From: Subject: Acute Renal Failure Date: Wed, 4 Oct 2006 16:45:46 +0530 MIME-Version: 1.0 Content-Type: text/html; charset="iso-8859-1" Content-Transfer-Encoding: quoted-printable Content-Location: file://C:\WINNT\Profiles\Administrator\Desktop\1sep\paediatrics\ARF.htm X-MimeOLE: Produced By Microsoft MimeOLE V5.00.2314.1300 Acute Renal = Failure

Acute Renal=20 Failure

Name=20 of the specialty: Pediatrics

 

Name of=20 topic/case: Acute Renal Failure

 

Name=20 of the expert : Dr.Sanjeev Rai B

 

Name of the = hospital: Father=20 Muller     = Medical=20 College Hospital

 

Introduction

   Acute renal failure = (ARF) is a=20 transient problem due to functional or organic injury to the = kidneys.  Occurs in 2-3 % of hospital = admissions=20 and 10% of pediatric intensive care admissions. Early recognition and = prompt=20 treatment of ARF is of paramount importance.

 

   Acute renal failure is = triad of=20 inability of the kidneys to excrete wastes, reduction in the GFR and = alterations=20 in the serum electrolytes.

 

  The Acute Dialysis Quality = Initiative=20 (ADQI) group has classified  = the=20 ARF, depending upon the  = baseline=20 changes in serum creatinine level or glomerular filtration rate (GFR), = urine=20 output (UO), or both and called it as The RIFLE classification=20

They=20 are as follows.

Risk=20 (R) - Increase in serum = creatinine=20 level X 1.5 or decrease in GFR by 25%, or UO <0.5 mL/kg/h for 6 hours =

Injury=20 (I) - Increase in serum = creatinine=20 level X 2.0 or decrease in GFR by 50%, or UO <0.5 mL/kg/h for 12 = hours=20

Failure=20 (F) - Increase in serum = creatinine=20 level X 3.0, decrease in GFR by 75%, or serum creatinine level > 4 = mg/dL; UO=20 <0.3 mL/kg/h for 24 hours, or anuria for 12 hours =

Loss=20 (L) - Persistent ARF, = complete loss=20 of kidney function >4 wk

End-stage=20 kidney disease (E) - Loss = of kidney=20 function >3 months

 

 

Pathophysiology:=20

   Main mechanism of = development=20 of  renal failure is the = reduction=20 of renal blood flow regardless of etiology. This reduction in the  RBF  leads to ischemia and cell = injury and=20 death. The decreased GFR  = leads to=20 oliguria ,failure to excrete the nitrogenous waste material and = alteration in=20 electrolyte and acid base mechanism.

  The renal failure develops in = three=20 phases Initiation phase, maintenance phase and the recovery phases, = however=20 there is no clear cut demarcation for these three phases and it may = occur in a=20 rapid succession and one may not be able differentiate the different = phases in=20 every case of ARF, usually it lasts for 6-7 days. Once RBF is restored = to=20 normal, the GFR increases and renal function recovers. However, it = depend upon=20 the number of functional nephrons =20 remaining after the initial insult.

 

The=20 ARF can occur due to primary renal diseases or non renal causes. It can = be pre=20 renal, renal or post renal failures

   Prerenal failure often = called as=20 functuional renal failure ,is due to the compromised renal perfusion = resulting=20 in decrease in GFR. In this type of renal failure the tubular and = glomerular=20 functions are nornal.

 The Intrinsic renal failure or = organic=20 renal failure and is due to the diseases of the glomerulus or tubule, = which are=20 associated with release of renal afferent vasoconstrictors. The Post = renal=20 failure or obstructive real failure, is due to the obstruction to the = urine=20 flow. The increase in tubular pressure resulting in  decreasing the filtration = driving force=20 in turn causes renal afferent vasoconstriction and the GFR is  altered.. 

Cause of ARF=20

Pre=20 renal ARF:

The=20 common causes for pre renal ARF are hypovolemia, hypotension and hypoxia.  Hypovolemia may be secondary = to=20 hemorrhage, gastro-intestinal loss, hypopretinemia, burns etc = Hypotension may be=20 due to septicemia, hemorrhage, and hypothermia or due to heart failure. = The=20 common causes of Hypoxia are due to respiratory distress syndrome, = pneumonias=20 etc

A=20 cause of renal failure varies with age. =20 In the Newborns and Infants common cause of Pre renal ARF are = hemorrhage,=20 Perinatal asphyxia and hyaline membrane disease .In older children it is = due to=20 the causes resulting in hypovolemia or hypotension thus decreasing renal = perfusion.

Intrinsic=20 ARF:

Mainly=20 due to the diseases of the = renal=20 parenchyma, specifically involving the glomeruli, renal tubules, interstitium =

Glomerulopathies=20 are the commonest cause, it can be post infectious, due to drug = reactions,=20 autoimmune diseases , infiltrative disease, Vascular diseases.  Acute tubular necrosis (ATN) = can occur=20 in perinatal asphyxia and secondary to medications like penicillin=92s,=20 sulfonamides, aminoglycosides, NSAIDs etc. it can also be seen in = Hemolytic=20 uremic syndrome associated with a diarrhea. Developmental anomalies of = the=20 kidneys like agenesis, hyoplasia and dysplastic kidneys, genetic = diseases like=20 sickle cell, trisomy can also cause renal failure.

 

Postrenal=20 ARF: Congenital malformations of = urinary=20 collecting systems and diseases=20 causing urinary obstruction from the level of the renal tubules to = the=20 urethra. Congenital Pelvi uretric junction obstruction and bladder neck=20 obstructions are the most common causes, Tubular obstruction from uric = acid or=20 calcium crystals, Ureteral obstruction due to tumor, urolithiasis or = Urethral=20 obstruction valves, strictures, hematoma, stones and neurogenic bladder = are the=20 other causes of post renal failure.

 

Clinical features

  

History:=20

    A=20 detailed history and proper clinical examination can able to diagnose = the=20 underlying cause for the renal failure in majority of cases. This is = very=20 important to initiate the treatment and prevent the progress of=20 ARF.

Prerenal=20 failure:

 History of excessive fluid loss = via=20 hemorrhage, GI losses suggests hypovolemia. Orthopnea and paroxysmal = nocturnal=20 dyspnea to rule out cardiac causes. Respiratory distress to hypoxic=20 ARF.

 Query about prior throat or = skin=20 infections with Hematuria, edema, and hypertension suggests glomerular=20 pathology.

Exposure=20 to nephrotoxic  = medications,=20 exposure to radiologic contrast agents, seizures, excessive exercise, = limb=20 ischemia or hemolysis recent blood transfusion may suggest impending = Acute=20 tubular necrosis.

Flank=20 pain and hematuria should raise a concern about renal calculi  use of acyclovir, = methotrexate,=20 triamterene, indinavir, or sulfonamides implies the possibility of = tubular=20 obstruction by crystals of these medications.

Poor=20 urinary stream suggests posterior urethral valves, triple micturation=20 suggests =20 reflux.

 

Physical=20 examination:

Physical=20 examination should include a search for the following =

Skin:  Livido reticularis, digital ischemia, = butterfly=20 rash, palpable purpura - Systemic vasculitis , Maculopapular rash - = Allergic=20 interstitial nephritis

Eyes :=20 Keratitis,=20 iritis, uveitis, dry conjunctivae - Autoimmune vasculitis , = Jaundice,Signs of=20 hypertension =96retinopathy.

Ears:   Hearing loss - Alport disease and = aminoglycoside=20 toxicity , Mucosal or cartilage ulcerations - Wegener = granulomatosis

Cardiac : Irregular rhythms (ie, = atrial=20 fibrillation) =96 Atheroemboli , Murmurs =96 Endocarditis , Increased = jugulovenous=20 distention, rales,

Pulmonary:  Rales - Goodpasture syndrome, Wegener=20 granulomatosis  Hemoptysis = - Wegener=20 granulomatosis

Abdomen :  Flank mass may suggest renal vein = thrombosis,=20 hydronephrosis, cystic disease or renal tumors

Costovertebral angle tenderness is seen in Nephrolithiasis

Distended bladder  = suggests  urinary obstruction

Limb=20 ischemia, edema indicates rhabdomyolysis

 

 

 

 

Investigations

Urine=20 output:=20 Changes in urine output generally are poorly correlated with changes in = GFR.=20 Approximately 50-60% of all causes of ARF are nonoliguric. However, = categories=20 of anuria, oliguria, and nonoliguria may be useful in differential = diagnosis of=20 ARF.

Anuria  - Urinary tract obstruction, = renal=20 artery obstruction, rapidly progressive glomerulonephritis, bilateral = diffuse=20 renal cortical necrosis

Oliguria  - Prerenal = failure,=20 hepatorenal syndrome

Nonoliguria  - Acute interstitial = nephritis, acute=20 glomerulonephritis, partial obstructive nephropathy, nephrotoxic and = ischemic=20 ATN, radiocontrast-induced ARF, and rhabdomyolysis

 

Urinalysis:=20 Microscopic examination of urine is essential in establishing = differential=20 diagnosis.

Normal=20 urinary sediment without hemoglobin, protein, cells, or casts generally=20 consistent with prerenal and postrenal failure.

Granular=20 casts  suggests ATN,=20 glomerulonephritis, interstitial nephritis

RBC=20 casts are seen in Glomerulonephritis.

WBC=20 casts are present in acute interstitial nephritis,=20 pyelonephritis

Eosinophiluria=20 is suggestive of acute allergic interstitial nephritis Crystalluria may = present=20 in children on Acyclovir, sulfonamides, methotrexate medications.=20

Complete blood count

Anemia  suggests SLE, HUS, renal vein=20 thrombosis,TTP or multiple .

Leukocytosis=20 is common in ARF.

Leukopenia=20 may be present in SLE or TTP.

Eosinophilia=20 suggests allergic interstitial nephritis, polyarteritis nodosa.=20

Thrombocytopenia=20 suggest HUS, renal vein thrombosis, SLE, TTP

Coagulation=20 disturbances indicate liver disease or hepatorenal=20 syndrome.

Serum  Chemistry

BUN: The urea=20 concentration correlates poorly with the GFR. However

this=20 can be used to differentiate prerenal failure from other type of ARF. In = pre=20 renal conditions disproportionate rise of BUN  occurs compare to creatinine, = thus the=20 serum BUN-creatinine ratio >20 in pre renal = failure.

Creatinine:=20 Serum creatinine is the accurate and consistent estimation of GFR. Rate = of=20 change in serum creatinine is an important tool in estimating GFR. Small = changes=20 with low baseline levels of creatinine are important clinically much = more than=20 large changes with high basal creatinine. Significant decrements in GFR = can=20 occur in the normal range of creatinine.

Serum=20 Electrolytes:=20 Hyperkalemia is a common complication of ARF. Hyponatremia may be = present it is=20 maily dilutional.

Serum=20 Bicarbonate: metabolic  acidosis is often associated = with renal=20 failure

Serum=20 Calcium-=20 Hypocalcemia is common in ARF.

Serum=20 Phosphorus-=20 Hyperphophatemia is one of the associated problem in = ARF

Creatine=20 phosphokinase (CPK)=20 elevations are seen in rhabdomyolysis.

Liver=20 enzymes:=20 Elevations in liver transaminases are seen in rapidly progressive liver = failure=20 and hepatorenal syndrome.

Serum C3 levels: Decrease in C3 = levels=20 suggestive of post streptococcal glomerulomnephritis

Urinary  indices

Differentiation=20 of pre renal azotemia from ATN is very important for  early management of these=20 patients.

Urine=20 indices that suggest pre renal and renal ARF are as=20 follows

 

Pre=20 renal

Intrinsic=20 renal

Urine=20 specific gravity

>1.020

<1.010

Urine=20 osmolality (mOsm/kg H2O)

>500

<500

Urine=20 sodium (mEq/L)

<15-20

>40

Plasma=20 BUN/creatinine ratio

>20

<10-15

Urine/plasma=20 creatinine ratio

>40

<20

FeNa=20

<1%

>=20 1%

 

FeNa  may be less than 1% in certain = intrinsic=20 renal failures  such as = urinary=20 tract obstruction, acute glomerulonephritis ,Hepatorenal = syndrome,Radiologic=20 contrast=96induced ATN ,Myoglobinuric and hemoglobinuric = ARF

 

Imaging=20 Studies:

Ultrasound=20 :Imaging studies in ARF are most important for the workup of suspected = postrenal=20 azotemia.-hydronephrosis, hydroureter, PUJ obstructions, posterior = urethral=20 valve  = etx

Chest radiography

Chest x-ray can give an evidence of volume = overload.=20 Findings of lung infiltration can lead to pulmonary/renal syndromes, = such as=20 Wegener granulomatosis and Goodpasture syndrome.

Electrocardiography:  ECG is one of the mode to know = the=20 levels of hyperkalemia  = and also use=20 full to detect the arrhythmias and cardic status.

Renal biopsy

 Often helpful in finding = specific cause=20 of renal failure,however it is rarely performed for the diagnosis of=20 ARF.

 

Mangaement

  = Management of=20 ARF ideally should begin before the diagnosis of ARF.  High index of suspicion often = is=20 necessary to diagnose early ARF. Significant decreases in GFR frequently = occur=20 before indirect measures of GFR reveal a problem. All seriously ill = children=20 should have ARF included early in their differential diagnosis.

 

Catheterisation:=20 Children=20 with featues of urinary obstruction dueto suspected bladder neck = obstruction=20 needs immediate catheterisation to reliv the discompfort as well as = reieve the=20 obstructions to the urine  = flow,=20 this can aslo help in nonambulatory PICU patients.

 

Fluid management

Accurate=20 determination of a patient's volume status is essential and it is = challenging=20 problem.  Hypovolemia=20 potentiates and exacerbates all forms of ARF.  Reversal of hypovolemia by = infusion of=20 isotonic saline at the rate of 20ml/kg should be done over 30 minutes = time. This=20 often  helful to = diffrentiate=20 hypovolemic renal failure. However, rapid fluid infusion can result in=20 life-threatening fluid overload in patients with ARF. The daily intake = of fluid=20 should be restricted to  20 ml/kg  will be given in addition to = amount=20 equivalent to the previous days urine output.

 

Diuretics :=20 Diuretics are useful only in management of fluid-overloaded = patients  and  in nonoliguric  ARF

 Furosemide=20 (Lasix)  2 mg/kg PO/IV, = once; may=20 increase by 1-2 mg/kg once in 6-8 hrs; not to exceed 6 mg/kg.

Large bolus dose may be given provided if the = urine out put=20 is not achieved with 1 hour patient should be dialysed immedeiatly.

 

Vasodilators=20 :=20 Low-dose dopamine is a potent vasodilator, increasing RBF in ARF.   After initiating = therapy, dose may=20 be increased by 1-4 mcg/kg/min q10-30min until satisfactory response = attained;=20 maintenance doses <20 mcg/kg/min usually satisfactory for 50% of = patients=20 treated. Low renal dose: 1-5 mcg/kg/min IV

 

Atrial natriuretic factor , Calcium channel = blockers ,=20 Infusion of mannitol have been shown in to be protective in ARF .

 

Correction of Dyselectrolytemia and Acid base imbalance

Common  problems encountered are = Hyperkalemia=20 and metabolic =20

Hyperlkalemia=20

Avoid  = or=20 restrict potassium containing foods

Aerosol of salbutamol is also used to decrease = the=20 potassium levels. Infusion of sodium bicarbonate 1-2 mEq/Kg over 5-10 = minutes=20 can correct the mild acidosis and the hyperkalemia.

The other measures include infusion of calcium = gluconate=20 10% solution at a dose of 1ml/kg as a slow IV infusion to counteract the = effect=20 of potassium on heart.

Infusion of regular Insulin 0.1U/kg and 50% = glucose  at 1mk/kg over a period of one = hour is=20 also advocated in severe hyperkalemia which will drive the extracellular = potassium into intracellular, thus reducing the serum potassium = levels.

Potassium exchanging resins Sodium polystyrene = sulfonate=20 resign 1gm/kg by orally or by enema to decrease ythe potassium = levels.

If the above method fails to control the = potassium level=20 then dialysis is indicated.

Hyponatremia:=20 There is no need to correct the hyponatremia unless it is symptomatic, = most of=20 the hyponatremia are dilutional. Corection of Potassium and = acidosis  will take care of = hyponatremia.

Acidosis: mild=20 metabolic acidosis is common ,however therapy is needed only if the = serum=20 bicarbonate is less than 12mEq/L.

Hypocalcemia:=20 There is no need to correct the Hypocalcemia. Low posphorous diet or = rarely=20 posphorous binders like aluminium hydroxide can be used. Still = hypocalcemia=20 isnot correcte calcium carbonate prepaertionas can be given orally.

 

Diet:   Child should be given = adequate=20 calories every day. Diet should contain minimal of protein with increase = of=20 sugars and fat  to = maintain the=20 calorie requirements.

 

Renal replacement therapy

Approximately=20 20% of patients experiencing ARF require dialysis during their hospital = stay.=20 The majority of these patients recover.

The=20 principal methods of renal replacement therapy (RRT) are peritoneal = dialysis=20 (PD).  intermittent = hemodialysis=20 (IHD) and continuous venovenous hemofiltration (CVVH), =

Peritoneal=20 dialysis is inexpensive, widely available, and does not result in = hypotension.=20 Its use may be most common in children.

IHD is=20 the most efficient way of removing a volume or solute from the vascular=20 compartment quickly.

Continuous=20 RRT techniques are more expensive and not universally available;  they are believed to achieve = better=20 control of uremia and clearance of solute from the extravascular = compartment.=20 Because it continues around the clock, CVVH is able to remove larger = fluid=20 volumes, which is a significant advantage with critical care patients on = parenteral nutrition and multiple infusions. CVVH may also preserve = cerebral=20 perfusion pressure more effectively.

Indications=20 for initiation of RRT include the following:

Volume=20 overload

Hyperkalemia=20 (K+ >6.5 or rising)

Acid-base=20 imbalance

Symptomatic=20 uremia (pericarditis, encephalopathy, bleeding dyscrasia) =

Uremia=20 (BUN>100)

Dialyzable=20 intoxications -theophylline, aspirin, lithium)

Severe=20 dysnatremia (<115 or >165), dysthermia may also be appropriate = indications=20 for RRT.

 

 

Prognosis:=20

Deaths=20 from ARF are related directly to the patient's underlying disease = process.  Mortality is about 25%, = Mortality rates=20 are generally lower for nonoliguric than for oliguric ARF.=20

 

References

 

1.=20 Bellomo R, Ronco C, Kellum JA: Acute renal failure - definition, outcome = measures, animal models, fluid therapy and information technology needs: = the=20 Second International Consensus Conference of the Acute Dialysis Quality=20 Initiative (ADQI) Group. Crit Care 2004 Aug; 8(4): R204-12=20

 

2.=20 Bonventre JV: Mechanisms of ischemic acute renal failure. Kidney Int = 1993 May;=20 43(5): 1160-78.

 

3.=20 Druml W: Prognosis of acute renal failure 1975-1995. Nephron 1996; = 73(1): 8-15.=20

 

4.=20 Kaufman J, Dhakal M, Patel B, Hamburger R: Community-acquired acute = renal=20 failure. Am J Kidney Dis 1991 Feb; 17(2): 191-8.

 

5.=20 Kellum JA, M Decker J: Use of dopamine in acute renal failure: a = meta-analysis.=20 Crit Care Med 2001 Aug; 29(8): 1526-31.

 

6.=20 Klahr S, Miller SB: Acute oliguria. N Engl J Med 1998 Mar 5; 338(10): = 671-5.=20

 

7.=20 Korevaar JC, Jansen MA, Dekker FW: Evaluation of DOQI guidelines: early = start of=20 dialysis treatment is not associated with better health-related quality = of life.=20 National Kidney Foundation-Dialysis Outcomes Quality Initiative. Am J = Kidney Dis=20 2002 Jan; 39(1): 108-15

 

8.=20 Levy EM, Viscoli CM, Horwitz RI: The effect of acute renal failure on = mortality.=20 A cohort analysis. JAMA 1996 May 15; 275(19): 1489-94. =

 

9.  Lewis J, Salem MM, Chertow GM, = et al:=20 Atrial natriuretic factor in oliguric acute renal failure. Anaritide = Acute Renal=20 Failure Study Group. Am J Kidney Dis 2000 Oct; 36(4): 767-74=20

 

10.=20 Liano F, Pascual J: Epidemiology of acute renal failure: a prospective,=20 multicenter, community-based study. Madrid Acute Renal Failure Study = Group.=20 Kidney Int 1996 Sep; 50(3): 811-8

 

11.=20 Moghal NE, Brocklebank JT, Meadow SR: A review of acute renal failure in = children: incidence, etiology and outcome. Clin Nephrol 1998 Feb; 49(2): = 91-5=20

 

12.=20 Molitoris BA, Sandoval R, Sutton TA: Endothelial injury and dysfunction = in=20 ischemic acute renal failure. Crit Care Med 2002 May; 30(5 Suppl): = S235-40.=20

 

13.=20 Nash K, Hafeez A, Hou S: Hospital-acquired renal insufficiency. Am J = Kidney Dis=20 2002 May; 39(5): 930-6.

 

14.=20 Ragaller MJ, Theilen H, Koch T: Volume replacement in critically ill = patients=20 with acute renal failure. J Am Soc Nephrol 2001 Feb; 12 Suppl=20

17:=20 S33-9

 

15.=20 San A, Selcuk Y, Tonbul Z, Soypacaci Z: Etiology and prognosis in 438 = patients=20 with acute renal failure. Ren Fail 1996 Jul; 18(4): 593-9 =

 

16.=20 Schiffl H, Lang SM, Fischer R: Daily hemodialysis and the outcome of = acute renal=20 failure. N Engl J Med 2002 Jan 31; 346(5): 305-10

 

17.=20 Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS: Renal considerations = in=20 angiotensin converting enzyme inhibitor therapy: a statement for = healthcare=20 professionals from the Council on the Kidney in Cardiovascular Disease = and the=20 Council for High Blood Pressure Research of the American Heart = Association.=20 Circulation 2001 Oct 16; 104(16): 1985-91

 

18.=20 Shilliday IR, Quinn KJ, Allison ME: Loop diuretics in the management of = acute=20 renal failure: a prospective, double-blind, placebo-controlled, = randomized=20 study. Nephrol Dial Transplant 1997 Dec; 12(12): 2592-6. =

 

19.=20 Stapleton FB, Jones DP, Green RS: Acute renal failure in neonates: = incidence,=20 etiology and outcome. Pediatr Nephrol 1987 Jul; 1(3): 314-20=20

 

20.=20 Thadhani R, Pascual M, Bonventre JV: Acute renal failure. N Engl J Med = 1996 May=20 30; 334(22): 1448-60.

 

21.=20 Thurau K, Boylan JW: Acute renal success. The unexpected logic of = oliguria in=20 acute renal failure. Am J Med 1976 Sep; 61(3): 308-15. =

 

 

 

 

Address=20 for correspondence:

Dr.B=20 Sanjeev Rai

Dean=20 & Prof of Pediatrics

Father=20 Muller Medical College

Father=20 Muller Road

Mangalore=20 575002