AKI/CKD Flashcards
(23 cards)
Define the following
- oliguria
- anuria
- AKI (labs)
stages of AKI
oligouria: little urine output: less than 400-500 ccs/day or less than 20cc/hour
Anuria: < 100 cc/day, no urine output
AKI: Acute Kidney Injury
- an increase in SCr > 0.3 mg/dL in 48 hours
- an increase in SCr > 1.5x their baseline Cr within 7 days (CKD pts. with naturally high Cr levels)
- < 0.5 cc/kg/hr urine output for 6-12 hours
we use SCr as our measure because Cr usually should be completely excreted through the urine: completely filtered out of blood: when theres an increase in SCr that means the kidneys arent doing their job
Classification of AKI comes from the KDIGO criteria and AKI is very common in the ICU and in the hospital
Stages of AKI
stage 1: the above criteria are met
stage 2: longer time of injury essentially
stage 3: can be an indication for dialyisis ish but not only the stage
Prerenal AKI
Etiology
most common type of AKI
Etiology
- a result of renal hypoperfusion; lost blood flow to the kidneys due to…
1. hypovolemia (any state of dehydration: fever, GI issue, dec. PO intake)
2. hypotensions & shock (shunting from kidneys)
3. hemorrhage
4. low cardiac output
5. over-diuresis
6. third spacing of fluid: edema to the liver, abdomen, burn pts. (there is a decrease in oncotic pressure; no pull of fluid into vessel and tehreofre low volume)
quick patho
- if there is a decrease in influx of blood to the glom. you have a decrease in pressure: but the glom. relies on the pressure gradient to force things from high (vessel) pressure to low (filtrate bowmnes space) pressure
- wihtout this pressure gradeint: you dont have proper renal function, poor filteration, reabsorption, excretion, etc.
Prerenal AKI
Diagnosis
Treatment
Diagnosis
- need a SCr level which meets criteria for dx.
- BUN/Cr ratio > 20:1 : because there is low flow, want to increase pressure so the body HOLDS ONTO the proteins (urea here) to try to increase oncotic pressure and try to fix the problem : results in lots of BUN in the blood
- urine sodium concentration LOW: < 10-20 mEq/L with hypovolemia because the body isnt letting any of those solutes go! trying to reabsorb them
- FENA < 1%: (fraction excreted of sodium) low because the body is holding onto more sodium than usual
FENA could be fasley high if they were given diueretics in the past 24 hours – check Feurea < 35% for these ppl.
- Urine Microscopy: bland urine, occasional hyline casts (protein)
Treatment
- ACHIEVE EUOVOLEMIA!! fix teh hypotension
- increase fluids
- if septic: give abx., pressures & maybe fluids
- if HF: improve cardiac output
- if hemmorahing: balanced receccitation (with lac. ringers)
Postrenal AKI
- etiology
- presentation
Etiology
- urine OBSTRUCTION of flow from both or one kidney (if thye only have 1) OR can be so downstreatm that its blocking all flow from both kidneys
- least common AKI
- can be a result of …
1. urinary retention
2. uretheral/ureter obstruction
3. BPH (most commonly)
4. bladder/cervical cancer
5. neurogenic bladder issues
6. bilateral stones in urethra
the obstruction leads to an increase in intratubular pressure (backflow) and therefore a decrease in GFR since theres now too high of pressure in the filtrate bowmans capsule to filter
Postrenal AKI
Diagnosis
Treatment
Diagnosis
- BUN:Cr ratio will be > 20:1 : poor urine output so kidneys think its bad pressure and tries to increase pressure with increase in reuptake of BUN
- FeNa < 1%
Imaging
- renal/bladder ultrasound!!: see hydronephrosis, large bladder volume or hydroureter
- can get CT if suspicious for cancer or malignancy
Treatment
- place an indwelling cath. to release the increase urine volume downstream
- treat the underlying conditions
- BPH: surgery or meds
- stones: lithotripsy
- cancer: chemo, radiation, surgery
- obstriction: stent
- pts. may have post-obstrutive diueresis, watch electrolytes and hypovolemia
Intrinsic AKI
Etiology
the post-renal or prerenal causes are excluded: or lead to intrarenal issues
Etiology
- damage is within the interstitum, vasculature, tubules or glomeruli of the kidney
each type of intrinsic AKI develops as its own
Itrinisic AKI
ATN
etiology
diagnosis
treatment
ATN: damage to the TUBULES most common intrinsic AKI
- ischemic or nephrotoxic agents (either exogenous or endogenous)
- abx (aminoglycosides, vancomyinc, amphotericin B)
- contrast
- hemolysis
- MM
- myoglombinuria (to rhabodomyolysis) see muscle breakdown by elevated CK, urine dipstick can show heme (but itrs really myoglobin) but no U/A with blood fix this with severe hydration
Diagnosis
- BUN:Cr ratio < 20:1 because now there is damage to the tubule and the ability to reuptake BUN –> thus it cant reabsorb anything
- FENA > 1%: excreting lots of sodium: body wants to hold on but damaged walls so it cant
- muddy brown casts with renual tubular epithelial cells
Treatment
- ischemic: avoid hypotension and treat underlying issue
- nephrotoxi: avoid agents, renally does
Intrarenal AKI
Acute Interstital Nephritis
(ANI)
Etiology
Presentation
Diagnosis
Treatment
Etiology: intrinsic AKI due to inflammatory interstitial reaction
- medication induced: penicillins, NSAIDS
Presentation
- rash, fever, arthralgias
Diagnosis
- eosinophilia (allergic response)
- white blood cell casts & eosinophils in urine
Treatment
- medication: remove it
- infection : treat it
- glucocorticoids can help
-
Acute Glomerular Nephritis
labs
damange which is occurring at the glomerulural level (least common)
Labs
- RBC casts!!
- hematuria
- proteinuria
- crecents seen in rapidly progressing nephritis
(referring i think to nephrotic and nephritic here) any injury at the glomerulus)
Vascular Intrinisic AKI
- large vessel
- small vessel
Large Vessel
- bilateral renal artey stenosis
- bilateral rein vein thrombosis
Small Vessel
- malignant hypertension
- atherosclerosis or thombotic emboli (thrown from somewhere else)
- HUS
- TTP
Indications for Dialysis
AEIOU!!!!
A: acidosis: refractory – pH < 7.1
E: electrolytes that are refractory – hyperkalemia > 6-6.5
I : intoxications - dialyazable (S: saliclates, L: lithium, I: isopropynol, M: magnesium E: ethylene glycosol, barbituates too)
O: overload of volume : refractory to dieuritics and affecting OXYGENATION STATUS
U: uremia and symptomatic (pericarditis ,AMS: brain risk!!)
Chronic Kidney Disease (CKD)
Etiology
definition
most commony etiology of CKD in the US is HTN and DM
Etiology
- Glomerular: diabetic nephropathy, renal amyloidosis, post-strep glomerulonephritis
- Tubulointersistial: drug incuded, sickle cell, chronic kidney infections
- Cystic: Polycystic Kidney Disease
- obstructive: prostate, stones, congenital
- vascualar: hypertension, renal artery stenosis
Definition
- Injury: kidney damage OR decreased function
Kidney Damage
- albuminuria (proteinuria)
- urinary sediment abnormalities (liks casts)
- imaging abnormalites (cysts)
- pathology: vai biopsy
- history of kidney transplant
Kidney Function
- assess using GFR (a decrease)
- Duration: greater than 3 months
Diagnosis of CKD
4 layers of
Labs
- BMP: look at Cr & electrolytes
- urinalysis/microscopy: broad, waxy casts & proteinuria because the tubules are damange so they’re windened (broad) and waxy = scarring
Imaging
- US: small, ecogenic kidney
- CT: shows abnormalities
Determine level of Proteinuria
- Albumin-Creatinine Ratio: via a spot check of the urine
- normal ACR is < 30 –> CKD will have > 30
Determine GFR
- eGFR: an estimate of GFR to stage CKD
- note: remember that CrCl is NOT an eGFR used to dx. CKD – CrCl is used for medication adjustments as it tells you the rate of flow through
- eGFR: via CKD-EPI equation, diet renal disease, etc.
Staging: CKD stages 1-5 (GFR) (3A & 3B) but also accounts for albumin to creatinine ration to account for progression and effect of teh disease progrnosis
- more severe albumin to creatitine ratio (> 300) is worse outcome
- CKD stage 5: GFR < 15
- CKD stage 1: GFR > 90
Management of CKD (primarily)
- management of DM
- wathc BP
- weight loss
- avoid nephrotoxic medications (NSAIDS)
- dietary modifications
- ACE/ARBS good for proteinuria (until late stages)
- SGLT-2 good for proteinuria (until into late stages of CKD – then you cant use)
Dialysis: for some
- helpful to improve life expectancy
- hemodialysis: access point of cathete or AV fistula; risk of infection
- peritoneal dialysis: done through the peritoneum via catheter; risk of peritonitis cannot have hyperkalemia and do this takes too long
Complications of CKD
- electrolytes
- hyperkalemia signs and treatment
first electrolyte to be disturbed with CKD is phosphorous
last one: when you know youre in trouble uremic syndrome
Hyperkalemia
- muscule weakeness, parlysis
- get BMP ASAP & EKG: peaked T waves fis asap wide QRS: you have minutes before they’re dead
Treatment of Hyperkalemia in CKD
1. intracellular shift of K+ (temporay fix)
- push insulin & D50: insulin forces K+ into the cell and pulls H+ out
- albuterol shifts K+ into cells
- bicarb if they come in acidotic
- stabilize the cardiac membrane (for those who have the peaked T waves and/or wide QRS)
- calcium gluconate - potassium binding/excreting thearpy (to actaully get the potassium out of the body)
- kayexalate (gut ischemia risk)
- lokelma (excrete through the bowel)
- loop diuretic (but id the CKD is bad this might not work)
- dialysis if you have tried everything
chronic hyperkalemia management
- potassium sparing diet (2g/day)
- avoid meds that increase K+
( k+ sparing diueretics, aldosterone antoagonists, ACE/ARB or beta blocker)
Complications of CKD
Uremia
Uremia: accuulation of uremia toxins can casue symptoms at a GFR < 10
- see increase in BUN (significant) on BMP
symptoms
- N/V
- ITCHY: puritis
- metallic taste
- uremic fector: hailtosis, twitching
- lethragy, confusion, seizure, coma
treatment
- dialysis
Complications of CKD
Cadriovascular
HTN: LV hypertrophy, vascualr remodeling, electrolyte issues, RAAS activation, volume overload/edema
treatment: low salt, fluid restriction, diuretics, ACE/ARB (unless hyperkalemia then no)
goal BP: < 130/80 outpt. < 120-125/80 via KDIGO
Cornary Artery Disease
Heart Failure (HFpEF)
Pericarditis: because uremia!!!!
Complications of CKD
Mineral and Bond Disorder (MBD)
pathology
disruptions in phosphorous excretion– because the kidney is dropping its GFR – it cant excrete the phosphate –> increased phosphate in the serum
increase in phosphate will trigger a block in PTH and a block in activating Vit D (called calcitriol)
lacking calcitrol –> cant absorb calcium from the intestines = lack of calcium
also with increased phosphate: it will bind to calcium (thuse reducing the avalible free calcium)
low calcium will stimualte PTH production more than the blocking that phosphate will do
PTH will trigger a release of calcium from the bone stores – leading to osteitis fibrosa cystica
additionally: high phosphate binds to calcium and leads to complex formation in the arteries and CAD
Complications of CKD
MBD
treatments- phosphorous
Phosphorous
once GFR gets to < 30 — see increased levels
- start with reducing phosphorous in the diet: to about 900mg
- phosphate binders can be used (if increased levels despite dietary changes)
Phosphate binders
- calcium carbonate, calcium acetate (but have calcium, can be an issue because if you add calcium to the pt. then you increase the risk of calcifications and CAD)
- preferred agents are non-calcium containing phosphate binders: sevelamer, lanthanum
complications of CKD
MBD
Vitamin D Treatment
what if they have secondary hyperparathyroidism
Vitamin D: only replenished if serum phosphorous is controlled from the phosphate binders AND the pt. is NOT hypercalcemic
treatment: Vitamin D2 (ergocalciferol) and Vitamin D3 (cholecalciferol)
these are not activte Vit D – need good enough renal function to convert the inactivte to active
Secondary Hyperparathyroidism (they need active vit D)
cacitriol: can be given (the active vit D)
cinacalet: for those on dialysis: a calcimimetic who binds to calcium receptors (CAPR) ; lowering the PTH production
-cinacalet for pts. who have high serum calcium, high serum phosphate, high serum PTH
Types of bone complications with CKD - MBD
osteitis fibrosa cystia: high bone turnover
adynamic bone disease: low bone turnover
osteoperosis
find which kind via bone biopsy
symptoms
- bone pain
- muscle weakness
- increased pathologic fractures
Hematologic complications of CKD
anemia
platelt dysfunctions
Anemia
- direct reduction in EPO production from the kidneys due to disease
- see anemia on CBC: MCV will be normal or decreased = anemia of chronic disease
Treatment:
- iron supplementation
- EPO via epoetin when Hgb < 9
Platelet Dysfunction
- uremia impacts the ability to clot
- CKD 4-5 : increased risk of bleeding
- give desmopressin to those with increased risk of bleeding pre-op
CKD & Metabolic Acidosis
- patho
- labs
- treatment
Metabolic Acidosis: due to a reduction in the kidneys ability to excrete the byproducts of amino-acids
- around GFR 40-50: ammonia buffer system in kidneys starts to decline
- bicarbonate amounts in serum begin to decrease because its being all used up to buffer the increasing ammonia
Labs
- once the bicarb is being used up to help at the kidneys = serum bicarb < 22
- can have a normal anion gap (because lost bicarb) but over time can create an anion gap (because acids are being added)
Treatment
- limit protein in diet
- supplement with bicarb
