Acute Renal Failure

ACUTE RENAL FAILURE

DEFINITION:
It is abrupt decrease in renal function which developed over a period of days or weeks and usually accompanied by reduction in urine volume and retention of nitrogenous waste (( eg. Blood urea and creatinine ))
CAUSES:
Pre renal:
Absolute decrease in effective blood volume eg. Hemorrhage, burns, diarrhea, vomiting.
Relative decrease in effective blood volume eg. Congestive heart failure, sepsis, anaphylaxis
Arterial occlusion
Renal:
Acute tubular necrosis (( ATN ))
Ischemic insult ( prolonged hypotension )
Nephrotoxic insult which is either:
Exogenous nephrotoxins eg. Aminoglycosides, amphotericin B, contrast agents.
Endogenous substances: Haemoglobuline, myoglobulin, uric acid, bacterial toxins.
Acute interstitial nephritis
Acute glomerulonephritis
3. Post renal
a. Obstructive uropathy
b. Bladder neck obstruction.
Clinical presentations & evaluation:
**Reversible pre renal ARF:
Marked hypotension and signs of poor peripheral perfusion
Postural hypotension ( fall > 20/10 mmHg )
Evidence of the underlying cause but some time concealed blood loss can occur eg GI-bleeding, pelvic fracture
Metabolic acidosis and hyperkalaemia are often present
Significant oliguria with concentrated urine
Elevated blood urea level with no or minimal increase in serum creatinine. ( blood urea/serum creatinine ratio more than 40 ).
Low urine sodium < 20 meq/L.
*Management:
Establish and correct the underlying cause of ARF.
If the patient is hypovolaemic, restore the blood volume as rapidly as possible with blood, plasma or normal saline.
Vital signs monitoring and central venous pressure monitoring.
Correct metabolic acidosis by:
a. Restoration of blood volume.
b. Isotonic Sodium bicarbonate may be used.
* If the treatment given sufficiently early, renal
function will improve rapidly but in some cases the
treatment is ineffective and renal failure become
established.
**Established ARF:
CLINICAL FEATURES:
1. Features of the underlying cause eg. Trauma, sepsis
2. Alteration in urine volume usually started as oliguric phase followed by polyuric phase which carry better prognosis and may indicate regeneration and recovery from ATN.
3. GIT symptoms ((early uremic symptoms)) include: anorexia, nausea, vomiting and hiccoughs.
4. Neurological manifestations: drowsiness, apathy, confusion, muscle twitching, fit and comma.
5. Cardiovascular features: pericarditis and arrhythmias which may be due to uremia itself or as a result of electrolyte disturbances.
6. Electrolytes and metabolic abnormalities:
a. Hyperkalemia: particularly with massive tissue break down or haemolysis, ECG changes ((tinted T-wave, absence of P-wave, wide QRS complex and Sine wave)), elevated serum potassium.
b. Metabolic acidosis.
c. Dilutional hyponatermia.
d. Hypocalcaemia & Hyperphosphatemia.
7.Increased respiratory rate due to acidosis, pulmonary oedema or respiratory infection.
8. Anaemia may be present due to excessive blood loss or it may indicate acute exacerbation on CRF.
9. Severe infection may complicate ARF due to decreased immunity.
10. Volume overload: bilateral leg oedema, pulmonary oedema, Pericardial effusion.
** Clinical approach to the diagnosis of ARF:
The clinical evaluation of ARF is achieved by answering the following five questions :
Is it ARF or an acute on chronic renal failure?
Is there renal tract obstruction?
Is there reduction in effective ECF volume?
Has there been a major vascular occlusion?
Is there parenchymal renal disease other than ATN?
A complete history, physical examination and chart review, as well as a careful urinalysis, a renal ultrasound, and a few routine blood tests should be performed in all patients with ARF .
This approach will reveal the likely cause of ARF in most patients. In a few carefully selected patient ,additional ,selected special investigations-imaging, serology, renal biopsy-may be necessary to establish the cause of renal dysfunction.
History
The diagnosis of prerenal failure is often facilitated by careful evaluation of the patient fluid balance during the few days preceding the onset of ARF.
H/O vomiting or diarrhea provides useful clues to the source of loss of ECF volume.
Symptoms of dry cough,orthopnea, or ankle swelling may indicate the possibility of early volume overload.
Frequency, urgency, and hesitancy are important symptoms in patient with bladder dysfunction or bladder neck obstruction.
H/O ingestion of a nephrotoxic drugs
Systemic symptoms such as fever, malaise or fatigue, and joint pain or skin rash raise the possibility of ARF caused by acute GN associated with SBE, vasculitis or connective tissue disease like SLE
H/O previous renal disease or hypertension may point to pre-existing chronic renal insufficiency .
Chart review
Since most ARF occurs in patients in hospital,the hospital record represent an extremely an important source of information regarding the possible cause. A chart review should be considered as an extension of the history, daily record of vital signs, changes in body weight and records of fluid intake and out put. The record of all drugs taken by the patient must be examined for potentially nephrotoxic drugs.
PHYSICAL EXAMINATION
Loss of skin turgor and postural hypotension when fluid loss exceed 5-10% of ECF volume.
Supine hypotension when the fluid loss exceed 20% of ECF volume.
Raised JVP ,pedal edema and pulmonary crackles indicate cardiac failure.
Skin:
Jaundice and other evidence of acute or chronic liver disease
Maculopapular skin rash may indicate drug induced AIN or acute GN.
Malar rash or photosensitivity in SLE
Livedo reticularis associated with cryoglobulinemia or atheroembolic disease
Palpable purpura commonly caused by cutaneous vasculitis or atheroembolic disease
Nonpalpable purpura may suggests the presence of thrombocytopenia associated with SLE or thrombotic microangiopathy.,
Eye examination
Jaundice, hypertensive retinopathy, Roth spots (endocarditis)or cholesterol emboli (atheroembolic disease)
Abdominal examination:
Ascites may indicate chronic liver disease or congestive cardiac failure
Bruits over the anterior abdomen or confirmed to the renal angles
Any evidence of bladder neck obstruction
Rectal or pelvic examination
The presence of large postvoid residual (more than 200-300 ml) is strongly suggestive of functionally significant urinary retention.
Urine volume
Patient with prerenal azotemia almost always have oliguria, but non oligureic ARF seen in :
1. diabetes insipidus
2. sodium wasting disease such as adrenal insufficiency
3. hyperglycemia
4. malnutrition
5. chroniclly ill patient
6. urinary tract obstruction ( unilateral or partial )
7. contrast induced ARF
8. aminoglycosid induced ARF
Anuria is unusual in patient with ATN but it is more common with rapidly progressive GN, acute interstitial nephritis or vascular catastrophes such as renal artery embolism or renal vein thrombosis .
If patient thought to have ATN have persistent anuria lasting more than 24 -48 hours, these other causes of ARF must be reconsidered.
SERUM CHEMISTRY
Blood urea nitrogen
The clearance of urea is always less than the GFR. This is because of the back diffusion of urea which is inversely related to the rate of urine flow and is enhanced by vasopressin .
BUN rises more rapidly than the creatinine in patient with prerenal failure
The ratio BUN : Cr is normally 15:1 (mg:mg) (60:1 mmol:mmol)


High ratio > 20:1caused by:
1. Prerenal failure
2. GI bleeding
3. increased protein intake
4. catabolic state
5. infusion of amino acids
6. corticosteroid therapy
7. tetracycllines

Low ratio < 5-10 :1 caused by:

1. severe liver disease
2. malnutrition
3. rhabdomyolysis
4. cimetidine
5. trimethoprim
6. cephalosporins

SERUM CREATININE

As renal function deteriorates ,the Cr becomes progressively less reliable as an index of GFR..
BUN rarely exceeds 30mg/dl.and serum Cr > 2 mg/dl.unless there is concurrent underlying chronic renal insufficiency.


OTHER SERUM CHEMISTRY:
They are usually unhelpful in the diagnostic process. Hyperkalemia, hyperuricemia, hypocalcemia and hyperphosphatemia are all common in ARF of any cause also they are not useful in distinguishing ARF from CRF
URINALYSIS:
Microscopy
Hematuria
protienuria
condition
normal
-
-
Prerenal azotemia
normal
-
-
Vascular occlusion
Dysmorphic RBC
RBC cast
Granular cast
+++
+++
GN
Pyuria,WBC cast
eosinophiluria
+
++
AIN
Normal


+
-/+
HUS/TTP
Muddy brown granular cast,epithelial cast, sometime NONE in nonoliguric ATN
-
-
ِATN
GUE may shows evidence of underlying renal pathology eg. GN, Interstitial nephritis or evidence of underlying cause eg DM, Multiple myeloma

URINE CHEMISTRY

ATN
Prerenal
Index
>40
<20
Urine sodium
<20
>40
U. cr / P.cr. (mg/dl)
<300-350
>500
U.osm
<1.1
>1.5
U./ P. osmolality
<1.015
>1.018
Specific gravity
<3
>8
U. / P. urea
.>2
<1
FeNa=U.Na/Ucr×Pcr/PNa×100
>1
<1
RFI=U.Na/ (U.cr/P.cr)


Hematological indices
-the hematocrit is not useful discriminate between ARF and CRF.
-High WBC count may point to systemic infection, lymphoma and leukemia
- Eosinophelia may suggest a drug induced ATN or atheroembolic disease
- Thrombocytopenia suggest HUS,TTP, SLE,myeloma,sepsis,and DIC.

RENAL ULTRASOUND

- It is a key investigation for the diagnosis of obstruction or CRF.
- It is not a reliable method for identifying the anatomical site of obstruction
- Even if the kidneys are reduced in size , the possibility of prerenal ARF or ATN superimposed on CRF must always be considered.
SEROLOGY
- ANA, ANCA, anti GBM, RF, complement levels
- They are useful for vascullitic or glomerular process
- Hepatitis and HIV serology (especially if dialysis is indicated)
CXR: may shows Pulmonary oedema, pericardial effusion
ECG: evidence of pericarditis, arrhythmia, hyperkalaemia
CT scan
It can delineate the level of obstruction and define retroperitoneal inflammation or retroperitoneal malignant mass
RENAL ANGIOGRAPHY:
It is indicated when renal artery occlusion is suspected or as a useful investigation in diagnosing classical PAN
Renal venography may be indicated to confirm the diagnosis of renal vein thrombosis.
RENAL BIOPSY
It is unnecessary in ARF but can be useful in patient in whom parenchymal renal disease other than ATN is suspected.( AIN or RPGN)
Renal biopsy also indicated in presence of systemic illness manifestations or for unexplained ARF.or for unexpected cause for ARF.
After 4-6 weeks , a renal biopsy may be In patient with ATN who do not recover renal function, renal biopsy indicated to determine the cause of ARF and clarify the prognosis.
*Treatment of ARF
1. Fluid balance (input and output chart) with central venous pressure monitoring, daily body weight and treatment of fluid over load with diuretics.
2. Emergency treatment of Hyperkalemia with ca-gluconate
3. Correction of acidosis by giving Sodium bicarbonate.
4. Bolus dose of loops diuretics to initiate dieresis but if it fail, No farther diuretics should be given.
5. Restriction of salt intake & protein intake into 40-60 gm/day.
6. vigorous treatment of infection.
7. Drugs that are nephrotoxic should be omitted or dose adjustment.
8. Dialysis ( When ever indicated should not be delayed ) Which is indicated in:
a. Severe Hyperkalemia
b. Severe acidosis not corrected by sodium bicarbonate.
c. Fluid overload not corrected by diuretics.
d. Blood urea > 200mg/dL. Or rapidly rising blood urea more than 40mg/dL. over 24hr.
e. Uremic encephalopathy
f. uremic pericarditis
g. severe uremic symptoms not controlled by medical treatment.
**Outcome & Prognosis
-The oliguric phase last 1-2 weeks.
- Those with oliguria more than 3 weeks carry poor prognosis.
- Uncomplicated ARF due to simple hemorrhage or drug carry better prognosis and low mortality.
- ARF associated with serious infection and multiple organ failure carry poor prognosis with 50-70% mortality.
- Outcome is usually determined by the severity of the underlying disorder other complication rather than by renal failure itself.