Pathophysiology
hyperfiltration theory
damage to nephrons somehow (where does this damage come from?)
increase in blood flow to intact nephrons
increase in SNGFR (single nephron glomerular filtration rate
increase in hydrostatic pressure
hyperfiltration injury
further nephron damage
protein leaks out --> proteinuria and microalbuminuria
Staging of CKD
stage 1
stage 2
stage 3
stage 4
stage 5
Subtopic 6
Causative Factors
diabetes
diabetes
hyperglycemia increases capillary endothelial dysfunction and membrane thickening
glucose-protein conjugates accumulate in tissue causing abnormal structural protein function and vascular permeability resulting in renal damage
glycemic control
type 1
goal is Hgb A1C < 6 %
type 2
ACCORD
A1C of 7 - 7.5 is new target
glomerular diseases (SLE, system infections, drugs)
interstitial disease/cystic disease
interstital diseases/cystic disease
kidney grafts
acute renal failure
Risk Factors for Progression of CKD (WHAT IS DIFFERENCE BETWEEN CAUSATIVE, RISK AND SUSCEPTIBLE)
proteinuria
hypertension
second leading cause of CKD
MRFIT and HDFP
suggest good target mean arterial pressure of 98 mmHg (BP < 130/80)
with proteinuria (>1gm/d) a BP target of 125/75
HTN control
diabetic HTN
recommended treatment protocol
use ACEI or ARB as primary treatment
ACEI
reduces glomerular capillary pressure and volume and preserves renal function
begin w/ low dose; increase at 4 week intervals to reduce microalbuminuria
ARBs
work similarly to ACEI
dose drug to albumin levels; don't just target BP
if BP < 130/80 not met (JNC VII) add thiazide or loop diuretic
add Ca channel blocker or B blocker if above does not work
nondihydropyridine Ca channel blockers
drugs
verapamil
diltiazem
MOA
decreases glomerular injury without changing renal hemodynamics
mainly dilates afferent arterioles
affects proteinuria
many px will require 2-3 agents
non-diabetic HTN
ALLHAT trial
diuretics, ACEI, ARBs all work
ACEI have most data against progression to CKD
recommended treatment protocol
BP reduction is key to decreasing CV and renal complications
ACEIs or ARBs 1st line in CKD px
smoking
hyperlipidemia
obesity
Lab Tests
Early Detection of CKD
tests recommended for those at risk
Susceptible for CKD (WHY??)
advanced age
reduced kidney mass/low birth weight
ethnic minorities
family history
low income
dyslipidemia
tests
BP
glucose
Scr to estimate GFR
spot urine specimen for protein or albumin
in selected px
ultrasound
electrolytes
full urinalysis
Expected Lab Abnormalities in CKD
elevated BUN
elevated Cr
anemia
hyperparathyroid hormone
hypocalcemia
hyperphosphatemia
hyperkalemia
hyponatremia
low bicarbonate
low pH (acidosis)
Lab Tests for Proteinuria and Microalbuminuria
for px not at increased risk
std. dipstick for protein (> 1+) - (spot urine test)
then perform protein:creatinine ratio
< 200 mg/g recheck periodically
> 200 mg/g go to a diagnostic evaluation
for px at increased risk
albumin specific dipstick (+) - (spot urine test)
then perform albumin:creatinine ratio using 24-hr urine (ACR)
if < 30 mcg/mg recheck periodically
30-300 mcg/mg considered microalbuminuria; go to diagnostic evaluation
a 24 hr urine collection having > 300 mg/day albumin is considered clinically significant (albuminuria)
Nutritional Management
for px w/ low GFR < 25, 0.6 gm protein/kg/day associated w/ decreased rate of progression of kidney function decline
for avg. person change in protein doesn't help that much
Complications of CKD
sodium and water balance
pathophysiology
lose ability ot adjust to abrupt changes in Na intake
Na balance is maintained but in a volume-expanded state
kidneys ability to dilute/concentrate urine is impaired
volume overload may lead to HTN or pulmonary edema
treatment
significant sodium/water restrictions are not necessary
maintain urine output with loop diuretics
thiazides ineffective is GFR < 30 ml/min
combination of thiazide + loop can act synergistically
metabolic acidosis
pathophysiology
potassium homeostasis
anemia of CKD
secondary hyperparathyroidism (SHPT)