Lecture 6.2 MJ slides Flashcards
List and describe the first 3 steps of prerenal AKI
Step 1: Low Blood Flow to Kidneys
-Filtration is impaired
-Resorption in the tubules is intact
Step 2: Blood Urea Nitrogen is not adequately filtered out
-Creatinine is not adequately filtered out
Step 3: Some BUN is resorbed
-Therefore, both values (BUN and Cr) go up, but BUN goes up higher
-This occurs at a ratio of about 20:1
-Clinically significant laboratory finding
During step 1 of prerenal AKI, there’s impaired blood flow to the kidneys.
1) What does this do to filtration?
2) What does this do to resorption in the tubules?
1) Filtration is impaired
2) Resorption in the tubules is intact
In step 2 of prerenal AKI, what 2 things are not adequately filtered out?
Blood Urea Nitrogen + Creatinine
Step 3 of prerenal AKI:
1) What is reabsorbed? What does this do?
2) What ratio does this occur at?
3) Can you see this in labs?
1) Some BUN; both values (BUN and Cr) go up, but BUN goes up higher
2) ~20:1
3) Clinically significant laboratory finding
1) In prerenal AKI, because filtration is down, what is also down?
2) List the path of ADH release
1) GFR is down
2) Renin > ang I > ang II > Aldo/ADH
Prerenal AKI:
1) What is being reabsorbed?
2) Describe the amount of solute and sodium in urine in this state.
3) What is the sodium status evidence of?
1) Water and salt are resorbed in the collecting duct
2) Elevated osmolality (high solute); low sodium
3) The action of aldosterone (your kidneys kept the salt too!)
Urine has elevated osmolality (high solute) in prerenal AKI. What is this a marker of?
Increased reabsorption, secondary to the effect of ADH
(Concentration of urine solute is high, because your kidneys kept the water!)
List and describe the 3 steps of post renal AKI
Step 1: There is an obstruction of the urine outflow
Usually this is a stricture, cancer, or other mechanical “blockage”
Step 2: Urine volume grows from the point of obstruction backwards
Urethra > bladder > ureter > renal pelvis > collecting ducts > Bowman’s capsule
Step 3: The normal direction of hydrostatic force which favors filtration is met with a significant “backwards pressure”
What is the impact of post renal AKI on filtration and resorption?
1) Filtration = impaired
2) Resorption = intact
Toxic type ATN:
1) What occurs?
2) What happens to the cells that slough off?
1) A blood borne toxin is delivered to the glomerulus where is it filtered out; toxin is then dumped directly into the proximal convoluted tubule. Epithelial cells are damaged beyond repair and slough off
2) Despite the name (necrosis) these cells undergo apoptosis, but they are unable to be resorbed, and local inflammation still ensues
(called “Acute Tubular Injury”)
Toxic type ATN: What are 3 common causes?
1) Rhabdomyolysis
-Disease of muscle breakdown; toxic element is myoglobin
2) Amphotericin (medication)
3) Contrast dye
Ischemic type ATN:
1) What is it? Describe what happens
2) What makes the cells in the renal tubules very susceptible to ischemia?
3) What further decreases GFR?
1) Impaired renal blood flow; the peritubular capillaries are not supplied with blood
2) Highly ATP-dependent (so ischemia-prone) because the pump moves ions against their concentration gradient
3) Massive vasoconstriction in hemorrhage
What are the 2 jobs of the peritubular capillaries (affected by ischemic ATN)?
1) Reabsorb nutrient back into systemic circulation after it has been filtered
2) Perfuse the cells of the renal tubules
List the steps of the course of ATN
1) Because tubules are damaged, resorption is impaired
2) Obstruction > pt becomes oligouric
3) Retrograde flow > now filtration is impaired
4) The epithelium regenerates
Acute pyelonephritis:
1) What is it?
2) What is the principal pathogen? Give examples
1) Common suppurative bacterial infection of the kidney and renal pelvis
2) Gram neg. bacilli
-E.coli, Proteus, Klebsiella, Enterobacter, & Pseudomonas
Acute pyelonephritis:
1) What is usually the cause?
2) What is this cause secondary to? Define this term.
3) What are 3 other potential causes?
1) Ascending infection following UTI
2) Vesicoureteral Reflux: incompetence of the vesicoureteral orifice
3) Obstruction; Abnormality of urinary tract; Hematogenous spread ( far less common)
Acute pyelonephritis:
1) What are the systemic Sx?
2) Lower UTI Sx?
3) Other Sx?
1) Fever, chills, malaise
2) Frequency, dysuria, urgency
3) CVA tenderness and flank pain
Chronic pyelonephritis
1) What leads to CKD?
2) What are the 2 types of chronic pyelonephritis?
1) Interstitial inflammation and scarring in patients UTI
2) Chronic obstructive & Chronic-Reflux Associated
Pyelonephritis Pathology:
1) What is it an infection of? (etiology). Give examples
2) Can these be seen in urine?
3) Where can the infection ascend?
1) Infection of Gram-negative organisms
-E coli; Klebsiella/Proteus/enterobacter
2) These organisms will be present in the urine, and are often detectable on urinalysis
-E. Coli converts N03 into N02, nitrites may be found in urine as well
3) Infxn Ascends the tubules > spreads to the interstitium
Pyelonephritis Pathology:
1) What do neutrophils lead to?
2) Where do neutrophils go?
3) What happens when they die?
1) Macrophages
2) Neutrophils will eventually occupy the tubules as well as the interstitium
3) When they are done causing local damage, they die, forming “WBC casts” in the tubules
-This is a clinically important finding on urinalysis
Pyelonephritis Pathology:
1) What is the fate of the neutrophils and macrophages?
2) Is any of this detectable in urine?
1) Some neutrophils and macrophages are transmitted back into excreted urine
2) WBC on urine is another clinically relevant finding
-Leukocyte esterase = enzyme produced by WBC; also detectable in urine
Allergic Nephritis:
1) What occurs?
2) What will be elevated on blood WBC count? Describe
1) Infiltration of interstitial space with leukocytes (eosinophils)
2) Their level will be elevated & they’ll spread to tubules and transmit to urine
What can cause allergic nephritis?
1) Exposure to Sulfur!: Bactrim; some diuretics
2) Also PCN, cephalosporin
Allergic Interstitial Nephritis:
1) Why can it occur? Give examples
2) What mediates it?
3) When does it start?
4) What usually leads to recovery?
1) Occurs from an adverse reaction to any number of drugs
2) Immune mediated (mixed)
3) Syndrome starts about 15 days after drug exposure.
4) Withdrawal of drug
NSAID Nephropathy:
1) What is less sensitive to the effect of angiotensin II? Why?
2) What happens if you take an NSAID?
3) What does this allow for?
4) What does that reduce?
1) Afferent tubule (as mentioned) is less sensitive to the effect of angiotensin II
One reason is that the afferent tubule can block the effect of angiotensin II with prostaglandins that allow it to remain dilated
2) You block prostaglandins
3) Both the afferent and efferent tubules to become constricted at once
4) Blood flow through the glomerulus which injures the kidney
Nephrotic syndrome:
1) What does it result from?
2) What does it lead to?
1) Damage to the basement membrane in the glomeruli with loss of filtration slits “podocyte effacement”
2) Increased permeability to plasma proteins, which leave circulation and are lost through the kidneys
Nephrotic syndrome is marked by what 4 crucial findings?
1) Proteinuria
2) Hypoalbuminemia
3) Generalized edema
4) Hyperlipidemia (lipidurea)
1) Define nephritic syndrome
2) What are its 4 crucial clinical features?
1) Acute onset of inflammatory lesions in the glomeruli
2) Hematuria, Proteinuria (less than nephrotic syndrome), Azotemia, HTN
