Nephro 2 Flashcards
Bricker’s Intact Nephron Hypothesis
Compensation depends on adaptive changes produced by renal hypertrophy and adjustments in tubuloglomerular feedback and glomerulotubular balance
Bricker’s Trade-Off Hypothesis
Physiologic adaptations to nephron loss also produce unintended clinical consequences
Brenner’s Hyperfiltration Hypothesis
Some adaptations accelerate the deterioration of residual nephrons
Acute Kidney Injury
A rise of at least 0.3 mg/dL or 50% higher than baseline within a 24-48-hour period; or
Reduction in urine output to 0.5 mL/kg per hour for longer than 6 hours
Oliguria
Defined as
High bone turnover with increased PTH levels
Osteitis fibrosa cystica: CLASSIC lesion for secondary hyperparathyroidism
Low bone turnover with LOW or NORMAL PTH levels
Includes adynamic bone disease and osteomalacia
Calciphylaxis (calcific uremic arteriolopathy)
Devastating condition seen almost EXCLUSIVELY in patients with advanced CKD; heralded by livedo reticularis
“Restless leg syndrome”
Ill-defined sensations of sometimes debilitating discomfort in legs/feet relieved by frequent leg movement
Uremic factor
A urine-like odor on the breath; derives from the breakdown of urea to ammonia in saliva and is often associated with an unpleasant metallic taste (dysgeusia)
Nephrogenic Fibrosing Dermopathy
Seen in patients with CKD who have been exposed to gadolinum
Current recommendation regarding gadolinum
CKD Stage 2 (GFR 30-59 mL/min) should MINIMIZE exposure to gadolinum
CKD Stages 3-5 (GFR
By light microscopy, glomeruli (at least 10 and ideally 20) are reviewed individually for discrete lesions
50% involvement is DIFFUSE
Injury in each glomerular tuft can be:
SEGMENTAL: involving a PORTION of the tuft (50%)
Endocarditis-associated GN
Kidneys have subscapular hemorrhages with a “flea-bitten” appearance