Nephro 2 Flashcards
(31 cards)
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
Granulomatosis with Polyangitis (Wegener’s)
Classically present with fever, purulent rhinorrhea, nasal ulcers, sinus pain, polyarthralgias/arthritis, cough, hemoptysis, shortness of breath, microscopic hematuria, and 0.5-1 g/24h of proteinuria
Microalbuminuria
Albuminuria in the range of 30-300 mg/24h
Anti-GBM Disease
Autoimmune disease where antibodies are directed agaisnt alpha-3 NC1 domain of collagen IV
Bartter’s Syndrome
May result from mutations affecting any of five ion transport proteins in the TAL. Clinical syndrome mimics the effects of chronic ingestion of LOOP DIURETICS
Gitelman’s Syndrome
Due to mutations in the thiazide-sensitive Na-Cl cotransporter, NCCT, in the DCT. Resembles the effects of thiazide diuretics
Hyperprostaglandin E syndrome
Sever form of Bartter’s syndrome in which neonates present with pronounced volume depletion and failure to thrive, fever, vomiting, and diarrhea from PGE2 overproduction
Liddle’s Syndrome
Mimics a state of aldosterone EXCESS by the presence of early and severe hypertension, often accompanied by hypokalemia and metabolic alkalosis, but plasma aldosterone and renin levels are LOW
The Triad of heavy metal (lead) nephropathy
Saturnine gout
Hypertension
Renal Insufficiency
Analgesic Nephropathy
Results from the long-term use of compound analgesic preparations containing phenacetin, aspirin, and caffeine
