Acute Renal Failure

Acute Renal Failure Stephanie Chieng Mei Ling 22/7/09

Introduction Deterioration of renal function over a period of hours to days which result in the failure of kidney : (i) To excrete nitrogenous waste product (urea & creatinine) (ii) To maintain fluid & electrolyte homeostasis  Glomerular filtration rate (GFR): is the rate at which ultrafiltrate is formed at the glomerulus.  Normal value of GFR: 100-120mls/min 

Introduction (cont’) 

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3 classes ARF: prerenal/hypoperfusion state, intrarenal/intrinsic renal parenchymal injury & postrenal/ urinary obstructive disorder. Can be further described according to the amount of urine produced per day as anuric (<50mL/d), oliguric (50400mL/d), non-oliguric (>400mL/d)

Types & Causes of ARF Prerenal ARF > Intravascular volume depletion is the most common cause. - Sudden & severe drop in BP (shock) or interruption of blood flow to the kidneys due to injury/ illness. - eg blood loss/fluid loss (vomiting, diarrhoea), cardiac failure, sepsis, dehydration etc. > Prerenal azotemia- due to diseases that leads to a decrease in the effective arterial blood volume. These diseases include HF, liver failure, and nephrotic syndrome. - Drugs: NSAIDs & ACE I are known to cause prerenal azotemia.

Intrinsic ARF Intrinsic renal parenchymal injury - Direct damage to the kidneys by inflammation, toxins, drugs, infection or reduced blood supply. - Classified as tubular, glomerular, interstitial & vascular.  Injury to tubules most often caused by ischemia or nephrotoxins. If not treated, can lead to ‘acute tubular necrosis’-more severe ischemic insult to kidneys.  Glomerulonephritis- uncommon cause of ARF. Can be due to diseases such as SLE.  Acute interstitial nephritis- often results from an allergic rxn to a drug. Can also be due to autoimmune disease, infection.

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Vascular disease- microvascular & macrovasular. Depending on location(s), vascular causes can be pre or intrarenal. Microvascuar commonly present as microangiopathic hemolytic anemia & ARF secondary to small vessel thrombosis or occlusion. Macrovascular causes of ARF in elderly should be suspected renal artery stenosis or thrombosis, aortic disease or acute dissection

Post-renal ARF Postrenal/ urinary obstructive disorder - Obstruction of the outflow tracts of the kidneys such as at renal pelvis, ureter or bladder neck. - Causes: prostatci hypertrophy, catheters, tumors etc. - Recovery of renal function is directly proportional to the duration of the obstruction.

Investigation Markers Urea (1.7- 8.3 mmol/L) -Poor marker of renal fn: variable reabsorption in renal tubules, varies with diet & hydration state, level increases w protein breakdown & decreased in other disease (eg liver disease)  Serum Creatinine (64-122 micromol/L) - Fairy constant daily production w minimal tubular reabsorption. -However, may vary with dietary intake (higher level2 hrs post high red meat intake). Levels peak in the evening, low in morning. -Generally, elevations implies impairments of RF & reduction of GFR. 

Investigation Marker (2) Creatinine Clearance (105-150ml/m) - Based on Cockcroft & Gault formula CrCL= (140-age) x IBW (kg)/ Serum Cr (micromol/l) x 0.814 For female= multiple the whole equation with 0.85 Mild RF : 25-50ml/min Moderate: 10-25ml/min Severe: <10ml/min 

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Any abnormalities of electrolytes values

Management The initial care –focus on reversing underlying cause, correcting fluid & electrolyte imbalances, and preventing further renal injury by providing supportive measures. Fluid Management - In oliguric RF, strategy is to have fluid restriction. - Hypovolaemia must be corrected - Hypotension must be quickly corrected with fluid challenge, or if there is no volume deficit, use of an appropriate inotrope is advocate 

Patients with volume deficit (i) In hypotensive patients -Fluid challenge with 250ml of NS over 15min. If BP does not improve or CVP measurement does not increase by 2cm repeat fluid challenge (up to 500-1000ml of NS may be required). Stop if CVP increases to satisfactory level i.e 5-10cm H2O -If volume is restored, with gd BP , but urine outflow is poor (<40mL/hr), IV frusemide can be given either by slow bolus of 40120mg repeated as necessary or by infusion (dilute in NS) at a rate of 10-30mg/hr with max daily dose of 1g.

Patients with volume deficit (2) -If vol is restored, with gd BP , but urine output remains poor despite frusemide & inotrope, restrict fluid to 500ml/24hr plus measured losses. Avoid K+ & food rich in K+. -If good BP is obtained & good urine flow is established (>40ml/hr), continue with a slower fluid replacement regimen. -If volume is restored, but BP is still low, use an appropriate inotrope (eg dopamine)

Patients w/hout volume deficit (ii) In normotensive patients -Fluid challenge should also be given to correct fluid deficit. -If gd urine flow is established (>40m/hr), continue with slower fluid replacement regimen. -If vol restored but urine outflow is poor (<40ml/hr), start IV frusemide as mentioned above. -Start IV frusemide & if necessary with an inotrope as mentioned before. -If urine flow does not improve, restrict fluid.

Metabolic acidosis pH< 7.1 or with HCO3 <10mmol/L may need to be treated with Sodium Bicarbonate. A rough estimation of the amount (mmol) required can be calculated by: 0.5 X body weigh (kg) X Base deficit base deficit= 24- actual HCO3 1ml of 8.4% NaHCO3 provides 1mmol of NaHCO3  Treatment usually titrated slowly by infusing bicarbonate (eg 1ml of 8.4% NaHCO3 per kg over 30min) & regularly checking the plasma pH & bicarbonate. 

Nutrition 

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In patients with ARF the main determinants of nutrient requirements (and outcome) are the degree of hypercatabolism caused by the disease associated with ARF, the nutritional state, and the type and frequency of dialysis therapy. Protein- 0.8-1.2g/kg/d (high intake if in hypercatabolic state) NaCl- 2-4g/d Caloric intake- 35-50kcal/kg/d Potassium- 40mmol/d (if dialysed) Oral feeding should be initiated whenever possible.

Dialysis Needed if medical Tx fails to control fluid/electrolyte derangement eg fluid overload, metabolic acidosis Indications for initiating dialysis are:  BU> 30mmol/l  Severe hyperK (>6mmol/l)  Severe metabolic acidosis (pH<7.1)  Volume overload +/- pulmonary oedema not responsive to diuretics  Development of uremic Sx eg CNS (asterixis, neuromuscular irritability,coma, seizure) and GI (nause & vomiting, haemorrhage) symptoms.  GFR< 10-15ml/min 

Types of dialysis Depending on clinical situations- haemodialysis, peritoneal dialysis, CRRT (continuous renal replacement therapy)  Patients with severe tissue breakdown (eg rhabdomyolysis, trauma, burns, sepsis) gave enhanced urea production- require haemodialysis or CRRT.  In other cases of ARF in which the catabolic component is less prominent, peritoneal dialysis may be adequate. 

Diuretic resistance Decreased response to loop diuretics- diuretic resistance  Some common causes of resistance in ARF: excessive Na intake, inadequate diuretics dose or inappropriate regimen, reduced bioavailability (from GI oedema), reduced RBF (drugs, intravascular depletion), nephrotic syndrome (diuretics bind to proteins in renal tubule, reducing diuretic effects)  Strategies to overcome: increasing the dose/ dosing frequency; continuous IV infusion of the diuretic; concomitant administration of loop diuretic with diuretics that act on distal convoluted tubule (thiazides) or the collecting duct (spironolactone, amiloride) for synergistic effect 

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Helms R.A., Quan D.J., Herfindal E.T et al. Textbook of Therapeutics: Drug and Disease Management. Sarawak Handbook of Medical Emergencies Needham E. Management of Acute Renal Failure. American Family Physician. 2005 November; 72: 1739-46. Adapted from http://www.aafp.org/afp/20051101/1739.pdf Druml W. Nutrition and Metabolism in Acute Renal Failure. Adapted from http://www.kidneyatlas.org/book1/adk1_18.pdf Mitch E.W., Klahr S.Handbook of Nutrition and Kidney:Nutritional Support in Acute Renal Failure. 3rd edition.