Transcript Acute and Chronic Renal Failure

Acute and Chronic
Renal Failure
ACUTE RENAL FAILURE
• Acute renal failure (ARF) is defined as an
abrupt and significant decrease in glomerular
filtration rate (GFR) and tubular function.
• This may lead to decreased excretion of waste
products (creatinine, urea, phosphate) and
water, resulting in azotemia and altered body
fluid homeostasis.
• Urine output may be low, normal, or high.
• Early recognition and management are crucial.
• ARF may be oliguric (<1 mL/kg/hour in
neonates and infants, <0.5 mL/kg/hour in
children) or nonoliguric.
• Nonoliguric ARF can be easily missed.
• Despite normal urine output, electrolyte
disturbances and uremia may become
significant.
• Urine osmolality is typically similar to serum
osmolality in such patients.
Causes of Acute Renal Failure
• PRERENAL
• POSTRENAL (OBSTRUCTION)
• INTRINSIC
PRERENAL
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Dehydration
Septic shock
Heart failure
Hemorrhage
Burns
Peritonitis, ascites, cirrhosis
POSTRENAL (OBSTRUCTION)
• Urethral obstruction (stricture, posterior
urethral valves, diverticulum)
• Ureteral obstruction (calculi/crystals, clot)
• Ureterocele
• Extrinsic tumor compressing bladder outlet
• Neurogenic bladder
• Tumor lysis syndrome
INTRINSIC
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Acute tubular necrosis
Nephrotoxins (drugs)
Acute cortical necrosis
Glomerulonephritis/interstitial nephritis
Vascular (renal vein thrombosis, arterial emboli-umbilical
artery catheter)
• Disseminated intravascular coagulation
• Vasculitis (Schönlein-Henoch purpura, lupus, Wegener
granulomatosis)
• Hemoglobinuria/myoglobinuria
• Acute tubular necrosis (ATN) is the most
common cause of ARF in children and is
usually the consequence of renal
underperfusion.
• Hypoxia-ischemia resulting from poor
perfusion leads to early renal vasoconstriction
and eventual tubular injury.
• Toxic injury secondary to drugs, exogenous
toxins (ethylene glycol, methanol), or
endogenous toxins (myoglobin, hemoglobin)
also result in ATN.
• Severe vascular compromise with or without
secondary arterial or venous thrombosis may
result in acute cortical necrosis.
• A precipitating illness associated with
vomiting and diarrhea or inadequate oral
intake resulting in oliguria are consistent with
prerenal causes.
• Postrenal causes may be occult and are not
associated with hypoperfusion or dehydration.
• With obstructive causes, flank masses or a
distended bladder may be present on
examination.
• Intrinsic renal failure can be associated with
signs of volume overload (hypertension,
cardiac enlargement, a gallop rhythm).
• Urine output characteristically is decreased,
and signs of systemic involvement may be
evident.
• Urinalysis usually reveals red blood cells
(RBCs) and granular casts, with mild to
moderate proteinuria.
Diagnostic Studies
• In oliguric states, differentiation between prerenal azotemia
and intrinsic renal disease is aided by determining the
fractional excretion of sodium (FENa).
• The FENa is the percentage of sodium filtered by the glomeruli
that is reabsorbed by the tubules and is calculated by the
following equation: [U/P Na/U/P creatinine]x100
where U and P are the urine and plasma concentrations.
• Values under 1% are consistent with prerenal azotemia (as the
kidney maximizes water and salt reabsorption).
• Values greater than 2% are consistent with intrinsic renal
dysfunction.
• A ratio of serum blood urea nitrogen (BUN)
and creatinine greater than 20:1 is typical of
prerenal states.
• Urinalysis may identify hematuria,
proteinuria, or casts, which further support
intrinsic or postrenal causes of ARF.
Prerenal
Child
Neonate
Renal
Child
Neonate
Postrenal
Postrenal
<20
<20-30
>40
>40
FENa* (%)
<1
<2-5
>2
>2-5
Urine osmolality
(mOsm/L)
BUN/serum Cr ratio
>500
>300-500
∼300
∼300
>20
≥10
∼10
≥10
Urinalysis
Normal
Normal
RBCs/WBCs, protein,
casts
Hypotension, anoxia
Nephrotoxins
Hypertension, edema
Variable, may be
>40
Variable, may be
>2
Variable, may be
<300
Variable, may be
>20
Variable
Laboratory/Clinical
Feature
Urine Na+ (mEq/L)
History
Physical examination
Diarrhea, vomiting
Diuretics
Dehydration,
hemorrhage
Poor urine
stream/output
Flank mass,
distended bladder
• Hyperkalemia can be seen in patients with
ARF as a result of decreased potassium
excretion.
• Acidosis is due to impaired secretion of
hydrogen ions and catabolic waste products.
• Hypocalcemia in ARF is often exacerbated by
hyperphosphatemia and, if untreated, can
lead to tetany or seizures.
• Ultrasound imaging may reveal increased
echogenicity with ATN and loss of
corticomedullary differentiation with more
severe involvement.
• Radiologic studies (ultrasound, voiding
cystourethrogram [VCUG], computed
tomography [CT], nuclear imaging) are often
helpful in determining the cause of
obstruction in postrenal cases.
• Renal biopsy, usually performed
percutaneously, may be indicated if the
presentation of ARF is atypical to assess the
severity of systemic disease involvement, to
guide therapy, or establish a prognosis.
• Light microscopy should be augmented by
immunofluorescence and electron
microscopy.
Treatment
• Careful assessment of intake and output
should be augmented with serial
measurements of body weight.
• Initial fluid and electrolyte therapy provides
water to equal insensible losses; water and
electrolytes are then added to replace
ongoing losses.
• If hypovolemia is present, intravascular
volume should be expanded by intravenous
(IV) administration of physiologic saline.
• If hypervolemia is present, 1 to 2 mg/kg of
furosemide may be attempted.
• Severe fluid overload in the presence of
marked oliguria or anuria is one indication for
dialysis.
• Serum electrolyte levels should be determined
frequently during the acute phase of ARF.
• Foods, fluids, and medications that contain
potassium should be restricted until renal
function is re-established or dialysis initiated.
• The major risk of hyperkalemia is arrhythmias.
• Intravenous calcium will block the acute
cardiac toxicity of hyperkalemia while
measures to shift potassium onto cells
(bicarbonate, beta-agonists, glucose/insulin)
and hasten removal (diuretics, sodiumpotassium exchange resins, dialysis) are
initiated.
• Although sodium bicarbonate counteracts
acidosis, it engenders a risk of fluid overload,
hypernatremia, and hypertension.
• Treatment of hypocalcemia and
hyperphosphatemia primarily involves efforts
to lower the serum phosphorus by dietary
phosphorus restriction and administration of
phosphate binders (calcium acetate and
calcium carbonate).
• Symptomatic hypocalcemia can be treated
with IV calcium; it must be given cautiously to
avoid precipitation with circulating
phosphorus.
• In children with ARF, dialysis has three major
indications:
• 1. Hypervolemia unresponsive to fluid
restriction or diuretics
• 2. Major electrolyte abnormalities
unresponsive to medical therapy
(hyperkalemia, acidosis)
• 3. Signs of uremia
• Renal replacement therapies in children
include peritoneal dialysis, hemodialysis, and
continuous renal replacement therapy
(continuous venovenous hemofiltration).
• Careful monitoring of blood levels of drugs
excreted by the kidney and appropriate
adjustment of either the total dose or dosing
intervals are necessary to prevent
complications or further renal injury.
Prognosis
• Recovery from ARF depends on the etiology,
availability of specific treatments, and other
aspects of the patient's clinical course.
• Sepsis and infections are major complications
of ARF.
CHRONIC KIDNEY DISEASE
Etiology and Epidemiology
• Congenital and obstructive abnormalities are
the most common causes of chronic kidney
disease (CKD) that present between birth and
10 years of age.
• After age 10, acquired diseases, such as FSGS
and chronic GN, are more common causes of
CKD.
• The risk of progression to ESRD is related to
the cause of CKD and modifiable factors, such
as UTI and hypertension.
• During puberty, renal function may
deteriorate if the damaged kidneys are not
able to grow and adapt to the increased
demands of larger body size.
• GFR(ml/min/1.73m2)=k x L(cm)/Pcr(mg/dl)
• The value for k, derived from the creatininelength-GFR correlation, is 0.33 in preterm
infants, 0.45 in full-term infants, 0.55 in
children and adolescent girls, and 0.7 in
adolescent boys.
Classification of the Stages of Chronic Kidney Disease
Stage GFR (mL/min/1.73
m2)*
1
≥90
2
60-89
3
4
5
30-59
15-29
<15 (or dialysis)
Description
Minimal kidney damage
Kidney damage with mild reduction of
GFR
Moderate reduction of GFR
Severe reduction of GFR
Kidney failure
Clinical Manifestations
• The factors associated with growth failure in
children with CKD include poor nutrition, renal
osteodystrophy (ROD), acidosis, anemia,
hormonal abnormalities, medication toxicity
(steroids), and the growth hormone/IGF-1
resistance seen in uremia.
• Anemia results primarily from a failure of the kidney
to produce adequate erythropoietin and an impaired
response to erythropoietin due to uremia.
• Renal osteodystrophy is common and is related to
phosphate retention from low GFR and diminished
1,25-dihydroxyvitamin D production in the kidney.
• Secondary hyperparathyroidism and poor bone
mineralization may ensue and lead to fractures and
bone deformities.
• Delayed puberty may be due to altered
gonadotropin secretion and feedback
patterns.
• Hypertension is relatively common in CKD and
may be asymptomatic or associated with
headaches, left ventricular hypertrophy (LVH),
and heart failure.
• Learning and school performance may also be
impaired in CKD.
Treatment
• The management of children with CKD requires a
multidisciplinary team of pediatric practitioners to address
their growth and development.
• Adequate nutrition should be provided even if this requires
dietary supplements and tube feedings.
• With very low GFR, maintenance dialysis may be needed for
growing children to allow adequate fluid and recommended
daily allowance of protein and calories.
• In infants with CKD, a low-solute formula with a phosphate
binder may be indicated.
• When acidosis develops, sodium bicarbonate
or sodium citrate is indicated.
• Unless a child is oliguric, fluid restriction is not
necessary.
• Sodium intake depends on the particular
sodium handling aspects of the renal disease.
• Many children with congenital renal disorders
waste sodium in their urine and require
supplemental salt.
• Conversely, children with GN tend to retain
sodium and may become hypertensive or
edematous if given excess salt.
• High-potassium foods should be avoided in
advanced CKD.
• The initial therapy for ROD is to restrict
phosphate in the diet.
• Oral phosphate binders are used if this is not
sufficient.
• Supplemental calcium may be needed.
• Parathyroid hormone levels should be kept in
the normal range and this may require
supplemental vitamin D analog (calcitriol,
paricalcital) therapy.
• Recombinant-produced erythropoietin is used
to maintain near normal hemoglobin levels in
children with CKD.
• Effective erythropoiesis requires iron and
typically depletes iron stores.
• Parenteral iron is often needed for children on
erythropoietin.
• Growth failure is more common with
advanced stages of CKD.
• Recombinant-produced growth hormone is
useful in children with CKD who are not
growing well despite proper management.
• The optimal treatment of ESRD is renal
transplantation.
• Maintenance dialysis is effective for a child
awaiting renal transplantation or for whom
renal transplantation is not possible.
• Peritoneal dialysis (PD) is effective in even
small infants, and about 40% of children who
require chronic dialysis use this modality in
the United States.
• Hemodialysis is used more often for older and
larger children, when intravascular access is
less of a concern, and for children whose
parents cannot provide home PD.
Prognosis
• Infants and children with ESRD have a good
prognosis, given the effectiveness of dialysis
and transplantation.
• Kidney transplants have an excellent success
rate.
• More than 90% of transplants in children
(living or deceased donor) function 1 year
after transplant; more than 50% still function
20 years later.
• Lifelong immunosuppressive medications are
necessary.
• The major complications relate to side effects
of medications: infections, cardiac
complications (left ventricular hypertrophy
[LVH], atherosclerosis, arrhythmias), and
increase in malignancies.
• Children after renal transplant who have not
had prior Epstein-Barr virus (EBV) infection are
more susceptible to develop an EBV-mediated
post-transplant lymphoproliferative disorder
(PTLD) that resembles malignant lymphoma.
• With early detection, PTLD and other
malignancies can usually be treated
successfully.