Chronic renal failure It is defined as either kidney damage or a decreased kidney glomerular filtration rate (GFR) of less than 60 mL/min/1.73 m2 for 3 or more months.

Etiology Cause may be congenital, acquired, inherited, or metabolic renal disease. children younger than 5yr is most commonly a result of congenital abnormalities such as renal hypoplasia, dysplasia or obstructive uropathy.

Etiology After 5yr, acquired diseases (GN) & inherited disorders (Alport syndrome) predominate. CRF related to metabolic disorders (cystinosis, hyperoxaluria) & polycystic kidney disease may present throughout the childhood years.

GFR(ML/MIN/1.73M²) = K X Ht cm s. Creatinine mg/dl K= 0.45(neonate)- 0.7 (adolescence)

Clinical manifestations There is accumulation of nitrogenous waste products, acidosis, sodium retention or sodium wasting, urinary concentrating defect, hyperkalemia. Renal osteodystrophy ( hyperphosphatemia, hypocalcaemia, secondary hyperparathyroidism)

Growth retardation inadequate caloric intake, renal osteodystrophy, metabolic acidosis, anemia, growth hormone resistance Anemia decreased erythropoietin production, iron, folate, B12 deficiencies, and decreased RBC survival Bleeding tendency defective platelets function

Clinical manifestations Neurologic symptoms (fatigue, poor concentration, headache, drowsiness, memory loss, seizures, peripheral neuropathy) GI symptoms (feeding intolerance, abdominal pain). hypertension, hyperlipidemia, pericarditis/ cardiomyopathy, & glucose intolerance.

Treatment The medical care of patients with chronic kidney disease should focus on the following: Delaying or halting the progression of chronic kidney disease by: Treatment of the underlying condition if possible

It requires close monitoring of patients clinical & lab It requires close monitoring of patients clinical & lab. Status including Hb level, serum electrolytes, blood urea nitrogen, creatinine, calcium, phosphorus, & alkaline phosphatase. Periodic measurement of parathormone level & X-ray studies of bone, echocardiography to identify left ventricular hypertrophy & cardiac dysfunction.

Fluid & electrolyte balance: Children with CRF due to renal dysplasia may be polyuric with significant urinary sodium losses, these children may benefit from high volume, low caloric density feedings with sodium supplementation. While children with high blood pressure, edema, or HF may require sodium restriction & diuretic therapy.

Fluid restriction is rarely necessary in children with CRF until the development of end stage RF. Hyperkalemia needs restriction of potassium intake, giving oral alkalizing agents or Kayexalate.

Acidosis: Treated by giving either Bicitra(1mEq sodium citrate/ml) or sodium bicarbonate tablets, dose 45-65 mg/kg/d PO divided qid to maintain serum bicarbonate >22mEq/L.

Nutrition: Dietary phosphorus, potassium, & sodium should be restricted according to individual patient's lab. Study Protein intake should be 2.5 g/Kg/day & should consist of high biologic value that is metabolized primarily to usable amino acids rather than to nitrogenous wastes. e.g. of high biologic value protein eggs, milk followed by meat, fish.

Supplements given of water soluble vitamins (nephrocaps) Supplements given of water soluble vitamins (nephrocaps). Zinc & iron added only if deficiencies are confirmed. Growth: Children who remain less than -2 SD for height despite optimal medical support) may benefit from recombinant human growth hormone

Renal osteodystrophy: It is a spectrum of bone disorders seen in patients with CRF caused by secondary hyperparathyroidism. The decrease in the functional renal mass leads to decline in renal 1α-hydroxylase activity, with decreased production of activated vitamin D (1,25-dihydroxycholecalciferol).

decreased intestinal calcium absorption, hypocalcaemia, & increased parathyroid gland activity, excessive PTH secretion (to correct hypocalcaemia) will increase bone resorption.

Clinically the child will be presented with muscle weakness, bone pain, & fractures with minor trauma. In growing children rachitic changes, varus & valgus deformity of the long bones. Radiograph of the hands, wrist & knees show subperiosteal resorption with widening of metaphysis. Treatments by low phosphate diet with phosphate chelation using calcium carbonate & calcium acetate, with administration of vitamin D 0.01-0.05μg/Kg/day of calcitriol.

Anemia in CRF is primarily the result of inadequate erythropoietin production by the failing kidneys Recombinant human erythropoietin those patients should also receive iron supplement and folic acid.

Hypertension: ACE inhibitors (enalapril, lisinopril) Immunization: Patients should receive all standard immunizations (except in those patients receiving immunosuppressive medications for GN). Adjustment in drug dosage: Because many drugs are excreted by the kidneys, their dosing may need to be adjusted to reduce risk of toxicity.

Uremic manifestations should be treated with chronic renal replacement therapy (hemodialysis, peritoneal dialysis, or renal transplantation)