BŁONIASTE KŁĘBUSZKOWE ZAPALENIE NEREK

Acute Renal Failure (AKI)
Abrupt onset of reduction in kidney function (6-12 weeks)
• usually detected by laboratory evaluation
serum creatinine rise >0.5 g/dl, GFR reduction >50%
• associated with
– oliguria (<400 ml urine/day)
– significant morbidity and mortality
• Incidence
– 2-5% of hospitalised pts
– 2- 25% of ICU pts
RIFLE Criteria for Acute Renal Dysfunction
Risk
GFR
creatinine x 1.5 or
GFR > 25%
Urine Output
UO < 0.5ml/kg/h
x 6 hr
Mortality risk
2.4
Injury
creatinine x2 or
GFR > 50%
UO < 0.5ml/kg/h
x 12 hr
4.1
Failure
creatinine x3 or
GFR > 75%
UO < 0.3ml/kg/h
x 24 hr or
Anuria x 12 hrs
6.3
Acute Kidney Injury Network criteria
• abrupt (within 48 hours)
increase in the serum creatinine of ≥ 0.3 mg/dL
• percentage increase in the serum creatinine concentration
of ≥ 50%
• oliguria of less than 0.5 mL/kg per hour for more than six
hours
Medical and surgical admissions to ICU
and factors contributing to AKI
Mortality in ARF
Risk factors for dying in patients with AKI
0.4 0.5
age (+10 yrs increment )
mechanical ventilation
vasopressors/inotropes
septic shock
hematologic vs cardiovasc
medical group
0.6
0.7 0.8
0.9
1
1.2
1.4 1.6 1.8
2.0
2.2 2.4
2.6 2.8
5,5
Risk factors
Uchino, S. et al. JAMA 2005;294:813-818
Prerenal ARF- pathophysiology
Ischemic stimulus:
decreased glomerular filtration pressure
– afferent vessel dilation
– efferent vessel constriction
– net effect = increase filtration rate
Autoregulatory mechanisms of kidney vasculature operate
between systolic blood pressure 170 - 70 mm Hg
Ischemia–reperfusion results in reversible or
irreversible injury to the proximal tubular cell
Male recipient –female kidney
Resolving ATN
Male recipient –
Female kidney with ATN
Female patient
with minimal change
- control
Male recipient
–male donor
+ control
Extrarenal cells participate in the regeneration
of renal injury in human ARF
Gupta S, Verfaille C et al, Kidney Int 62 (4), 1285-1290, 2002.
Clinical and cellular phases in ischemic ARF
•BBM loss
•Exfoliation
•Tubular obstruction
Cell injury
hypoxia
Microvascular injury
•Obstruction
•Inflammation
•Coagulation
Maintenance
•Dedifferentiation
•Migration
•Proliferation
•Redifferentiation
•Repolarization
Sutton et al Kidney Int 62:1539-1549,2002
Intrinsic renal disease
 40-50% of all ARF
 involving one or more of 4 major anatomic parts of the kidney
vasculature, interstitium, glomeruli, tubules
 most common cause:
Acute Tubular Necrosis
ischemia
nephrotixic agents
Renal function
5 yrs after AKI
good
Cause of AKI
Henoch Schonlein purpura
Tubulointerstinal nephritis
Post-infectious nephritis
ATN
Diffuse proliferative lupus GN
MPGN
HUS/TTP
bad
Extracapillary GN
Acute cortical necrosis
Postrenal ARF
Obstruction of urinary tract at any level
occurs in:
5-10% of all ARF
obstructive lesion in urinary bladder or below
in patients with solitary functioning kidney
- early stage filtration continues
increasing ureteral and tubular pressure
- prolonged obstruction
vasoconstriction in afferent arterioles
results in diminished blood flow, filtration, interstitial
oedema
Acute renal failure differentiation - urinalysis
Intrinsic renal
Prerenal
Postrenal
Dipstic Blood
-
-
Dipstic
Protein
-
-
RBC
-
-
WBC
-
-
Casts
-
-
Other
Hyaline casts
-
Vasculitis, GN
Interstitial
ATN
+++
+++
+
+
-
+++
+
+
+++
-
RBC and
WBC casts
WBC casts
-
Eosinophils
Tubular cells
Brown casts
-
Microscopy
-
ARF - clinical course
Prerenal or postrenal azotemia
Prompt diagnosis and treatment – fully reversible
Intrinsic renal failure – prolonged course
Most common - ATN
- initial phase (usually not noticed)
- maintenance phase (2-3 weeks)
- recovery
50% of patients oliguric, 5-10% anuric
mortality 50-60% of non-renal causes: sepsis, cardiovascular complications
ARF – clinical manifestation
Cardiovascular complications
hypertension, oedema, pulmonary congestion, pericarditis
Hematologic manifestations
• anaemia – decreased production of erythropoetin, excessive
blood loses, haemolysis, shortened RBC half-life
• bleeding diathesis - impaired platelets aggregation, adhesion
• impaired immunity- lymphopenia, chemotaxis defect, cellular
immunity
defect
Neurologic symptoms
disorientation, asterixis, seizures, coma, peripheral neuropathy
GI tract symptoms: hiccups, nausea, vomiting, anorexia, ileus,
bleeding
Treatment of ARF
 eliminate or control underlying primary disease
 restore effective renal blood low
 eliminate obstruction of urine flow
 eliminate nephrotoxic agents
Supportive treatment
Renal replacement treatment
Indications for dialysis in ARF
•
•
•
•
•
•
Hyperkalemia
Fluid overload
Acidosis
Uremic symptoms
Pericarditis
Poisoning with toxins eliminated by dialysis (methanol
ethylene glycol)
• Blood urea >140-200 mg/dl
Supportive treatment, early beginning
ATN prophylaxis
• Careful evaluation of fluid status, cardiac output,
nephrotoxins elimination
• Special attention to patients with compromised renal
blood flow or kidney function
–
–
–
–
–
–
elderly
heart failure
kidney disease
liver disease
renal artery stenosis
diabetes mellitus
Prevention or reversal of ATN
High dose furosemide, low dose dopamine, mannitol
–data controversial
–effective in maintaining diuresis
–mortality unchanged
Experimental therapies
–ANF, EGF, antibodies to adhesion molecules
–Free radicals scavengers
–Calcium channel blockers
Contrast nephropathy risk factors
intra-arterial contrats administration
Age >75 years
Baseline creatinine cleareance <60ml/min/1.73m2
Coronary catheterization in an emergency setting
 Diabetes mellitus
Congestive heart failure
Peripheral vascular disease and
Volume of administered contrast > 300 ml
Prevention of Contrast Nephropathy
The major preventive actions
• Identification of high risk patients
• Withdraw nephrotixic medications prior to planned procedure
• Hydration with 0.45%/ 0.9% saline administered at a rate of 100 ml/hr
beginning 12 hours before and continued 12 hours after angiography
use LOCM or IOCM
aditionally
• oral acetylcysteine, 1200 mg twice daily the day before and on the day of
administration of contrast
ACR Committee on Drugs and Contrast Media 2010
ATN secondary to rhabdomyolysis
•
•
•
•
•
crush syndrome
caused by medication (statins, zidovudine, ephedrine)
alcohol abuse
seizures
insect bite
baseline serum creatinine (≥1.7mg/dl and ≥1.5mg/dl)
maximum CPK value
predictive for AKI and sustained kidney failure
AKI in oncology
Prerenal , Post renal
Renal
 ATN due to medication (cisplatin, ifosfamide,
interleukin-2) or sepsis
 TTP/HUS after stem cell transplantation
 Infiltration of the renal parenchyma from cancer cells
(leukemia, lymphoma, myeloma)
 Intratubular obstruction (cast nephropathy-multiple
myeloma, tumor lysis syndrome, methotrexate)
Tumor lysis syndrome
high rate of tumor cell turnover
tumor lysis syndrome
uric acid nephropathy
prevention
• establishing a urine output > 3 to 5 L/24 hr
• allopurinol
• rasburicase*
*recombinant urate oxidase, a nonhuman proteolytic enzyme oxidizing uric acid to allantoin
AKI after cardiac surgery
Risk factors
• CKD, diabetes mellitus, congestive heart failure, age >70 years,
cardiopulmonary bypass (with artificial perfusion) >3 hours
Prevention
• clonidine improved creatinine clearance and was associated
with greater hemodynamic stability
• atrial natriuretic peptide (ΑΝΡ) reduces the need for dialysis or
the risk of death compared to placebo
• furosemide increases urine output but it decreases GFR
and the filtration fraction
• dopamine doesn’t prevent AKI
Potential consequences
of late refferal to nefrologist
• Missing potentially reversible non-ATN cause of AKI
(example: RPGN)
• Delayed diagnosis
increased
• Deayed treatment
mortality
• Increased risk of complications
• Increased risk of ESRD
Which is the best`method for RRT
in the AKI setting?
ARF simple
1 organ failure
Alternate day
dialysis
ARF severe
ARF MOF
2 organs failure
3 or more organs failure
Kidney + shock or other organ
Kidney + shock + other organ
Daily dialysis
Continuous dialysis
Slow Extended Dialysis
Which is the best method
for RRT in the AKI setting?
Hemodialysis
CRRT
PD
Advantages
effective (K/h)
Commonly used
Easy to use
Short duration
Very effective (K/w)
Hemodynamic stability
Restores acid-base balance
continuosly
allows iv fluids
administration
Does not increase IP
Hemodynamic stability
Low cost
No anticoagulation
No vascular access
Does not increase IP
Disadvantages
-Coagulation
-Risk of increase d IP
-Hypotension episodes
- Limited fluid removal
- Continuous coagulation
- Loses from the dialyser
- High cost
- Reduced dialysis dose
- Infection risk
- Affects respiration