AKD Flashcards
SEVERITY
- asymptomatic
- fatal
- sudden
- Renal function
- Retention of nitrogenous wastes
AKD
duration of AKD
- acute
- chronic
Categories of Acute Kidney Injury
- Hypovolemia
- Decreased cardiac output
- Decreased effective circulating vol
+ Congestive heart failure
+ Liver failure - Impaired renal autoregulation
+ NSAIDs
+ ACE-VARB
+ Cyclosporine
PRERENAL
Categories of Acute Kidney Injury
INTRARENAL
- Glomerular
+ Acute glomerulonephritis - tubules and interstitium= sepsis/ infection, ischemia, Nephrotoxins
- Vascular
+Vasculitis
+ Malignant hypertension
+ TTP-HUS
Categories of Acute Kidney Injury
POSTRENAL
- Bladder outlet obstruction
- Bilateral pelvoureteral obstruction (or unilateral obstruction of a solitary functioning kidney)
Factors that affect the autoregulatory response:
- Atherosclerosis
- Age
- long standing hypertension
- SBP <80 mm Hg
narrowing and
impaired vasodilation
Hyalinosis and myointimal
hyperlasia
ecreased perfusion pressure in the presence of NSAIDs
- Decreased vasodilatory prostaglandins
- increased angiotensisn II
creased perfusion pressure in the presence of ACE-I or ARB
- slightly increased vasodilatory prostaglandins
- decreased angiotensin II
- Arterial vasodilation in the splanchnic circulation despite volume overload
- Reduced systemic vascular resistance
- Vasoconstriction: Hypovolemia
HEPATORENAL SYNDROME
perturbations in the microcirculation
occlusion of small vessels
HYPOXIA
directly
generation of free radicals
CYTOTOXIC DAMAGE
Nephrotoxins: Antibiotics
Exogenous:
high trough levels
Vancomycin
Nephrotoxins: Antibiotics
Exogenous:
both cause tubular necrosis
(vasoconstriction and direct tubular injury)
Aminoglycosides & Amphotericin B
Nephrotoxins: Antibiotics
Exogenous:
tubular obstruction
Acyclovir
Nephrotoxins: Antibiotics
Endogenous
- intrarenal vasoconstriction,
- direct proximal tubular toxicity
- mechanical obstruction
- Intratubular crystals
Intrinsic: Glomerulonephritis
- glomerular podocytes
- mesangium
- endothelial cells
Where is WBC cast found in urinary?
Distal
Where is Epithelial cell cast found in urinary?
Distal
Where is hyaline cast found in urinary?
Loop of Henle
History of poor fluid intake or fluid
loss (hemorrhage, diarrhea, vomiting, sequestration into extravascular
space); NSAID/ACE-I/ARB; heart failure;
evidence of volume depletion (tachycardia, absolute or postural hypotension, low jugular Venous pressure,
dry mucous membranes), decreased ffective circulatory volume (cirrhosis,
heart failure)
Prerenal azotemia
- BUN/creatinine ratio above 20,
-FeNa <1%, - hyaline casts in urine sediment,
- urine specific gravity >1.018,
- urine osmolality >500 mOsm/kg
Prerenal azotemia
epsis, sepsis syndrome, or septic
shock. Overt hypotension not always
seen in mild to moderate AKI
Sepsis-associated AKI
Positive culture from normally sterile
body fluid; urine sediment often
contains granular casts, renal tubular epithelial cell casts
Sepsis-associated AKI
Systemic hypotension, often superimposed upon sepsis and/or reasons for limited renal reserve such as older age, CKD
Ischemia-associated AKI
Urine sediment often contains granular casts, renal tubular epithelial cell casts FeNa typically >1%
Ischemia-associated AKI
Nephrotoxin-Associated AKI: Endogenous
- Traumatic crush injuries, seizures, immobilization
- Elevated myoglobin, creatine kinase; urine heme positive with few red blood cells
- FeNa may be low (<1%)
Rhabdomyolysis
Nephrotoxin-Associated AKI: Endogenous
- Age >60 years, constitutional symptoms, bone pain
- Monoclonal spike in urine or serum
electrophoresis; low anion gap; anemia - Bone marrow or renal biopsy can be
diagnostic
Multiple myeloma
Nephrotoxin-Associated AKI: Endogenous
- Recent chemotherapy
- Hyperphosphatemia, hypocalcemia,
hyperuricemia
Tumor lysis
Nephrotoxin-Associated AKI: Endogenous
- Recent blood transfusion with transfusion reaction
Recent chemotherapy - Anemia, elevated LDH, low haptoglobin
- FeNa may be low (<19%); evaluation for transfusion reaction
Hemolysis
Nephrotoxin-Associated AKI: Exogenous
- Exposure to iodinated contrast
- Characteristic course is rise in SCr within 1-2 d, peak within 3-5 d, recovery within 7 d
- FeNa may be low (<1%)
Contrast nephropathy
Nephrotoxin-Associated AKI: Exogenous
- Aminoglycoside antibiotics, cisplatin, tenofovir, zoledronate, ethylene glycol,
aristolochic acid, and melamine - Urine sediment often contains granular casts, renal tubular epithelial cell casts. FeNa typically > 19%.
- Can be oliguric or nonoliguric
Tubular injury
- skin rash, arthralgias, sinusitis (AGBM disease) lung hemorrhage, recent skin infection or pharyngitis (poststreptococcal)
- ANA, ANCA, AGBM antibody, hepatitis
serologies, cryoglobulins, blood culture, decreased complement levels,
ASO titer (abnormalities of these tests depending on etiology)
Glomerulonephritis/ vasculitis
- Nondrug-related causes include tubulointerstitial nephritis-uveitis (TINU) syndrome, Legionella infection
- Eosinophilia, sterile pyuria; often
nonoliguric - Urine eosinophils have limited diagnostic accuracy; kidney biopsy may be necessary
Interstitial nephritis
- Neurologic abnormalities and/or AKI;
recent diarrheal illness; use of calcineurin inhibitors; pregnancy or postpartum; spontaneous - Schistocytes on peripheral blood
smear, elevated LDH, anemia, thrombocytopenia - Typical HUS
TTP/HUS
- Recent manipulation of the aorta or other large vessels; may occur spontaneously or after anticoagulation; retinal plaques, palpable purpura, livedo reticularis, GI bleed
- Hypocomplementemia, eosinophiluria (variable), variable amounts of
proteinuria
Atheroembolic disease
- History of kidney stones, prostate
disease, obstructed bladder catheter,
retroperitoneal or pelvic neoplasm - specific findings other than AKI;
may have pyuria or hematuria
Postrenal AKI
MANAGEMENT OF ACUTE KIDNEY INJURY
General Issues
. Optimization of systemic and renal hemodynamics through volume resuscitation and judicious use of vasopressors
2. Elimination of nephrotoxic agents (e.g., ACE inhibitors, ARBs, NSAIDs, aminoglycosides) if possible
3. Initiation of renal replacement therapy when indicated
MANAGEMENT OF ACUTE KIDNEY INJURY
Hyperkalemia
a. Restriction of dietary K intake
b. Discontinuation of K-sparing diuretics, ACE inhibitors, ARBs, NSAIDs
c. Loop diuretics to promote urinary potassium loss
d. Potassium binding ion-exchange resin (sodium polystyrene sulfonate)
e. Insulin (10 units regular) and glucose (50 mL of 50% dextrose) to promote entry of potassium intracellularly
f. Inhaled beta-agonist therapy to promote entry of potassium intracellularly
g. Calcium gluconate or CaCl (1 g) to stabilize the myocardium
MANAGEMENT OF ACUTE KIDNEY INJURY
- Hyponatremia
a. Restriction of enteral free water intake, minimization of hypotonic intravenous solutions including those containing dextrose
b. Hypertonic saline is rarely necessary in AKI. Vasopressin antagonists are generally not needed.
MANAGEMENT OF ACUTE KIDNEY INJURY
- Volume overload
a. Salt and water restriction
b. Diuretics
c. Ultrafiltration
MANAGEMENT OF ACUTE KIDNEY INJURY
- Nephrotoxin-specific
a. Rhabdomyolysis:
b. Tumor lysis syndrome:
a. Rhabdomyolysis: aggressive intravenous fluids; consider forced alkaline
diuresis
b. Tumor lysis syndrome: aggressive intravenous fluids and allopurinol
or rasburicase
MANAGEMENT OF ACUTE KIDNEY INJURY
Metabolic acidosis
a. Sodium bicarbonate (if pH <7.2 to keep serum bicarbonate >15 mmol/L)
b. Administration of other bases, e.g., THAM
c. Renal replacement therapy
MANAGEMENT OF ACUTE KIDNEY INJURY
Hyperphosphatemia
a. Restriction of dietary phosphate intake
b. Phosphate binding agents (calcium acetate, sevelamer hydrochloride,
aluminum hydroxide—taken with meals)
MANAGEMENT OF ACUTE KIDNEY INJURY
Hypocalcemia
Calcium carbonate or calcium gluconate if symptomatic
MANAGEMENT OF ACUTE KIDNEY INJURY
Hypermagnesemia
Discontinue Mg?* containing antacids
MANAGEMENT OF ACUTE KIDNEY INJURY
Hyperuricemia
Acute treatment is usually not required except in the setting of tumor
lysis syndrome
MANAGEMENT OF ACUTE KIDNEY INJURY
Nutrition
Sufficient protein and calorie intake (20-30 kcal/kg per day) to avoid negative nitrogen balance. Nutrition should be provided via the enteral route if possible.
MANAGEMENT OF ACUTE KIDNEY INJURY
Drug dosing
a. Careful attention to dosages and frequency of administration of
drugs, adjustment for degree of renal failure
b. Note that serum creatinine conc. may overestimate renal function in the non-steady state characteristic of patients with AKI
