September 2 nd, 2010

Acute Renal Failure Prerenal (Most Common) Results from hypoperfusion to kidney Dehydration, CHD, Sepsis Decreased perfusion -> ischemic injury -> fall in GFR Compensation: 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 ARF History should fit Renal imaging normal PrerenalRenalTubular Function U Na+<20>40Sodium Retention U osm>500<400Urine Concentration FE Na+<1%>3%Na retention+urine concentration BUN/Cr RatioIncreased

Intrinsic Renal Disease Parenchymal injury (ischemic or toxic) ATN, interstitial nephritis, HUS, glomerulonephritis, nephrotoxic drugs May see RBC or granular casts

Intrinic Renal Failure Renal scans (Mg-3) may identify areas of poor function Bx may be needed PrerenalRenalTubular Function U Na+<20>40Sodium Retention U osm>500<350Urine Concentration FE Na+<1%>3%Na retention+urine concentration BUN/Cr RatioIncreased

Postrenal Failure Obstruction to urinary flow Calculi, posterior urethral valves, UPJ obstruction Renal damage results from increased pressure Urinary sediment findings variable Imaging U/S Radioisotope scan

ARF: Management Renal perfusion Balancing fluid/ electrolytes Controlling BP Anemia Adequate nutrition Renal dosing of meds Dialysis (when needed) *Plan the initial treatment for a child with acute renal failure *Recognize the complications of ARF

Renal Perfusion Adequate CVP May require fluid administration Vasoactive agents Low-dose dopamine can improve renal blood flow, but the actual benefit is debated in literature

Fluid Management If unstable, bolus! If stable but ?volume depleted, gentle bolus Once intravascular volume re-established, minimal fluids Know that coexisting volume depletion should be corrected in patients with acute renal failure

Fluid Management Diuretics (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

Lytes Hyponatremia Hyperkalemia Acidosis Hypocalcemia

Anemia Consider transfusion: Active bleeding Hemodynamic instability Hct < 25

Hypertension Secondary to volume overload, increased vasc tone Diuresis or dialysis may be required IV antihypertensives if >99%ile Labetalol, nicardipine, enalapril

Nutrition Patients are in catabolic state, malnutrition is common For infants, low phos formula Older kids, may need low phos, K+, Na+ Balance nutrition with fluid restriction TPN Know the importance of nutrition in a child with ARF

Meds Renal dose and interval Know that drug dosages must be modified in ARF

Dialysis Indications CHF Anemia Hyperkalemia Severe acidosis Pericarditis Inadequate nutrition CVVH most commonly used acutely Can use with low BPs

Determine the Pattern Nephrotic Pattern: No inflammation on histology Nephrotic range proteinuria Inactive urine sediment (few cells or casts) Nephritic Pattern: Inflammation by histology Urine sediment: RBCs, WBCs, granular and RBC casts, variable proteinuria

Indicators of Glomerular Bleeding

What about function? Reduction in GFR Progression of disease Superimposed insult Decreased perfusion Possibly reversible Schwartz formula May overestimate GFR

Schwartz Formula GFR = k X Ht(cm) / Serum Creat k = 0.33preterm infants k = 0.45infants k = 0.55children/ adolescent girls k = 0.7adolescent boys

Blood Tests TestDisease Low C3PSGN, MPGN-II, Low C3, C4Lupus, MPGN-I, shunt nephritis, SBE ANCASystemic vasculitis (Wegner’s) IgAIgA nephropathy, HSP Anti-GBMGoodpasture’s ANA, antiDNALupus *Differentiate acute post-strep GN from other forms

Renal Biopsy Goals Confirm Dx Determine extent of injury Predict outcome Timing Dependant on clinical setting

Rapidly Progressive (Crescentic) GN Clinical Syndrome Features of glomerular disease Progressive loss of renal function (days, weeks) May be presentation of many underlying dx Tx Pulse methylprednisolone Cyclophosphamide Consideration of plasmapheresis (anti-GBM)

Membranoproliferative GN Most common chronic GN in older kids and adults May present with nephrotic syn OR acute nephritic syndrome Renal function normal to severely decreased 50% progress to end stage renal disease in 10yrs No proven therapy

Post-Streptococcal Glomerulonephritis Acute nephritic syndrome 1-2wks after strep pharygitis, or up to 6wks after impetigo Strep Antibody titers positive Hematuria, edema, HTN, renal insufficiency. U/A: RBC casts, proteinuria, WBC Low C3 Very 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 GNPost-strep GN

Post-Streptococcal Glomerulonephritis Treatment: 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 Glomerulonephritis Prognosis 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