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