Acute Renal Failure

Jayanti Jasti, M.D.

Emory Johns Creek Hospital

Definition
Sudden decrease in GFR over a period of
hours to days resulting in the failure of the
kidney to excrete nitrogenous waste
products and maintain fluid and electrolyte
homeostasis.
Clinically seen as rise in serum creatinine
by 50% above baseline or increase by 0.5
mg/dl.
Measurement of Renal Function
Cockroft-Gault Formula
GFR = (140-age in yrs) x Lean body wt(kg)/ S.Cr x 72
Adjustment made for the gender.
MDRD and modified MDRD
Complicated, Laboratory reports it!
Adjustment made for the gender and race.
Creatinine Clearance
CrCl = U.Cr x U.vol/ S.Cr x 1440
Serum Creatinine as a marker
Steady state between creatinine production and
excretion is required.
Creatinine production is dependent on muscle
mass
Drugs which interfere with proximal tubular
secretion of creatinine.
Trimethoprim, Triamterene, Cimetidine,probenecid, amiloride etc.,
Drugs which interfere with creatinine
measurement in the lab.
Ascorbic acid, cephalosporins etc.,

Blood Urea Nitrogen
BUN increases in volume depleted states
due to reabsorption in the proximal tubules
and in the collecting ducts.
BUN can be high with out RF.
Hypercatabolic states, protein loading, steroids etc.,
BUN can be low even with RF
Severe malnourishment, liver disease, low protein diet
etc.,
Types of ARF
ARF
ARF/CKD

Anuric (<50ml of urine output/day)
Oliguric (<400 ml/day)
Non-oliguric (>400 ml/day)
Etiology of ARF
Prerenal
Renal hypoperfusion, no structural damage to the kidneys, Cr
normalizes in 24-72 hours with correction of hypoperfused state.
Post-renal
Obstruction to the urine flow, either unilateral/bilateral, intra-ureteral
or extra-ureteral or bladder neck or intra-pelvis (renal pelvis).
Intra-renal
Damage or inflammation within the kidney, may be primary renal or
part of systemic disease.
Prerenal ARF
Decreased
Extra cellular
Volume
Hemorrhage
Volume losses
Either renal, GI
or other (skin)
Hyperthermia etc.,
Third spacing
Peritonitis, pancreatitis,
SIRS, hypoalbuminemia
etc.,
Prerenal ARF
Increased ECV with
Arterial underfilling
Reduced Cardiac
Output
Cardiogenic shock, MI, PE
Tamponade, constrictive
Pericarditis etc.,
Peripheral Vasoldilatation
Sepsis, anaphylaxis, anaesthesia,
Cirrhosis, other liver diseases.
Intrarenal hemodynamic changes
ACEI and ARB associated ARF
These medications cause ARF where angiotensin
is playing a major crucial protective role in
maintaining GFR by constricting the glomerular
efferent arteriole.
Volume Depletion
B/L Renal artery stenosis
CHF
Diuretic use
Cirrhosis etc.,

NSAIDs associated ARF
Vasomotor in nature.
In the presence of conditions with
increased renal vasoconstrictor activity like
CHF, Cirrhosis, Nephrotic Syndrome,
Sepsis, Volume depletion, HTN, CKD, DM,
Anaesthesia etc.,
No RF seen in Euvolemic conditions with
normal kidney, liver and cardiac functions.
Postrenal ARF
Intra Ureteral
Stones, Clots, Pyogenic debris, Sloughed papillae in
analgesic nephropathy, sickle cell disease etc.,
Extra Ureteral
Malignancy, Retroperitoneal fibrosis, accidental ligation
etc.,
Bladder neck/Urethral
BPH, Prostate Ca, Bladder Ca, Autonomic neuropathy
with urinary retention, Urethral stricture, Blood
clots/bladder stones.
Intrarenal ARF
Vascular
Glomerular
Interstitial
Tubular
Vascular causes of Intrarenal ARF
Large and Medium size vessels
Renal artery thrombosis or emboli
Renal vein thrombosis
Polyarterial nodosa
Small vessel disease
Atheroembolic phenomenon
Microangiopathies like TTP, HUS, HELLP and malignant
HTN.
Glomerular causes of Intrarenal
ARF
Nephritis
Hematuria
Proteinuria (1-2gm/d)
ARF
May present as Rapidly
progressive
Glomerulonephritis
Renal Biopsy to diagnose

Nephrosis
Massive
proteinuria(>3gm/d)
Minimal hematuria
Uncommon to present as
ARF
Renal Biopsy needed to
diagnose.

Interstitial causes of Intrarenal ARF
Focal/diffuse edema and infiltration of the renal
interstitium with inflammatory cells.

Acute
Interstitial
Nephritis

Drugs
Antibiotics, NSAIDs,
Phenytoin, allopurinol,
diuretics etc.,
Systemic
Diseases
SLE etc.,
Infections
Staph, Strepto, CMV,
EBV, TB etc.,
Tubular causes of Intrarenal ARF,
Acute Tubular Necrosis
Ischemia induced
Shock
Hemorrhage
Sepsis
Trauma
Pancreatitis
Nephrotoxin induced
Drugs like IV contrast,
Aminoglycosides, Ampho
B, pentamidine, Acyclovir,
Ehtylene Glycol etc.,
Endogenous Toxins in
the case of
Rhabdomyolysis,
Hemolysis, uric acid
nephropathy
Epidemiology of ARF
Community acquired ARF seen in 1% of all
hospitalized patients on admission.50% of those
patients have underlying CKD.
Development of ARF in hospitalized patients is
common and carries independent mortality risk.
In patients with normal renal function, the
incidence of ARF is about 5%.
In patients with underlying CKD, the incidence is
about 16%
Epidemiology of ARF
Hospital acquired ARF
40% is due to ATN
15% related to medication associated
ARF.
10% due to contrast induced nephropathy.
AIDS associated ARF account for 5%.

Mortality associated with ARF
ICU associated ARF along with
respiratory failure requiring
hemodialysis, the mortality is >90%.
ICU associated ARF with out
respiratory failure or hemodialysis, it
is 72%
Non-ICU renal failure associated
mortality is around 32%.
Evaluation of ARF
Careful History and tabulation of data
including u.o, weights, vitals, medications
etc.,.
Physical Examination findings including
signs of vol. depletion etc.,
Urinalysis
Urinary indices(Urine sodium, creatinine,
FeNa, FeUrea etc.,)
Urinary Indices
Prerenal
High SpGr
No
proteinuria/hematuria
U.Na <20
U.Cr/P.Cr >40
U.Osm >500
FeNa <1%
FeUrea <35%

ATN
Sp Gr 1.010
Variable proteinuria
U.Na >40
U.Cr/P.Cr <20
U.Osm <350
FeNa >1%
FeUrea >50%

Urinalysis and Urine Sediment
UA positive for heme and proteinuria seen
in Glomerular and Interstitial renal failure.
Urine eosinophils are seen in AIN,
Atheroembolic disease etc.,
Urine sediment positive for red cell casts
seen in Glomerulonephritis.
UA bland in Post Renal ARF.


Laboratory Data
Peripheral eosinophilia in AIN,
Atheroembolic disease.
Hypocomplementemia seen in SLE,
MPGN, Atheroembolic disease etc.,
Elevated ESR seen in Atheroembolic
disease.
Serologies positive in glomerular diseases,
like ANA, ANCA, Anti GBM, Hepatitis, HIV
Elevated LDH seen in RVT.

Laboratory Data (contd)
Thrombocytopenia with microangiopathic
hemolysis seen in TTP, HUS etc.,
Low Haptoglobin, High retic count seen in
microangiopathic states.
Schistocytes (red cell fragmentation).
CPK, uric acid levels etc., to evaluate for
rhabdomyolysis, uric acid nephropathy.
Evidence of hepatic insufficiency in
diagnosing hepatorenal syndrome.

Imaging
Ultrasound
Useful in Post renal ARF.
Early obstruction may not show significant
hydronephrosis.
External obstruction encasing the whole urinary
system may not show hydronephrosis, for e.g.,
retroperitoneal fibrosis.
U/S doppler useful in diagnosing Renal vein
thrombosis.

Imaging (contd)
CT scan
Useful for detecting stones, location of the
obstruction, Tumours etc.,
Isotope renography
To evaluate the function significance of
obstruction.
Done with lasix and Mag3 isotope for evaluatine
obstruction.
Imaging (contd)
Cystoscopy and Retrograde
Pyelography
To evaluate patients with high clinical suspicion
of obstruction esp., in unique cases of calculi,
pyogenic debris, blood clots, bladder cancer
etc.,
Renal Angigraphy
In emergent cases of anuria with suspicion of
renal embolization.
Renal Biopsy
Only in patients with no clear etiology.
In patients with active urinary sediment
(RBCs, red cell casts etc., )
RPGN (rapidly progressive
glomerulonephritis).
Refractory ATN with out recovery despite
no further renal insults.
Acute Interstitial nephritis.

Management of ARF
Volume repletion with isotonic fluids to improve
renal perfusion pressures in prerenal states.
CVP/ PAWP monitoring.
Supportive measures for sepsis with pressors,
antibiotics etc.,
Colloidal substances like blood products in
hemorrhagic shock.
Management of heart failure by improving
cardiac output.




Management (contd)
Drugs need to be dosed according to the
renal clearance.
Electrolyte and acid base correction.
Renal diet, if K+ high.
Diuretics in overt fluid overload states.
Foley catheterization in bladder neck
obstruction/prostatic obstruction.



Management (contd)
Avoid nephrotoxic agents like Contrast
dye, NSAIDs, Aminoglycosides etc.,
Also avoid ACEI/ARB unless the
underlying problem is decompensated
heart failure.
Nutritional support with parenteral or
enteral feeding.
Management (contd)
Renal replacement therapy
Modes of dialysis:
IHD (Intermittent Hemodialysis)
Quick removal of solutes over 3-4 hours,
possible hemodynamic instability. ICU,
hypotensive patients are probably not the best
candiadtes for this type of HD.
CRRT (Continuous renal replacement therapy).
Modality of choice in critically ill patients.
Management (contd)
Vascular access needed for Hemodialysis.
Peritoneal dialysis uncommonly used for
managing ARF
It may be used in locations where IHD or
CRRT are not available.
Any Questions?