ACUTE RENAL FAILURE

&
CHRONIC RENAL FAILURE
Maj Htain Lynn
M.B;B.S,
M.Med Sc(Int: Medicine)
M.R.C.P(UK)
Consultant Physician
 ACUTE RENAL FAILURE

the situation where there is

a sudden and often reversible
loss of renal function,
which
develops over days or weeks
and is usually accompanied by
a reduction in urine volume.
Causes of Acute Renal Failure
 Pre-renal
Acute Renal Failure
(Renal hypo-perfusion)

 Intrinsic
Acute Renal Failure
(Renal damage)

 Post-renal
Acute Renal Failure
(Acute obstructive uropathy)
Pre-renal Acute Renal Failure
(Renal hypoperfusion)
 Cardiac failure
 Sepsis
 Blood loss
 Dehydration
 Vascular occlusion
 Intrinsic Renal Failure
 Acute tubular necrosis (ATN) due to renal
hypoperfusion
 Toxic ATN
 Drugs (Gentamycin), Radio-contrast
nephropathy, Snake & venoms
 Rhabdomyolysis, Haemolysis, Infections
(malaria,leptospirosis etc.)
 Glomerulonephritis and vasculitis
 Interstitial disease (Diabetes mellitus,
pyelonephritis)
 Intrinsic Renal Failure
 Drugs
 Penicillins, cephalosporins, rifampicin,
sulphonamides, erythromycin, ciprofloxacin,
NSAIDs, frusemide, thiazides, chlorthalidone,
anticonvulsant drugs – phenytoin,
carbamazepine, allopurinol
 Mushrooms
 Myeloma, Sjogren's syndrome, Sarcoidosis
 Renal large and small vessels oclusion
 Accelerated Hypertension, Pre-eclampsia
Post-renal Acute Renal Failure
(Urinary tract obstruction)

- Urinary calculi,
Retroperitoneal fibrosis,
Benign prostatic enlargement,
Prostate cancer,
Cervical cancer,
Urethral stricture/valves,
Meatal stenosis/phimosis
Be aware that ARF may develop as a
complication in any seriously or critically
ill (medical, surgical or obstetrical and
gynaecological) patients.

Routinely check the daily fluid

intake and output, measure blood
urea, creatinine and electrolytes
daily in any seriously ill patient.
Clinical assessment and
investigations are directed to
answering two questions!

IS DIALYSIS NEEDED URGENTLY ?

IS THERE ANY CORRECTABLE

CAUSE ?
IS THERE ANY CORRECTABLE
CAUSE ?
 Shock and renal hypo-perfusion
 Urinary tract obstruction – percutaneous
nephrostomy
 Accelerated hypertension
 Any nephrotoxic medication being used
 Infection
 Any treatable underlying cause – indication of
steroids, immunosuppressive, immunophresis,
plasma exchange?
If blood urea and creatinine are rising
in spite of measures correcting pre-
and post renal cause, the diagnosis of
established ARF (Intrinsic renal
damage) should be considered
irrespective of urine volume.

Oliguria may not be present in

hypercatabolic state!
OLIGURIC PHASE
- 30 – 60% of ARF are of the non-oliguric type. This phase
may last from several hours up to 2- 4 weeks.
. If it exceeds 6 weeks, other causes such as bilateral
cortical necrosis should be suspected.

POLYURIC PHASE
- need to maintain fluid and electrolytes balance
- need to prevent and treat infection
- despite a high urine output (often 3- 4 litres/day) plasma
urea and creatinine may continue to rise for variable period
and require continued dialysis

RECOVERY PHASE
 OLIGURIC PHASE
- Optimize fluid balance

INADEQUATE VOLUME EXCESSIVE VOLUME

REPLACEMENT REPLACEMENT

RENAL HYPOPERFUSION PULMONARY OEDEMA

AND AND
PRE-RENAL FAILURE CEREBRAL OEDEMA

THERE IS DANGER OF EXCESSIVE VOLUME EXPANSION

IN OLIGURIC PATIENTS AND A RISK OF INADEQUATE
VOLUME REPLACEMENT IN PRERENAL PATIENTS
 This will depend
on the hydration
Fluid usually 300 – 500 ml + urine output in
intake status of the previous 24 hours
patient – may
need restriction
or replacement
Assessment of HYDRATION
[Dehydration or fluid overload]

 Skin turgor and mucus membrane

 Any oedema
 Blood pressure (supine and sitting or
upright) (postural drop of BP >20/10
mmHg is reliable sign of IVF depletion)
 Pulse rate
 Jugular venous pulsation, JVP +/- CVP,
PCWP
 Intake-output chart
 Daily body weight
Features of dehydration
 Thirst
 Dry tongue and mouth
 Reduced skin turgor
 Postural hypotension &
hypotension
 Rapid and low volume pulse
 Decreased JVP+/- CVP, PCWP
 Negative intake-output balance
 Rapidly decreased body weight
Features of fluid overload
 Puffy face & conjunctival oedema
 Generalized oedema
 Pulmonary and cerebral oedema
 Hypertension
 Raised jugular venous pulsation
 Increased JVP+/- CVP, PCWP
 Positive intake-output balance
 Rapidly increased body weight
If volume is depleted

Expand volume until

CVP is 5 -10cm

If dehydrated, replacement of fluid and

electrolyte is essential. Infusion of
dextrose water alone may aggravate the
situation.
When adequately filled (CVP >10cm),
reassess urine output

- If oliguric, give i.v. frusemide 120mg-1g

slowly (max. 4mg/min) +/- metolazone 5-
10mg PO. Consider low dose dopamine
(2- 5μg/kg/min)

If hypotension persists (mean arterial

pressure < 60mmHg) in spite of volume
replacement (CVP >10cm), commence
inotropic support
If fluid overloaded (Fluid overload is
common especially with prior unsuccessful and
repeated fluid challenges) -

In case of pulmonary and cerebral oedema -

consider urgent HD. Consider venesection if there
is delay for dialysis;remove 250- 500cc
Fluid restriction (Intake = Output + 500cc or less)
i.v. frusemide 120mg-1g (max. 4mg/min) +/- low
dose dopamine +/- nitrate

In case with dyspnoea, Give O2 to maintain SiO2

>95%. Consider CPAP
Monitor (serum K+ and ECG evidence of
hyperkalaemia) and correct
Hyperkalaemia
 Restrict dietary potassium or drugs containing K+
 Exchange resins (Na+/Ca++) –orally or retention enema
(for maintenance therapy only)
 Glucose-insulin infusion (insulin 10- 30U + 50%
dextrose 50-100ml)(increase cellular K+ uptake – onset
30 mins)
 iv NaHCO3 8.4% 40- 60ml and repeat prn.
(shift of K+ into the cells – onset 5-10 mins)
 iv Calcium gluconate 10% 10-20ml and repeat
prn.(antagonize cardiotoxic effects of K+ - onset 2-3
mins)
 If above measures fail – dialysis treatment
Monitor (observing acidotic breathing and
cardiac dysfunction) and correct
acidaemia

If pH is <7.2, give 100cc of 8.4% NaHCO3

via central line over 15- 30min (or 400cc
2.1%HCO3 peripherally)

If above measures fail – dialysis treatment

Maintain nutrition
 Protein intake should be limited to
approximately 0.5g/kg/day to decrease
nitrogenous waste production.
 Patients who are highly catabolic (e.g.
postsurgical and burn patients) or
malnourished require higher protein intake
and should be considered for early
institution of dialysis or CAVH.
 Total calories intake should be 35-
50kcal/kg/day to avoid catabolism.
Blood pressure

 Hypotension – should be promptly evaluated

and corrected with volume expansion or
vasopressors, depending on the patient's
intravascular volume status.

 Hypertension – correct hypervolumia, can

use calcium-antagonist, clonidine, prazosin,
i.v. sodium nitroprusside, i.v. labetalol
 Correct anaemia

 Treat infection and sepsis (Nephrotoxic drugs

should be avoided and dose of the drugs
should be adjusted according to GFR.)

 Treat the underlying renal disease e.g. RPGN

 Identify and correct precipitating factors (E.g.-

hypovolumia, hypotension, hypertension,
urinary tract obstruction, nephrotoxic drugs
and substances, infection, renal diseases)

 Treat associated problems

Indications of Dialysis therapy
(Early intervention is better)
 Severe fluid overload not responding to fluid
restriction and diuretic therapy
 Dangerous hyperkalaemia (rapidly
developed in severe infection and massive
tissue destruction)
 Metabolic acidosis
 Rapidly rising or very high blood urea and
creatinine
 Pericarditis
Main modalities of dialysis

1. Acute peritoneal dialysis

2. Intermittent haemodialysis (IHD)
3. Continuous renal replacement
therapy (CRRT)
(Venovenous or arteriovenous HD)
An irreversible deterioration
in renal function which
classically develops over a
period of years.
Initially, it is manifest only as a
biochemical abnormality.
Eventually, loss of the
excretory, metabolic and
endocrine functions of the
kidney leads to the
development of the clinical
symptoms and signs of renal
failure.
Once the plasma Creatinine
exceeds about 300 μmol/l

There is usually progressive

deterioration in renal function
irrespective of aetiology
When renal function
deteriorates slowly,
patients may remain
asymptomatic until the
GFR is 20 ml/min or less.
[Normal 80 – 120 ml/min]
Clinical Features
A. Signs & symptoms of uraemia
• vague ill-health (lethargy, generalised
weakness)
• breathlessness on exertion
• anorexia, nausea, vomiting, disordered
intestinal motility
• headaches, visual disturbances
• pruritus, loss of libido
• pallor, pigmentation
• polyuria, nocturia, oliguria, oedema
 B. Endocrine
 Hyperparathyroidsm, hyper-
prolactinaemia, prolonged insulin half-
life
 C. Myopathy
 Muscle cramp, restless leg syndrome
 D. Neuropathy
 Sensory – paraesthesia
 Motor – foot drop

 Autonomic – delayed gastric emptying,

dyspepsia, diarrhoea, postural
hypotension
 May resolve once dialysis is
established.
E Anaemia
•(causes)
 dietary intake of iron & haematinic
impaired intestinal absorption of iron
 erythropoiesis due to toxic effects on bone
marrow
 red cell survival
 blood loss d/t capillary fragility & poor
platelet function

• normochromic normocytic anaemia usually

• associated iron deficiency anaemia is not
uncommon
F. Cardiovascular disorders
• hypertension in about 80% of patients
(LVH may develop)
• atherosclerosis is common & accelerated
by hypertension
pericarditis in untreated ESRF
G. Metabolic bone disease
(Renal osteodystrophy)
• osteomalacia, hyperparathyroid bone
disease (osteitis fibrosa), osteoporosis,
osteosclerosis
• hypocalcaemia, hyperphosphataemia
H. Acidosis
• metabolic acidosis (aggravate renal
osteodystrophy)
I. Susceptibility to infection
• both cellular & humoral immunity
impaired
• UTI are very common
 Clinical Features of
End Stage Renal Failure

• ill and anaemic

• oedematous or dehydrated
• acidotic breathing, pruritus
• anorexia, nausea, vomiting,
dysphagia, hiccough
• muscle twitchings, fits, drowsiness,
coma
Management of CRF

• Identify the underlying renal disease

• Attempt to prevent further renal
damage
• Look for reversible factors which are
making renal function worse
• Attempt to limit the adverse effects
of the loss of renal function
• Institute renal replacement therapy
[dialysis, renal transplantation]
when appropriate
 Identify the underlying renal disease
 History
 Clinical examination
 Testing of biochemistry
 Testing of immunology
 Radiology [USG, KUB, IVU, Renal
scan, CT scan]
 Biopsy

In some cases, the cause may be amenable

to specific therapy, e.g. immunosuppression
in some types of glomerulonephritis
Correct the causes of rapid
deterioration of renal function in
CRF
 Decrease in effective arterial blood volume
(volume depletion, worsening congestive heart
failure)
 Alterations in BP (hypertension, hypotension)
 Urinary tract obstruction
 Infection
 Nephrotoxic agents
 Renal vascular events (renal vein thrombosis,
progression of renal artery stenosis, cholesterol
embolization)
- Optimize fluid balance

INADEQUATE VOLUME EXCESSIVE VOLUME

REPLACEMENT REPLACEMENT

Renal hypo-perfusion Exacerbate generalized

and oedema and hypertension
Further deterioration of
renal function

Maintaining minimal peripheral oedema is

appropriate to prevent renal hypo-perfusion.
 In oliguric patient or late phase
of CRF when there is evidence
of fluid accumulation

Fluid
usually 300 – 500 ml + urine output daily
intake
If volume is depleted

If dehydrated, replacement of fluid and

electrolyte is essential. Infusion of
dextrose water alone may aggravate the
situation.
If fluid overloaded

In case of pulmonary and cerebral oedema

- Give O2 to maintain SiO2 >95%. Consider CPAP
- i.v. frusemide 120mg-1g (max. 4mg/min)
- Fluid restriction (Intake = Output + 500cc or less)
- Control hypertension
- may consider urgent HD.
- Consider venesection if there is delay for dialysis;
remove 250- 500cc
Na+
 Extra-salt may be required in salt losing
nephropathy
 It is usual to start with 2-3 g/day and increase
the dose as required.
 Salt restriction should be considered when
 systemic or pulmonary oedema developed

 aggravation of hypertension occurred

K+
 Restricted to 40 mEq/day when GFR falls
below 20 ml/min
 Acidosis
 Declining renal function is associated with
metabolic acidosis, which is often asymptomatic.
 Sustained acidosis
 Aggravates metabolic bone disease

 Increase tissue catabolism

 Produce multi-organ dysfunction

 When s' bicarbonate falls below 18 mEq/l

give oral NaHCO3 300- 600 mg p.o. tid (CaCO3
up to 3 g daily instead in case of hypertension)
 Diet
 Moderate restriction (< 50 g protein/day) should be
accompanied by adequate intake of calories to
prevent malnutrition.
 Adequate caloric intake – 35- 50kcal/kg/day
 Protein restriction – 0.6- 0.7 g/kg/day of high
biologic value protein when GFR falls below
30ml/min
 Anorexia and muscle loss may indicate a need to
commence dialysis treatment.
 Prevent and treat hyper-cholesterolaemia and
hyper-triglyceridaemia
Hypertension may be due to
 Expanded ECF volume
 Increased sympathetic activity
 Erythropoietin administration
 RAA stimulation, prostaglandins/bradykinins
 Parathyroid hormone secretion
 Calcified arterial tree
 Renal vascular disease
 Rapid decline in serum K+ while on dialysis
Drug treatment for hypertension
• Diuretics (chlorthalidone, loop diuretics) –
hypovolaemia, electrolyte imbalances
• Calcium antagonists (nifedipine, amlodipine) –
headache, palpitation, fluid retention
• Vasodilators (prazosin, hydralazine) – postural
hypotension, first dose effect
• Beta blockers (atenolol, carvidelol) –
bradycardia, bronchospasm, sleep disturbances
• ACEI/ Angiotensin II receptor antagonists –
exclude renovascular disease, monitor renal
function regularly
Anaemia
 Correction of any iron and vitamin deficiency
 Erythropoietin 50 U/kg sc 2- 3 times/week
(S.E – hypertension)
 Target haemoglobin of >10 g/dl
 Diminished conversion of
25hydroxy cholocalciferol to
1.25 dihydroxy cholecalciferol

Impaired
Impaired renal mineralization
function of bone
Decreased
GI calcium
Impaired phosphate absorption
excretion

Reduced s' Ca Increased

Raised s' PO4
bone
resorption
Parathyroid gland
 Renal osteodystrophy
 Plasma calcium and phosphate should
be kept as near to normal as possible.
 Hypocalcaemia
 1-α-hydroxylated synthetic
anologues of vitamin D
 Hyperphosphataemia
 Dietary restriction of foods with high
phosphate content (milk, cheese,
eggs)
 Phosphate binding drugs (CaCO3 )
 Parathyroidectomy in case of tertiary
hyperthyroidism
Renal Replacement Therapy

 Haemodialysis
 Continuous ambulatory
peritoneal dialysis [CAPD]
 Renal transplantation