Renal Tubular and Interstitial Diseases Flashcards
(36 cards)
Definition of AKI
Loss of renal function over hours or days
Clinically as retention of nitrogenous waste products (rising creatinine and urea)
Causes of AKI in hospital setting
ATN
ATN
Most common cause of AKI in hospitalized
Ischemia or exposure to substance directly toxic to tubular epithelial cells
Types of nephrotoxic injury
Ischemic injury
Aminoglycosides
IV contrast media…other random medicines..also .ethylene glycol
Endogenous - myoglobin from rhabdomyolysis
Ischemic - spetic, burns, homrrhage, prolonged dehydration, CHF
Most susceptible areas of injury of the PCT
S3 segment and TALH (thick ascending loop of Henle)
High tubular energy requirement (ATP)
Decreased O2 supply
Minimal glycolytic machinery
Pathology of ATN…early
Loss of apical brush borders
Blebbing of atypical cytoplams into lumen with eventual loss
Vacuoolization of cytoplasm
Pathology of ATN
Luminal ectasia
Epithelial simplification from loss of cytoplasm
Granular casts (of cellular debris and Tamm-Horsfall prtoein)
With renal tubular epithelial casts
ATN regnerative phase
Mitotic figures
increased N/C ratio
Prominent nucleoli
U/A of ATN
Tubular epithelial cells
Tubular epithelial casts
Granular casts “muddy brown”
Multiple granular casts
GFR and ATN
DECREASED because
Vasoconstriction - AA via increased NaCl and flow to the macula densa
Tubular obstruction - casts and cell debris
Denuded tubular epithelium - back leak of filtrate to the interstitium
Direct toxocity to glomerular vasculature
FENa
Frctional excretion of Na
Urinary (Na)/plasma (Na) *GFR
U(na)P(cr)/(PnaUcr)
When conserving Na, would be below 1%…in ATN, over 1-2%
ATN clincal
Sustained decrease in urine output
some do NOT have oliguria
Sodium and H2O overload - hypervolemia
Elevated BUN, creatinine, K+
Acidosis
ATN management
Prevention is key**
Na, H2O, and K restriction
Diuretics will not alter the outcome but will assist in management
Close assement of dosing
ATN recovery phase
Steady increase in urine volume…solute diuresis, eliminating the accumulated Na and water…decreased ability of kindye to concentrate (loss of medullary osmolarity and ADH)
Hypokalemia
BUN and cr return to normal
More infections
Atn outcome
Prognosis depends on clinical setting
Contrast neprhopathy
Renal vascular constriction caused by high osmolarity, endothelin and adenosine
12-24 hours after constrat
Non-oliguric and function reutnr in 5-7 days
Pts with diabetic nephropathy at higher risk
Contrast nephropathy managmeent
Prevention
Risk./benefit
Acetylcysteine not provem
Fluids - bicarb or normal saline…just hydrate them
Aminoglycoside toxicity
Accumulates in proximal tubular cells
Intracellular concentrations arem uch higher than plasam
5-7 days after initiating tx
Decreased istal ADH sensitivity, fanconi syndrome, hypomagnesemia
NON-oliguric
Drug associated AIN
INvolvement of kidney by immunologic response to medication
T-cell mediated or AB mediated
Acute renal fialure within 1-2 weeks of drug expoure
Also maybe to systemic AI ds of malignant neoplasms
Allergic reaction
Drug induced AIN
Fever, rash, eosinophilia
Mild flank pain
AKI
Leukocyturia with eosinophiluria
US - normal or enlarged kindey and increased cortical echogenecity
Acute pyelonephritis
Acute bacterial infection with suppurative inflammation
Most by ascending urinary tract infection (E coli)
Minority from hematogenous from Stpah
Does NOT cause AKI unless bilateral, septic, dehydrated or has one kidney
Acute pyelonpehritis urinalysis
WBCs and bacteria are nonspecific that could be found in cystitis
WBC casts are specific and localized to renal parenchyma
COmplications of acute pyeloneprhitis
Papillary necrosis - diabetics
Acute pyeloneprhtiis clinical
Fever, chills, severe unilateral flank pain, dysuria, urgency
Urine and blood culture
