Renal Material Flashcards
Things to look for to determine Prerenal
20:1 BUN/Scr ratio increase of BUN rapidly no evidence of cell death no RBC no WBC Urine Na < 20mEq/L FeNA % <1 (conserving)
Things to look for to determine Intrarenal
16:1 BUN/Scr ratio Scr doubles, BUN increases (not as rapidly as prerenal) muddy brown casts RBC, WBC Urine Na >40 mEq/L FeNA% >2 (wasting)
Things to look for to determine Postrenal
16:1 ratio BUN/Scr cellular debris RBC -variable WBC -1+ >40 mEq/L FeNA% >2 (wasting) blockage/ obstruction
Prerenal AKI also known as
Prerenal Azotemia
Prerenal involves changes in
Volume and tone
Prerenal occurs in
afferent and efferent arterioles (Glomerulus)
Risk factors for prerenal
Age Diuretic use Poor oral intake GI fluid loss CHF Renal Artery Stenosis ACEi/ARBs NSAIDs
Prerenal Treatment
Fluid replacement with NaCl
Intrinsic kidney injury also known as
Intrarenal AKI
What is intrinsic kidney injury
structural damage to glomerulus, tubules or interstitium which often occur due to prolonged prerenal causes
Intrinsic kidney injury leads to
renal cell necrosis by mechanisms of ischemia, infection or immune response that result in inflammation
3 types of intrinsic kidney injury
Acute tubular necrosis (ATN)
Acute interstitial nephritis (AIN)
Glomerulonephritis
Diagnosing with ATN
muddy brown casts
epithelial cells
no crystals
mild proteinuria (
Diagnosing with AIN
WBC casts, eosinophilic casts
WBCs 2-4+, eosinophils
No crystals
mild proteinuria (
Diagnosing with Glomerulonephritis
RBC casts RBCs Crystals may be present moderate-large proteinuria (.5-3g/day or >3g/day) slower development over 7-10 days
Drug induced postrenal AKI
Common drug causes include acyclovir, indinavir, sulfadiazine, chemotherapy causing high cell turnover (e.g., uric acid nephropathy)
kidney calculi (kidney stones)
Nephrolithiasis: the process of forming kidney stones
May or may not lead to postrenal obstruction
Who develops?
Family history of calcium oxalate stones or urate stones
Diabetes, gout, obesity
Leads to flank pain and hematuria; may lead to renal obstruction
Prevention is key through hydration and dietary modifications (low oxalate and low urate containing foods)
AKI clues:
Tenting of skin
prerenal
AKI clues:
Dark urine
prerenal
AKI clues:
Fever/high WBC
AIN or Glomerulonephritis
AKI clues:
Fever/Rash
AIN or Glomerulonephritis
AKI clues:
Blood in urine
Glomerulonephritis or postrenal obstruction (kidney stones)
Kidney regulatory function
Control composition and volume of blood volume
Maintain stable concentrations of cations such as sodium (Na), potassium (K), and calcium (Ca)
Maintain acid-base balance
Kidney Excretory function
Produce urine
Remove metabolic waste (e.g., urea and other waste products)
Kidney Hormone function
Produce renin for BP control
Produce erythropoietin which stimulates marrow production of red blood cells
Activate 25(OH)-D (inactive vitamin D) 1,25(OH)2D (active vitamin D)
Kidney Metabolic function
Gluconeogenesis
Metabolize drugs and endogenous substances (e.g., insulin)
Normal kidney sodium reabsoprtion
Normal kidney = 99% of sodium is reabsorbed with a net loss of 1% or less into urine
Afferent Arteriole
Looking at volume and tone
Efferent Arteriole
looking at tone
What is AKI?
200% increase of the serum creatinine over 24 hours
Acute ↑ in creatinine with or without↓ in urine output over a short period of time
Nonoliguria
urine output > 500 mL in 24-hours (per day)
oliguria
Urine output 100-500 mL in 24-hours (per day)
Anuria
urine output < 100 mL in 24-hours (per day)
Non-modifiable risk factors for AKI
Chronic kidney disease Diabetes Older age Chronic liver disease (e.g., cirrhosis) Congestive heart failure (CHF) Renal artery stenosis Peripheral vascular disease
Modifiable risk factors for AKI
Volume depletion (e.g., poor oral intake/dehydration, diarrhea, vomiting) Hypertension/Hypotension Hypoalbuminemia Sepsis/shock Nephrotoxic medications Major surgery/anesthesia
Drugs associated with prerenal AKI
ACEi/ARBs * NASAIDs * Cyclosporine Tacrolimus SGLT-2 inhibitors
impaired regulation with NSAIDs in prerenal
NSAIDs inhibit prostaglandins –> constriction of afferent arteriole -> reduced flow and pressure –> decreased perfusion pressure and filtration
impaired regulation with ACEi/ARBs
ACEi/ARBs block angiotensin 2 –> dilation of efferent arterioles –> reduction in back pressure –> decrease perfusion pressure and filtration
Drugs associated with ATN
Radiocontrast media
Aminoglycosides (AG)
Contrast induced nephropathy (CIN)
↑ in SCr by ≥0.5 mg/dL or 25% from baseline
Usually begins 24-48 hrs post-procedure; Peaks in 3-5 days and begins downtrending; Returns to baseline in 7-10 days
CIN risk factors
Age anemia HF hypotension volume depletion
drug induced ATN
Major cause of drug-induced ATN
Variable incidence of nephrotoxicity, 1.7-58%
Onset: 5-10 days after initiation of therapy; serious; largely preventable
Proposed pathogenic mechanism
Cationic charge (heavily filtered into tubule) binding and uptake by PCT cells disrupt normal cell function tubular cell death
Stimulate Ca sensing receptor in the apical membrane induction of cellular signaling and cell death
Presentation: ATN (oliguric or non-oliguric), magnesium wasting, FeNa >2%, presence of muddy brown casts
ATN MOA
rupture proximal tubular epithelial cell
ATN patient related risk factors
CKD Advanced age Liver disease Dehydration Hypotension Magnesium or potassium deficiencies
ATN drug related risk factors
Prolonged course Cumulative dose Trough concentration >2 mcg/mL Repeated courses (14-day wash out) Concomitant nephrotoxic agents
Drugs associated with AIN
Allergenic medication
penicillins, cephalosporins, fluoroquinolones, sulfamides, NSAIDs, PPIs
Drug induced AIN onset
7-20 days due to sensitizing
drug induced AIN treatment
Stop drug and start prednisone 1 mg/kg/day
Drugs associated with Postrenal
Acyclovir
Sulfonamides
Indinavir
Management of DIKD
stop offending agent
avoid nephrotoxins
maintain hydration
