ICU Nephro/AKI Flashcards
KIM-1 (Kidney Injury Molecule 1) is a marker of what
transmembrane glycoprotein: undetectable in normal kidney tissue or urine but is expressed at high levels in proximal tubular cells after ischaemic or toxic injury.
NGAL is what?
Neutrophil gelatinase- associated lipcalin (NGAL): NGAL is predominantly detected in proliferating nuclear antigen - positive proximal tubular cells.
What is IGFBP7 + TIMP2
Tissue insulin like growth factor binding protein 7 and tissue inhibitor of metalloproteinase 2 function as both autocrine and paracrine signals to arrest cell cycle and shut down cell function with early kidney injury. They are both increase in early kidney injury
Red blood cell casts on urine microscopy
Acute GN until proven otherwise. May be seen on acute TIN but must rule out GN
What do hyaline casts mean on urine microscopy
Reduced renal perfusion (volume depletion, hypotension, acute cardiopulmonary event, drug induced reduction in glomerular function, abdominal compartment syndrome
White blood cell casts on microscopy
pyelonephritis or tubulointersititial nephritis
FeNa <1%
FeUrea <35%
In nonoliguric AKI generally indicates prerenal AKI as opposed to ATN
(Low fractional excretion indicates sodium retention by the kidney, suggesting pathophysiology extrinsic to the urinary system such as volume depletion or decrease in effective circulating volume… i.e. the kidneys - the tubules are working to hold onto sodium.
Higher values can suggest sodium wasting due to ATN
In terms of intraglomerular haemodynamic compromise , what are predominant afferent vasoconstrictors
NSAIDs, calcineurin inhibitor, amphoteracin, contrast agents
In terms of intraglomerular haemodynamic compromise , what are predominant efferent vasodilators
ACEi/ARB.
Definition of intraabdominal hypertension
IAH is defined as having sustained intra-abdominal pressure (IAP) ≥ 12 mm Hg. IAP is measured at endexpiration in supine position after ensuring absence of abdominal muscle contractions, with transducer zeroed
at level of midaxillary line
Definition of abdominal compartment syndrome?
ACS is defined as having a sustained IAP ≥ 20 mm Hg (± abdominal perfusion pressure (APP) < 60 mm Hg)
that is associated with new-organ dysfunction/failure.
• APP = mean arterial pressure (MAP) – IAP
How do you manage intraabdominal hypertension/ abdominal compartment syndrome?
Management of IAH/ACS: If IAP ≥ 12 mm Hg, begin medical therapy to reduce IAP:
• Measure IAP ≥ every 4 to 6 hours. Titrate therapy to maintain IAP ≤ 15 mm Hg
• Therapeutic measures to reduce IAP:
■ Evacuate intraluminal contents: nasogastric and/or rectal tube, initiate gastro-/colo-prokinetic agents,
minimize or discontinue enteral nutrition, lower bowel decompression with enemas, or even colonoscopy
as needed.
■ Evacuate intra-abdominal space occupying lesions or fluids as applicable (e.g., large volume paracentesis
if safely tolerated)
■ Improve abdominal wall compliance: ensure adequate sedation and analgesia: remove constrictive
dressings, consider reverse Trendelenburg position +/– neuromuscular blockade.
■ Minimize fluid administration, remove excess fluids with use of diuretics or even ultrafiltration (UF),
consider hypertonic fluids, colloids.
■ Optimize systemic/regional perfusion: goal-directed fluid resuscitation with hemodynamic monitoring to
guide resuscitation
■ If IAP > 20 mm Hg and new-organ dysfunction/failure occurs despite maximal medical intervention,
consider surgical abdominal decompression
Criteria for diagnosing hepatorenal syndrome
- Diagnosis of cirrhosis with ascites
- AKI defined per AKIN (increase in sCr> 0.3 from stable baseline in less than 48 hours) or >50% incrase in stable baseline SCr within the prior 3 months.
- No improvement of creatinine after 2 days of diuretic withdrawal and volume expansion with albumin
- Absence of shock
- No current or recent nephrotoxic drugs
- Absence of parenchymal disease as indicated by proteinuria > 500mg/ d, haematuria or abnormal renal US
What is the difference between type 1 and type 2 HRS?
Type 1: > Doubling of initial scR> 2.5 or a 50% reduction of initial creatinine clearance to <20ml/min within 2 weeks.
Type 1 may occur spontaneously but frequently occurs in close relationship with a precipitating factor: severe bacterial infections, GI haemorrhage, major surgical procedure.
Type 2: Moderate and stable reduction in GFR. Renal failure does not have a rapidly progressive course.
Dominant feature is severe ascites with poor or no response to diuresis.
What are the 5 types of cardiorenal syndrome
Heart first. Then kidney.
CRS type 1 - Abrupt worsening of cardiac function –> AKI
(ACUTE HEART &ACUTE)
CRS type 2 - chronic abnormalities in cardiac function –> progressive CKD
(CHRONIC HEART &CHRONIC)
CRS type 3 - Abrupt worsening of renal function –> acute cardiac dysfunction
(ACUTEKIDNEY &ACUTE)
CRS type 4 - CKD –> decreased cardiac function, cardiac hypertrophy, and/ or increased risk of adverse cardiovascular events.
CRS type 5 - (secondary CRS) systemic condition –> both cardiac + renal dysfunction.
Nephrotoxin induced AKI -assoc with “formation of tubular cell cytoplasmic small uniform vacuoles”
Radiocontrast agents,
Cylosporine
Tacrolimus
Sucrose based IVIG.
Nephrotoxin induced AKI - with mitochondrial DNA injury with large atypical tubular cell mitchondira
Tenofovir.
Nephrotoxin induced AKI with intracytoplasmic inclusions
gold
Nephrotoxin induced AKI with intracytoplasmic inclusions
lead
Nephrotoxin induced AKI EM reveals proximal tubular cell” myeloid bodies” which are
multilamellar lysosomes filled with undigested drug–phospholipid complexes or drug-bound cytoplasmic
structures.
Gentamicin
Atheroembolic AKI triad
Clinical history of an invasive procedure or arteriography -
Livedo reticularis
AKI
Eosinphilia with or without low complements.
Fundoscopy may reveal hollenhorst plaque ( cholesterol emboli)
Histopathology: as cholesterol dissolves during tissue processing, cholesterol crystal embolization is seen as
clear needle-shaped structures within vascular lumens or walls, sometimes with surrounding multinucleated
giant cells. They may be in large or small arteries, arterioles, or capillaries
Do not anticoagulate or use thrombolytics.
What are the theorectical benefits of alkalinisation with sodium bicarb over normal saline in rhabdo?
Urine pH> 6.5 may reduce heme- induced renal toxicity +pigment cast formation.
Sodium bicarbonate may reduce the release of free iron from myoglobin.
But no clear evidence of benefits. Do not use in hypocalcaemia, hypokalaemia, existing carbon dioxide retention, or
Benefit of dialysis in rhabdoto remove myoglobin or hemoglobin has not been shown
Biopsy - Proximal tubular cell with small uniform ( isometric ) vacuoles + AKI
Contrast induced AKI
Low versus high osmolal agents in reduction of contrast nephropathy
Use low (iohexol) or iso- osmolal ( iodixanol) agents preferentially.
“Controversy: iso-osmolal iodixanol may be better than low-osmolal iohexol among patients with DM and
CKD, but not better than other low-osmolal agents”
Criteria for diagnosing tumour lysis syndrome
Criteria for laboratory TLS > 2 of the following:
- High uric acid - > 8 or greater than 25% increase from baseline.
- K > 6 or greater than 25% increase from baseline.
- High phosphate > 6.5 or 25% increase from baseline.
LOW calcium. calcium < 7 or greater than 25% decrease from baseline.
Criteria for clinical TLS -
Meeting lab criteria plus
One or more of the assoc. complications involving AKI, cardiac arrhythmias, seizures or death.
How does rasburicase work?
Rasburicase: recombinant form of urate oxidase, converts uric acid to the more soluble metabolite,
allantoin, which can be renally excreted.
• NOTE: Rasburicase is contraindicated in patients with glucose- 6-phosphate dehydrogenase and
catalase deficiencies due to the development of hemolytic anemia and methemoglobinemia.
• Rasburicase is associated with hypersensitivity (including anaphylaxis) in 1% of patients.
• Rasburicase effectively reduces hyperuricemia, but not shown to reduce incidence of clinical TLS.
