Acute Kidney Injury Flashcards
Definition of AKi
the impairment of kidney filtration and excretory function over days to weeks, resulting in the retention of nitrogenous waste products normally cleared by the kidneys
Common causes of community-acquired AKI
Volume depletion
Heart failure
Adverse effects of medications
Obstruction of Urinary Tract
Malignancy
Common causes of hospital-acquired AKI
Sepsis
Major surgical procedures
Critical Illness involving heart or liver failure
Nephrotoxic medical administration
Classification of major causes of AKI
Most common form of AKI
Pre-renal azotemia
Decreased perfusion pressure in the presence of NSAIDS
loss of vasodilatory prostaglandins increases afferent resistance
Decreased perfusion pressure in the presence of ACE-i or ARB
loss of angiotensin II action reduces efferent resistance
Threshold of systolic blood pressure when renal autoregulation falls
80 mmHG
Type 1 Hepatorenal Syndrome
defined as >two-fold increase in SCr to >2.5 mg/dL within 2 weeks without alternate cause, persists despite volume administration and withholding of diuretics
Type 2 Hepatorenal Syndrome
less severe from characterized mainly by refractory ascites
Most common causes of intrinsic AKI
Sepsis
ischemia
Nephrotoxins
At risk to develop ischemia-associated AKI
limited renal reserve (older age),
Coexisting insults:
-Sepsis
-Vasoactive or nephrotoxic drugs
-Rhabdomyolysis
-Systemic inflammatory states associated with burns and pancreatitis
Procedures most commonly associated with AKI
Cardiac surgery with cardiopulmonary bypass,
Vascular procedures with aortic cross clamping,
Intraperitoneal procedures
Common risk factors for postoperative AKI
Underlying CKD
Older age
Diabetes Mellitus
Congestive heart failure
Emergency procedures
Risk factors for Nephrotoxin associated AKI
Older age
CKD
Pre renal azotemia
Hypoalbuminemia (in some)
Most common clinical course of contrast nephropathy
rise in SCr beginning 24-48h following exposure, peaking within 3-5 days, and resolving within 1 week
Most common findings in CI -AKI
low fractional excretion of sodium (FeNa) and relatively benign urinary sediment without features of tubular necrosis
Clinical features of amphotericin B nephrotoxicity
Polyuria
Hypomagnesemia
Hypocalcemia
Nongap metabolic acidosis
Chemotherapeutic drugs that accumulates in the proximal tubular cells and cause necrosis and apoptosis
Cisplatin and carboplatin
Ifosfamide nephrotoxicity
Cause hemorrhagic cystitis and tubular toxicity manifested as type II renal tubular acidosis (Fanconi’ syndrome), polyuria, hypokalemia, and a modest decline in GFR
Chemotherapeutic drugs that cause thrombotic microangiopathy
Bevacizumab
Mitomycin C
Gemcitabine
Tumor lysis syndrome
Hyperuricemia
Hyperkalemia
Hyperphosphatemia
Hypocalemia
Occurs when the normally unidirectional flow of urine is acutely blocked either partially or totally, leading to increased retrograde hydrostatic pressure and interference with glomerular filtration
Post-renal AKI
Common cause of postrenal AKI which impacts both kidneys
Bladder neck obstruction
Definition of AKI
-elevation in the SCr concentration or reduction in urine output
-a rise from baseline of at least 0.3 mg/dL within 48h or at least 50% higher than baseline within 1 week or a reduction in urine output to <0.5 ml/kg per h for longer than 6h
Key differences from CKD
Clues suggestive of CKD:
1. Radiologic studies
-small shrunken kidneys with cortical thinning on renal ultrasound
-evidence of renal osteodystrophy
- Laboratory findings
-normocytic anemia in the absence of blood loss
-secondary hyperparathyroidism with hyperphosphatemia and hypocalcemia
Clinical and laboratory features of prerenal azotemia
Clinical and laboratory features of sepsis-associated AKI
Clinical and laboratory features of ischemia-associated AKI
Clinical and laboratory features of endogenous nephrotoxin-associated AKI
Clinical features of exogenous nephrotoxin associated AKI
Clinical features of other causes of intrinsic AKI
Urinary sediments in AKI
Definition of Oliguria
defined as <400 ml/24h
AKI conditions that may present with complete anuria
Complete urinary tract obstruction,
Renal artery occlusion,
Overwhelming septic shock,
Severe ischemia,
Severe GN or vasculitis
AKI conditions that may present with preserved urine output
Nephrogenic DI (longstanding urinary tract obstruction),
Tubulointerstitial disease,
Nephrotoxicity from cisplatin or aminoglycosides, etc/
Characteristic urine sediment of AKI from ATN (sepsis, ischemic injury, or certain nephrotoxins)
pigmented “muddy brown” granular casts and tubular epithelial cells
Causes of disproportionate BUN elevation compared to creatinine
Prerenal azotemia
UGIB
Increased tissue catabolism
Glucocorticoid use
the fraction of filtered sodium load that is reabsorbed by the tubules, and is a measure of both the kidney’s ability to reabsorb sodium as well as endogenously and exogenously administered factors that affect tubular reabsorption
FeNa
Diagnostic and therapeutic in prerenal azotemia
Response of urine output to crystalloid or colloid fluid administration
Conditions with urinary tract obstruction that can present without radiologic abnormalities
Volume depletion,
Retroperitoneal fibrosis,
Encasement with tumor,
Early in the course of obstruction
CKD conditions with normal kidney size on radiologic evaluation
Diabetic nephropathy,
HIV-associated nephropathy,
Infiltrative disease
AKI conditions with enlarged kidneys
Acute interstitial nephritis
Infiltrative diseases
A rare but serious complication seen most commonly in patients with ESRD and severe AKI undergoing MRI with gadolinium based-contrast agents
Nephrogenic system fibrosis
Provide definitive and prognostic information about AKI and CKD
Kidney biopsy
Renal failure indices
BUN
Crea
FeNa
Urine osmolality
Can be used as a prognostic test for Oliguric AKI
urinary flow rate in response to bolus IV furosemide 1.0-1.5 mg/kg
UO <200 ml over 2h post furosemide ->higher risk for progression to more severe AKI and the need for RRT
a type 1 transmembrane protein that is abundantly expressed in proximal tubular cells injured by ischemia or nephrotoxins such as cisplatin
Kidney injury molecule-1 (KIM-1)
a novel bioimarker that is highly upregulated after inflammation and kidney injury and can be detected in the plasma and urine within 2h or cardiopulmonary bypass-associated AKI
Neutrophil gelatinase associated lipocalin (NGAL)
aka Lipocalin-2 or siderocalin
Predictive biomarkers for higher risk of the development of moderate to severe AKI in critically ill patients
Insulin-like growth factor binding protein 7 (IGFBP7),
Tissue inhibitor of metalloproteinase 2 (TIMP-2)
Hallmark of AKI
Build of nitrogenous waste products , manifested as an elevated BUN concentration
Polyuric phase of recovery from AKI
may be due to an osmotic diuresis from retained urea and other waste products as well as delayed recovery of tubular reabsorptive functions
Fluid contraindicated in AKI
Hydroxyethyl starch solutions
Management of AKI - general principles
Definitive treatment of hepatorenal syndrome
Orthotopic liver transplantation
Bridge therapies that have shown promise in HRS
Terlipressin (a vasopressin analog),
Combination tx with octreotide (A somatostatin analog),
Midodrine (an a1 adrenergic agonist), and
norepinephrine in combination with IV albumin (25-50 g, max 100 g/d)
Treatment for scleroderma renal criis
ACE inhibitors
Treatment for idiopathic TTP-HUS
plasma exchange
Treatment for rhabdomyolysis
Early and aggressive volume repletion , may initially require 10L of fluid per day
- alkaline fluids may be beneficial
Management in severe cases of volume overload
Furosemide may be given as a bolus (200 mg) followed by an intravenous drip(10-40 mg/h), with or without a thiazide diuretic
General threshold of treatment of metabolic acidosis
Severe metabolic acidosis:
pH< 7.20
serum hco3 <15 mmol/L
Total energy intake of patients with AKI
20-30 kcal/kg per day
Protein intake of noncatabolic AKI without the need for dialysis
0.8-1.0 g/kg/day
Protein intake of patients with AKI on dialysis
1.0-1.5 g/kg/day
Protein intake of patients with AKI with hypercatabolic state receiving continuous renal replacement therapy
1.7 g/kg/day
Indications for dialysis in AKI
When medical management fail to control volume overload, hyperkalemia, or acidosis; in some toxic ingestions; and when there are severe complications of uremia (asterixis, pericardial rub or effusion, encephalopathy, uremic bleeding)
Small solutes are removed across a semipermeable membrane down thier concentration gradien
“Diffusive clearance”
Solutes are removed along with the movement of plasma water
“Convective clearance”
Conditions when CRRT is preferred in patients with AKI
Severe hemodynamic instability
Cerebral edema
Significant volume overload
