INTRODUCTION.
Kidney failure :
also known as renal failure is the partial or
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complete impairment of kidney function.It result in an inability to excrete metabolic
waste products and water, and it contributes to
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disturbances of all body system.uremic syndrome and renal failure:
are used synonymously. The term uremic syndrome
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describes a set of manifestations that result from loss
of renal function.
ACUTE RENAL FAILURE
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Acute kidney injury is a syndrome characterizedby-
Sudden decline in GFR(hours to day)
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Retention of nitrogenous wastes product in
blood (Azotemia).
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Disturbance in extracellular fluid volumeDisturbance in electrolyte and acid base
homeostasis.
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ACUTE RENAL FAILURESudden decrease in function ( hrs-days)
Often multifactorial.
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Pre-Renal and intrinsic renal cause-70%
Oliguric, UOP-<400ml
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Associated with high mortality and morbidityPRESENTATION.
Often no sign or symptom
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OliguriaAt risk group
Patient with chronic renal disease, Diabetes,
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hypertension.
Increased creatinine and urea.
ASSESSMENT.
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ARF vs CRF
CRF more likely if Acute illness , long duration,
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of symptom, intra-abdominal mass, palpablebladder.
If patient euvolaemic?
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Renal Parenchymal disease?Urine dipstick and microscopy
Major vessel occlusion?
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CAUSEPre-renal 40-70 %
Renal 10- 50 %
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Post- renal 10 %.
DIFFERENCE BETWEEN ACUTE AND CHRONIC RENAL
FAILURE.
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ACUTE RENAL FAILURECHRONIC RENAL FAILURE
1.ONSET-OVER DAYS TO WEEKS
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OVER WEEK TO MONTH
2.INVARIABILY REVERSIBLE
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USUALLY IRREVERSIBLE3.CAUSE-PRE-RENAL OR RENAL
MOSTLY RENAL
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4.URINARY VOLUME
POLYUREA AND NOCTURIA
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OLIGURIC AND ANURIA5.RENAL FAILUR CAST -ABSENT
PRESENT
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6.SPECIFIC gravity--HIGHLOW AND FIXED.
7.DIALYSIS REQUIRED FOR SHORT
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REPEATEDLY.
PERIOD
PRERENAL ARF.
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Cause of pre- Renal--Due to reduced blood delivery to the
kidney.
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Volume depletion-hemorrhage
dehydration
GI fluid loss
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Decrease effective circulatory bloodvolume
Decrease cardiac output(CHF,MI,
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Hypotension.)
Liver failure
Functional `
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ACEIs, NSAID,ARBsCorrection of volume depletion can restore kidney function.
CAUSE OF POSTRENAL ARF.
Due to obstruction of urinary outflow.
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Bladder outlet obstruction
Benign prostatic hypertrophy
Prostate cancer
Ureteral obstruction
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MalignancyPelvis or Renal obstruction
Rapid resolution of Post-renal ARF without
structural damage restore kidney function.
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INTRINSIC RENAL DISEASESDue to damage is within the kidney( structure of the
nephron)
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CAUSES--
Vascular damage( Renal thrombosis)
Glomerular damage( Nephrotic/Nephritic,
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Glomerulonephritis)Acute tubular necrosis(ATN)- Acount for 50% of
all cases of ARF.
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Ischemia(Hypotension)
Endogenous toxin(Hb, uric acid)
Exogenous toxin(Aminoglycosides, contrast
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induced nephropathy)Acute interstitial nephritis
NSAID, Infection
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Pre renal ARF can progress to intrinsic ARF if the the condition is notcorrected.
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CLINICAL FEATURES ACUTE RENALFAILURE(ARF).
It depends upon the cause of ARF and
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the stage of the disease at which the
patient presents.
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It includes one of these 3 major pattern-Syndrome of Acute nephritis
Syndrome accompanying tubular pathology
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-Oliguric phase-Diuretic phase
-Recovery phase
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Pre- Renal syndrome
SYNDROME OF ACUTE
NEPHRITIS
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This is associated with acute glomerulonephritis (Inflammation of glomerulus)
Results in increase glomerular permeability and
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decrease in glomerular filteration rate
Features?
mild proteinurea
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Haematureaoedema
SYNDROME ACCOMPANYING PATHOLOGY
ARF is caused by destruction of the tubule cells of the
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nephrons?
Desease progress in three stages?
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Oliguric phase?Last for 7-10 days with urine output less
400ml/day.
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Accumulation of waste product of protein metabolism
in the blood and resultant.
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Metabolic acidosisAzotaemia
Hyperkalaemia
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Hyponatremia.Hypervolaemia
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Diuretic phase--Healing of tubules results in improving the
urinary output
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Effect?
Dehydration and electrolyte imbalance.
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Recovery phase--Full recovery of tubule cells occurs in half cases
Time period--upto one year.
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Pre- Renal syndromeBecause of secondary disorders like ischaemia(
Decreased blood flow to tissue) and not due to
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glomerular or tubular damage.Cause of ischaemia--
Renal arterial obstruction
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hypovolaemia
hypotension
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Due to decrease renal flow, there is decrease inGFR causing oliguria, azotemia(elevation of
BUN and creatinine) and oedema.
SIGNANDSYMPTOMSOFACUTERENALFAILURE
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Decreased urine output--Anuria / Oliguria.
Acidic breathing.
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Electrolyte imbalance--Hyperkalemia.Nausea, vomiting ------Dehydration.
Hypertension
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Hematuria
Ascitis
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Pale skinPoor appetite
DIAGNOSIS OF ACUTE RENAL
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FAILURERoutine laboratory test
(Creatinine and blood urea nitrogen)
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Ultrasound of kidney - Ultrsonography helps to see the
presence of two kidney, for evaluating kidney size and
shape, and for detecting hydronephrosis or hydroureter,
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renal calculi and renal vein thrombosis.Kidney biopsy.
ACUTE RENAL FAILURE
DIAGNOSTIC.
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Laboratory EvaluationBlood urea and creatinine - Both are raised due to diminished renal blood flow.
URINE ROUTINE EXAMINATION
If Glomerulonephritis--
Hematurea
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ProteinureaRBC cast.
Serum Creatinine reliable marker of GFR
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BUN- generally follows Serum CreatinineBUN/ Creatinine -- helpful in classifying cause of ARF--
Ratio > 20 : 1-- suggest pre-renal cause
Ratio 10-15:1-- suggest intrinsic renal cause.
LAB. INVESTIGATION
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Blood exam :
Anemia
Leucopenia
Thrombocytopenia
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serum electrolytes:-
Hyponatremia
Hyperkalemia
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HypocalcemiaHyperphosphatemia
Metabolic acidosis.
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ACUTE RENAL FAILURE
DIAGNOSTIC
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UrinolysisUnremarkable in pre- renal and post-
renal cause.
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Differentiates ATN vs AIN vs AGN.
Muddy brown cast in ATN
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WBC cast in AIN .RBC cast in AGN.
INVESTIGATION.
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RBCs and RBC cast in Glomerular disease.
Crystals , RBC and WBC in post-renal ARF.
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HB % -- Haemolysis, GI bleeding/ Total Leucocyte count---Infection.
LFT: Albumin imply proteinurea--GN.
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Elevated Blood urea, Serum creatinine ratio
indicate Pre-renal ARF.
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HCO3: Metabolic acidosis.OTHER BIOMARKER.
Cystatin C
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Neutrophil gelatinase- associated lipocalin(NGAL).Interieukin
Kidney injury molecule-1
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N-acetyl-D-glucosaminidase.
CYSTATIN C
Superior to serum creatinine, as a surrogate
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marker of early and subtle changes of kidney
function.
It identifies kidney injury while creatinine levels
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remain the normal range.
Allows detection of AKI,24-48 hours earliers than
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serum creatinine.KIDNEY INJURY
MOLECULE-1
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KIM-1 is a type 1 trans membrane glycoprotein.Served as a marker of severity of AKI.
NEUTROPHIL gelatinase- associated
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lipocalin(NGAL).
NGAL can be detected in the plasma and urine
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within 2 hrs of cardiopulmonary bypass-associated AKI.
Considered equivalent to troponin in acute
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coronary syndrome.ACUTE RENAL FAILURE
DIAGNOSTIC
TEST
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FAVOURS PRERENAL FAVOURS ATN
DISEASE
BUN/CREATININE
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>20:1
10-15:1
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RATIOUosm
>500mosol/kg
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<350 mosol/kg
Una
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<20 meq/L>40 meq/L
FEna
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<1 percent
>2 percent
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