September 2nd, 2010

Acute Renal FailurePrerenal (Most Common)

Results from hypoperfusion to kidney Dehydration, CHD, Sepsis

Decreased perfusion -> ischemic injury -> fall in GFRCompensation:

Relax afferent arterioles (decreasing renal vasc resistance) Increased catecholamines Increased vasopressin Renin-angiotensin system

Enhanced Na and water reabsorption to increase perfusion May secondarily worsen oliguria

Vasodilatory prostaglandins -> relax microvasculature

*Recognize the causes of acute renal failure in infants and children

Diagnosis: Prerenal ARFHistory should fitRenal imaging normal

Prerenal Renal Tubular Function

U Na+ <20 >40 Sodium Retention

U osm >500 <400 Urine Concentration

FE Na+ <1% >3% Na retention+urine concentration

BUN/Cr Ratio Increased

Intrinsic Renal DiseaseParenchymal injury (ischemic or toxic)

ATN, interstitial nephritis, HUS, glomerulonephritis, nephrotoxic drugs

May see RBC or granular casts

Intrinic Renal FailureRenal scans (Mg-3) may identify areas of

poor functionBx may be needed

Prerenal Renal Tubular Function

U Na+ <20 >40 Sodium Retention

U osm >500 <350 Urine Concentration

FE Na+ <1% >3% Na retention+urine concentration

BUN/Cr Ratio Increased

Postrenal FailureObstruction to urinary flow

Calculi, posterior urethral valves, UPJ obstruction

Renal damage results from increased pressure

Urinary sediment findings variableImaging

U/SRadioisotope scan

ARF: ManagementRenal perfusionBalancing fluid/ electrolytesControlling BPAnemiaAdequate nutritionRenal dosing of medsDialysis (when needed) *Plan the initial treatment for a child with acute renal failure *Recognize the complications of ARF

Renal PerfusionAdequate CVPMay require fluid administrationVasoactive agents

Low-dose dopamine can improve renal blood flow, but the actual benefit is debated in literature

Fluid ManagementIf unstable, bolus!If stable but ?volume depleted, gentle bolusOnce intravascular volume re-established,

minimal fluids

Know that coexisting volume depletion should be corrected in patients with acute renal failure

Fluid ManagementDiuretics (Furosemide, Mannitol)

Benefit: May help volume overload Decrease intratubular obstruction Remove K+ (furosemide)

Downfall: Do not prevent need for dialysis Could worsen renal perfusion and injury

Restore intravascular volume and measure urine lytes prior to diuretics

LytesHyponatremiaHyperkalemiaAcidosisHypocalcemia

AnemiaConsider transfusion:

Active bleedingHemodynamic instabilityHct < 25

HypertensionSecondary to volume overload, increased

vasc toneDiuresis or dialysis may be requiredIV antihypertensives if >99%ile

Labetalol, nicardipine, enalapril

NutritionPatients are in catabolic state, malnutrition is

commonFor infants, low phos formulaOlder kids, may need low phos, K+, Na+Balance nutrition with fluid restrictionTPN

Know the importance of nutrition in a child with ARF

MedsRenal dose and interval

Know that drug dosages must be modified in ARF

DialysisIndications

CHFAnemiaHyperkalemiaSevere acidosisPericarditisInadequate nutrition

CVVH most commonly used acutelyCan use with low BPs

Glomerular Disease

Determine the PatternNephrotic Pattern:

No inflammation on histologyNephrotic range proteinuriaInactive urine sediment (few cells or casts)

Nephritic Pattern:Inflammation by histologyUrine sediment: RBCs, WBCs, granular and

RBC casts, variable proteinuria

Indicators of Glomerular Bleeding

What about function?Reduction in GFR

Progression of diseaseSuperimposed insult

Decreased perfusion Possibly reversible

Schwartz formula May overestimate GFR

Schwartz FormulaGFR = k X Ht(cm) / Serum Creat

k = 0.33preterm infantsk = 0.45infantsk = 0.55children/ adolescent girlsk = 0.7 adolescent boys

Blood TestsTest Disease

Low C3 PSGN, MPGN-II,

Low C3, C4 Lupus, MPGN-I, shunt nephritis, SBE

ANCA Systemic vasculitis (Wegner’s)

IgA IgA nephropathy, HSP

Anti-GBM Goodpasture’s

ANA, antiDNA Lupus

*Differentiate acute post-strep GN from other forms

Renal BiopsyGoals

Confirm DxDetermine extent of injuryPredict outcome

TimingDependant on clinical setting

Rapidly Progressive (Crescentic) GNClinical Syndrome

Features of glomerular diseaseProgressive loss of renal function (days, weeks)May be presentation of many underlying dx

TxPulse methylprednisoloneCyclophosphamideConsideration of plasmapheresis (anti-GBM)

Membranoproliferative GNMost common chronic GN in older kids and

adultsMay present with nephrotic syn OR acute

nephritic syndromeRenal function normal to severely decreased50% progress to end stage renal disease in

10yrsNo proven therapy

Post-Streptococcal GlomerulonephritisAcute nephritic syndrome 1-2wks after strep

pharygitis, or up to 6wks after impetigoStrep Antibody titers positiveHematuria, edema, HTN, renal insufficiency.U/A: RBC casts, proteinuria, WBCLow C3Very similar presentation to MPGN, but

resolves by 2mos

•Acute onset•Hematuria, edema, HTN•Impaired renal function•U/A: RBC casts, proteinuria, WBC•Low C3•Lasts longer than 2 months•Confirmed on Biopsy

•Acute onset•Hematuria, edema, HTN•Impaired renal function•U/A: RBC casts, proteinuria, WBC•Low C3•Strep antibodies positive•Resolves by 2 months

Membranoproliferative GN Post-strep GN

Post-Streptococcal GlomerulonephritisTreatment:

Manage the acute effects of renal insufficiency, HTN

Amoxicillin Prevent spread of nephritogenic organisms Does not affect natural course of disease

*Plan the initial management of PSGN

Post-Streptococcal GlomerulonephritisPrognosis

Complete recovery 95% Renal function and C3 normalize by 6wks HTN up to 3mos Hematuria/proteinuria for prolonged periods

If chronic, think MPGN *Know sequence of resolution: C3, hematuria, proteinuria