Download MBBS Renal Failure Lecture PPT

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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 characterized

by-

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 volume

Disturbance in electrolyte and acid base

homeostasis.

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ACUTE RENAL FAILURE

Sudden 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 morbidity
PRESENTATION.

Often no sign or symptom

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Oliguria

At 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, palpable
bladder.

If patient euvolaemic?

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Renal Parenchymal disease?

Urine dipstick and microscopy

Major vessel occlusion?

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CAUSE

Pre-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 FAILURE

CHRONIC RENAL FAILURE

1.ONSET-OVER DAYS TO WEEKS

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OVER WEEK TO MONTH

2.INVARIABILY REVERSIBLE

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USUALLY IRREVERSIBLE

3.CAUSE-PRE-RENAL OR RENAL

MOSTLY RENAL

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4.URINARY VOLUME

POLYUREA AND NOCTURIA

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OLIGURIC AND ANURIA
5.RENAL FAILUR CAST -ABSENT

PRESENT

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6.SPECIFIC gravity--HIGH

LOW 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 blood

volume

Decrease cardiac output(CHF,MI,

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Hypotension.)

Liver failure
Functional `

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ACEIs, NSAID,ARBs
Correction 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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Malignancy
Pelvis or Renal obstruction
Rapid resolution of Post-renal ARF without

structural damage restore kidney function.

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INTRINSIC RENAL DISEASES

Due 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 not

corrected.

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CLINICAL FEATURES ACUTE RENAL

FAILURE(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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Haematurea
oedema
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 acidosis

Azotaemia

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 syndrome

Because 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 in

GFR 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 skin

Poor appetite
DIAGNOSIS OF ACUTE RENAL

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FAILURE

Routine 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 Evaluation
Blood urea and creatinine - Both are raised due to diminished renal blood flow.
URINE ROUTINE EXAMINATION
If Glomerulonephritis--
Hematurea

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Proteinurea
RBC cast.

Serum Creatinine reliable marker of GFR

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BUN- generally follows Serum Creatinine
BUN/ 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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Hypocalcemia

Hyperphosphatemia

Metabolic acidosis.

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ACUTE RENAL FAILURE

DIAGNOSTIC

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Urinolysis

Unremarkable 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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RATIO

Uosm

>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