ACUTE RENAL

FAILURE
 Acute renal failure (ARF) is a syndrome
characterized by rapid decline in GFR
hours to days, retention of nitrogenous
waste products and disturbances in the
extra cellular volume, electrolyte and
acid base homeostasis.
 Is seen as a complication in about 5% of
hospital admissions, and up to 30% of
intensive care admissions.
 Oliguria is a common finding but not
necessary. ARF is sometimes asymptomatic
and is diagnosed by increase in the urea and
creatinine.
CLASSIFICATION AND MAJOR CAUSES
OF ACUTE RENAL FAILURE (ARF)
 I: PRERENAL ARF:
 A: Hypovolemia
 1: Hemorrhage, burns, dehydration
 2: GIT fluid loss; vomiting, surgical drainage,
diarrhea
 3: Renal fluid loss; diuretics, osmotic diuresis
(Diabetes mellitus), hypoadrenalism
 4: Sequestration in extravascular space;
pancreatitis, peritonitis, trauma, burns, severe
hypoalbuminemia
 B: Low cardiac output:
 1: Diseases of myocardium, valves, and
pericardium, arrhythmias, tamponade
 2: Other: pulmonary hypertension, massive
pulmonary embolus, positive pressure
mechanical ventilation
 C: Altered Renal systemic vascular
resistance ratio
 1: Systemic vasodilation; Sepsis,
antihypertensives, afterload reducers,
anesthesia, anaphylaxis
 2: Renal vasoconstriction: Hypercalcemia,
norepinephrine, epinephrine, cyclosporine,
FK 506, amphoterecin B
 3: Cirrhosis with ascites (hepatorenal
syndrome)
 D: Renal hypoperfusion: with impairement of
renal autoregulatory responses
 1: Cyclooxygenase inhibitors, ACE inhibitors

 E: Hyperviscosity syndrome
 1: Multiple myeloma, macroglobenemia,
polycythemia
 II: INTRINSIC RENAL ARF
 1: Reno-vascular obstruction (Bilateral or
unilateral in the setting of one functioning
kidney)
 A: Renal artery obstruction: Atherosclerotic
plaque, thrombosis, embolism, dissecting
aneurysms, vasculitis
 B: Renal vein obstruction: Thrombosis,
compression
 2: Diseases of the glomeruli or renal
microvasculature
 A: Glomerulo nephritis and vasculitis
 B: Hemolytic uremic syndrome: Thrombotic
thrombocytopenic purpura, DIC, toxemia of
pregnancy, accelerated hypertension, radiation
nephritis, SLE, scleroderma
 3: Acute tubular necrosis:
 A: Ischemia: As per pre-renal ARF, Obstetric
complications (abruption placenta, post partum
hemorrhage)
 B: Toxins:
 1: Exogenous: radio contrast, cyclosporine,
antibiotics (aminoglycosides), chemotherapy
(cisplatin), organic solvents (Ethylene glycol),
acetaminophen, illegal abortificients
 2: Endogenous: Rhabdomyolysis, hemolysis,
uric acid, oxalate, plasma cell dyscrasia
(myeloma)
 4: Interstitial nephritis
 A: Allergic; Antibiotics (beta lactums, sulfonamides,
trimethoprim, rifampicin), NSAID, diuretics, captopril
 B: Bacterial; (acute pyelonephritis, leptospirosis), viral
(cytomegalovirus), fungal (candidiasis)
 C: Infiltration: Lymphoma, leukemia, sarcoidosis.
 D: Idiopathic:
 5: Intratubular deposition and obstruction
 Myeloma proteins, uric acid, oxalate, acyclovir,
methotrexate, sulphonamides
 6: Renal allograft rejection
 III: POST RENAL ARF (OBSTRUCTION)
 1: Ureteric: Calculi, blood clot, sloughed
papillae, cancer, external compression
(retroperitoneal fibrosis)
 2: Bladder neck ; Neurogenic bladder, Prostatic
hypertrophy, calculi, cancer, blood clot
 3: Urethra: stricture, Congenital valve, phimosis
 Clinical features and differential diagnosis
 1: Determine whether decline in GFR it is acute
or chronic. Findings that suggest of chronic renal
failure are anemia, neuropathy, and radiologic
evidence of osteo-dystrophy, small scarred
kidney.
 2: Once ARF is established identify the
cause of ARF, eliminate the triggering
insult (nephrotoxin) and/or institution of
disease specific therapies, prevention and
management of uremic complications
 Clinical assessment
 Prerenal ARF: Thirst, orthostatic dizziness,
tachycardia, reduced jugular venous pressure,
decreased skin turgor, dry mucous membrane,
reduced axillary sweating,
 Intrinsic renal ARF: Ischemic and nephrotoxic
causes should be ruled out which constitute 90%
of causes
 Post renal ARF: Suprapubic and flank pain,
colicky pain, Neurogenic bladder should be ruled
out in patients on anticholinergic.
 Urine analysis
 Anuria suggests complete urinary tract
obstruction
 Prerenal: contains transparent hyaline casts
formed in concentrated urine from normal
constituents of urine mainly Tamm-Horsfall
protein secreted by the epithelial cells of the
loop of Henle.
 Labarotary findings:
 Creatinine: peak creatinine is observed
after 3-5 days after contrast nephropathy,
and 7-10 days after ischemic ARF and
athero embolic disease.
 Hyperkalemia, hyperphosphatemia,
hypocalcemia, increased uric acid, and
creatinine kinase at the time of
presentation suggests diagnosis of
rhabdomyolisis.
 Hyperurecemia > 15mg/dL in association with
hyperkalemia, hyperphophatemia, and raised
levels of LDH indicate acute urate nephropathy
and tumor lysis syndrome following
chemotherapy.
 Radilogy:
 Renal biopsy
 Complications
 ARF impairs renal excretion of Na, K, and water,
disturbs divalent cation homeostasis and urinary
acidification mechanisms.
 Hence ARF presents with intravascular volume
overload, hyponatremia, hyperkalemia,
hyperphosphatemia, hypocalcemia,
hypermagnesemia, and metabolic acidosis, rise
in nitrogenous waste products leading to uremic
syndrome
 Expansion of Extracellular fluid volume:
 Diminished salt and water excretion in oliguric or
anuric patients is characterized by weight gain
 Bilateral basal crepts
 Raised JVP
 Dependent edema
 Pulmonary edema
 Cerebral edema
 Neurologic abnormalities including seizures
 Hyperkalemia
 Serum K rises by 0.5 mmol/L per day in oliguric
and anuric patients due to impaired excretion of
ingested or infused K and K released from the
injured tissue. Coexisting metabolic acidosis will
exaggerate hyperkalaemia by promoting K efflux
from cells.
 Metabolism of dietary protein yields 50-100
mmol/d of fixed non volatile acids.
 Mild hyperphosphatemia is always seen in ARF,
and also in patients with rhabdomyolysis,
hemolysis, tumor lysis. Metastatic deposition of
calcium phosphate leads to hypocalcemia.
 Anemia: is due to impaired erythropoesis,
hemolysis, bleeding, hemodilution, and reduced
red cell survival time
 Increased bleeding time, leukocytosis.
 Infection
 Cardiopulmonary complications
 GIT bleeding
 Uremic syndrome
 TREATMENT
 Prevention:
 No specific therapy for ischemic or nephrotoxic
ARF except preventing the etiologic factors.
 Preventing hypotension by aggressive volume
replacement
 Judicious use of nephrotoxic drugs
 Adjusting dosage of the nephrotoxic drugs
 Allupurinol and forced alkaline diuresis in
patients at high risk of urate nephropathy
(cancer chemotherapy, hematologic
malignancies)
 N-acetylcysteine limits acetaminophen induced
injury
 Dimercaprol prevents the metal nephrotoxicity
 Specific therapies
 Prerenal:
 Correction of hypovolemia depends upon the
etiology that has caused it.
 Corrected with blood if it is due to hemorrhage
 Isotonic saline is appropriate replacement for
mild to moderate hemorrhage or plasma loss.
 Serum K and acid base status should be
corrected
 Cardiac failure needs aggressive
management with positive ionotropes,
preload and afterload reducing agents,
antiarrhythmic agents, IABP.
 Fluid management may be difficult in
patients with cirrhosis and ascites.
Hepatorenal syndrome should be ruled out
 Intrinsic renal ARF
 ANP therapy
 Low dose dopamine
 Loop diuretic
 Calcium channel blockers
 Alpha adreno-receptor blocker
 Prostaglandin analogues
 Antioxidants
 Antibodies against leukocyte adhesion
molecules
 Insulin like growth factors
 ARF due to glomerulonephritis, and vasculitis
respond better with glucocorticoids, alkylating
agents, and plasma pheresis
 Hypertension and ARF due to scleroderma is
sensitive to ACE inhibitors
 Post Renal ARF
 Can be detected by collaboration of
nephrologists, urologist, and radiologist.
Obstruction of the urethra and bladder neck is
managed initially by catheterization.
 Supportive measures:
 Salt water intake is titrated as required
 Diuretics to correct hypovolemia
 Management of hyperkalemia
 Correction of metabolic acidosis
 Hyperphosphatemia is corrected by
Alluminium hydroxide, calcium carbonate
 Nutrition therapy to prevent the catabolism
and starvation ketoacidosis, by restricting
the protein intake to 0.6g/kg, and giving
high carbohydrate diet
 Blood transfusion if anemia
 Dialysis
 Outcome and long term prognosis
 Mortality rate with ARF is about 50%,
patients usually die of the sequelae of
primary illness that lead to ARF and not
ARF per say.
 Patients with oliguria UOP< 400ml/d and
rise in serum creatinine > 3mg/dl at the
time of admission have a poor prognosis