Renal Pathophysiology Flashcards
(87 cards)
Kidneys receive ___% total CO
15-25%
95% directed to the renal cortex (glomerulus)
5% to the medulla
Renal Autoregulation
INTRINSIC - intact even in denervated kidneys
Tubuloglomerular feedback
Renal Blood Flow
Afferent arteriole → glomerular capillary → Bowman’s capsule → proximal tubule → loop of Henle descending → ascending → macula densa → distal tube collecting duct
Glomerulus
Separates the afferent from efferent arterioles
Resistance in efferent arterioles creates hydrostatic pressure w/in glomerulus
Capillaries lined w/ podocytes
GFR
Glomerular filtration rate
Rate blood filtered through all glomeruli
Measures overall kidney function
SNS Activation
↓RBF
Blood shunted to skeletal muscle during exercise
Surgical stimulation ↑vascular resistance
Stimulates adrenal medulla → catecholamine release
↓BP → RAAS activation
ADH
Vasopressin
Antidiuretic hormone Released in response to ↓stretch receptors in atrial/arterial wall & ↑plasma osmolality Synthesized in hypothalamus Released from posterior pituitary Half-life 16-24 minutes Constrict efferent arteriole H2O reabsorption
ADH Primary Functions
- ↑renal H2O reabsorption (osmolality)
2. Vasoconstriction ↑SVR ↑BP
Periop Release ADH Causes
Hemorrhage PPV + Upright position Nausea Medications
Renin
Enzyme secreted by kidneys Hydrolyzes angiotensin → angiotensin I Released from JG cells near afferent arterioles - ↓arterial BP - ↓Na+ load delivered to distal tubules - SNS β1 receptors
Angiotensin
Angiotensin I converted in the lungs by ACE into angiotensin II
Angiotensin II potent vasoconstrictor & stimulates hypothalamus to secrete ADH
Aldosterone
Mineralocorticoid hormone released from the adrenal gland
Plasma half-life 20 minutes
Stimulates epithelial cells in distal tubule & collecting ducts to reabsorb Na+ & H2O (exchanges K+ to maintain electroneutrality)
Spironolactone
K+ sparing diuretic that blocks the aldosterone receptors
Acute Renal Failure
AKI
Sudden inability to produce urine
Develops rapidly but may resolve
50% mortality rate
Pre-Renal
Hemodynamic or endocrine factors impair perfusion
Causes - hypotension, shock, hypovolemia, hemorrhage, burns (fluid shift), vascular occlusion (thrombosis or clamping), ↓RBF (heart failure or renal artery stenosis), hepato-renal syndrome
Activate RAAS → ADH
Low urine Na+ ↑osmolality
Possible to progress to permanent parenchymal damage
Intra-Renal
Acute Tubular Necrosis
Direct kidney tissue damage
Causes - inflammation/infection, reduced blood supply, prolonged ischemia, nephrotic injury (antibiotics, chemo, contrast dye), glomerulonephritis
Parenchymal disease difficult to concentrate urine
↑urine Na+ ↓osmolality
Post-Renal
Urinary outflow obstruction
Causes - kidney stones (calculi), stricture, blood clots, neoplasm, bladder/pelvic tumor, prostate enlargement, or injury
Less common in OR setting
Anuria
<100mL/day
Oliguria
<400mL/day
<0.5mL/kg/hr
OR oliguria indicates inadequate systemic perfusion
Polyuria
> 2.5L/day
Non-concentrated urine
Acute Renal Failure
AKI Risk Factors
↓renal reserve w/ age
Each year after 50 creatinine clearance ↓1.5mL & renal plasma flow ↓8mL
Pre-existing renal dysfunction
Surgical procedures
- Cardiac bypass >2 hours
- Aortic aneurysms (supra-renal aortic clamping)
- Ventricular dysfunctions
Sepsis - hypovolemia, hemolysis, DIC, infections, acidosis
Nephrotoxic agents
Diabetes
Hypertension
AKI Prevention
Prevention renal insult more successful than management
Hydration
Maintain blood pressure
Euvolemia
Contrast-Induced Nephropathy
3rd most common cause hospital acquired AKI
Results from iodinated contrast media admin
Transient & reversible acute renal failure
1° supportive treatment
- Fluid & electrolyte management
- Dialysis
Low incidence in normal renal function patients 0-5%
Pre-existing renal impairment 12-27%
Diabetic neuropathy up to 50%
CIN Risk Factors
Pre-existing renal disease Diabetes Hypertension Volume-status (dehydration) Obesity Hepato-renal injury