Renal Pathophysiology Flashcards
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
CIN Pathology
Unclear
Hypoxia & hypo-perfusion exacerbate injury
Direct contrast media toxicity r/t harmful effects free radicals & oxidative stress
Excreted contrast in renal tubules generates osmotic force causing ↑Na+/H2O excretion
Diuresis ↑intratubular pressure ↓GFR → acute renal failure
CIN Treatment
Supportive
Prevention = key
Contrast media diagnostic studies or interventional procedures weigh risk against benefit
Intraop Monitors
Rapid recognition & treatment to prevent renal insult Foley Transesophageal echocardiogram CVP (less accurate) Blood pressure Stroke volume variation
Oliguria Treatment
Assume pre-renal oliguria r/t fluid until proven otherwise
Blood
Selective dopamine receptor agonists cause renal arteriolar vasodilation - Fenoldopam & low-dose dopamine <3mcg/kg
Diuretics - Furosemide or Mannitol (do not admin in patient w/ intravascular hypovolemia)
Chronic Renal Failure
Slow, progressive, & irreversible
↓nephron function ↓RBF ↓GFR
Causes - glomerulonephritis, pyelonephritis, diabetes, vascular or hypertensive insults, or congenital defects
Renal Insufficiency
↓renal reserve asymptomatic until <40% normal nephron remain
Insufficiency when 10-40% functioning nephrons remain
Compensated w/ minimal renal reserve
ESRD
End-stage renal disease/failure
>95% nephrons non-functioning
GFR <5-10% normal
Severely compromised electrolyte, hematologic, & acid-base balance
Uremia - urine in the blood eventually lethal
Dialysis dependent
Chronic Renal Failure S/S
Hypervolemia Acidemia Hyperkalemia Cardiorespiratory dysfunction Anemia Bleeding disturbances
Chronic Renal Failure Treatment
Hemodialysis HD
Peritoneal dialysis PD
Kidney transplant
Urine Specific Gravity
Measure solutes present in urine
Indicates kidneys ability to excrete concentrated urine
Reflects tubular function