineralization)
Adynamic bone disease (decreased rate of bone turnover without mineralization defect; worse in DM)
PTH effects on cardiovascular system and potential tx
Elevated PTH —> cardiac muscle fibrosis
Increased vascular calcification and atherosclerosis
Tx includes supplemental calcitriol (vit D analog) to suppress PTH
Number one cause of mortality in pts with CKD
Cardiovascular disease
[likely associated with increased inflammatory state with cytokines and CRP]
Requires aggressive interventions including BP management, lipid management, exercise, smoking cessation, weight reduction, etc.
What causes the anemia associated with CKD?
What kind of anemia is it?
Decreased erythropoietin production
Normochromic, normocytic anemia with associated neocytolysis (premature RBC death)
Signs/symptoms of anemia associated with CKD
Fatigue, decreased exercise tolerance
Decreased cognition and mental acuity
Impaired host defense against infection
Left ventricular hypertrophy (LVH) — d/t chronic low O2 delivery activating SNS to increase HR and SV
Neuromuscular effects are seen by stage ____ of CKD and include WHAT signs/symptoms?
STAGE 3
Neuromuscular irritability = twitches, hiccups, cramps
Peripheral neuropathy by stage 4 — sensory predominates until later stages, LE > UE
GI effects of uremia
Uremic fetor — urine-like breath odor associated with unpleasant metallic taste
Gastritis, peptic disease and mucosal ulcerations
Anorexia, N/V
Constipation
[pts also become calorie depleted d/t new dietary restrictions including sodium, potassium, etc]
Endocrine effects of CKD include increased plasma levels of _____ (which is usually cleared by the kidney), ______ levels of estrogen in women, and _____ levels of testosterone in men
Insulin; decreased; decreased
How do endocrine effects of CKD affect young women? What about young children?
Young women: Fertility changes, irregular menstrual cycles
Children: growth retardation, failure to thrive
Skin changes associated with CKD
Hyperpigmentation (likely d/t decreased excretion of pigments)
Pruritis — intense itching is hallmark if uremia!! Worse with hyperphosphatemia
Tx/management of CKD
Control BP — ACE-I and ARBs are first line
Monitor volume status for edema (I/Os, daily weights)
Dietary changes (Na+ restriction, protein restriction but monitor for malnutrition)
Assess and tx cardiac risk factors
Monitor for extra-renal complications — anemia, GI, bone changes, etc.
What nephrotoxic drugs must be avoided in CKD?
NSAIDs
Antibiotics (aminoglycosides)
Antiarrhythmics
Radiocontrast agents and gadolinium
At what CKD stage/GFR should you refer your pt to nephrology for possible dialysis or renal transplant?
Nephrology referral at CKD stage 4 — when GFR is <30
[dialysis or transplant must be initiated when GFR is 15 or less]
Describe dialysis
Goal is volume and toxin reduction
Solute diffusion and water transport across a selectively permeable membrane; can be intermittent (3-4 hrs, 3x/week)
