Diseases Flashcards
Defined as a sudden decline in kidney function causing disturbances in fluid, electrolytes and acid-base balance due to a loss of small solute clearance and
decreased GFR
acute kidney injury
Increased mortality even if renal function returns to normal**
AKI is defined as
Reduction of renal function within 48 hrs as defined by:
Absolute increase in serum creatinine > or equal to 0.3 mg/dl
Percentage increase in serum creatinine > or equal to 50%
Reduction in urinary output, with documented oliguria of less than 0.5 ml/kg per hour for more than 6 hours
stages of AKI
Stage 1-Inc. in Serum Cr >.3 or 150-200% from baseline, along with oliguria for
>6 hrs
Stage 2-Inc. in Serum Cr 200-300% from baseline, along with oliguria for >12 hrs
Stage 3-Inc. in Serum Cr >300% from baseline, need for RRT, and/or oliguria for 24 hrs/anuria > 12 hrs
An adaptive response to severe volume depletion and hypotension, with structurally intact nephrons
**Most common form of AKI, accounts for 55% AKI
pre-renal
what can cause prerenal failure
- volume depletion
- decreased CO
- arteriole vasoconstriction
- systemic vasodilation
M/C caused by acute tubular injury (ATN), either ischemic or cytotoxic
intrinsic
what can cause intrinsic renal failure
- drugs
- vascular
- AI
- tubular
Mechanical obstruction of urinary collecting system resulting in obstructive uropathy
postrenal
S/S chronic renal failure
fatigue, weight loss, anorexia, nocturia, and pruritis
acute tubular necrosis casts
granular, muddy brown
epitheleal
glomerulonephritis casts
RBC, tea colored
prerenal failure will have a FENa of
< 1%
how to tx AKI
volume expansion
decrease potassium intake, insulin & glucose, albuterol, kayexelate, lasix, IV calcium (cardiac instability)
when is dialysis indicated
volume expansion that cannot be controlled by diuretics Hyperkalemia refractory to medication
Severe acid-base imbalances refractory to medication Severe azotemia (BUN > 80-100), uremia,
Seizure/coma
CC <10 and serum Cr >9
how long after AKI is a pt dx with chronic renal failure
no improvement after 6-8 weeks
Accounts for 85% of Intrinsic AKI
Death of tubular cells that form the tubule that
transports urine to the ureters while reabsorbing 99% of the water (and highly concentrating the salts and
metabolic byproducts)
ATN
ischemic ATN shows
skip lesions through tubules
toxic ATN
Characterized by proximal tubular epithelium necrosis due to a toxic substance, necrotic cells fall into the tubule lumen, obliterating it
BM intact, so regen is possible
MC drug causing toxicity
aminogylcosides
acute interstitial nephritis usually caused by
acute allergic reaction to a medication, including antibiotics and nonsteroidal anti-inflammatory drugs (NSAIDs)
Also linked to infections, diseases, and transplant rejection
Clinical presentation hallmark:
Fever, Rash, Eosinophilia **
Also arthralgias, proteinuria, hematuria, and Sterile pyuria
AIN
AGN
Acute glomerular Nephritis always have some urinary
protein, hematuria with RBC casts, and sometimes pyuria with WBC casts….this is known as nephritic or active urine. Dark tea colored urine
CGN
Chronic Glomerular Nephritis is noted for heavy
proteinuria and urine fat (oval fat bodies)….this is known as nephrotic urine.
low vs normal complement for AGN
low-Post infectious, SLE, MPGN
normal-Iga nephropathy, Good pastures,
Young men > women (6 X )
Hemoptysis , SOB, anemia, reddish urine
High bun/creat. , high anti serum anti GMB
Often have pulmonary & renal symptoms
Goodpasture’s Syndrome
tx w/plasmapharesis and steorids
Patients tend to be s/p pharyngitis, impetigo, sub acute
endocarditis…. Group A beta hemolytic streptococcal infections
1-3 weeks after infection
Patient becomes lethargic slight edema,oligiuric, HTN, red urine “cola colored”.
post infectious GN
Most common form of Acute GN
Children and young adults, M>W
Occurs 1-3 days af ter throat infection with reddish
“cola” urine.
IgA Nephropathy (Berger’s dx)
MCC Cryoglobulin Associated GN (Necrotizing skin lesions, Arthralgias, Fever, Hepatosplenomegaly, Low complement levels)
Hep B/C
Effects the basement membrane becomes thickened due to immune deposition and mesangial proliferation.
BM “double layer” appearance
membranoproliferative GN
type one is more nephrotic
type two is more nephritic
Heavy proteinuria (>3.5gr./24hr) Hypoalbuminemia (<3gr./dl)
Fat bodies in urine (“maltase cross”)
nephrotic syndrome
MC cause of N.S. in kids (<10 y/o) and can follow a viral URI
Loss / fusion of epithelial cell foot processes
In adults its MC associated NSAIDS, and less commonly associated with Hodgkin’s Dx.
Proteinuria with no hematuria
minimal change disease (nil’s)
M.C. primary Cause of N.S. in adults, 5-6th decade of life
membranous nephropathy
Characterized by scaring of mesangial cells on microscopy and is diagnostic
May see decreased renal function at time of diagnosis in 30-50% of patients
Focal Segmented Glomerulur Sclerosis
MCC end stage renal disease
Diabetic nephropathy
chronic renal failure
GFR will increase to nl as a result of hyper filtration of remaining nephrons… this eventually leads to scaring and progressive rapid loss of GFR
broad waxy casts
when should diabetics start dialysis
GFR is 15 or serum Cr. Is
