W2 Acute Kidney Injury 2 Flashcards
Basics of intra-renal
FeNa will be?
RBUS will show/not show?
UA micro will show?
Which is more commonly a/w AKI, nephrotic or nephritic?
Intrarenal AKIs are AKIs that result from a problem within the kidney itself (essentially leading to a functional problem at the level of the nephron resulting in the clinical presentation of AKI - but that’s vague - and a lot can be wrong here - so stay tuned)
● Potential causes of intrarenal AKIs are so profoundly abundant
■ Note that nephritic syndromes are for more commonly a/w AKI than nephrotic syndromes (however there still are nephrotic syndromes that are associated w/ AKI)
○ In (sole) intrarenal AKIs, the FeNa will still be >1%
kidney is not reabsorbing 99% of Na+
○ In (sole) intrarenal AKIs, the RBUS will not demonstrate hydronephrosis
○ The UA micro w/ sediment to see blood would typically be very abnormal, and variably so (which we will cover, as it’s an important aspect of characterizing if an Intrarenal AKI is a nephrotic syndrome, a nephritic syndrome, or neither)
○ For intrarenal AKI w/u, you will also need a CBC (which you likely would already have)
Note that nephritic syndromes are for more commonly a/w AKI than nephrotic syndromes (however there still are nephrotic syndromes that are associated w/ AKI)
What are the 4 types of intra-renal injuries
● Classification & Organization of Intrarenal AKIs (the 4 big ones):
○ Tubular Injuries:
damage to the nephro-tubular structures themselves
○ Vascular: (focal areas)
Non-glomerular vaso-occlusive syndromes and microangiopathies that lead to renal ischemic events (*this one gets tough to organize as it actually may be considered part of the intrarenal classification systems, as well as potentially being considered a prerenal AKI too depending on the rate of onset of disease & size / location of the affected vessels, however in the context of intrarenal AKIs, this of this more so being related to an acute impairment in blood flow within the vessels to a focal region of the kidney)
○ Glomerular Disease / Injury:
essentially exclusively a sequela of immune-mediated vasculitis processes that lead to functional impairment of the impact the glomerulus / glomeruli’s ability to filter serum into the bowman’s capsule
Areas along the nephron for appropriate exchange of molecules
■ What is the glomerulus?
○ Interstitial Disease:
inflammation of the interstitial tissues within the nephron itself, leading to an inflammatory-mediated functional impairment of the nephron secretion and reabsorption
● Given so many potential causes though, how will I know ?
Algorithm again for reference
Intra-renal AKI
ATN: 3 main causes
Tubular injuries are defined as injuries directly to the cellular & structural tubular aspects of the nephron lumen, which surprise ( ! ), also happen to be incredibly important to their reabsorption and secretion functions. ATN injuries are typically either ischemic or chemically toxic in nature.
- ⭐️Medications: aminoglycosides, displaying
- ⭐️ Contrast-induced AKI
- ⭐️ Rhabdomyolysis or massive hemolysis
❗️[must know]
Intra-renal: tubular injuries
2 types of tubular injuries?
UA w/ micro would show?
FeNa?
-
ATN:
—leading to the superficial tubular cell damage/death. Nephron dysfunction -
Tubular obstruction:
—Literal obstruction of the nephron tubule leading to poor outflow of filtrate from that nephron unit typically 2/2 either ATN cellular death casts obstructing the lumen or from large luminal crustal formation like CaOx stone
findings
—UA w micro and sediment demonstration epithelial cells / casts MUDDY BROWN CASTS and dead metabolised luminal epithelial cells and crystals
—FeNa would be HIGH
—RUS would NOT demonstrate hydronephrosis
Intra-renal: tubular injuries
Treatments
● Like most causes of AKI, treatment plan for ATNs is typically dependent on removing the offending agent and/or treating the primary cause, and providing fluid resuscitation
(FYI for your future pharmacology talks re: AKI & volume status, there are some more rare instances when a patient has BOTH an AKI and are volume overloaded, in which case the patient may not benefit from fluid resuscitation, may even need to be diuresed)
Individual Examples of Treatment for Tubular Injuries would be (aside f/ giving fluids):
—Stop the aminoglycoside
—Stop the nephrotoxic chemo
—Stop the NSAID that is causing direct toxicity to the tubular cells
—Don’t give patient any more iodinated contrast (or if you know they have tenuous renal function at baseline or have had prior episodes of AKI w/ contrast, seriously weigh your risks and benefits of giving that patient contrast in the first place)
● IVF here (if pt is euvolemic or volume down) can be super helpful here though as if there is an obstructive tubular component (not just a ATN component), then the IVF may help flush out these
obstructive products and help improve outflow of filtrate from those obstructed nephrons)
Intra-renal: tubular injuries
● If the kidney is met with an ATN-mediated Intrarenal AKI, and if pt has minimal other renal disease risk factors (lower severity of the AKI, none or infrequent prior episodes of AKI) and the workup is performed and causative process is addressed appropriately through workup-guided treatment, then the nephro-tubular structure may be able to regenerate, hopefully leading to return to b/l nephron function (not always so lucky)
● ATN is considered a reversible form of intrarenal AKI (but takes 1-3 weeks for cells to recover)
Intrarenal AKI
Vascular occlusion injury
Which two associated conditions?
Peripheral smear would show?
TTP (thrombo-embolic)
HUS (thrombotic)
leads to acute ischemia of nephrons
CBC peripheral smear: schistocytes
Intrarenal Acute Kidney Injuries: Common & Significant Causes pt. 2: (micro) Vascular Occlusion / Injury
Small vessel / microscopic renovascular occlusive processes are a major complication of TTP, this may lead to acute ischemia of nephrons → intrarenal AKI
Small vessels:
Thrombotic microangiopathies: hemolytic uremic syndrome (HUS) thrombotic thrombocytopenia purpura (TTP)
Thrombotic microangiopathies describes a specific pathological lesion in which abnormalities in the vessel wall of arterioles and capillaries lead to microvascular thrombosis.
Intra-renal
Common & Significant Causes pt. 2: Vascular Occlusion / Injury
Intrarenal AKI W/U & Findings: (sole) Vascular Injuries:
● CBC peripheral smear (our new friend): would demonstrate < plts and schistocytes (like in other microvascular occlusive disease states)
● UA w/ micro and sediment: less helpful and variable here, but may show everything that you see in ATN
● FeNa: would be HIGH (>1%)
● RUS would NOT demonstrate hydronephrosis
- Take Homes: TTP & HUS may cause micro-occlusive angiopathies that may result in intrarenal AKI. TTP is more systemic (and mixed thrombo - embolic), HUS more focal to the renal microvasculature (and predominantly thrombotic).
Intrarenal AKI 2/2 (micro) Vascular Occlusion: TREATMENTS ↓
● Like most causes of AKI, the treatment plan for Vascular Intrarenal AKI is typically dependent on removing the offending agent and/or treating the primary cause, and providing fluid resuscitation
● Individual Examples of Treatment for Vascular Intrarenal AKIs would be (aside f/ giving fluids):
○ TTP: Thrombotic Thrombocytopenic Purpura
■ Treat the specific cause of the TTP (whatever is causing the TTP to occur in the 1st place)
● Ex: address any autoimmune components, address any contributory medications
■ Supportive therapy (IVF), remove all nephrotoxic agents, renally dose really cleared meds
○ HUS: Hemolytic Uremic Syndrome (more common in peds population)
■ Treat the ST-Producing E. coli infection
■ Supportive therapy (IVF), remove all nephrotoxic agents, renally dose really cleared meds
■ If profoundly hyperuremic or otherwise having severe AKI, these pts may need HD
● See your pre-class readings / access med for further key point specifics on these disease states (testable), and if you have any questions please feel free to come chat with me about them!
Common & Significant Causes pt. 3: Glomerular Disease / Injury
This is where most of the immunologically-mediated glomerulonephritis syndromes come into play and cause acute kidney injury (broad examples below, more specific examples in the pre-class readings)
● A post-infectious GN (like post-streptococcal - the m.c. post-infxn cause of GN), IgA nephropathy, Goodpasture Syndrome
The workup for these syndromes is complicated and often involves assessing for immunologic / autoimmune disease specific serum markers (which you will likely get to in more detail during your rheumatology / immunology courses).
For now, remember:
● The standard AKI workups
● That most current-day immune mediated microvascular syndromes and immune mediated nephropathies fall
under the nephritic syndrome umbrella, meaning they are commonly associated with microhematuria.
● The info on GD in this slide set, & the generalized overview information in the pre-class readings for glomerular dz are still testable material (including the listed names of disease states a/w acute GN in the orange box 2 slides from now, however for my recommended final exam questions, no need to memorize any
additional specifics like specific serum markers for dz states - though FYI they may show up on PANCE)
Intrarenal AKI W/U & Findings: (sole) Glomerular Disease / Injuries:
● UA w/ micro and sediment: the UA will show microhematuria (with DYSMORPHIC RBCs on MICROSCOPY), the sediment may be variable (see orange box on next slide)
● CBC peripheral smear is variable
● FeNa: would be HIGH (>1%)
● RUS: would NOT demonstrate hydronephrosis
!! GLOMERULAR DISEASE-RELATED INTRARENAL AKI WILL
Microhematuria: Glomerular or Extraglomerular ?
Microhematuria: Glomerular or Extraglomerular ?
Glomerular Bleed: Bleed coming from the glomeruli more likely to have….
● Urine micro showing
DYSMORPHIC RBCs (abnormally shaped and sized RBCs, also you may see a wider potential range of abnormal appearance of the RBCs, even in the same sample)
Extraglomerular: Bleed from elsewhere in the urinary tract more likely to have …
● Urine micro showing
ISOMORPHIC RBCs (more normally shape and size, also the variability between differences in shape and size are much more narrow)
Intrarenal AKI 2/2 Glomerular Disease: TREATMENTS ↓
● Like most causes of AKI, the treatment plan for GD-associated Intrarenal AKI is typically dependent on removing the offending agent and/or treating the primary cause, and providing fluid resuscitation
● Otherwise the treatments are HIGHLY VARIABLE depending on etiology and may involve needing steroids, HD, among others and is otherwise beyond the scope of this talk
Intra-renal AKI
Interstitial disease
Common & Significant Causes pt. 4:
Interstitial Disease
80% attributed to?
What will the UA show?
What will the CBC show?
How do you diagnose?
Acute interstitial nephritis
—(80%) medications: NSAIDs, PPIs, Allopurinol, methicillin induced
—infections: cytomegalovirus, strep, legionella
—systemic diseases
—UA w/ micro and sediment in the UA will show microhematuria, pyruvate, urine, WBC casts, eosinophiluira
—CBC will show eosinophilla
—FeNa: would be high >1%
—RUS: would NOT demonstrate hydronephrosis
—Renal bx is required for official dx of an AIN
Intrarenal AKI 2/2 Interstitial Disease: TREATMENTS ↓
● Like most causes of AKI, the treatment plan for AIN-associated
Intrarenal AKI is typically dependent on removing the offending agent and/or treating the primary cause, and providing fluid resuscitation
● Like HD, otherwise the treatments are HIGHLY VARIABLE and
may involve needing steroids, HD, among others and is otherwise beyond the scope of this talk (however the basic info outlined in the pre-class readings are testable material)
Intra-renal image for reference
Post renal — all covered in previous slides
Rhabdomyolysis
Nephrotic vs nephritic
Nephrotic and nephritic syndrome
