Download MBBS Renal Failure Lecture PPT

Download MBBS (Bachelor of Medicine and Bachelor of Surgery) Latest Renal Failure Lecture PPT


INTRODUCTION.
Kidney failure :
also known as renal failure is the partial or

complete impairment of kidney function.

It result in an inability to excrete metabolic

waste products and water, and it contributes to
disturbances of all body system.

uremic syndrome and renal failure:

are used synonymously. The term uremic syndrome

describes a set of manifestations that result from loss
of renal function.
ACUTE RENAL FAILURE

Acute kidney injury is a syndrome characterized

by-

Sudden decline in GFR(hours to day)

Retention of nitrogenous wastes product in

blood (Azotemia).

Disturbance in extracellular fluid volume

Disturbance in electrolyte and acid base

homeostasis.
ACUTE RENAL FAILURE

Sudden decrease in function ( hrs-days)

Often multifactorial.

Pre-Renal and intrinsic renal cause-70%

Oliguric, UOP-<400ml

Associated with high mortality and morbidity
PRESENTATION.

Often no sign or symptom

Oliguria

At risk group

Patient with chronic renal disease, Diabetes,

hypertension.

Increased creatinine and urea.
ASSESSMENT.

ARF vs CRF

CRF more likely if Acute illness , long duration,

of symptom, intra-abdominal mass, palpable
bladder.

If patient euvolaemic?

Renal Parenchymal disease?

Urine dipstick and microscopy

Major vessel occlusion?
CAUSE

Pre-renal 40-70 %

Renal 10- 50 %

Post- renal 10 %.
DIFFERENCE BETWEEN ACUTE AND CHRONIC RENAL
FAILURE.

ACUTE RENAL FAILURE

CHRONIC RENAL FAILURE

1.ONSET-OVER DAYS TO WEEKS

OVER WEEK TO MONTH

2.INVARIABILY REVERSIBLE

USUALLY IRREVERSIBLE

3.CAUSE-PRE-RENAL OR RENAL

MOSTLY RENAL

4.URINARY VOLUME

POLYUREA AND NOCTURIA

OLIGURIC AND ANURIA
5.RENAL FAILUR CAST -ABSENT

PRESENT

6.SPECIFIC gravity--HIGH

LOW AND FIXED.

7.DIALYSIS REQUIRED FOR SHORT

REPEATEDLY.

PERIOD
PRERENAL ARF.

Cause of pre- Renal--Due to reduced blood delivery to the

kidney.

Volume depletion-
hemorrhage
dehydration
GI fluid loss

Decrease effective circulatory blood

volume

Decrease cardiac output(CHF,MI,

Hypotension.)

Liver failure
Functional `
ACEIs, NSAID,ARBs
Correction of volume depletion can restore kidney function.
CAUSE OF POSTRENAL ARF.

Due to obstruction of urinary outflow.

Bladder outlet obstruction
Benign prostatic hypertrophy
Prostate cancer
Ureteral obstruction
Malignancy
Pelvis or Renal obstruction
Rapid resolution of Post-renal ARF without

structural damage restore kidney function.
INTRINSIC RENAL DISEASES

Due to damage is within the kidney( structure of the

nephron)

CAUSES--
Vascular damage( Renal thrombosis)
Glomerular damage( Nephrotic/Nephritic,

Glomerulonephritis)

Acute tubular necrosis(ATN)- Acount for 50% of

all cases of ARF.

Ischemia(Hypotension)
Endogenous toxin(Hb, uric acid)
Exogenous toxin(Aminoglycosides, contrast

induced nephropathy)

Acute interstitial nephritis
NSAID, Infection

Pre renal ARF can progress to intrinsic ARF if the the condition is not

corrected.


CLINICAL FEATURES ACUTE RENAL

FAILURE(ARF).

It depends upon the cause of ARF and

the stage of the disease at which the

patient presents.

It includes one of these 3 major pattern-
Syndrome of Acute nephritis

Syndrome accompanying tubular pathology

-Oliguric phase

-Diuretic phase

-Recovery phase

Pre- Renal syndrome
SYNDROME OF ACUTE
NEPHRITIS

This is associated with acute glomerulonephritis (

Inflammation of glomerulus)

Results in increase glomerular permeability and

decrease in glomerular filteration rate

Features?
mild proteinurea
Haematurea
oedema
SYNDROME ACCOMPANYING PATHOLOGY

ARF is caused by destruction of the tubule cells of the

nephrons?

Desease progress in three stages?

Oliguric phase?

Last for 7-10 days with urine output less

400ml/day.

Accumulation of waste product of protein metabolism

in the blood and resultant.

Metabolic acidosis

Azotaemia

Hyperkalaemia
Hyponatremia.

Hypervolaemia


Diuretic phase--

Healing of tubules results in improving the

urinary output

Effect?

Dehydration and electrolyte imbalance.

Recovery phase--

Full recovery of tubule cells occurs in half cases

Time period--upto one year.
Pre- Renal syndrome

Because of secondary disorders like ischaemia(

Decreased blood flow to tissue) and not due to
glomerular or tubular damage.

Cause of ischaemia--

Renal arterial obstruction

hypovolaemia

hypotension

Due to decrease renal flow, there is decrease in

GFR causing oliguria, azotemia(elevation of
BUN and creatinine) and oedema.
SIGNANDSYMPTOMSOFACUTERENALFAILURE

Decreased urine output--Anuria / Oliguria.

Acidic breathing.

Electrolyte imbalance--Hyperkalemia.

Nausea, vomiting ------Dehydration.

Hypertension

Hematuria

Ascitis

Pale skin

Poor appetite
DIAGNOSIS OF ACUTE RENAL

FAILURE

Routine laboratory test

(Creatinine and blood urea nitrogen)

Ultrasound of kidney - Ultrsonography helps to see the

presence of two kidney, for evaluating kidney size and
shape, and for detecting hydronephrosis or hydroureter,
renal calculi and renal vein thrombosis.

Kidney biopsy.
ACUTE RENAL FAILURE
DIAGNOSTIC.
Laboratory Evaluation
Blood urea and creatinine - Both are raised due to diminished renal blood flow.
URINE ROUTINE EXAMINATION
If Glomerulonephritis--
Hematurea
Proteinurea
RBC cast.

Serum Creatinine reliable marker of GFR

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

Blood exam :
Anemia
Leucopenia
Thrombocytopenia

serum electrolytes:-
Hyponatremia
Hyperkalemia

Hypocalcemia

Hyperphosphatemia

Metabolic acidosis.

ACUTE RENAL FAILURE

DIAGNOSTIC

Urinolysis

Unremarkable in pre- renal and post-

renal cause.

Differentiates ATN vs AIN vs AGN.

Muddy brown cast in ATN

WBC cast in AIN .

RBC cast in AGN.

INVESTIGATION.

RBCs and RBC cast in Glomerular disease.

Crystals , RBC and WBC in post-renal ARF.

HB % -- Haemolysis, GI bleeding

/ Total Leucocyte count---Infection.

LFT: Albumin imply proteinurea--GN.

Elevated Blood urea, Serum creatinine ratio

indicate Pre-renal ARF.

HCO3: Metabolic acidosis.
OTHER BIOMARKER.

Cystatin C

Neutrophil gelatinase- associated lipocalin(NGAL).

Interieukin

Kidney injury molecule-1

N-acetyl-D-glucosaminidase.
CYSTATIN C

Superior to serum creatinine, as a surrogate

marker of early and subtle changes of kidney
function.

It identifies kidney injury while creatinine levels

remain the normal range.

Allows detection of AKI,24-48 hours earliers than

serum creatinine.
KIDNEY INJURY

MOLECULE-1

KIM-1 is a type 1 trans membrane glycoprotein.

Served as a marker of severity of AKI.

NEUTROPHIL gelatinase- associated

lipocalin(NGAL).

NGAL can be detected in the plasma and urine

within 2 hrs of cardiopulmonary bypass-
associated AKI.

Considered equivalent to troponin in acute

coronary syndrome.
ACUTE RENAL FAILURE
DIAGNOSTIC

TEST

FAVOURS PRERENAL FAVOURS ATN
DISEASE

BUN/CREATININE

>20:1

10-15:1

RATIO

Uosm

>500mosol/kg

<350 mosol/kg

Una

<20 meq/L

>40 meq/L

FEna

<1 percent

>2 percent

This post was last modified on 30 November 2021