Renal Flashcards
(15 cards)
What are the indications for CRRT
(continuous renal replacement therapy)
Acidosis
Electrolytes (esp. HyperK+)
Intoxication
Overload (refractory to diuresis)
Uremia (uremic encepalopathy, pericarditis)
What is ATN?
Acute tubular necrosis is an intrarenal inury most often caused pre-renally by sepsis/hypovolemia, but it can also be caused directly by toxins.
How do kidneys maintain glomelular pressure?
Glomelular pressure ranges from a MAP of 80-180 mmHg.
If MAP falls, the kidney compensates by vasodilating the afferent arteriole, and vasoconstricting the efferent arteriole.
Goal is to have enough pressure to filter 125mL/min.
What affects GFR?
- Blood flow
- Pressure in the Bowman’s space
- Plasma oncotic pressure
What does creatinine clearance indicate?
Indicator of GFR. Levels below 50 mL/min signal severe kidney dysfunction.
Can be calculated using the Cockcroft-Gault Formula:
CrCl (mL/min) = [(140 - age) * weight (kg)] / (72 * serum creatinine (mg/dL))
For women, multiply the result by 0.85
How does aldosterone exert its effects?
Angiotensin II stimulates the adrenal glands to release aldosterone, which act on the distal tubule to facilitate Na+ & H2O reabsorbtion to increase BP.
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Na+ is exchanged with K+, which means more K+ in cells, more Na+ in blood, but is also adds a K+ channel to the apical surface of a principal cell in order to release more K+ in urine.
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Bonus: aldosterone is produced in the cortex, which use cholesterol in the production of aldosterone.
Describe the parts of the nephron
Proximal convoluted tubule reabsorbs organic nutrients, proteins, glucose, water and electrolytes (phosphate, bicarbonate, K+, Cl-, Ca+)
In the distal ascending Loop of Henle, electrolytes are reabsorbed, based on feedback from the macula densa cells.
Distal convoluted tubule reabsorbs Na+ and Cl- as needed to make urine hypotonic.
The collecting duct manages H2O absorbtion or elimination, and secretion of H+ and HCO3. It’s permeability is affected by ADH.
Functions of the Kidney
- Excretion and removal of metabolic waste and foreign substances.
- Activate vitamin D
- Maintain fluid volume, pH, blood pressure and electrolyte balance
- Secrete hormones (i.e. erythopoietin to increase RBC production)
3 RASS Steps
- Juxtoglomelular cells release renin
- Renin meets with circulating angiotensin (which is produced in the liver), and cleaves it to make Angiotensin I
- Angiotensin I interacts with endothelial cells containing angiotensin converting enzyme in capillaries to form Angiotensin II, which exerts its effects on tissues.
ACE inhibitors, which end with the “pril” suffix, prevent the conversion of Angiotensin I to Angiotensin II.
What does Angiotensin II do?
- Vasoconstriction by acting on peripheral vascular receptors in arterioles.
- Na+ reabsorbtion to retain more H2O
- Stimulates release of ADH (vasopressin), causing further vasoconstriction and retention of H2O
- Stimulates release of aldosterone, which acts on distal convoluted tubule to retain Na+ (uses ATP to increase Na+ in the blood, exchanged for K+)
What are the triggers for juxtoglomelular release of renin?
- Reduction of BP sensed by JG cells in afferent arteriole.
- Sympathetic nerve stimulation from neighbouring cells.
- Release of prostaglandins from macula densa cells located in distal convoluted tubule. This is triggered in response to sensing less circulating Na+ due to lower BP.
Stages of AKI
Stage 1: creatinine rises 0.3 mg/dL in 48 hours, urine output is < 0.5 ml/kg/hr for 6-12 hours.
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Stage 2: creatinine reaches 2-3x baseline, urine output is < 0.5ml/kg/hr for 12 hours.
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Stage 3: creatinine levels are above 4mg/dL, urine output <0.3ml/kg/hr for over 24 hours OR anuria for 12 hours.
Goal is >60ml/hr urine output.
Causes of AKI
Prerenal
Sepsis causes approximately 50% of prerenal AKI cases. Anything that reduces blood flow to the kidney, i.e. trauma and persistent hypotension.
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Infrarenal
Most often caused by ischemia (see footnote) or nephrotoxic drugs: antibiotics, cyclosporin, corticosteroids, furosemide, some anesthetics and contrast dye. NSAID’s and ACE inhibitors affect the kidney’s ability to regulate renal perfusion. Rhabdomyalysis blocks tubules and affects ability to reabsorb.
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Postrenal
Most often caused by abdominal compartment syndrome or trauma.
During periods of ischemia, ATP is not available for active transport of molecules across tubule membrane. After 60 - 90 minutes, membrane damage becomes irreversible.
What triggers the release of ADH?
Released by the pituitary in response to:
- High blood osmolarity
- Low blood volume as indicated by stretch receptors in the RA and vena cava
- Decrease in BP as noted by baroreceptors in the aortic arch and carotid sinuses
- Circulating Angiotensin II
How does ADH work?
- Smooth muscle of systemic arteries to vasoconstrict
- Increased reabsorbtion of H2O in the kidney: works on the collecting duct by opening up channels in cells (aquaporin, normally H2O impermeable) to return H2O to the bloodstream.
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Note: volume will increase, and osmolarity will decrease.
