Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.

1. Management of
Acute Renal Failure
Dr. Sachin Verma MD, FICM, FCCS, ICFC
Fellowship in Intensive Care Medicine
Infection Control Fellows Course
Consultant Internal Medicine and Critical Care
Web:- http://www.medicinedoctorinchandigarh.com
Mob:- +91-7508677495
References
 Brenner & Rector’s The Kidney, 7 th ed.
 Harrison’s Principles of Internal Medicine, 16th ed.
29/9/05

2. Definition
 Acute renal failure is a syndrome
characterized by a rapid (hours to week)
decline in GFR and retention of
nitrogenous waste products such a BUN
and creatinine

3. Etiology & Classification of ARF
A. Pre renal azotemia (55-60%)
 Intravascular volume depletion
 Decreased cardiac output
 Renal vasoconstriction
B. Acute intrinsic renal azotenia
 Disease involving large renal vessels
 Diseases of glomeruli and renal microvasculature
 Injury to renal tubules. Exogenous toxins and
endogenous toxins
 Acute disease of tubulo interstitium.

4. Etiology & Classification of ARF
C. Post renal azotemia
 Ureteric obstruction (Intraluminal, intramural,
Extraureteric, periureteric)
 Bladder neck obstruction
 Uretheral obstruction

5. Clinical Approach to the
Diagnosis of ARF
History (Drug history)
↓
Physical examination (Fundus & Weight)
↓
Urinanalysis
↓
Flow chart of serial BP, Wt, BUN, S. Cr.
Major clinical events interventions
↓
Routine blood chemistry
↓
Radiologic evaluation (plain abdominal film)
Renal USG, IVP, renal angiography, MR angiography
↓
Renal Biopsy

6. Clinical Assessment
Pre renal
 Fluid loss in any form
 Symptoms of thirst
 Orthostatic dizziness and hypotension
 Tachycardia
 Decreased skin turgor dry mucus membrane
 Decreased axillary sweating
Definitive diagnosis
 Resolution of ARF after restoration of renal
perfusion

7. Intrinsic
 Increased muscular activity (Rhabdomyolysis)
 Recent transfusion (Hemolysis)
 Flank pain
 Hyperreflexia and asterixis
Post renal
 Suprapubic pain (Acute distension of bladder)
 Colicky flank pain radiating to groin
Definitive diagnosis
 Radiologic investigation and rapid improvement
in renal function after relief of obstruction

8. Urinanalysis
1. Urine volume
2. Urine sediment
 Acellular / Transparent hyaline cast (pre renal)
 Pigmented “muddy brown” granular cast, tubule
epithelial cell cast (renal)
 Benign sediment, hematuria, pyuria (post renal)
 Broad granular cast characteristics of chronic renal
disease and reflect interstitial fibrosis and dilatation of
tubules
 Granular cast
 ATN, GN / vasculitis, Interstitial nephritis
 RBC cast
 GN / Vasculitis, Malignant hypertension

9.  WBC cast
 Acute interstitial nephritis, Severe pyelonephritis,
Marked leukemic or lymphomatous infiltration
3. Eosinophiluria (>5%)
 Drug induced allergic interstitial nephritis
4. Crystalluria
 Uric acid crystals (pleomorphic), oxalate (envelop
shaped), Hippurate (needle shaped)
5. Tubule proteinuria (<1g/d) : proximal tubule cell injury,
glomerular proteinuria (>1g/d) injury to glomerular
ultrafiltration barrier
6. Haemoglobinuria
7. Myoglobinuria

10. Confirmatory test
 Plain abdominal film
 USG
 CT Scan
 Radio nuclide scan
 MRA
Doppler USG and Spiral CT
 Contrast angiography (Gold standard)
 Renal biopsy

11. FENa (Fractional Excretion
of Na+(%)
 Most sensitive index to differentiate pre renal
azotemia from ATN
UNa X Pcr <1 prerenal
X100
PNa X Ucr >1 ATN

12. Treatment
Pre renal azotemia
 Correction of Hypovolemia by packed red cells,
isotonic saline, Hypotonic saline (0.45%)
 Loop blocking diuretic, (Frusemide high dose 20
– 160 mg orally or IV twice daily) to effect
adequate diuresis and convert oliguric to non-
oliguric RF.
 ARF with cirrhosis (fluid challenge) paracentesis
with albumin administration
 Renal dose dopamine (1-3 mg/kg/min)

13. Treatment
Intrinsic ATN
 Optimization of CV function & intravascular
volume
 Prophylactic oral acetylcysteine (600 mg BD 24
hour before and after procedure)
 Use of less nephrotoxic contrast agent
(Gadolinium and CO2)
 Cautious use of diuretics, NSAIDs, ACE inhibitors
 Lipid encapsulated formulation of amphotericin B
 Allopurinol (Acute urate nephropathy)
 Amifostine an organic thiophosphate (Cisplatin)

14.  Forced diuresis and alkanization of urine
(Rhabdomyolysis)
 N Acetylcysteine within 24 hour
(Acetaminophen)
 Dimercaprol (Chelating agent) (heavy metal)
 Ethanol (ethylene glycol toxicity)
 Plasma pharesis (Myeloma cast nephropathy)
 Systemic arterial pressure control (malignant
htpertensive nephrosclerosis)
 Acute GN (pulse glucocorticoid therapy)

15. ANP
 28 amino acid polypeptide. Synthesized in
cardiac atrial muscle. Increased GFR by
triggering afferent arteriolar vasodilatation and
increasing ultrafiltration. Inhibits Na transport
and lower oxygen requirement.
Post renal ARF
 Transuretheral or suprapubic placement of
bladder catheter (obstruction of urethra or
bladder neck)
 Percutaneous catheterization of dilated renal
pelvis or ureter (ureteric obstruction)
 Removal of obstructing lesion percutaneously or
bypassed by insertion of ureteric stent

16. Management of complication
Intravascular volume overload
 Salt (1-2 gm/day) and water (<1 lt/day) restriction
 Diuretics, usually loop + thiazide
 Ultrafiltration or dialysis
Hyponatremia
 Restriction of enteral free water intake (<1lt/day)
 Avoid hypotonic intravenous solution (including
dextrose)

17. Hyperkalemia
 Restriction of dietary K+ intake (<40 mmol/day)
 Eliminate K+ supplement and K+ sparing diuretic,
 Potassium binding ion-exchange resin (Na
polystyrene sulphonate)
 Glucose (50 ml of 50% Dextrose) and insulin (10
U regular)
 NaCO (50-100 mmol)
3
 Calcium gluconate (10 ml of 10% solution) over 5
minute
 Dialysis (with low K+ dialysate)

18. Metabolic acidosis
 Restriction of dietary protein (0.6 g/Kg/day of high
biologic value)
 Na bicarbonate (maintain serum bicarbonate >15
mmol/L or arterial pH >7.2)
 Dialysis
Hyperphosphatemia
 Restriction of dietary phosphate intake (<800
mg/day)
 Phosphate binding agents (Ca carbonate,
Aluminium hydroxide)

19. Hypocalcemia
 Calcium Carbonate
 Calcium gluconate (10 – 20 ml of 10% solution)
Hypermagnesemia
 Avoid Mg2+ containing antacids
Hyperuricemia
 Treatment usually not necessary (<15 mg/dl)
Nutrition
 Restriction of dietary protein (0.6 g/kg/day)
 Carbohydrate (100 g/day)
 Enteral / Parenteral nutrition

20. Indication for Dialysis
 Clinical evidence (signs & symptoms) of uremia
 Intractable intravascular volume over load
 Hyperkalemia
 Severe acidosis (resistant to conservative
measures)
 Prophylactic dialysis when urea >100-150 mg/dl
or creatinine >8-10 mg/dl

21. Outcome
 Mortality rate approximately 50%
 Poor prognosis – Oliguria (<400 mg) or serum
creatinine (>3 mg/dl), older debilitated patient
and multiple organ failure at the time of
presentation
 50% subclinical impairment of renal function
 5% never recover (require dialysis or
transplantation)
 5% progressive decline in GFR