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Acute Renal Failure

• Definition: sudden rapid potentially reversible decrease in renal function sufficient to cause
nitrogenous waste accumulation occurring over days to weeks.
• Epidemiology: 1% of hospital admissions
• Aetiology:
o Prerenal
 Volume depletion
• Renal losses (diuretics, polyuria)
• GI losses (vomiting, diarrhea)
• Cutaneous losses (burns, Stevens-Johnson syndrome)
• Hemorrhage
• Pancreatitis
 Decreased cardiac output
• Heart failure
• Pulmonary embolus
• Acute myocardial infarction
• Severe valvular disease
• Abdominal compartment syndrome (tense ascites)
 Systemic vasodilation
• Sepsis
• Anaphylaxis
• Anesthetics
• Drug overdose
 Afferent arteriolar vasoconstriction
• Hypercalcemia
• Drugs (NSAIDs, amphotericin B, calcineurin inhibitors,
norepinephrine, radiocontrast agents)
• Hepatorenal syndrome
• Efferent arteriolar vasodilation – ACEIs or ARBs
o Intrinsic
 Vascular (large and small vessel)
• Renal artery obstruction (thrombosis, emboli, dissection, vasculitis)
• Renal vein obstruction (thrombosis)
• Microangiopathy (TTP, hemolytic uremic syndrome [HUS], DIC,
preeclampsia)
• Malignant hypertension
• Scleroderma renal crisis
• Transplant rejection
• Atheroembolic disease
 Glomerular
• Anti–glomerular basement membrane (GBM) disease (Goodpasture
syndrome)
• Anti–neutrophil cytoplasmic antibody-associated
glomerulonephritis (ANCA-associated GN) (Wegener
granulomatosis, Churg-Strauss syndrome, microscopic polyangiitis)
• Immune complex GN (lupus, postinfectious, cryoglobulinemia,
primary membranoproliferative glomerulonephritis)
 Tubular
• Ischemic
• Cytotoxic
o Heme pigment (rhabdomyolysis, intravascular hemolysis)
o Crystals (tumor lysis syndrome, seizures, ethylene glycol
poisoning, megadose vitamin C, acyclovir, indinavir,
methotrexate)
o Drugs (aminoglycosides, lithium, amphotericin B,
pentamidine, cisplatin, ifosfamide, radiocontrast agents)
 Interstitial
• Drugs (penicillins, cephalosporins, NSAIDs, proton-pump inhibitors,
allopurinol, rifampin, indinavir, mesalamine, sulfonamides)
• Infection (pyelonephritis, viral nephritides)
• Systemic disease (Sjögren syndrome, sarcoid, lupus, lymphoma,
leukemia, tubulonephritis, uveitis)
o Postrenal
 Ureteric obstruction (stone disease, tumor, fibrosis, ligation during pelvic
surgery)
 Bladder neck obstruction (benign prostatic hypertrophy [BPH], cancer of the
prostate [CA prostate or prostatic CA], neurogenic bladder, tricyclic
antidepressants, ganglion blockers, bladder tumor, stone disease,
hemorrhage/clot)
 Urethral obstruction (strictures, tumor, phimosis)
• Risk factors:
o NSAIDs x3 risk of ARF.
o Hypertension
o Congestive cardiac failure
o Diabetes
o Multiple myeloma
o Chronic infection
o Myeloproliferative disorder
• Pathology:
o Prerenal: there is impaired perfusion of the kidneys with blood leading to a
depression in GFR.
o Intrinsic: this is due to damage to the renal parenchyma due to causes mentioned
above, the most common pathology is acute tubular necrosis where there is
 Intrarenal microvascular constriction  tubular cellular injury  disrupted
basement membrane
 This leads to: reduction of surface area available for filtration, back-leak of
infiltrate into the proximal tubule and obstruction of the tubule due to
debris shed from ischaemic tubular cells.
o Postrenal: in this case there is obstruction in the urinary tract  build up of urine in
the urinary tract  back flow into the kidney and damage to the basement
membrane occurs if this obstruction is not relieved.
• History: Enquire about causes!
o Symptoms of uremia - anorexia, early satiety, nausea, vomiting, pruritus, fatigue,
weakness
o If fever and abdominal pain, consider abdominal sepsis with glomerulonephritis
o History of trauma, blood transfusions
o History of Oliguria <400mL/day. Abrupt anuria  acute urinary obstruction, acute
and severe glomerulonephritis, or embolic renal artery occlusion. A gradually
diminishing urine output  a urethral stricture, bladder outlet obstruction due to
prostate enlargement
o History of NSAIDs or ACE inhibitor use.
• Examination: Looks for signs of causes!
o General Physical:
 hypertension (Na+ retention, disturbed renin-angiotensin axis),
hypervolemia
 connective tissue abnormalities suggest SLE, scleroderma, MCTD
 fever suggests acute interstitial nephritis (especially with penicillins or
allopurinol)
 check postural BP and pulse changes to rule out hypovolemia (prerenal
azotemia)
o Skin:
 Purpura suggests Henoch-Schonlein purpura, vasculitis
 Maculopapular or petechial skin eruption suggests acute interstitial nephritis
(especially with penicillins or allopurinol)
 check skin turgor to rule out hypovolemia
o HEENT:
 check mucous membrane moisture and intraocular pressure (i.e. sunken
eyeballs) to rule out hypovolemia
o Cardiac:
 cardiomyopathy (with chronic fluid overload, concentric hypertrophy
common), pericarditis
 heart murmur suggests subacute bacterial endocarditis with
glomerulonephritis
o Lungs:
 pulmonary disease suggests Wegener's, Goodpasture's, SLE, vasculitis
o Abdomen:
 distended, tender bladder or bilaterally hydronephrotic kidneys suggests
postrenal causes
o Extremities:
 muscle tenderness or edema suggests rhabdomyolysis
o Neuro:
 neuromuscular irritability, asterixis, coma
o Rectal:
 digital exam of prostate to rule out postrenal causes
• Investigations:
o Bloods:


 FBC  normocytic anaemia (suggestive of chronic disease  acute on
chronic RF?)
 U&E  markedly raised urea & creatinine
 ESR/CRP  raised in inflammatory conditions
 LFTs  liver disease?
 CK  rhabdomyolysis?
 MSU & Urine cultures  haematuria & proteinuria (GN?), Infection
(pyelonephritis)
 Urine drug screen for nephrotoxic drugs
o ECG: hyperkalemia (tall tented T wave, small or absent P wave, increased P-R
interval)
o Imaging:
 CXR  pulmonary oedema (fluid overload)
 Renal ultrasound  excluding postrenal pathology (obstruction?)
 Renal Doppler  checking for renal blood flow (intrinsic and prerenal
pathology?)
 Nuclear scan: radionuclide imaging with technetium-99m-
mercaptoacetyltriglycine (99m Tc-MAG3),99m Tc-diethylenetriamine
pentaacetic acid (99m Tc-DTPA), or iodine-131 (131 I)–hippurate can be used
to assess renal blood flow and tubular functions.
 Aortorenal angiography: renal artery stenosis?
o Invasive:
 Renal biopsy: useful in establishing the diagnosis of intrinsic causes.
• Management:
o Medical management:
 General management:
• Correct volume depletion with IV fluids
• If the patient is septic, take appropriate cultures and treat
empirically with antibiotics
• Stop nephrotoxic drugs; adjust doses of renally excreted drugs
(p295).
• Nutrition is vital: aim for normal calorie intake (more if catabolism,
eg burns, sepsis) and protein ~0.5/kg/d. If oral intake is poor,
consider nasogastric nutrition early (parenteral if NGT impossible,
p574).
 Monitor for complications
• hyperkalemia and correct it:


• Pulmonary oedema: correct it with Furosemide 40-80 mg IV, if it’s
not corrected with dieresis consider renal replacement therapy
• Bleeding: Impaired haemostasis due to uremia
o Fresh frozen plasma & platelets as needed if there are
clotting problems.
o Blood transfusion to maintain Hb >10g/dL and haematocrit
>30%.
o Desmopressin to increase factor VIII activity, normalizing
bleeding time.
 Prerenal causes:
 Intrinsic
 Postrenal
• Renal replacement therapy (RRT) in acute renal failure :
o Indicated in:
 Refractory pulmonary oedema
 Persistent hyperkalaemia (K+ >7mmol/L), severe metabolic acidosis
(pH<7.2 or base excess <10)
 Uraemic encephalopathy
 Uraemic pericarditis (pericardial rub).
o Types of RRT:
 peritoneal dialysis,
 intermittent haemodialysis (HD) combined with ultrafiltration
o Continuous therapy is superior to intermittent therapy
o Comparison between HD/CRRT (continuous renal replacement therapy) and
PD:
o Peritoneal dialysis (PD): Drawbacks to the use of PD in ARF are:
 Low efficiency in fluid and solute removal compared to CRRT or
intermittent HD;
 ARF complicating intra-abdominal pathology is unsuitable for PD;
 Increasing intra-abdominal pressure can compromise lung function;
 Use of dialysis fluids with a high dextrose content may produce
hyperglycaemia and other metabolic derangements.
• Prognosis:
o Worse if oliguric. Mortality depends on the cause: burns (80%);
trauma/surgery (60%); medical illness (30%); obstetric/poisoning (10%).

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