0 0 5 5 10 10 15 15 20 20 1 1220 90 90 0 660 0 330 0 115 5 55 m m g g / / d d l l GFR in ml/min GFR in ml/min S. creatinine vs GFR S. creatinine vs GFR S. S. creatinincreatinin ee OUTLINE OUTLINE I.
I. Definition: ARFDefinition: ARF II.
II. Pre-Renal FailurePre-Renal Failure a.
a. EtiologyEtiology b.
b. PathophysiologyPathophysiology III.
III. Intrinsic Renal FailureIntrinsic Renal Failure a. a. ClassificationClassification b. b. EtiologyEtiology c. c. PathologyPathology IV.
IV. Post-RenalPost-Renal V.
V. Approach to Renal FailureApproach to Renal Failure Acute Ren
Acute Renal Failureal Failure Definition:
Definition: •
• characterized by a rapid decline in glomerular filtrationcharacterized by a rapid decline in glomerular filtration rate
rate (GFR)(GFR) over hours to daysover hours to days •
• complicates approximately 5complicates approximately 5––7% of hospital7% of hospital
admissions and up to 30% of admissions to intensive admissions and up to 30% of admissions to intensive care units
care units •
• usually asymptomatic and diagnosed when biochemicalusually asymptomatic and diagnosed when biochemical monitoring of hospitalized patients reveals a new monitoring of hospitalized patients reveals a new increase in
increase in blood urea and serum creatinineblood urea and serum creatinine concentrations.
concentrations. •
• ARF is often considered to be reversible but may ARF is often considered to be reversible but may alsoalso contribute to progression to chronic kidney disease contribute to progression to chronic kidney disease Clinical Features
Clinical Features:: •
• Retention of nitrogenous waste products (BUN)Retention of nitrogenous waste products (BUN) •
• oliguria (urine output <400 mL/doliguria (urine output <400 mL/dfluid overloadfluid overload •
• electrolyte and acid-base abnormalitieselectrolyte and acid-base abnormalities Three major Categories:
Three major Categories: 1.
1. Prerenal ARF(55%)-Prerenal ARF(55%)- diseases that causes renal diseases that causes renal hypoperfusion, resulting in decreased function without hypoperfusion, resulting in decreased function without frank parenchymal damage
frank parenchymal damage 2.
2. Intrinsic ARF (40%)-Intrinsic ARF (40%)- diseases that directly involve thediseases that directly involve the renal parenchyma
renal parenchyma 3.
3. Postrenal ARF (5%)-Postrenal ARF (5%)- diseases associated with urinary diseases associated with urinary tract obstruction
tract obstruction eGFR = ml/min
eGFR = ml/min (140
(140–– age) age) x x kg kg BW BW *eGFR ( *eGFR ( 0.85 0.85 ) ) for for femalefemale S cr (mg/dl) x 72
S cr (mg/dl) x 72
Pre-Renal Failure/Pre-renal Azotemia Pre-Renal Failure/Pre-renal Azotemia •
• The most common form of ARF which occurs in theThe most common form of ARF which occurs in the setting of
setting of renal hypoperfusionrenal hypoperfusion. (55%). (55%) •
• reversible when renal perfusion is restored reversible when renal perfusion is restored •
• renal parenchymal tissue is not damaged.renal parenchymal tissue is not damaged. •
• can complicate any disease that induces hypovolemia,can complicate any disease that induces hypovolemia, low cardiac output, systemic vasodilatation, or selective low cardiac output, systemic vasodilatation, or selective intrarenal vasoconstriction
intrarenal vasoconstriction •
• more severe or prolonged hypoperfusion may lead more severe or prolonged hypoperfusion may lead toto ischemic injury, often termed as
ischemic injury, often termed as Acute tubular Acute tubular Necrosis(ATN)
Necrosis(ATN) •
• Manifestation of renal hypoperfusionManifestation of renal hypoperfusion →prerenal ARF and →prerenal ARF and ischemic ATN
ischemic ATN Etiology of Prerenal Failure Etiology of Prerenal Failure I.
I. HypovolemiaHypovolemia
A. Increased extracellular fluid losses: hemorrhage A. Increased extracellular fluid losses: hemorrhage B. Gastrointestinal fluid loss: vomiting, diarrhea, B. Gastrointestinal fluid loss: vomiting, diarrhea, enterocutaneous fistula
enterocutaneous fistula
C. Renal fluid loss: diuretics, osmotic diuresis, C. Renal fluid loss: diuretics, osmotic diuresis, hypoadrenalism,nephrogenic diabetes insipidus hypoadrenalism,nephrogenic diabetes insipidus D. Extravascular sequestration: burns, pancreatitis, D. Extravascular sequestration: burns, pancreatitis, severe hypoalbuminemia (hypoproteinemia) severe hypoalbuminemia (hypoproteinemia)
E. Decreased intake: dehydration, altered mental E. Decreased intake: dehydration, altered mental status
status II
II.. Altered ren Altered renal hemodyal hemodynamics renamics resulting in hsulting in hypoperfusionypoperfusion A. Low cardiac output state:
A. Low cardiac output state:
B. Systemic vasodilation: sepsis, antihypertensives, B. Systemic vasodilation: sepsis, antihypertensives, afterload reducers, anaphylaxis
afterload reducers, anaphylaxis
C. Renal vasoconstriction: hypercalcemia, C. Renal vasoconstriction: hypercalcemia,
catecholamines, calcineurin inhibitors, amphotericin B catecholamines, calcineurin inhibitors, amphotericin B D. Impairment of renal autoregulatory responses: D. Impairment of renal autoregulatory responses: cyclooxygenase inhibitors (e.g., nonsteroidal cyclooxygenase inhibitors (e.g., nonsteroidal anti-inflammatory drugs), angiotensin-converting enzyme inflammatory drugs), angiotensin-converting enzyme inhibitors, or angiotensin II receptor blockers
inhibitors, or angiotensin II receptor blockers E. Hepatorenal syndrome
E. Hepatorenal syndrome Pathophysiolog
Pathophysiology of y of Prerenal FailurePrerenal Failure Hypovolemia
Hypovolemia fall in mean systemic arterial pressure(decreased fall in mean systemic arterial pressure(decreased stretch in carotid sinus)
stretch in carotid sinus) neurohormonal responses (SNS, RAA,neurohormonal responses (SNS, RAA, AVP stimulation)
AVP stimulation) renal salt & water retentionrenal salt & water retention •
• In mild renal hypoperfusion, compensatory mechanismsIn mild renal hypoperfusion, compensatory mechanisms preserve glomerular pressure and filtration
preserve glomerular pressure and filtration fraction.fraction. Reduction in perfusion pressure, stretch receptors in Reduction in perfusion pressure, stretch receptors in afferent arterioles trigger afferent arteriolar afferent arterioles trigger afferent arteriolar vasodilatation
vasodilatationthrough a local myogenic reflexthrough a local myogenic reflex ((autoregulationautoregulation).).
•
• Relatively non-essential vascular beds (such asRelatively non-essential vascular beds (such as
muskulocutaneous and splanchnic circulations) undergo muskulocutaneous and splanchnic circulations) undergo vasoconstriction in an attempt to preserve cardiac and vasoconstriction in an attempt to preserve cardiac and cerebral perfusion pressure.
cerebral perfusion pressure. •
• Salt loss through sweat glands is inhibited Salt loss through sweat glands is inhibited LEGEND
LEGEND
Normal text : lecture Normal text : lecture Italics : book and recording Italics : book and recording
Blood Urea Nitrogen
Blood Urea Nitrogen CreatinineCreatinine
•
• Protein intakeProtein intake •
• Catabolic rateCatabolic rate •
• Tissue InjuryTissue Injury •
• GI bleedingGI bleeding •
• DrugsDrugs
•
• Muscle mass andMuscle mass and breakdown breakdown •
• Drugs that inhibit Drugs that inhibit tubule secretion tubule secretion •
• Lab interactionLab interaction •
• Prerenal FailurePrerenal Failure
ACUTE RENAL FAILURE
ACUTE RENAL FAILURE
Ma. Martina F. Alcantara, MD
• Angiotensin II : increases filtration fraction and preserves GFR, maintains glomerular pressure • Increases biosynthesis of vasodilator prostaglandins
(e.g., prostaglandin E2 and prostacyclin), also resulting in afferent arteriolar vasodilation.
• induces preferential constriction of efferent arterioles.
• With more severe hypoperfusion, these
compensatory responses are overwhelmed and GFR falls, leading to prerenal ARF.
Who are at risk?
• the elderly
• patients with diseases that affect the integrity of afferent arterioles
• hypertensive nephrosclerosis,
• diabetic vasculopathy
• occlusive (including atherosclerotic)/ renovascular disease)
• Drugs that inhibit renal prostaglandin biosynthesis: NSAIDs, ACE inhibitors, ARB’s
• NSAIDS do not complicate GFR of healthy individuals, only those patients with volume depletion and chronic kideney disease (in whom GFR is maintained, in part, through prostaglandin hyperfiltration by the remaining functional nephrons)
Hepatorenal Syndrome
• unique form of prerenal ARF that frequently
complicates advanced cirrhosis as well as acute liver failure
• is a life-threatening medical condition that consists of rapid deterioration in kidney function in individuals with cirrhosis or fulminant liver failure
• kidneys are structurally normal but fail due to splanchnic vasodilation and arteriovenous shunting, resulting in profound renal vasoconstriction.
• Coreection of underlying liver disease (e.g. Liver
transplantation) results in resolution of the acute r enal failure
2 forms:
1. Type 1- more aggressive form, ARF progresses even after optimization of systemic hemodynamics and carries mortality rate of >90%
2. Type II- associated with ascites that does not improve with standard diuretic medications.
Intrinsic Renal Failure
PreRenal ARF prolonged hypoperfusion Intrinsic
Renal Failure Other Names: Ischemic or Nephrotoxic ARF/ Acute Tubular Necrosis/ Acute Kidney Injury)
• renal tubular epithelial/endothelial cells are injured • 40% of acute renal failure cases
• More severe or prolonged hypoperfusion may lead to
ischemic injury, often termed acute tubular necrosis, or ATN.of renal hypoperfusion.
• Although many patients with ischemic or nephrotoxic ARF do not have morphologic evidence of cellular necrosis, this disease is often referred to as acute tubular necrosis, or ATN.
• More recently,because of the important role of sublethal injury to tubular epithelial and other renal cells (e.g., endothelial cells) in the pathogenesis of this syndrome, the term acute kidney injury (AKI) has been proposed. Classsification of Intrinsic Renal Failure
(1) ischemic or nephrotoxic tubular injury– termed acute tubular necrosis eventhough there is no morphologic evidence of cellular necrosis
(2) tubulointerstitial diseases
(3) diseases of the renal microcirculation and glomeruli, and (4) diseases of larger renal vessels
Etiology of Intrinsic Renal Failure
I. Renovascular obstruction (bilateral, or unilateral in the setting of one kidney)
A. Renal artery obstruction: atherosclerotic plaque, thrombosis, embolism, dissection aneurysm, large vessel vasculitis
B. Renal vein obstruction: thrombosis or compression II. Diseases of the glomeruli or vasculature
A. Glomerulonephritis or vasculitis
B. Other: thrombotic microangiopathy, malignant hypertension, collagen vascular diseases (systemic lupus erythematosus, scleroderma), disseminated intravascular coagulation, preeclampsia
III. Acute tubular necrosis
A. Ischemia: causes are the same as for prerenal ARF, but generally the insult is more severe and/or more prolonged
B. Infection, with or without sepsis syndrome C. Toxins: intrarenal vasoconstriction/ generate reactive oxygen species/direct toxicity/ obstruction
1. Exogenous: radiocontrast, calcineurin inhibitors, antibiotics ( aminoglycosides), chemotherapy (cisplatin), antifungals (amphotericin B), ethylene glycol
2. Endogenous: rhabdomyolysis, hemolysis IV. Interstitial nephritis
A. Allergic: antibiotics (β-lactams, sulfonamides, quinolones, rifampin), nsaid’s, diuretics)
B. Infection: pyelonephritis (if bilateral)
C. Infiltration: lymphoma, leukemia, sarcoidosis D. Inflammatory, nonvascular: Sjögren’s syndrome, tubulointerstitial nephritis with uveitis
V. Intratubular obstruction
A. Endogenous: myeloma proteins, uric acid (tumor lysis syndrome), systemic oxalalosis
B. Exogenous: acyclovir, gancyclovir, methotrexate, indinavir
Etiology and Pathophysiology of Ischemic ATN • part of manifestation of renal hypoperfusion
• in most severe form, ischemia leads to bilateral renal cortical necrosis and irreversible renal failure
• differs from prerenal ARF in that the renal tubular epithelial cells are injured in ischemic ATN
• recovery typically takes 1 – 2 weeks after normalization of renal perfusion, as it requires repair/regeneration of renal cells
• 4 phases:
o Initiation- lasting hours to days.
- GFR declines because of 1) reduced
glomerular ultrafiltration pressure as blood flows falls, 2)flow of filtrate within tubules is obstructed by casts, epithelial cells and necrotic debris, 3)backleak of glomerular filtrate though injured tubular
epithelium .
- Ischemic injury most prominent in the S3
segment of proximal tubule and medullary portion of thick ascending loop of Henle .
These segments are sensitive to ischemia because of high rates of active(ATP-dependent) solute transport and location in outer medulla where partial pressure of oxygen is low
o Extension- continued ischemic injury and
inflammation secondary to endothelial damage.
o Maintenance
- typically 1-2 weeks. GFR stabilizes at its
nadir (typically 5-10 ml/min), urine output at its lowest, and uremic complications.
- Persistent intrarenal vasoconstriction
and medullary ischemia triggered by
dysregulated release of vasoactive mediators
o Recovery- repair and regeneration as well as a
gradual return of GFR toward premorbid levels Etiology and Pathophysiology of Nephrotoxic ARF
• Nephrotoxic ATN may complicate exposure to many
structurally diverse pharmacologic agents. With most nephrotoxins, the incidence of ARF is increased in the elderly and in patients with preexisting chronic kidney disease, true or “effective” hypovolemia, or concomitant exposure to other toxins.
• Radiocontrast agents, cyclosporine, and tacrolimus (FK506) cause kidney injury through intrarenal vasoconstriction →acute fall in renal blood flow and GFR, relatively benign urine sediment, and a low fractional excretion of sodium.
• Contrast nephropathy is also thought to result from the generation of reactive oxygen species that are directly toxic to renal tubular epithelial cells. (preexisting chronic kidney disease, diabetes mellitus, congestive heart failure, hypovolemia, or multiple myeloma.) • Antibiotics and anticancer drugs typically cause ATN
through direct toxicity to the tubular epithelial cells and/or intratubular obstruction.
- Aminoglycoside- cause oxidative stress and cell
injury. Damage occurs in proximal and distal
- Amphotericin B-dose related through intrarenal
vasoconstriction and direct toxicity to proximal tubules
- Foscarnet and pentamidine
- Cisplatin and carboplatin- similar to
aminoglycoside
- Ifosphamide- leads to hemorrhagic cystitis
• Endogenous nephrotoxins include calcium, myoglobin,
hemoglobin, urate, oxalate, and myeloma light chains. Hypercalcemia can compromise GFR, predominantly by inducing intrarenal vasoconstriction as well as volume depletion from obligate water loss.
Pathology of Intrinsic Renal Failure (ATN)
• patchy and focal necrosis of the tubular epithelium, with detachment of cells from the basement membrane, • Occlusion of tubule lumens with casts composed of intact
or degenerating epithelial cells, Tamm-Horsfall protein, and pigments.
• Leukocyte accumulation is frequently observed in vasa recta
• glomeruli and renal vasculature is characteristically normal.
Postrenal Failure
• Urinary tract obstruction accounts for fewer than 5% of cases of hospital-acquired ARF
• Bladder neck obstruction is the most common cause of postrenal ARF and is usually due to Prostatic disease, neurogenic bladder, or therapy with anticholinergic drugs
• Ureteric obstruction may result from intraluminal obstruction (e.g., calculi, blood clots, sloughed renal papillae), infiltration of the ureteric wall (e.g., neoplasia), or External compression (e.g., retroperitoneal fibrosis, neoplasia or abscess, inadvertent surgical ligature)
Approach to Renal Failure
1. Acute or Chronic ARF?
- Acute-If review of lab records demonstrates recent rise
in BUN and crea
- Chronic- anemia, evidence of renal osteodystrophy
(radiologic or laboratory) and small scarred kidney 2. Etilogy and specific treatment?
3. Prevention and management? Diagnostics:
• Urinalysis
• BUN, Creatinine
• Na, K, Cl
• CBC
Approach to Renal Failure: Acute or Chronic?
Approach to ARF: Clinical Assessment
• Prerenal ARF
- thirst and orthostatic dizziness. - orthostatic hypotension, tachycardia,
- ↓jugular venous pressure
- decreased skin turgor
- dry mucous membranes
• Intrinsic/ Ischemic ARF
- Hypovolemia, septic shock, and major surgery
- Persistence of ARF despite restoration of
hemodynamics
- Fever, arthralgias, and a pruritic erythematous
rash following exposure to a new drug suggest allergic interstitial nephritis
- Flank pain may be a prominent symptom following
occlusion of a renal artery or vein
- Oliguria, edema, and hypertension, with an “active”
urine sediment (nephritic syndrome), suggests acute gomerulonephritis or vasculitis
- Malignant hypertension may result in ARF, often
in association with hypertensive injury to other organs (e.g., papilledema, neurologic dysfunction, left ventricular hypertrophy)
• PostRenal ARF
- Suprapubic and flank pain due to distention of
the bladder and of the renal collecting system and capsule
- Colicky flank pain radiating to the groin suggests
acute ureteric obstruction
- Prostatic disease - nocturia, frequency, and
hesitancy and BPH on rectal examination
- Neurogenic bladder - anticholinergic
medications or with physical evidence of autonomic dysfunction.
Urinalysis
• PreRenal ARF:
- acellular & contains transparent hyaline casts
(“bland,” “benign,” “inactive” urine sediment)
- Hyaline casts are formed in concentrated urine
from normal constituents of urine—principally Tamm-Horsfall protein, which is secreted by epithelial cells of the loop of Henle
• Intrinsic ARF:
- Pigmented “muddy brown” granular casts and
casts containing tubule epithelial cells are characteristic of ATN ( ischemic/ nephrotoxic)
- mild “tubular” proteinuria (<1 g/d),
- RBC casts indicate glomerular injury or acute
tubulointerstitial nephritis
- WBC casts and nonpigmented granular casts
suggest interstitial nephritis
- broad granular casts are characteristic of CKD - Eosinophiluria (>5% of urine leukocytes) is a
common finding (~90%) in antibiotic-induced allergic interstitial nephritis
- Lymphocytes may predominate in allergic
interstitial nephritis induced by NSAIDs,and some other drugs (i.e., ampicillin, rifampicin, and
interferon )
- uric acid crystals – prerenal or urate
nephropathy
- Proteinuria of >1 g/d suggests glomerular
proteinuria or excretion of myeloma light chains.
- Hemoglobinuria or myoglobinuria should be
suspected if urine is strongly positive for heme by dipstick but contains few red cells
- Bilirubinuria may provide a clue to the presence
of Hepatorenal Syndrome
• Postrenal ARF
- Anuria/ wide fluctuations in urine output
- inactive sediment, although hematuria and pyuria
are common in patients with intraluminal obstruction or prostatic disease.
Prerenal vs Renal
- The fractional excretion of sodium (FENa) is most
useful in this regard. The FENa relates sodium clearance to creatinine clearance.
- Sodium is reabsorbed avidly from glomerular filtrate in
patients with prerenal ARF, in an attempt to restore intravascular volume.
- creatinine is not reabsorbed in either prerenal or
intrinsic renal failure.
- The FENa tends to be high in ischemic ATN but is often
low in patients with sepsis-induced, contrast-associated).
- Patients with prerenal ARF typically have a FENa of
<1.0% (frequently <0.1%). In patients with metabolic alkalosis, where there may be obligate losses of sodium in the urine to maintain electroneutrality, the fractional excretion of chloride (FECl) may be more sensitive than the FENa in detecting prerenal azotemia.
Ur Na/ P Na X 100 Ur Crea/ P Crea
- The FENa tends to be high in ischemic ATN
patients with prerenal ARF typically have a FENa of <1.0% (frequently <0.1%).
BUN/Creatinine CREATININE
- rises rapidly (within 24–48 h) in patients with ARF
following renal ischemia, atheroembolization, and radiocontrast exposure ( 3-5days)
- peak later (7–10 days) in ATN and atheroembolic
disease
- Rises late until the second week of therapy with many
tubular epithelial cell toxins (e.g., aminoglycosides, cisplatin
BUN/ CREATININE ratio
- Normal is 10:1
- Prerenal is > 20:1 - Intrinsic Renal is < 10:1
Radiology
• Ultrasound– to rule out postrenal ARF
• CT and MRI are alternative imaging modalities
- plain film of the abdomen or unenhanced
helical CT scan is a valuable initial screening technique
• Retrograde or anterograde pyelography - more
definitive investigations in complex cases and provide precise localization of obstruction.
• Magnetic resonance angiography (MRA) is often used to
assess patency of renal arteries and veins
- Doppler ultrasound
- CT-based angiography/ Catheter-based
angiography Kidney Biopsy
• diagnoses other than ischemic or nephrotoxic injury that may respond to disease-specific therapy
- glomerulonephritis, vasculitis, and allergic
interstitial nephritis Complications of ARF
• Expansion of extracellular fluid volume is an
inevitable consequence of diminished salt and water excretion in oliguric or anuric individuals.
- weight gain, bibasilar lung rales, raised jugular
venous pressure, and dependent edema, continued volume expansion may precipitate life-threatening pulmonary edema.
• hypoosmolality and hyponatremia from excessive
ingestion of free water
• Hyperkalemia is a frequent complication of ARF.
- Severe hyperK : rhabdomyolysis, hemolysis,
and tumor lysis syndrome.
- Milk hyperK : < 6.0 mmol/L; asymptomatic
• metabolic acidosis , often with an increased anion gap may exacerbate hyperkalemia
- diabetic or fasting ketoacidosis; lactic acidosis;
sepsis; liver ds; ethylene glycol / methanol
• Hyperphosphatemia (highly catabolic states),
hypocalcemia ( tissue resistance to the actions of parathyroid hormone and reduced levels of 1,25-dihydroxyvitamin D
• Anemia (impaired erythropoiesis, hemolysis, bleeding, hemodilution, and reduced red cell survival time); bleeding diathesis (mild thrombocytopenia, platelet dysfunction, and/or clotting factor abnormalities • Infection is a common and serious complication of ARF
• Cardiopulmonary complications include
arrhythmias, pericarditis and pericardial effusion, and pulmonary edema.
• Uremic syndrome
Intravascular volume depletion during recovery phase of Intrinsic ARF
Management of Prerenal ARF
• Composition of replacement fluids for hypovolemia should be tailored according to the composition of the lost fluid
- isotonic / hypotonic (0.45% saline) fluids for
urine and GIT losses
- PRBC’s
• Treatement of cardiac failure, Invasive hemodynamic monitoring may be required
• Fluid management may be particularly challenging in patients with cirrhosis complicated by ascites (HRS)
- use jugular venous pressure/ central venous
pressure
- Large volume paracentesis with albumin infusion - transjugular intrahepatic portosystemic shunting
Management of Postrenal ARF
• close collaboration between nephrologist, urologist, and radiologist
• Foley catheter, transurethral or suprapubic placement of a bladder catheter, percutaneous catheterization of the dilated renal pelvis or ureter, ureteric stent
Management of Intrinsic Renal Failure
• Reversal of Renal Insult
- Ischemic ATN - Restore systemic
hemodynamics and renal perfusion through volume resuscitation and use of vasopressors
- Nephrotoxic ATN - Eliminate nephrotoxic
agents, Consider toxin-specific measures: (e.g., forced alkaline diuresis for rhabdomyolysis, allopurinol/rasburicase for tumor lysis syndrome
- Other Diseases ( Glomerulonephritis/
vasculitis) - Immunosuppresion
(Glucocorticoids, alkylating agents, and/or plasmapheresis)
• Supportive Measures:
1. Salt & Water restriction 2. Diuretics/ Ultrafiltration
3. Low K diet/ K-binding resins/ Insulin+glucose 4. Sodium bicarbonate
5. Protein and calorie intake to avoid net negative nitrogen balance 6. Avoid other nephrotoxins 7. Drug dosing 8. Dialysis • Dialysis: Indications: uremic syndrome refractory hypervolemia, hyperkalemia, or acidosis
empirically, blood urea levels of >100 mg/dL
2 types: Hemodialysis and peritoneal dialysis According to harrisons, hemodialysis appears to
be somewhat more effective than peritoneal dialysis for management of ARF, but Dr. Alcantara said their just the same. Hemodialysis
Hemodialysis
- Internal Jugular Catheter - Arterio-venous Fistula/ Graft
- Subclavian vein is avoided because of risk of
subclavian stenosis Peritoneal Dialysis
- Preferred if there is diificulty obtaining vascular
access
- Associated with more protein loss
- Contraindicated in those who have undergone
recent surgery or those w ith ongoing infection
ARF Acute Kidney Injury
• new terminology considers the disease as a spectrum
of injury.
• Acute Dialysis Quality Initiative (ADQI) and devised the RIFLE definition and staging system
• Acute Kidney Injury Network (AKIN) group modified
the RIFLE staging system
• Kidney Disease: Improving Global Outcomes
(KDIGO) harmonises the previous definitions and staging systems proposed by both ADQI and AKIN5
KDIGO staging system for acute kidney injury
Biomarkers of AKI
• serum creatinine and urine output remain the best
biomarkers for AKI.
• despite the fact that serum creatinine represents a poor biomarker
• Serum crea has poor correlation with estimated GFR ( e GFR )
• Serum creatinine should be measured using the
enzymatic technique to avoid analytical interference.
• Serum and/or urinary biomarkers currently being
researched include neutrophil gelatinase-associated lipocalin (NGAL), Kidney Injury Molecule-1 (KIM-1), interleukin-18 (IL-18), and cystain C
• 25-kD protein that is covalently bound to gelatinase from neutrophils.
• normally expressed at very low levels in several human tissues, such as the kidney, lungs, stomach, and colon • One of the earliest and most robustly induced genes and
proteins in the kidney after ischemic or nephrotoxic injury vs. very low levels in CKD
• proinflammatory cytokine that is induced and cleaved in the proximal tubule after AKI.
• The active form of IL-18 exits the cell and may enter the urine after being activated in proximal tubules.
Biomarkers of AKI- Tubular Proteins
• Kidney Injury Molecule-1.
o (KIM-1) is a transmembrane protein that is
overexpressed in proximal tubular cells in ischemic or nephrotoxic AKI in animals
• Na+/H+Exchanger Isoform 3.
o most abundant sodium transporter in the
renal tubules and is located in the apical
membrane of proximal tubular cells and thick ascending limb cells. After ischemia and/or necrosis in experimental animals, NHE3 abundance decreasesexcretion into the urine
---END---Shoutouts!!!
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Roseanne,..hello!=)yey! lapit ng matapos ang mga interview natin..Mau, friends na ba tayo? Magkasama pa tayo sa JI ah..=) teng, sama ka na sa baguio!!! Cge na mas maganda ka na talga..haha..=) hi faye!thanks sa b-day treat mo..hi joy and jecs..hello carlo! Hi Celina..♡hello fau, ung kwento mo sakin ha..hello lea..
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Hello kay Vincent,Dianne, anna, and kxi..anna, di ka pa kumanta dba? Kxi, kwentuhan tau ulit kasama si bhoy..hehe=)
hello robin! At sa mga section A every Wednesday! Hello Alvin! Hi JM/Mark..wala ba discount ang painting mo? Hehe=)
