IRIS Staging Acute Renal Failure Flashcards
LÄS: http://www.iris-kidney.com/pdf/4_ldc-revised-grading-of-acute-kidney-injury.pdf
http://www.iris-kidney.com/pdf/4_ldc-revised-grading-of-acute-kidney-injury.pdf
Generellt
Acute kidney disease represents a spectrum of disease associated with a sudden onset of renal parenchymal injury most typically characterized by generalized failure of the kidneys to meet the excretory, metabolic, and endocrine demands of the body, i.e. acute renal failure (ARF).
Acute kidney disease typically is recognized clinically
by its advanced and most overt manifestations, ARF.
Acute renal failure is characterized by rapid hemodynamic, filtration, tubulointerstitial, or outflow injury to the kidneys and subsequent accumulation of metabolic toxins (uremia toxins) and dysregulation of fluid, electrolyte, and acid-base balance. However, ARF reflects only a subset of patients with kidney injury who have the highest morbidity and mortality.
The term “acute kidney injury” (AKI) has been adopted in human medicine to better reflect the broad spectrum of acute diseases of the kidney and to reinforce the concept that AKI encompasses a continuum of functional and parenchymal damage from its least to its most severe manifestations. Kidney injury may be imperceptible clinically at early stages and culminate with the requirement for renal replacement therapy (RRT, various forms of dialysis or renal transplantation) with the onset of overt failure of kidney function or death.
AKI oftast orsakat av toxis, iskemisk eller infektions orsak.
Oftast tubuli celler som drabbas, då mest beroende av oxygen och högt metabolic rate.
Generellt - Fortsatt
Animal patients most often are recognized with an acute uremia which must be differentiated subsequently into its prerenal, intrinsic renal parenchymal, and/or postrenal components for proper diagnostic evaluation, management, and staging.
Acute kidney injury typically affects intrinsically normal kidneys, but events predisposing to AKI frequently are superimposed on preexisting chronic kidney disease (CKD - Acute on chronic) to produce a seemingly acute uremia with similar clinical features.
Currently, there are no markers to define or stratify the conditions that constitute AKI, although some discrete biomarkers are showing promise. Precise definitions for AKI have not been established in veterinary medicine. There also is no formal categorization of the spectrum of the functional deficiencies to standardize its classification, severity, grade, clinical course, response to therapy, or prognosis for recovery.
Unlike the IRIS staging for CKD, grading of AKI would not imply the kidney disease is stable or at steady-state. On the contrary, the “grade” represents a moment in the course of the disease and is predicted to change as the condition worsens, improves, or transitions to CKD.
IRIS AKI Grade 1
defines non azotemic animals with historical, clinical, laboratory
(biomarkers such as: glucosuria, cylinduria, proteinuria, inflammatory sediment,
microalbuminuria, etc.), imaging evidence of AKI, and/or those with clinical oliguria/
anuria. IRIS AKI Grade I includes animals with progressive (hourly or daily) increases
in blood creatinine of ≥0.3 mg/dl (≥ 26.4 μmol/l) within the nonazotemic range
during a 48 hour interval. IRIS AKI Grade I also includes animals whose decreased
urine production is readily fluid volume-responsive. Fluid volume responsiveness
represents an increase in urine production to >1 ml/kg/hr within 6 hours; and/or
decrease in blood creatinine to baseline over 48 hours.
IRIS AKI Grade 2
Som ovan +
Mild azotemi (140-220 umol/L)
Fluid responsive
IRIS AKI Grade II includes animals with progressive (hourly or daily) increases
in blood creatinine of ≥0.3 mg/dl (≥ 26.4 μmol/l) during a 48 hour interval med pre-existing CKD (Acute on chronic).
IRIS AKI Grade 3-5
Beskriver djur med dokumenterat AKI, och progressiv större parenchymal skada och funktionell svikt (Uremi).
Grade 3: 221-439 umol/l
Grade 4: 440-880 umol/l
Grade 5: >880 umol/l
Underindelning
AKI underindelas även på bakgrund av urinproduktion som NO: non-oliguri eller O: oliguri/anuri, samt om behov för Renal Replacement Therapy (RRT).
Non-oliguri: >1 ml/kg/h
Oliguri: < 1ml/kg/h
Anuri: Ingen urin producerat på >6h
Gränsen på 1 ml/kg/h är en relevant cut-off i flesta hydrerade patienter som får parenteral vätska, och djur med nedsatt koncentrationsförmåga som följd av njurskada.
- NB! dock vissa normala friska katter som producerar så pass koncentrerat urin, att < 1mg/kg/h är normalt.
Underindelning baserat på behov av RRTär baserat på behovet för vätska för att korrigera livshotande konsekvenser av AKI inkl svår azotemi, hyoerkalemi, syr-bas rubbningar, överhydrering, oliguri/anuri eller för ett utskilja nefrotoxiner.
Behov av RRT kan uppstå vid alla grader av AKI.
Patofysiologi
Unikt mottagliga för akut skada, då mottager 20% av cardiac output -> högt i kroppen relaterat till vikten på organet.
Bark och yttre del av märg mottager mest blod, då även mest mottagliga för skada -> oftast prox. tubuli och tjocka ascenderande ben henles slynga.
Indelas i 4 faser: Initiation(minuter till timmer - skadan händer), Extension(timmer till dagar - fortsättning på initial skada, men samtidig börjande reperation), Maintenance(dagar till veckor) och Recovery(Veckor till månader - fortsatt reperation och funktion börja återkomma).
