CASE
4yr old with h/o uti, was fou d to have puv. His urea was 100mg% and creatinine 1.9mg% when diagnosed at 2yrs. He had fulgaration. His general condition improved but creatinine value slowly rising now rea hing 3mg%. Urinw out put was normal
Wt 10kg
Ht 80cm
Bp 114/76
Cbc- hb 9gm%, perioherl smear microcytic anemia
Ferritin 10 ng/ml
Calcium 7.1mg%, phis phorous 6 mgm %
Pth 300pg/ml, 25oh vit d 10 ng/ml
Creatinine 3.1mg%, urea 120mg%, sgpt 48iu, s albumin 2.4gm%
Abg ph 7.2 , tco2 22
Na 129 k 5 cl 99 hco2 14
List problems in this child
Wt <2sd
Ht <3rd centile
Anemia
Hypertension
Hyperphosphatemia
Vit d deficiency
High creatinine
Hypocalcemia?
Metabolic acidosis
What are the atages ofCKD?
What are the common causes of ckd?
In < 5 years of age
Congenital malformations: Hypoplastic/dysplastic kidneys /Re fl ux nephropathy /Obstructive uropathy Posterior urethral valves
Metabolic/genetic disorders:
Oxalosis /Polycystic kidney disease /Congenital nephrotic syndrome /Wilms’ tumor
In > 5 years of age
Glomerular disease: Focal segmental glomerulosclerosis /Hemolytic uremic syndrome /Chronic glomerulonephritis Alport’s syndrome
Tubulointerstitial disease: Chronic tubulointerstitial nephritis/ Cystinosis Nephronophthisis/ Nephrotoxic drugs
What are the clini al features?
How do you evaluate ckd?
Assessment of renal function:
• Serial measurements of creatinine : Serial measurement of serum creatinine is important. An abnormal serum creatinine value persisting for more than 3 months con fi rms CKD.
• Creatinine clearance : As per KDOQI guidelines, measurement of creatinine clearance using 24-h urine collections does not improve the estimate of GFR over that provided by predictive equations like Schwartz’s equation but may provide useful information in infants and malnourished children. Proteinuria:
• Persistent proteinuria is a marker of ongoing renal disease. Reduction of proteinuria may slow progression of CKD. Hence, early detection and intervention are important.
Although several novel urinary markers (such as tubular or low molecular weight
• proteins) show promise of future utility, they should not be used for clinical deci-sion making at present. Screening for microalbuminuria: In some speci fi c types of chronic kidney dis
•((eases (diabetic nephropathy, hypertension), one should evaluate for microalbu-minuria as an early marker of hyper fi ltration.
Imaging studies:
Renal ultrasound:––• Renal growth monitoring is feasible with serial ultrasonographic measurements of kidney length and volume. These measurements can be plotted against age or body height on reference graphs (nomograms). .
Ultrasonography in children with CKD may reveal normal sized/small or large kidneys; hydronephrosis; loss of corticomedullary differentiation.
Conditions that may present with normal-sized or enlarged kidneys in CKD are:
Nephronophthisis Focal segmental glomerulosclerosis Congenital nephrotic syndrome Polycystic kidney disease Obstructive uropathy
Renal Histopathology
In advanced stages of CKD, renal histopathology may be nonspeci fi c showing widespread glomerulosclerosis, tubular atrophy, and interstitial fi brosis.
How to assess nutrion and growth in ckd?
Height or recumbent length, weight, body mass index (BMI), and head circumference should be measured and plotted on the appropriate growth charts at regular intervals. Whoiap charts
It is recommended that the following growth and nutritional parameters be evaluated every 1–3 months in children under 3 years of age with CKD stages 2–5 and every 3–6 months in older children:
Dietary intake (3-day diet record or three 24-h dietary recalls)
Length- or height-for-age percentile or standard deviation score (SDS)
Length or height velocity-for-age percentile or SDS Estimated dry weight and weight-for-age percentile or SDS
Body mass index (BMI)-for-height–age percentile or SDS
How to manage nutrtion CKD?
Oral intake of an energy-dense diet is preferred especially in resource-poor countries before commercial nutritional supplements are prescribed in children with CKD stages 2–5 and children on dialysis (CKD stage 5D).
When energy requirements cannot be met with oral supplementation, tube feeding should be considered. Protein intake :
• Recommendations suggest relative restriction of protein intake as a means of reducing phosphorus intake.
Protein intake is prescribed according to severity of CKD, with intakes between 100 % and 140 % of the dietary reference intake suggested for children with CKD stage 3 and intakes between 100 % and 120 % for children with CKD stages 4–5.
Sodium and fl uid : • •
Restriction of sodium and fl uid is only absolutely necessary in children with oliguric or anuric renal failure (CKD stage 5). In lower stages of CKD, restriction is generally unnecessary. In contrast, children with polyuric renal failure often require sodium and water supplementation.
Sodium supplementation in the range of an additional 2–4 mmol/kg/100 ml of formula has been shown to be useful in improving growth in infants with polyuric CKD. Sodium supplementation must be accompanied by a high fl uid intake. In addition to the volume of formula required to meet caloric needs, these children should receive supplemental water, to take total fl uid intake of as high as 180–240 ml/kg/day.
Doses of sodium and water should be adjusted according to growth response and serum biochemistry.
Potassium : • Potassium restriction is usually required only for children with CKD stage 5. However, in some conditions, restriction may be necessary at lower CKD stages. Monitoring of serum potassium levels is essential to determine the need for potassium restriction.
Should we support growth withGH therapy?
Initiation of growth hormone therapy:Therapy with (recombinant) growth hormone (rhGH) is indicated in patients with GFR <75 ml/min/1.73 m 2 who have potential for growth, when height SDS is <1.88 (3rd percentile) or height velocity-for-age SDS is <1.88 (3rd percentile) despite adequate nutrition.
Dose: The initial dose of GH is 0.05 mg/kg/day SC or 30 IU/m 2 /week (0.35 mg/kg/week).
Baseline investigations
before starting GH therapy:––• Hip X-rays and wrist (left-hand wrist) bone age. Problems such as active rickets or a slipped capital femoral epiphysis should be resolved before starting growth hormone therapy.
Growth hormone therapy should not be initiated until the PTH level is no greater than twice the target upper limit for CKD stages 2–4 or one-and-a-half times the target upper limit in CKD stage 5.
What is the cause of anemia in CKD?
Erythropoietin (EPO) de fi ciency and iron de fi ciency are the most important causes for anemia in CKD. Other causes include in fl ammation, infection, dietary de fi ciencies, hyperparathyroidism, and aluminum toxicity. Serum iron and the % TSAT refl ect the amount of iron immediately available for hemoglobin synthesis. The serum ferritin refl ects total body iron stores. A low level of either of these indices may indicate the need for supplemental iron to support erythropoiesis. The TIBC represents the amount of iron, if added to transferrin that is needed to saturate Tf plus the iron that was already bound to the Tf.
Diagnosis of iron de fi ciency in CKD: • • • Low MCV with a high red cell distribution width (RDW) Serum ferritin of <20 ng/ml (target 100 ng/ml during iron or erythropoetin therapy) Transferrin saturation (serum iron / transferrin or total iron binding capacity ×100 %) of <20 % (0.2; not applicable when the TIBC < 200 m cg/dl (<36 mcmol/l)) Iron – replete state : TSAT > 20 % and serum ferritin >100 ng/ml (adults on HD: >200 ng/ml) Iron – deplete state : TSAT < 20 % and serum ferritin <100 ng/ml
Erythrocyte-stimulating agents (ESA) are indicated in CKD when the iron status is adequate and hemoglobin level is below recommended standards mentioned in Table 9.4
. Iron de fi ciency needs to be treated before administrating ESA.
• Iron therapy :–––– Oral iron therapy is indicated in doses ranging from 2 to 3 mg/kg up to 6 mg/ kg of elemental iron per day in two to three divided doses per day. Oral iron should be taken 2 h before or 1 h after all calcium-based phophate binders and food in order to maximize gastrointestinal absorption.
Intravenous (IV) iron therapy is indicated if children do not have a satisfactory response with oral iron therapy. The IV iron formulations currently available include iron dextran, iron sucrose, and sodium ferric gluconate. Sodium ferric gluconate complex in sucrose and iron sucrose appear to be safer than iron dextran.
Erythropoietin –
Stimulating Agents ( ESA ) Advantages of ESA: Minimization of blood transfusions Reduced sensitization to histocompatibility antigens Reduced risk of infections and iron overload Erythropoietin Dosage (per kg/week): <1 years: 350 IU, 1–5 years: 275 IU, 5–12 years: 250 IU, >12 years: 200 IU. –
Darbepoetin : Darbepoetin (starting dose of 0.5 m g/kg per week) is equally ef fi cacious for treating anemia associated with CKD. The extended half-life of darbepoetin does provide an advantage by allowing less frequent dosing at 1 m g /kg every 2 weeks.
What is bone mineral disease and renal osteodystrophy?
The term renal osteodystrophy (ROD) is exclusively used to de fi ne alterations in bone morphology associated with chronic kidney disease. The terminology bone mineral disease includes renal osteodystrophy and vascular calci fi cation. The three main abnormalities seen in renal osteodystrophy or bone mineral disease of CKD are (a) phosphate retention, (b) decreased free calcium level, and (c) decreased 1, 25 hydroxyvitamin D Phosphate retention and hyperphosphatemia : Phosphate retention begins early in the disease as the glomerular fi ltration rate (GFR) decreases. Hyperphosphatemia plays a central role in the development of secondary hyperparathyroidism.
Hypocalcemia : Total serum calcium usually decreases during the course of CKD due to phosphate retention, decreased calcitriol level, and resistance to the calcemic actions of PTH on bone. With compensatory hyperparathyroidism, PTH secretion varies inversely with serum calcium. Decreased calcitriol activity : Plasma calcitriol levels fall below normal when the GFR is less than 30 ml/min. Low calcitriol levels have also been found in earlier stages of CKD.
How do you assess bmd?
Assessment : 1. Clinical symptoms Children manifest with renal osteodystrophy in early stages of CKD, and it is recommended to begin screening for bone disease in stage 2 CKD. Symptoms may be subtle with bone pains, abnormal gait, hairline fractures, and bony deformities. Associated clinical entities such as slipped epiphysis, muscle weakness, and extra skeletal calci fi cation may be encountered. 2. Investigations • Serum levels of calcium, phosphate, alkaline phosphatase, total CO 2 , and parathyroid hormone should be measured in all patients with CKD stages 2 through 5 at regular intervals (see Table 9.5 ). The frequencies of measurement of PTH, calcium, phosphorus (phosphate), total CO 2 (bicarbonate), and alkaline phosphatase in stages of CKD are mentioned in Table 9.5 . These measurements should be made more frequently if the patient is receiving concomitant therapy for the abnormalities in the serum levels of calcium, phosphorus, or PTH in a transplant recipient or is a patient being treated with growth hormone therapy (rhGH). • • The target range of serum PTH in the various stages of CKD: Stages 2 and 3: 35–70 pg/ml (or ng/l in SI units) Stage 4: 70–110 pg/ml Stage 5: 200–300 pg/ml Other Aspects of Renal Osteodystrophy Newer markers of renal osteodystrophy: Markers of bone formation: bone-speci fi c alkaline phosphatase and osteocalcin. Markers of bone resorption: tartrate-resistant acid phosphatase and pyridinoline. They are not recommended in the routine evaluation of CKD ROD. Vitamin D de fi ciency: If serum PTH is above the target range for the stage of CKD and serum 25-hydroxyvitamin D (25-hydroxy cholecalciferol) should be measured. Vitamin D stores are categorized as vitamin D insuf fi ciency (levels of 25 OH vitamin D of 10–30 ng/ml [25–75 nmol/l]) and de fi ciency (levels <10 ng/ml [<25 nmol/l]).
Dual-energy X-ray absorptiometry (DXA) should not be used to monitor bone mineral density (BMD) in children with CKD. X-ray radiography is only indicated in stage 5 CKD and in high turnover bone disease. Bone biopsy The gold standard diagnostic test for determining the type of bone disease associated with CKD is iliac crest bone biopsy with double tetracycline labeling and bone histomorphometric analysis.
What is the management rod?
Phosphate Control
If serum phosphorus levels exceed upper limits of normal (see Chap. • 17.1 ) despite dietary phosphorus restriction, phosphate binders should be prescribed. Calcium-based phosphate binders are used as the initial therapy. Calcium carbonate, calcium acetate, and calcium gluconate are the preferred binders that need to be administered with meals (1 g of calcium carbonate binds 39 mg of phosphate and 1 g of calcium acetate binds 45 mg of phosphate). It is important to continue restriction of dietary phosphate during this therapy. Aluminum- and citrate-based phosphate binders should be avoided in children.
Sevelamer: Corrected serum calcium of >10.2 mg/dl (2.54 mmol/l) or serum PTH levels <150 pg/ml (150 ng/l) on two consecutive measurements are indications for the use of a non-calcium-, nonaluminum-containing phosphate binder, such as sevelamer. The dose recommended is 120–160 mg/kg/day in three divided doses along with meals. It can be used alone or in conjunction with the calcium-based phosphate binder.
How do you manage calcium in CKD?
Calcium Supplementation
• • • Patients whose serum levels of corrected total calcium are below the lower limit (<8.8 mg/dl [2.20 mmol/l]) should receive calcium supplements. Therapy for hypocalcemia should include calcium salts such as calcium carbonate or calcium acetate orally, or calcium gluconate or calcium chloride parenterally, and/or oral vitamin D.
Monitoring: If corrected total serum calcium level exceeds 10.2 mg/dl (2.54 mmol/l), therapies that increase serum calcium should be adjusted as follows: (a) Calcium-based phosphate binders to be discontinued and the use of noncalcium, nonmetal-based phosphate binders should be considered. (b) Active vitamin D sterols should be discontinued until the serum levels of corrected total calcium return to the target range (8.8–9.5 mg/dl [2.20–2.37 mmol/l]). (c)
If hypercalcemia (serum levels of corrected total calcium >10.2 mg/dl [2.54 mmol/l]) persists despite the discontinuation of therapy with vitamin and/or the modi fi cation of calcium-based phosphate binders, dialysis using lower dialysate calcium may be used for 3–4 weeks. The serum Ca X P should be maintained at <55 mg 2 /dl 2 (<4.4 mmol 2 /l 2 ) in adolescents >12 years and <65 mg 2 /dl 2 (<5.2 mmol 2 /l 2 ) in younger children. This is best achieved by controlling serum levels of phosphorus within the target range. Dietary Considerations Calcium and phosphorus
• • • Calcium intake should be limited to 100–120 % of the dietary reference intake for age, taking into account all sources of calcium, including phosphate binders. In CKD stages 3–5 and dialysis, dietary phosphorus intake should be limited to 100 % of the DRI for age when the serum parathyroid hormone (PTH) concentration is above the target range for CKD stage and the serum phosphorus concentration is within the normal reference range for age.
In CKD stages 3–5 and dialysis, dietary phosphorus intake should be limited to 80 % of the dietary reference intake for age when the serum PTH level is above the target range for CKD stage and the phosphorus concentration exceeds the normal reference range for age. Serum phosphate concentration should be monitored at least every 3 months in children with CKD stages 3–4 and monthly in children with CKD stage 5.
Vitamin D Therapy • 50,000 IU every week for 3 months In CKD stages 2–4: Measure PTH. If serum PTH is above the target range for the stage of CKD, serum 25-hydroxyvitamin D should be measured. • • • • •
If the serum level of 25-hydroxyvitamin D is <30 ng/ml (75 nmol/l), supplementation with vitamin D2 (ergocalciferol) should be initiated as mentioned below
The serum levels of corrected total calcium and phosphate should be measured after 1 month and then at least every 3 months.
If the serum levels of corrected total calcium exceed 10.2 mg/dl (2.54 mmol/l), discontinue ergocalciferol therapy and all forms of vitamin D therapy.
If 25(OH) vitamin D is normal, discontinue vitamin D therapy. Once patients are replete with vitamin D, continued supplementation with a vitamin D-containing multivitamin preparation should be used with annual reassessment of serum levels of 25(OH) vitamin D.
Active Vitamin D Therapy • •
In CKD stages 2–4: Active oral vitamin D (calcitriol) should be initiated when:
1. Serum levels of 25(OH) D are >30 ng/ml (75 nmol/l).
2. Serum levels of PTH are above the target range for the CKD stage.
3. Serum levels of corrected total calcium <10 mg/dl (2.37 mmol/l).
4. Serum levels of phosphorus less than age-appropriate upper limits. Dosage adjustments: 1.
If serum levels of PTH decrease to values below the target range for the CKD stage, active vitamin D sterol therapy should be held until serum levels of PTH increase to above the target range; treatment should then be resumed at half the previous dose of active vitamin D sterols. 2.
If serum levels of corrected total calcium exceed 10.2 mg/dl (2.37 mmol/l), active vitamin D sterol therapy should be held until serum calcium decreases to <9.8 mg/dl (2.37 mmol/l); treatment should then be resumed at half the previous dose.
If the lowest daily dose of the active vitamin D sterol is being given, alternate-day dosing should be used. 3. The dosage of active vitamin D sterols should be adjusted downward as follows:
If serum levels of phosphorus increase to greater than age-appropriate upper limits, active vitamin D therapy should be held; the dose of phosphate binders should be increased or initiated until the levels of serum phosphorus decrease to age-appropriate levels; then, treatment at half the prior dose of active vitamin D sterol should be resumed.
How to deal metabolic acidosis?
Metabolic Acidosis In children, overt acidosis is present when the estimated GFR is less than 30 ml/min per 1.73 m 2 . Acidosis may also be present in less severe CKD with conditions associated with renal tubular acidosis. Acidosis is associated with growth impairment because the body utilizes bone buffering to bind some of the excess hydrogen ions. In CKD stages 1–5, the serum level of total CO 2 should be measured. In patients >2 years of age, serum levels of total CO 2 should be maintained at >22 mEq/l (22 mmol/l); in neonates and young infants below age 2, serum levels of total CO 2 should be maintained at >20 mEq/l (20 mmol/l). If necessary, supplemental alkali salts should be given to achieve this goal.
Aluminum Bone Disease
Prevention: To prevent aluminum toxicity, the regular administration of aluminum should be avoided and the dialysate concentration of aluminum should be maintained at <10 m g/L.
Monitoring: In children with CKD lower than stage 5, serum levels of aluminum should be measured yearly if children have been exposed to aluminum for 3 months or more in the prior year. Baseline levels of serum aluminum should be <20 m g/l. A deferoxamine (DFO) test should be performed if there are elevated serum aluminum levels (60–200 m g/l) or clinical signs and symptoms of aluminum toxicity or prior to parathyroidectomy if the patient has had aluminum exposure for at least 4 months or more. Diagnosis: The presence of aluminum bone disease can be predicted by a rise in serum aluminum of >50 m g/l following DFO challenge combined with serum PTH levels of <150 pg/ml (150 ng/l). However, the gold standard for the diagnosis of aluminum bone disease is a bone biopsy showing increased aluminum staining of the bone surface (>15–25 %) using an aluminum-speci fi c stain and often the presence of adynamic bone disease or osteomalacia.
Therapy: In symptomatic patients with serum aluminum levels >60 m g/l but <200 m g/l or increase in aluminum after DFO >50 g/l, DFO should be given to treat the aluminum overload.
How to treat hypertension?
Measurement of blood pressure in children should be performed with age- and sizeappropriate equipment, and blood pressure values should be interpreted according to normal values adjusted for age, gender, and height percentile, as recommended by the Task Force Report on High Blood Pressure in Children and Adolescese
T)arget blood pressure in children should be lower than the 90th percentile for normal values adjusted for age, gender, and height or 120/80 mmHg, whichever is lower. M
ore recent randomized trial evidence suggests that maintaining BP below the 50th percentile may be effective in delaying progression of CKD. Intensi fi ed blood pressure control with target 24-h blood pressure levels in the low range of normal confers a substantial bene fi t with respect to renal function among children with chronic kidney disease.
The approach to using antihypertensive drugs and drug dose adjustments in CKD is mentioned below.
Antihypertensive Drugs in CKD When the GFR is >50 ml/min/1.73 m 2 , thiazides are indicated. When GFR <50 ml/ min/1.73 m 2 , loop diuretics can be tried.
If blood pressure readings are >75th percentile, treatment with angiotensin-converting-enzyme inhibitors/angiotensin receptor blockers is initiated. One may add calcium channel blockers or beta adrenergic blockers, and thereafter, if blood pressure readings are >75th percentile, clonidine, minoxidil, or prazosin may be added.
How to deal. Dyslipaedemia and cardiac issues?
Cardiovascular abnormalities such as left ventricular (LV) hypertrophy, LV dysfunction, increased arterial stiffness, increased carotid intima–medial thickness (IMT), and coronary calci fi cation are common in CKD, even in children and young adults. Individuals who are under dialysis are at particularly high risk for CV abnormalities. Hypertension, anemia, fl uid overload, hyperphosphatemia, and carnitine de fi ciency are risk factors contributing to cardiovascular morbidity.
KDOQI recommends the evaluation of dyslipidemia in adolescents upon presentation with CKD stage 5 (GFR <15 ml/min/1.73 m 2 or on dialysis), at 2–3 months after a change in treatment or other conditions known to cause dyslipidemia and at least annually thereafter.
The assessment of dyslipidemia should include a complete fasting lipid pro fi le with total cholesterol, LDL, HDL, and triglycerides.
Hyperlipidemia in children is de fi ned as lipid levels greater than the 95th percentile for age and gender. The normative data for lipids in children and adolescents currently used are from the Lipid Research Clinics Program from the NIH published in 1980 and can be found in the 2003 KDOQI guidelines for the management of dyslipidemia in chronic kidney disease. For adolescents with stage 5 CKD and a level of LDL ³ 130 mg/dl (3.36 mmol/l), KDOQI recommends treatment to reduce LDL to <130 mg/dl. If LDL is <130 mg/dl, fasting triglycerides ³ 200 mg/dl (5.18 mmol/l), and non-HDL cholesterol (total cholesterol minus HDL) ³ 160 mg/dl (4.14 mmol/l), treatment should be considered with gem fi brozil (1,200 mg/day) or feno fi brate (48 mg/day).
All children with dyslipidemia should follow the recommendations for therapeutic lifestyle changes (TLC), which include diet modi fi cation with a reduction in saturated fat intake and increase in fi ber intake and moderate physical activity
. If LDL cholesterol is ³ 160 mg/dl (4.14 mmol/l) and non-HDL cholesterol ³ 190 mg/dl, statin therapy (atorvastatin 5–10 mg/day, simvastatin 20 mg/day) is recommended in children older than 10 years.
How to Prevent infection in ckd?
Hepatitis B vaccine schedule (for <20 years): Recombivax hepatitis B: 5 m g, 0.5 ml IM, 3 doses at 0.1 and 6 months. Engerix B: 10 m g, 0.5 ml IM, 3 doses at 0, 1 and 6 months. The Advisory Committee on Immunization Practices (ACIP): recommends double standard doses to achieve a measurable antibody response. Serological testing for anti-hepatitis B antibody (anti-HBs) 1–2 months after the third dose. Anti-HBs levels <10 mIU/ml are an indication for revaccination. Live vaccines such as BCG, oral polio, and measles–mumps–rubella (MMR) are contraindicated while on immunosuppressive therapy or within 6 weeks of their discontinuation.
Children who have completed the pneumococcal vaccine (13-valent [PCV13] – if available – or 7-valent [PCV7] conjugate vaccine) series before 2 years of age and who have CKD should receive one dose of 23-valent pneumococcal polysaccharide vaccine (PPV23), ( ³ 2 months after the last dose of PCV). Children ages 24–59 months with CKD should receive two doses of PCV13 (or PCV7, if PCV13 is unavailable) administered 2 months apart followed by one dose of PPV23 administered ³ 2 months after the second dose of PCV. Children aged 24–59 months who have received PPV23 vaccine should receive two doses of PCV7 or 13 administered 2 months apart, 2 months of the last dose of PPV23.
What are the hematological issues?
Besides anemia, children with advanced CKD demonstrate altered platelet function and abnormal coagulation which may result in bleeding or thrombotic tendency.
Uremic bleeding is characterized by abnormal prolongation of bleeding time and hemorrhagic symptoms, like skin bleeds, epistaxis, and prolonged bleed from needle puncture sites, hemorrhagic pericarditis, and intracranial and retroperitoneal bleed. The factors responsible for platelet dysfunction are platelet abnormalities, uremic toxins, von Willebrand factor abnormalities, blood vessel abnormalities, and anemia.
Correction of uremic bleed: Correct anemia, maintain adequate dialysis, and withdraw antiplatelet agents. Desmopressin (DDAVP) is indicated 1 h before surgery at a dose of 0.3 m g/kg subcutaneously (or IV 30 min before surgery), or 2–3 m g/kg intranasally.
Cryoprecipitate can be administered as infusion of 10 units (bags) in adults in case of active bleed and prior to surgery. If unavailable, frozen plasma (10 ml/kg) may be tried. •
Thrombotic events: Children on hemodialysis are at risk to develop thrombosis at the site of vascular access as well as coronary, cerebral, and retinal arteries.
How to retard progression of CKD?
The modi fi able factors contributing to CKD progression are:
Hypertension • • • •
• Proteinuria
Dyslipidemia
Nephrotoxic drugs
Urinary obstruction
Hyper fi ltration
Lowering blood pressures to target systolic and diastolic blood pressures <90th percentile for age, height, and gender.
In a pediatric study from Europe, 29.9 % of patients who received intensi fi ed blood pressure control reached the end point of 50 % decline of renal function compared to 41.7 % of patients receiving conventional blood pressure control.
Reduction of proteinuria: Angiotensin-converting-enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB) have potential reno-protective effect by reducing proteinuria, lowering intra-glomerular pressure, and exerting antif i brotic effects. In children with CKD, ACEI have been bene fi cial in the presence of hypertension and proteinuria. The combination therapy of ACEI and ARB is not yet recommended as a part of standard care.
Phosphorus control: Studies in adults reveal that phosphorus restriction may help retard progression of CKD.
(d) Dietary protein restriction: Children are in a dynamic phase of growth and cannot afford to have restriction in calorie or protein intake. (e) (f) P
rophylactic antibiotics in children with recurrent UTIs; consider urological interventions (clean intermittent catheterization, surgery) when indicated.
Ensure adequate volume status (an issue in children with polyuric CKD).
What are the. Indication for. Tenal replacement therapy?
Laboratory criteria:
GFR <15 ml/min/m •
2, refractory hyperkalemia, hyperphosphatemia, and
metabolic acidosis.
Clinical criteria:
Children with symptoms of nausea, vomiting, malnutrition, growth retardation, fl uid overload, hypertension, and uremia, despite optimal medical management.
• Renal transplantation is the renal replacement therapy of choice in children, offering a near normal life to a child with end-stage renal disease ().
For children requiring dialysis while awaiting transplantation or for children unable to receive a transplant, peritoneal dialysis is generally the preferred choice as it is child friendly, potentially less costly than in-center hemodialysis, can be offered at home, preserves vascular access, and is more feasible in small infants than hemodialysis.
Superintendent, ICH.