RENAL FAILURE

DR..M.H.MUMTAZ

TYPES

1, REVERSIBLE DYSFUNTION

(acute R.failure)

2, IRREVERSIBLE DYSFUNTION

(Chronic R failure)

ACUTE RENAL FAILURE

• 1, PRE RENAL

• 2, RENAL

• 3, POST RENAL

PRE RENAL FAILURE

• CAUSES

a,total body water depletion

b,water redistribution

ivs--------iss

vasodilation,sepsis,anaphy.

c,low CO--------low BP (S,M.D)

RENAL

a, Interstitial nephritis

b, A.T.N.

hypoperfusion

chemical

trauma , toxins

sepsis

PATHOLOGY

T.obstruction

T.damage

T.backleakage

DIAGNOSIS

a,History

oligurea,concentrated U

b,Tests

lab. Serum,urine

radiodiagnostics

C.T. MRI. Ultrasount

ALTERNATIVE CLASS.

Filteration failure

Tubular dysfuntion

Oliguric/non oliguric

RISK FACTORS

• Acute diseases

sepsis

SIRS

jaundice

I.A.P.

renal trauma

transfusion DIC

Anaphylaxis

muscle injury

thermal burn

electrocution

RISK FACTORS

CHRONIC DISEASES advancing age diabetes mellitis renal disease vascular disease hyperuricaemia

RISK FACTORS

Physiological changes

1. ^ age

2. ^ HR hypotension

^ CVP, lowRVPP

high or low co,svr

abnormal OER

olig/polyurea

3. Fluid balance

Oedaema

high/low protein

intake

RISK FACTORS

Chronic drug therapy

NSAIDS

Diuretics

Cyclosporins

RISK FACTORS

Acute drug therapy

A. ATN

aminoglycosides

cephalosporins

diuretics contra.

rifampicin

lithium

cisplatin

B. Interstitial nephritis

cephalosporins

diuretics

aspirin,NSAIDS

cemetidine

captopril

RISK FACTORS

Proceedures

a. Aortic/renal cross clamping

b.Transfusion

c. Major surgery

RISK FACTORS

IMPAIRED RBF

hypotension/m.hypertension

renal art. Occlosion

hepatorenal failure

endotoxaemia

renal vein thrombosis

renal venous hypertansion

RISK FACTORS

Metaboic causes

1. Electrilytes

hyper-cal

hypo-k

hyper-phosphate

2. High oncotic P.

3. Metabolites

Pigments

bilirubin

myoglobin

haemoglobin

RISK FACTORS

Post-renal

urethral/blader obs.

bil.ureter obs.

stones/clot/tumur

papillary necrosis

Retroperitoneal fibrosis

Surgical ligation

Blader rupture

Renal pelvic trauma

Urethral trauma

ACUTE TUBULAR NECROSIS

PHASES

a,Initiation phase

b,Maintenance phase

INITIATION PHASE

ISCHAEMIA

^ symp.stimulation

^ renin activity

PGE2

ANH inhibition

^ ADH

^ adenosine

^ endothelin

NEPHROTOXINS

Ischaemia increases the

susceptibility to

nephrotoxic agents

MANTENANCE PHASE

• Factors acting to maintain filteration failure

1,tubular obstruction

2,tubular backleak

3,vasodilatation of efferent art.

4,decreased GMP

Mechanism of oligurea

a,glomerulo-tubular balance

b,decreased GMP

c,itratubular obstruction

d,interstitial oedema

e,cortical ischaemia

Complications of ARF/ATN

A,oligurea

absolute

relative

B, azotaemia

normal solute load

maximum

in catabolic states

in ARF

^ urea/d

^ cr/d

Complications

C,Biochamical

^NaCl/water

^ K

^ HPO4

hypocalcaemia

^ Mg

^ uric acid

M.acidosis

D,Haematological

Anaemia

Thrombocytopaenia

Leukocyte dysf.

Complications

E,Immunosupression

Lumphopaenia

Reduced IgG

Reduced comple.

Impaired PMN

R.I.response

Drug effects

Infections

F,C.V.S.

CCF

Hypertention

Arrhythmias

Pericarditis

Effusion

Complications

G, G.I.T.

Anorexia,Nausea,

Ileus,Hmge.

H,Neurological

Lethargy,somnolance

Confusion,

Convulsions

^ sensitivity to

anaesthetics

Complications

I,causes of pulmonary infilterates in ARF

1,LVF/CCF

2,bacterial pmeumonia

3,Atypical pneumonia

4,Septicaemia

5,ARDS

6,Autoammune diseases

Causes of Acidosis in ARF

A,Tubular dysfuntion

B,Glomerular dysfuntion

C,Other causes

low C.O.

Resp.F

Starvation

Rhabdomyolysis

Hyperkalaemia

Organic acids

INVESTIGATIONS IN ARF

• Biochemistry

INVESTIGATIONS

Investigations-1, Biochemistry

parameter Pre-renal ARF ATN

Urine osmol. >500 <350

U/P osmolality >1.8

<0.8-1.2

Urine SG >1.020 1.010-1.015

Urine(Na) <20 >40

Urine (Cl) <20 >20

U/P urea >8 <3

U/P creatinine >40 <20

FE Na <1 >1

Definitions

• RFI=RENA FAILURE INDEX

• =urine(Na)/(U/P creatinine)

• FEna=%fractional excretio Na

• =(U/P Na).100/(U/P creatinine)

Abnormal urea/creatinine ratio

• Normal U:C ratio 100:1( R;70-150)

• Pre-renal disease >200:1

Abnormal urea/creatinine ratio

• High Ratio

• ^ urea .dehydration/hypovol.

• .GIT.bleeding

• .Catabolic state

• .Hyperalimentation

• .Drugs

• low creatinie .elderly,low m. mass

Abnormal urea/creatinine ratio

• Low Ratio

• low urea. Liver failure

• hepato-renal synd

• Malnutrition

• High creatinie rhabdomyolysis

• acute m.disease

• ketones,drugs

CREATININE CLEARANCE

• 1, clearance(ml/min=(N-age[years])*BW(kg)/serum creat. N = 150 foe female N = 160 for male > 70 N = 170 for male < 70

2, clearance(ml/min)=UV*1000 /p*420 U=urine creatinine level V=urine volume (midnight &7 am) P= plasma creatinine level

2. Urinary sediment

• .Cast types

• i,hyaline casts, fever,diuretics,RD

• ii,red cell casts glomerulonephritis

• iii,w.cell casts pyelonephritis

• iv,waxy casts chronic renal disease

3,Imaging

• 1, Ultrasound

• 2, CT scan

• 3, IV pylogram

• 4, radio-isotope perfusion scan

• 5, renal angiogram

4,Renal biopsy

• 1, glomerulonephritis

• 2, vasculitis

• 3, SLE

• 4, Goodpasture syndrome

• 5, TTP

• 6, Interstitial nephritis

• 7, oligurea lasting > 8 weeks

Renal failureprophylaxis&protection

• Methods

• 1, physiological

• 2,physical

• 3,pharmacological

• 4,replacement therapies

Physiological methods

• a, normalise blood volume

• iv fluids,(Na containg)

• b,optimise cardiac output

• iv fluids.inotropes,vasopressors

• c, optimise O2 delivery

• Hb,Spo2,avoid acidosis

• d, high sodium excretion

Physical methods

• Detection/management of IOH• Detection/management-post renal obs.• Limitation of aortic clamp times• Avoidance of embolisation• Minimise direct trauma

Pharmacological methods

• Avoid nephrotoxins

• Avoid inhibitors of autoregulation

• Diuretics

• Renodilators

• Other agents• free radical scavengers

• Ca channel blockers

Renal replacement methods

• Haemo- filtration

• Haemo-diafiltration

• Haemodialysis

• R. Transplant.

Renal failure---Frusemide

• Beneficial effects• Increased tubular&urine flow• Increase Na &osmolar clearance• Decreased tubular O2 demand• Stimulate vasodilator prostaglandins

• Deleterious effects• Hypovolaemia• Hypokalamia,Hyponatraemia• Ototoxicity

Uses in non renal failure

• Fluid overload

• Cerebral oedema

• Hyperkalaemia

• Renal protection• ( decreased O2 demand)

Renal failure---Mannitol

• 1,Osmotic diuresis

• 2,Anti sludging ,tubular protect.

• 3,renal vasodilatory PG synthesis

• 4,Free radical scavenger

• 5,Decreased T. swelling

Renal failure---Dopamine

• Increases Fe Na excretion

• Increases urine out put

• Does not increase creatinine clearance

• Inotropic effect

• Doesnot prevent ac.renal failure

• Side effects,

• gastric stasis,inhibition of

• ant pit.hormones,hypoxic

• drive depression.

Renal failure---Nor-adrenaline

• Increases perfusion pressure by increase

• of efferent arteriolar resistance

• more than afferent art.resistance

Other therapies

• 1,Calcium channel blockers

• 2,Adenicine recepter antagonists

• 3,Oxypentifylline

• 4,Chlorpromazine

• 5,Clonidine

• 6,ATP-MgCl2

• 7,ANF

Conclusion,Renal rescue therapy

• Normalise;-

• Blood flow• blood volume

• blood pressure• O2 delivery• CO—CI

• Blood Pressure, s,m,d.