What are some ways that we can classify kidney disorders?
- Prerenal, intrarenal, & postrenal
- Intrinsic vs extrinsic
- Primary vs secondary
which biopsy is most beneficial
glomerular diseases, tubular diseases, vascular, interstitial
Acute kidney injury vs chronic process
- sometimes both can happen at the same time
When we’re thinking about prerenal, intrarenal, or postrenal, What is the general approach when trying to figure them out?
- post; how, sxs, timeline
- prerenal: what labs could you use
- Pre & post renal: No change in GFR
- Maybe in post there is an obstruction which you can see w/ US and patient will have low urine output with frequent urgency to urinate; Kinda depends but a lot of times if it is prostate hypertrophy you may see that it developed slowly over time but if it is something else like a stone it may be more acute presentation
- Creatinine ratio might give you an idea. Fractional excretion of Na+, Signs & sx
How do you start the evaluation of patient who presents with decreased urine ouput
- hx questions
- How do we gage the urgency of the situation?
- hx of prostate CA?
- Volume of urine output/body weight, 24 hr urine collection, US of bladder to look for obstruction, BUN and Cr (need baseline)
• What would be a cut off for this pt where you would be worried about his urine output? When do we diagnose AKI based on urine output?
○ Less than about 500mL per day
○ The cut off is .5mL/kg/hr
○ So over the past 12 hrs he should’ve put out 571.8mL at the minimum.
How to get UA with obstruction?
- catheter
- significant obstruction and sometimes you may not be able to pass a catheter so at that point that is more of an emergency where you would involve the urologist, pt may need to get a stent place or they may be able to scrape some of the internal lining of the prostate to debulk the prostate and get a diagnosis at the same time to confirm it is hyperplasia and not a cancer
Describe the pathophysiologic changes that resulted in post obstructive AKI
- compensatory mech
- results in
- if you have an obstructive process you’re gonna increase the pressure w/in the ureter which then increases w/in the nephron. Initially he can have compensatory mechanisms in the arterioles to help maintain GFR, but after a while the increased pressure in the nephron will overrule that and it reduces GFR and affects kidney function
- At the glomerulus you have high pressure to squeeze blood through that filter and so if you have this increased opposing pressure on bowmans space youre gonna have to offset that somehow so the initial response is dilating afferent arteriole so you can increase the pressure going through there
- ischemia (decreased perfusion to the tubules so you can end up with ischemic tubular damage), Infection
Predict the following laboratory findings in obstructive AKI
- Serum creatinine
- FENa
- best test
○ Serum creatinine: would be elevated. It depends on what phase he is (comp or not). Bc this has been going on for a while and with the really severely decreased urine output it is a good chance that his would be elevated
○ FENa: It can be less than 1 or greater, but in general at the time of diagnosis its gonna be greater than or equal to 1 but its usually not all that helpful
- imaging
If you had obstruction in 1 ureter, why are you not gonna have AKI
Usually the other kidney can compensate. Where that is not the case is if you only have 1 functioning kidney and then you get a stone in that kindey, or if you have bilateral stone, but it if is just one side it wont usually cause AKI
What are some of the other causes of post renal azotemia?
Stone, BPH, congenital deformities (will show up really early in life), pregnancy, intraabdominal tumors (particularly pelvic - tumors of the uterus, ovaries), lymphoma (abdominal that can cause obstruction bilaterally in the ureters)
Prerenal with motorcycle accident
- Etiologies
- causes
- Patho
- Diagnostic findings
- problem
- imaging
- Management
- Decreased blood volume due to blood loss or dehydration
- Hanta virus, post op clot
- increased blood loss or dehydration –> decreased perfusion of nephron
- Increased creatinine, increased BUN, decreased urine output; with more impact to BUN so ratio > 20
- impaired reabsorption –> GFR goes down so you having more reabsorption at the level of the proximal tubule and start having more reabsorption of BUN,
- to look for intraabdominal bleeding if there was an injury undiagnosed initially
- Go into OR to stop the bleeding, IV normal 0.9% saline to replace intravascular volume quickly
Intrarenal Etiologies with motorcycle accident
- drugs
- management
- Drug induced/antibiotic induced: It would be directly or indirectly toxic to the tubule, Aminoglycosides are the most notorious for this and causing tubular necrosis OR contrast-induced nephropathy
- Management: Stop antibiotic , Ensure that they’re receiving enough fluids
Postrenal Etiologies with motorcycle accident
Trauma that could’ve caused postrenal obstruction
Pt with severe crush injury
- most likely problem
- how does this cause injury?
- results on work up
- treatment
- rhabdomyolysis
- increased muscle breakdown and increased serum creatine kinase (surrogate marker for muscle breakdown); You’re also releasing myoglobin –> directly toxic to tubular epithelium
- Serum creatine kinase, Muddy brown casts
- Aggressive rehydration for supportive care as they clear out the myoglobin
Pt w/ hx of dementia, BPH, CHF, CKD and diabetes that presents with weakness, dysuria an difficulty passing urine what would happen if this was pre-renal azotemia
- etiologies
- Expected diagnostic findings
- Management
○ CHF with decreased ejection fraction could be decreasing perfusion to kidneys; Causes decreased filtration across the glomerulus, Decreased perfusion to everything including the tubules and interstitum
○ Type II diabetes could cause atherosclerosis at the renal artery; Can cause hylaine sclerosis of the renal arteries which decreases the caliper of those arteries and decreases the perfusion as well
○ Dehydration: low BP, dry mucosa; in an older patient it is not very specific; they could have a lot of mouth breathing causing the dry mucosa, but still very important to pay attention to; Patient has said they are so weak they are not getting out of bed, so they are not getting out of bed and oral intake could be another significant problem. This is very important in patients with weakness because it can cause significant dehydration which could be playing into decreased intravascular volume
○ Patient is on ACE i: directly hampers the GFR; Dilates the efferent arteriole and somewhat constricts afferent arteriole
- Elevated BUN/CR and FE Na
- CHF causing renal impairment -> use saline fluids since BP is low; Decrease afterload -> increase CO and increase perfusion to kidneys; Stop ACE inhibitor
Why are ACE inhibitors renal protective?
- progression of renal dx -> decrease in renal mass -> increase in intraglomerular pressure and so we are going to shift the balance and the flow through the glomerulus so you’re going to decrease the GFR to each glomerulus to try and protect it
Pt w/ hx of dementia, BPH, CHF, CKD and diabetes that presents with weakness, dysuria an difficulty passing urine what would happen if this was Post Renal azotemia?
- etiology
- management
- BPH: pt has prior history of benign prostatic hypertrophy, so thinking about obstruction
- put in foley cath ->Monitor output
Pt w/ hx of dementia, BPH, CHF, CKD and diabetes that presents with weakness, dysuria an difficulty passing urine what would happen if this was Intra-renal azotemia?
- etiology
- low hgb -> what does this do?
- dx
- complications
- management
- Ischemia associated AKI bc of systemic hypotension ->At some point the pre-renal azotemia becomes severe enough or long standing and shift into intra-renal problem bc intravascular supply problem will lead to ischemic tubular necrosis, etc.
- CKD causes decreased EPO production which leads to anemia of chronic renal insufficiency -> Exacerbates ischemia bc there will be even lower amount of O2 delivery
- Elevated creatinine: In a patient with chronic kidney disease will most likely have elevated creatinine at baseline, so would define an acute on chronic renal dx with even higher creatinine than baseline amount
○ Bicarb low and K is at high normal -> EKG with peak T waves - There are ways you could lower K acutely: give glucose and insulin and shift pathway intracellularly, give bicarb for acidosis but if patient already has EKG changes just take pt to dialysis
Creatinine levels for different stages of AKI
□ Stage 1 AKI: 1.5-1.9 X baseline
- Stage 2 AKI: 2X baseline
How does diabetes cause renal damage?
Significant intra-renal damage and some degree of pre-renal
What is interplay between AKI and chronic kidney injury
Older pt with chronic renal injury are a lot more susceptible and do not recover as fast from acute renal injury from hypoxia, particularly a patient with diabetes, is going to have slower healing response if they do have damage to their tubular epithelium or endothelium so they are already set up for having acute injury. They will have an acute renal injury go to the hospital and get through that but as we talked about in structures last week these acute injuries over time will lead to scarring. You’re damaging more nephrons and scarring them and as you lose those nephrons youre going to cause faster progression of chronic renal dx since damage to these nephrons is irreversible which can then lead to glomerular HTN and these patient will end up on chronic dialysis or renal transplantation.
55 y/o hispanic male w/ severe R flank pain, radiating to RLQ, dysuria, dark colored urine, less urine output, pain of 10/10, emesis. Elevated BP, no fever, unable to sit or lie still
- what additional tests would you order
- DX?
- how could you r/o nephritis
- Tx?
- UA, CBC, CMP/BMP
- Kidney stone on R side
- RBC casts; if there arent any then it is post-renal and problem is happening after glomerulus
- give IV hydration, pain mgmt (morphine), tamsulosin, and on discharge- catch & analyze stone.
What is leukocyte esterase
- confirms or denies WBC in urine which would indicate or exclude an infection
