Nephrology And Urology Flashcards
RIFLE criteria for AKI
R: risk of kidney injury
Cr- 1.5*base line
Uo- < 0.5 mL/kg/h for > 6 h
I: Injury to the kidney
2*base line
<0.5 mL/kg/h for > 12 h
F: failure of kidney function
3*baseline or SCr>4 with an acute rise >0.5 mg/dl
<0.3 mL/kg/h for > 24 h or anuria for >12 h
L: loss of kidney function
Persistent renal failure for >4 week
E: End-stage disease
Persistent renal failure for> 3 months
Causes of AKI
1- Prerenal
2- Renal
3- Postrenal
Prerenal causes:
( reduced renal perfusion)
True volume depletion :
a-hemorrhage
b-renal or extra-renal loss (GI, Skin)
Decreased effective blood loss (ebv)
a- CHF. b- Hepatorenal syndrome
c-third space fluid accumulation
Increased renal vascular resistance
A-Hypercalcemia
B-NSAIDs
C-Calcineurin inhibitors:
cyclosporine ,tacrolimus, ACEI, ARBs
Renal causes
A-Glomerular: RPGN, PSGN, HUS, ANTI-GBM
B- Tubular: ATN (ischaemic/toxin)
C- Interstitial: AIN
( Allergy, infection, infiltration)
D- Vascular: Renal artery stenosis/thrombosis
Post-renal causes:
1- INTRA-URINARY TRACT:
A- intraluminal: stone, blood clots, sloughed papillae, crystal
B- intramural: tumor, infection, neurogenic drug, stricture
2- EXTRA-URINARY TRACT:
Prostate: hypertrophy, cancer
Retroperitoneal fibrosis, lymphoma
AKI Complication
Metabolic acidosis
Pulmonary edema
Hyperkalemia
Pericarditis
Arrhythmias
Hypertension
Hyperuricemia
Mx of AKI
1-Pre-renal: correct volume depletion with fluid challenge/ improve circulatory volume
2- Renal: remove toxins/ ischemic insult
Supportive tx of : A- intravascular volume overload . B-hyperkalemia
C- metabolic acidosis
3- Post-renal : Relive obstruction (specific aetiology-dependent )
Possible therapy includes: @ in-dwelling bladder catheter. @nephrostomy. @Stenting
RRT indication for AKI
(RENAL REPLACEMENT THERAPY)
- EDEMA ( pulmonary)
-HYPERKALEMIA ( refractory)
-PERICARDITIS
-ACIDOSIS (refractory)
-ELEVATED BUN (>35mM)
-ENCEPHALOPATHY
Contrast Induced Nephropathy
Presentation:
Relatively common cause of AKI but is rarely associated with irreversible loss of kidney function.
1- It can present as oliguria or nonoliguria
2- THE ONSET OCCURS WITHIN 24-48 hr after exposure, reaches a peak within 3-5 days, and subsides within 7-10 days
Contrast induced nephropathy
RISK FACTORS:
- Age>55
-Preexisting renal insufficiency
-Diabetic nephropathy
-Volume depletion
-Low CO
-MM
-Large volume of contrast
CKD
Kidney damage or
GFR < 60 mL/min/1.73m2 for 3 months or longer