Renal Failure

Dr.MOHAMED SALEYE(MD,PEDITRICIAN)
• Acute kidney injury has been traditionally defined as an abrupt loss of kidney function

leading to a rapid decline in the glomerular filtration rate (GFR), accumulation of

waste products such as BUN and creatinine, and dys regulation of extracellular

volume and electrolyte homeostasis.

• The term AKI has largely replaced acute renal failure.

According to KDIGO AKI is defined as:

• Increase in serum creatinine by ≥ 0.3 mg/dL from baseline within 48 hr.

• Increase in serum creatinine to ≥ 1.5 times baseline within the prior 7 days.

• Urine volume ≤ 0.5 mL/kg/hr for 6 hr.

 The incidence of AKI varies from 2–5% of all hospitalizations to > 25% in critically ill

infants and children.

 The etiology of AKI varies widely according to age, geographic region, and clinical

setting.

 Functional AKI induced by dehydration is usually reversible with early fluid therapy.
 PATHOGENESIS

 AKI has been conventionally classified into three categories: prerenal, intrinsic renal,

and post renal.

 PRERENAL AKI,

 is characterized by a diminished effective circulating arterial volume, which leads to

inadequate renal perfusion and a decreased GFR.

 Evidence of structural kidney damage is absent.

 Common causes of prerenal AKI include dehydration, sepsis, hemorrhage, severe hypo

albuminemia, and cardiac failure.

 INTRINSIC RENAL AKI

• includes a variety of disorders characterized by renal parenchymal damage,

including sustained hypo perfusion and ischemia.
• Glomerulonephritis

• Hemolytic-uremic syndrome

• Acute tubular necrosis

• Cortical necrosis

• Rhabdomyolysis

• Tumor infiltration

• Toxin and drugs

• Tumor lysis syndrome

 POST RENAL AKI
 includes a variety of disorders characterized by obstruction of the urinary tract.

• Posterior urethral valves

• Ureter pelvic junction obstruction

• Ureter vesicular junction obstruction

• Tumors

• Urolithiasis

• Urethral strictures

• Neurogenic bladder

• Anticholinergic drugs
 Clinical Manifestations and Diagnosis
• History?
• P/E?
• Laboratory Findings:
• Anemia
• Leukopenia.
• Hyponatremia.
• Elevated BUN, creatinine, uric acid, potassium, and phosphate.
• hypocalcaemia.
• The serum C3 level may be depressed
• hematuria, proteinuria, and RBC cast.
 PRERENAL AKI INTRINSIC AKI

Urine SG (>1.020) Urine SG <1.010.

 urine osmolality (UOsm > 500 UOsm < 350 mOsm/kg).

mOsm/kg), UNa> 40 mEq/L.
 UNa < 20 mEq/L, fractional excretion of sodium > 2%
 fractional excretion of sodium < 1% (>10% in neonates).
(<2.5% in neonates).
 Treatment
Medical Management

• Catheterize for BOO

• intravascular volume should be expanded by intravenous administration of isotonic saline, 20

mL/kg over 30 min.

• After volume resuscitation, hypovolemic patients generally void within 2 hr; failure to do so
suggests intrinsic or post renal AKI.

• Furosemide (2-4 mg/kg) may be administered as a single intravenous dose after the adequacy
of the circulating blood volume has been established.

• Mannitol may be effective in the prevention of pigment (myoglobin, hemoglobin)-induced

renal failure.
• If there is no response to a diuretic challenge, diuretics should be discontinued and fluid
restriction is essential.

• Patients with a relatively normal intravascular volume should initially be limited to 400
mL/m2 /24 hr (insensible losses) plus an amount of fluid equal to the urine output for that
day.

• Management of Hyperkalemia

• Management of metabolic acidosis

• Management of hypocalcaemia

• Management of Hyponatremia

• Management of Hypertension
 INDICATIONS FOR DIALYSIS IN AKI :

• Anuria/oliguria

• Volume overload with evidence of hypertension and/or pulmonary edema

• refractory to diuretic therapy

• Persistent hyperkalemia

• Severe metabolic acidosis unresponsive to medical management

• Uremia (encephalopathy, pericarditis, neuropathy)

• Calcium: phosphorus imbalance, with hypocalcemic tetany that cannot be

controlled by other measures.

 CHRONIC KIDNEY DISEASE

 CKD is determined by the presence of kidney damage and level (or severity) of kidney

function (glomerular filtration rate, or GFR.

 End-stage renal disease (ESRD) is an administrative term used to define all patients

who are treated with dialysis or kidney transplantation, and is a subset of patients with

stage 5 CKD.
• The pediatric CKD prevalence is approximately 18 per 1 million children.

• childhood-onset ESRD still carries significant morbidity and a 30-fold increased

mortality rate as compared with healthy peers, with cardiovascular and infectious

diseases as the leading causes of death.

 Pathogenesis
 In addition to progressive injury with ongoing structural or metabolic genetic diseases,
renal injury can progress despite removal of the original insult.

 Hyper filtration injury may be an important final common pathway of glomerular

destruction, independent of the underlying cause of renal injury.

 Other pathologic etiologies of chronic kidney disease include proteinuria, hypertension,

hyperphosphatemia, and hyperlipidemia.
Clinical Manifestations
 Laboratory Findings

• Laboratory findings can include elevations in blood urea nitrogen and serum creatinine

in addition to hyperkalemia, hyponatremia (secondary to either renal salt wasting

versus volume overload), hypernatremia (loss of free water), acidosis, hypocalcaemia,

hyperphosphatemia, and an elevation in uric acid.

 Treatment and Management

• CKD treatment is supportive, with an aim to screen for and treat various metabolic

complications of CKD in hopes to improve the quality of life and potentially slow the

progression of renal dysfunction.

 Nutrition
• Patients should receive 100% of the estimated energy requirement for age, individually
adjusted for the physical activity level,body mass index, and response in the rate of
weight gain or loss.

• When oral supplemental nutrition with increased calories or fluid volume is

insufficient, tube feeding should be considered.

• the recommended protein intake is often 100% of the DRI .

• For Children with CKD stages 2-5 should receive 100% of the DRI of vitamins and
trace elements; water-soluble vitamin supplements are often required for patients
receiving dialysis.
 Fluid and Electrolyte Management
• Infants and children with renal dysplasia may be polyuric, with significant urinary
sodium and free water losses.

• These children benefit from high-volume, low-caloric-density feedings with sodium

supplementation.

• Children with high blood pressure or edema benefit from sodium restriction and diuretic
therapy.

• Fluid restriction is necessary in severe cases of nephrotic syndrome or when renal

function worsens to the point of requiring dialysis.
 Anemia
• Anemia in patients with CKD is primarily the result of inadequate erythropoietin
production by the failing kidneys and typically manifests when renal function falls
below 40 mL/min/1.73 m2.

• Other contributory factors for anemia in CKD include iron, folic acid, and/or vitamin
B12 deficiency, and decreased erythrocyte survival secondary to uremia.
 Anemia in pediatric CKD patients is defined when the hemoglobin falls to <5% for age
and gender; alternatively, anemia can be defined when the

hemoglobin falls to < 11g/dL (ages 0.5-5 yr of age), < 11.5 g/dL (5-12 yr of age),< 12
g/dL (females > 12 yr of age, males 12-15 yr of age), and < 13 g/dL (males > 15 yr of
age).

 Once anemia is diagnosed, the recommendation is to investigate for deficiencies in

iron and/or other vitamins (i.e., vitamin B12 , folate)
• Iron supplementation (oral or intravenous) is recommended for patients who

demonstrate a transferrin saturation ≤ 20% and ferritin ≤ 100 ng/mL.

• Erythropoiesis-stimulating agents (ESAs) have decreased the need for transfusion in

CKD patients, especially those receiving hemodialysis.

• Erythropoietin and darbepoetin alfa are common prescribed ESAs.

 Adjustment in Drug Dose

• Drugs excreted by the kidneys might need to be dose adjusted in CKD patients to

maximize their effectiveness and minimize the risk of toxicity.

• Strategies in dosage adjustment include lengthening of the interval between doses

or decreasing the absolute dose, or both.

THANK YOU