SM_206a: CKD Clinical Flashcards
Stage 1 CKD is GFR ____
Stage 1 CKD is GFR ≥ 90
(kidney damage with normal or increased GFR)
Stage 2 CKD is GFR ____
Stage 2 CKD is GFR 60-89
(kidney damage with mildly decreased GFR)
Stage 3 CKD is GFR ____
Stage 3 CKD is GFR 30-59
(moderately decreased GFR)
Stage 4 CKD is GFR ____
Stage 4 CKD is GFR 15-29
(severely decreased GFR)
Stage 5 CKD is GFR ____
Stage 5 CKD is GFR < 15 (or ESRD)
(kidney failure)
CKD is defined as _____ and classified based on _____
CKD is defined as abnormalities of kidney structure or function present for > 3 months with implications on health and is classified based on cause, GFR category, and albuminuria category
Serum creatinine is not entirely accurate for measuring GFR because of _____, _____, and _____
Serum creatinine is not entirely accurate for measuring GFR because of variable creatinine production, variable creatinine secretion, and extra-renal secretion
Relationship between GFR and creatinine is _____
Relationship between GFR and creatinine is non-linear
Describe the systemic consequences of CKD
Describe the reciprocal relationship between drugs and kidney function
Reciprocal relationship between drugs and kidney function
- Renal excretory capacity leads to drug accumulation
- Drug accumulation can accelerate kidney disease
Greater sodium intake is associated with ____ proteinuria in CKD
Greater sodium intake is associated with greater proteinuria (induces hyperinflation)
(interaction with profibrotic effects of aldosterone, activate local RAAS in vessels and enhance conversion of Angiotensin I to Angiotensin II)
Treatment with an ARB + thiazide _____ proteinuria in CKD
Treatment with an ARB + thiazide lowers proteinuria
Giving bicarbonate _____ creatinine clearance in CKD
Giving bicarbonate raises creatinine clearance
CKD can lead to _____ due to disorder iron balance
CKD can lead to iron deficiency anemia due to disorder iron balance
(chronic inflammation and reduced renal clearance in CKD -> increased hepcidin -> reduced duodenal iron uptake and enhanced iron release from cellular iron stores)
Roxadustat is an _____ that is used to treat _____ in CKD patients
Roxadustat is an HIP inhibitor that is used to treat iron deficiency anemia in CKD patients
(blocks hepcidin -> allows formation of RBCs -> stops anemia)
CKD leads to a _______ disorder due to abnormal Ca2+, P3-, PTH, and Vitamin D metabolism
CKD leads to a mineral bone disorder due to abnormal Ca, P, PTH, and Vitamin D metabolism
_____ fluctuates by the second to keep Ca2+ in a narrow range
PTH fluctuates by the second to keep Ca2+ in a narrow range
Hypoparathyroidism is ___ PTH and ___ Ca2+
Hypoparathyroidism is low PTH and low Ca2+
(hyperphosphatemia)
Hyperparathyroidism is ___ PTH and ___ Ca2+
Hyperparathyroidism is high PTH and high Ca2+
(hypophosphatemia)
_____ is associated with low PTH and high Ca2+
Malignancy is associated with low PTH and high Ca2+
Increased PTH leads to _____ calcitriol, which leads to _____ reabsorption of Ca2+ and P3-
Increased PTH leads to increased calcitriol, which leads to increased reabsorption of Ca2+ and P3-
____ inhibits calcitriol
Calcitriol inhibits calcitriol (is its own inhibitor)
FGF23 secreted by osteocytes _____, _____, and _____
FGF23 secreted by osteocytes stimulates phosphaturia, decreases 1,25-D levels, and inhibits PTH
The trade-off (Bricker) hypothesis states that PTH ____ so Ca2+ can fall as GFR decreases
The trade-off (Bricker) hypothesis states that PTH decreases so Ca2+ can fall as GFR decreases
____ is the first molecule to increase in CKD
FGF23 is the first molecule to increase in CKD
(inflammation, iron deficiency)
Glomerular _____ occurs in diabetes mellitus
Glomerular hyperinflation occurs in diabetes mellitus
(glucose load causes tubule to work harder and hypertrophy)
ACE-inhibitors and ARBs _____ glomerular hyperfiltration in CKD
ACE-inhibitors and ARBs decrease glomerular hyperinflation in CKD
Diabetes mellitus leads to glomerular _____
Diabetes mellitus leads to glomerular hypertension
(less Na+ delivery to macula densa -> less ATP converted to adenosine -> glomerular afferent vasodilation -> GFR increases)
SGLT2 inhibitors _____ intra-glomerular pressure
SGLT2 inhibitors decreases intra-glomerular pressure
(block hyperinflation)
SGLT2 inhibition leads to afferent _____, while RAAS blockade leads to efferent _____
SGLT2 inhibition leads to afferent vasoconstriction, while RAAS blockade leads to efferent vasodilation
SGLT2 slows progression of ____ and protects against _____
SGLT2 slows progression of CKD and protects against cardiovascular disease
Describe the clinical action plan for management of CKD
- Early stages: slow progression, reduce CVD risk
- Middle stage: reduce CVD risk, treat complications
- End stage: work up for transplant
(CKD progression defined based on drop in GFR category and/or decline of ≥ 25% in eGFR from baseline - rapid progression is sustained decline of eGFR of > 5 mL/min/1.73 m2/yr)
Once damaged, CKD progresses over time due to _______
Once damaged, CKD progresses over time due to increased work of the remaining nephron mass
Describe indications for dialysis
Indications for dialysis
- Acute: acidosis, electrolytes (hyperkalemia), ingestions (lithium, ASA), overload (volume overload causing hypoxia, decompensated HF), uremia, nutrition (pediatric)
- Chronic: acute indication in setting of CKD (GFR < 15 cc/min), general malaise or failure to thrive in patient with GFR < 10-15 cc/min
Azotemia is _____, while uremia is _____
Azotemia is high BUN level, while uremia is high BUN level with symptoms (confusion, encephalopathy, bleeding, asterixis)
