Acute renal failure

Definition
 A syndrome characterized by-
– Rapid decline in GFR(hours to days)
– Retention of nitrogenous waste products
– Abnormilities of extracellular fluid volume,
electrolytes and acid base.
 ARF complicates approx. 5% of
hospital admissions and upto 30% of
ICU admissions.
 Oliguria is present in only 50% of ARF.

 Frequently detected during

biochemical monitoring.
 Causes of ARF
 Prerenal ARF- renal hypoperfusion
without compromising the integrity of
renal parenchyma (~ 55%).
 Intrinsic Renal ARF- diseases that
directly involve the renal
parenchyma(~40%).
 Post renal ARF- diseases associated
with urinary tract obstruction(~5%).
 Most ARF is reversible.
 ARF is associated with 50%
mortality,due to diseases that
precipitates ARF.
 Pathophysiology and
Etiology of ARF
 Prerenal- reversile upon restoration of renal
blood flow, no parenchymal damage
– Hypovolemia
– Low cardiac output
– Systemic vasodialation- sepsis,
– Renal vasoconstiction- hypercalcemia,.
– Renal hypoperfusion with impairment of
autoregulation -NSAIDs, ACEI.
 Intrinsic renal ARF
 1.Acute tubular necrosis-
– Ischemic-severe trauma, burn, sepsis
– Toxins- eg- aminoglycosides,
acyclovir,amphotericin B,cisplatin,contrast
, rhabdomyolysis, hemolysis,uric acid.
 2.Acute interstitial nephritis-
– Drugs - penicillins, quinolone, diuretics,
– Infections
 3.Diseases of glomeruli and renal
microvasculature-
– Glomerulonephritis and vasculitis
– HUS, TTP,Malignant HTN,
Preeclampsia,DIC,
 4.Renovascular obstrucion- renal
artery or renal vein obstruction.
 Course of Ischemic
ARF-
 The initiation phase( hours to days)-
initial period of renal hypoperfusion during
which ischemic injury is evolving.
 Maintenance phase- (typically 1-2
weeks),during which injury is established,
GFR stabilizes to 5-10 ml/min.
 Recovery phase- gradual return of GFR to
normal. Diuresis due to retained solutes and
delayed recovery of interstitial function
compared to glomerular.
 Drug induced ARF
 Aminoglycosides- 10-30% cases of
courses, risk factors are-
– prolonged exposure,
– high doses,
– elderly,
– patients with pre existing ARF,
– volume depletion,
– hypokalemia.
Chronic kidney disease
 Defined as - disease duration of more than
3 months.
 Kidney damage is either functional or
structural with or without reduction in GFR
as identified by-
– Abnormal pathology- gross or microscopic
– lab,. Markers of kidney damage in blood, urine,
imaging tests
– GFR < 60 ml/min/1.73m2 in absense of any
other abn.
 D/D
 Features of chronicity-
 Anemia
 Nocturia
 Neuropathy
 Malnutrition
 Tolerance to uremia
 Radiological e/o Bone disease or Small
kidneys
 Diagnosis
 Pre renal- features s/o hypovolemia or
reduced ECV(cardiac failure,
sepsis),improves after normalization of
homodynamic.
 Intrinsic renal- ARF persist even after
normalization of systemic hemodynamics
h/o severe ischemic insult or toxin.(90%
either ischemic or toxic ATN).
 Post renal- obstruction in ureter, bladder or
urethra can cause.
 most common causes are- stones, tumor,
sloughed papilla, enlarged prostate, urethral
stricture, PUV in children.
 Radiological investigations are necessary.
 Complete anuria if bilateral obstruction.
 Urinalysis
 Prerenal- sediment is acellular (
bland), contain hyaline casts.
 Post renal – also bland, but
sometimes hematuria, pyuria in calculi,
prostatic ds.
 Intrinsic renal ARF-
– Sediment active- hematuria, proteinuria,
casts.
Renal failure indices
Diagnostic indices Prerenal Intrinsic
renal
FE Na- <1 >1
Una.Pcr/Ucr.Pna
Urinary Na <10 mEq >20mEq
Urine cret/plasma cr >40 <20
Urine sp. gravity >1.020 1.010
Urine osmolality >500 <350
Plasma bun/creat >20 <10
 Lab findings
 Serial creatinine measurment-
– Ischemic ATN and after contrast – rapid
rise in 1-2 days.
– Delayed rise in toxic ATN(
aminoglycoside) 7-10 days.
.
– Severe anemia in absense of
hemorrhage- hemolysis, multiple
myeloma, HUS.
 Radiologic findings
 USG – size of kidney and to exclude post
renal ARF, but in acute obstruction PCS
dialatation may be absent.
 Doppler for Renal artery stenosis.
 Renal biopsy- Patients in whom pre renal
and post renal cause excluded and ARF is
not recovering esp. for cause other than
ATN. Eg- glomerulonephritis, vasculitis,
HUS,AIN etc.
 Complications
 Intravascular volume overload
 Hyponatremia
 Hyperkalemia
 Hyperphosphatemia
 Hypocalcemia
 Hypermagnesemia
 Metabolic acidosis
 Anemia
 Prevention
– maintain normal intravascular volume.
– Adjusting doses of nephrotoxic drugs in
elderly, and renal impairment. Use GFR
measurment.
– Cautious use of drugs eg- ACEI, AngII R
blockers and NSAIDS in patients with
hypovolemia.
– Forced alkaline diuresis and allopurinol in
patients on chemotherapy.
 Formula to estimate
GFR
 Estimated Ccr (mL/min) =
(140 - age)(body weight in kg)
72 x serum creatinine in mg/dL
 Example: For man, age 70 years, weight 58
kg, serum creatinine 1.3 mg/dL, estimated
Ccr = 43 mL/min; for woman with similar
values, estimated rate would be 37 mL/min.
 For women, multiply result by 0.85 (see
text).
(Adapted from Cockcroft and Gault).
Volume replacement in
pre renal ARF
 Crystalloids- isotonic saline is the fluid of
choice for most patients with hypovolemia
leading to pre renal ARF.
 Lactated Ringer solution for hemorrhagic
shock.it produces less acidosis.
 Hypotonic saline can be used in case of
mild hypovolemia and hypernatremia.
 Crystalloids are preferred fluids in renal
failure.
 Colloids- colloid solutions ( albumin,
gelatins, dextrans contain oncotically active
molecules.
 Albumin- no obvious advantage of albumin
in critically ill patients with hypovolemia,
burns and hypoproteinemia.
 Dextrans should also be avoided in Pre
renal ARF.
 Specific therapy
 By definition prerenal ARF is reversible on
restoration of hemodyanamic abnormility
and post renal ARF after relief of
obstruction.
 There is no specific therapy for established
Intrinsic ARF due to ATN. Maintenance of
hemodyanamics and avoid the drug.
 For other Intrinsic ARF eg. Nonrecovering
AIN,AGN,vasculitis etc., kidney biopsy is
necessary.
Role of diuretics in ARF
 No role except ,for patient in fluid overload,
high doses of loop diuretics , furosemide
200 to 400 mg/day may promote diuresis in
patients who fail to respond to conventional
doses.
 Loop diuretics can be tried within 24- 48 hrs
of oligoanuria, if no response stop them.
 Manitol should not be given once ATN is
established as it can cause pulmonary
edema.
 Role of dopamine in
ARF
 It has been proved in various trials,that that
low dose dopamine(<5 microgm/kg/min)is
ineffective in ARF, on the contrary, it may
trigger arrythmia and sudden cardiac death
in critically ill patients. But it can be used as
vasopressor to increase BP.
 Norepinephrine is a better vasopressor than
dopamine.
 Treatment of
complications
 Hyponatremia- can be treated by fluid
restriction. And hypernatremia by
infusion of hypotonic fluids.
 Metabolic acidossi not treated until pH
is<7.2 or bicarb is <15 mMol/l. excess
sodabicarb can cause- hypervolemia,
hypocalcemia and hypokalemia.
 Nutrition in ARF
 Protein restriction to 0.6 gm/kg/wt-
day, of high biological value and to
provide most calories as
carbohydrates, but if patient is
hypercatabolic( sepsis), then high
protein diet – 1.5 gm/kg/wt.
 Indications of dialysis
 Symptoms and signs of uremia
 Hyperkalemia

 Refractory fluid overload

 Refractory acidosis

 Uremic pericarditis

 Uremic encephalopathy.
 Modalities of dialysis
 Hemodialysis-
 Peritoneal dialysis

 CRRT
Outcome and prognosis
 The mortality rate is approx- 50%.
 Mortality vary according to cause of ARF-
15% in obstetric causes, 30% in toxin
related ARF and 60% after surgery or
trauma (usually due to septicemia).
 Most patients of ARF recover , 5% require
regular RRT and another 5% develop
progressive deterioration of renal function.
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