NEPHROLOGY III.pptx

NEPHROLOGY III ACUTE KIDNEY INJURY(ACUTE RENAL FALIURE) AND CHRONIC KIDNEY DISEASE (CHRONIC RENAL FALIURE) Dr Ugolee Jerry .C. ACUTE KINDNEY INJURY Definition: Acute Kidney Injury (Acute renal failure) is an abrupt or sudden inability of the kidneys to excrete metabolic waste products as well as maintain normal body chemistry and fluid balance. 2 ACUTE KIDNEY INJURY It is characterised by a reversible increase in blood concentration of creatinine and nitrogenous waste products and failure of the kidney to regulate fluid and electrolyte homeostasis. 3 ACUTE KIDNEY INJURY It is commonly associated with - : Oliguria Abrupt Elevation in Serum Creatinine Dys-electrolyteamia and acid base disturbances. 4 ACUTE KIDNEY INJURY Classification: Multiple definitions for AKI obviously led to a great disparity in the reported incidence of AKI. Therefore, it became crucial to establish a consensual and accurate definition of AKI that could ideally be used worldwide, hence the various classifications by various nephrology bodies. 5 ACUTE KIDNEY INJURY Classification: The RIFLE classification is based on Serum Creatinine and Urine Output evaluation. It considers three severity classes of AKI (Risk, Injury and Failure), and two outcome classes (Loss of kidney function and Endstage kidney disease). 6 ACUTE KIDNEY INJURY RIFLE CLASSIFICATION: • R stands for Risk • I stands for Injury • F stands for Failure • L stands for Loss • E stands for End stage renal Disease 7 RIFLE CRITERIA (ADQI) Class GFR UO Risk ↑ SCr × 1.5 or ↓ GFR >25% <0.5 mL/kg/h × 6 h Injury ↑ SCr × 2 or ↓ GFR >50% <0.5 mL/kg/h × 12 h Failure ↑ SCr × 3 or ↓ GFR >75% or if baseline SCr ≥353.6 μmol/L(≥4 mg/dL) <0.3 mL/kg/h × 24 h or anuria × 12 h Loss of kidney Complete loss of kidney function >4 function weeks End-stage kidney disease Complete loss of kidney function >3 months 8 PAEDIATRIC RIFLE CRITERIA STAGE % REDUCTION IN DEGREE OF GFR CREATININE INCREASE URINE OUTPUT IN ML/KG/HR RISK 25 1.5 X BASELINE < 0.5 FOR HRS INJURY 50 2.0 X BASELINE < 0.5 FOR 16 HRS FAILURE 75 3.0 X BASELINE < 0.3 FOR 24 HRS OR ANURIA FOR 12 HRS OUTCOME PARAMETERS LOSS FAILURE >4 END STAGE FAILURE >3 8 WEEKS MONTHS 9 ACUTE KIDNEY INJURY Classification: The Kidney Disease Improving Global Outcomes (KIDIGO)work group in 2012, combined the RIFLE and AKIN classifications in order to establish one classification of AKI for practice, research and public health. 10 ACUTE KIDNEY INJURY Classification: KDIGO defines AKI as any of the following: •Increase in serum creatinine by 0.3mg/dL or more within 48 hours or •Increase in serum creatinine to 1.5 times baseline or more within the last 7 days or •Urine output less than 0.5 mL/kg/h for 6 hours. 11 Stage 1 Serum Creatinine 1.5-1.9 times baseline or Urine Output < 0.5 mL/kg/h for 6 h ≥0.3 mg/dL increase 2 2-2.9 times baseline < 0.5 mL/kg/h for 12 h 3 times baseline 3 or < 0.3 mL/kg/h for 24 h Increase in serum creatinine to ≥4 mg/dL or or Anuria for ≥12 h Initiation of renal replacement therapy 12 ACUTE KIDNEY INJURY Aetiology: It is customary to classify the causes of acute kidney injury into Pre renal Intrinsic Renal Post renal 13 ACUTE KIDNEY INJURY Pre-renal Circulatory insufficiency - Dehydration (gastroenteritis), blood loss, sepsis, cirrhosis, heart failure, burns, hypoalbuminemia. Intrinsic Renal -AGN, ATN, HUS, Drugs, PKD, Tumor lysis syndrome, Incompatible blood transfusion,. Post-renal -Posterior urethral valves, Stones, tumors, urogenic bladder. 14 ACUTE KIDNEY INJURY PATHOPHYSIOLOGY: Pre renal - AKI results from a decrease in renal blood ﬂow, leading to significant hypoperfusion. This may be due to a decrease in effective circulating volume, loss of vascular tone, or alternatively due to a redistribution of ﬂuid may occur from either reduced oncotic pressure within the blood or from an increased leakage of plasma fluid from vessels as seen in systemic inﬂammatory response syndrome/sepsis Leading ultimately to suboptimal renal perfusion. 15 ACUTE KIDNEY INJURY Pathophysiology: Decreased cardiac output as seen in heart failure or in blood delivery to the kidneys from narrowed or atonic blood vessels are possible causes. More commonly in children, severe dehydration from gastrointestinal tract losses is a leading cause in our environment. Blood loss from acute hemorrhage can also lead to direct reduction in volume and decreased renal perfusion. 16 ACUTE KIDNEY INJURY Pathophysiology: Intrinsic AKI refers to direct renal parenchymal damage or dysfunction. Categories include AKI associated with tubular, interstitial, glomerular, or vascular damage and nephrotoxin exposure. A common cause of intrinsic AKI is transformation of prerenal AKI to acute tubular necrosis (ATN) after prolonged hypoperfusion. The damage seen from prolonged hypoperfusion can range from mild tubular injury to cell death. Most intrinsic ARF cases are associated with ATN from prolonged ischemia or toxic injury. 17 ACUTE KIDNEY INJURY Pathophysiology: Nephrotoxin exposure is an increasingly common cause of intrinsic AKI, particularly in hospitalized patients. Common drugs implicated in AKI include aminoglycosides, amphotericin, chemotherapeutic agents. Radiocontrast agents used during radiological investigations are a signiﬁcant cause of nephrotoxin related AKI. 18 ACUTE KIDNEY INJURY Pathophysiology: Post renal AKI results from obstructive processes that block urine ﬂow. Obstruction of the urinary tract initially causes an increase in tubular pressure, which decreases the filtration driving force leading to stasis and a back pressure. 19 DIFFERENTIATING BETWEEN PRE RENAL AND RENAL AKI PARAMETER PRE RENAL AKI RENAL AKI Urine Osmolality > 500 mOsmols/kg < 350 mOsmols/kg Urine Specific gravity > 1020 < 1010 Urine Sodium < 20 mEq/l > 40 mEq/l Sodium < 1% > 1% Urine Plasma Creatinine ratio > 40 < 20 Urine Plasma Urea ratio >8 <3 Urine Microscopy Normal Many RBCs, Granular casts, RBC casts Fractional Excretion of 20 ACUTE KIDNEY INJURY Management: A quick history is taken to determine the most likely precipitating cause, ask about symptoms that may include diarrhoea and vomiting, bleeding from accidents, circumcision site, burns and fluid loss, body swelling, haematuria, following antecedent sore throat or skin infection, ingestion of drugs or poisonous agents (herbal concoctions), dysuria, poor urinary stream, abdominal pain, fever, convulsions. 21 ACUTE KIDNEY INJURY Clinical Features: Symptoms directly attributable to renal failure include - : • Oliguria/ anuria ( Oliguric Phase) • Body swelling • Tachypnea /dyspnea • Convulsions • Coma 22 ACUTE KIDNEY INJURY Clinical Features: physical findings usually results from the hypovolaemic state which follows loss of body fluids, the may include; loss of skin tugor, a dry buccal mucosa, sunken eyes, delayed capillary refill, a small pulse volume, low blood pressure and depressed anterior fontanelle. 23 ACUTE KIDNEY INJURY INVESTIGATIONS: Urine dipstick test for protein, blood, etc Urine specific gravity, Sodium content. Urine microscopy for RBC, casts, leucocytes. Serum Electrolytes, Urea, Creatinine. Serum Proteins, Total and albumin. 24 ACUTE KIDNEY INJURY INVESTIGATIONS: Serum calcium, Phosphate Magnesium. FBC, Blood Culture. ASO titre, Serum complement C3. Throat swab, Skin swab for MCS. Ultrasound scan ( KUB). 25 ACUTE KIDNEY INJURY Treatment: treatment goalsMaintenance of electrolyte balance. Maintenance of fluid balance. Treatment of cause of AKI. Treatment of hypertension. 26 ACUTE KINDNEY INJURY Treatment: Adequate nutrition. Treatment of emerging complications. Prevention of further nephrotoxicity – : - harmful drugs (genticin), poisons, concoctions. 27 ACUTE KIDNEY INJURY Treatment: In patients with depleted circulatory volume with severe dehydration and/or signs of shock, give fluid challenge with 20mls /kg of normal saline over 30 minutes ( 1hr for infants). Can be repeated if no urine in 1 hour. IV Frusemide 2mg/kg can be given as well, watch out for urine production with strict input/output charting. If urine is passed and vital signs are corrected, continue rehydration process. Subsequent days give equivalent of previous day’s fluid out put (urine) plus insensible loss (400mls/m²/day on the average). 28 ACUTE KIDNEY INJURY Correction of Electrolyte Derangement Hyperkalaemia is the most important electrolyte derangement ECG monitoring is useful in evaluation. For Levels above 6.5mmol/L -: Give 8.4% sodium bicarbonate 2 mmol/kg over 20minutes to correct acidosis, give 10% glucose 1gm/kg/hr and soluble insulin 0.1unit /kg/hr IV as continuous infusion (drives potassium into cells). Give 10% Calcium gluconate IV 0.5 ml/kg over 5-10 minutes (ameliorates the toxic effect of potassium on the myocardium). 29 ACUTE KIDNEY INJURY Correction of electrolyte derangement: Give IV Salbutamol 4 mcg/kg over 20mins(aids shift of potassium into cells).Can also be given by nebulizer. Sodium polystyrene sulfonate can be given orally with sorbitol or rectally as enema 1 gm/kg/dose twice daily. It exchanges potassium for sodium( ion exchange resins). Metabolic acidosis tends to correct itself over time. 30 ACUTE KIDNEY INJURY Treatment: Hypertension is a very important physical sign that can result in hypertensive encephalopathy. Severe hypertension is managed withHydrallazine 0.1 – 0.3 mg/kg IV over 5 -10 minutes. Diaxoxide 1 – 3 mg/kg IV bolus. Labetalol 0.2mg/kg IV bolus over 2mins. Nifedipine 0.2- 0.5 mg /kg oral. 31 ACUTE KIDNEY INJURY Nutrition • Adequate caloric intake (at least 100 kilocals/kg/day). • Protein diet beginning with 0.5 gm/kg/day on the second day. • Low salt diet. • Avoid food items rich in potassium and phosphates( banana, plantain) 32 ACUTE KIDNEY INJURY PARAMETERS MONITORED • Strict fluid input- output chart • Daily dipstick urinalysis • Daily weighing • Blood pressure - at least 2hrly on day 1 Modify interval subsequently as appropriate 33 ACUTE KIDNEY INJURY • If the patient deteriorates in spite of these measures, then dialysis, either peritoneal or haemodialysis has to be carried out. • In centers where facilities are readily available, dialysis is undertaken much earlier when a patient goes into acute renal failure. 34 ACUTE KIDNEY INJURY Indications for Dialysis • Fluid overload with pulmonary oedema and congestive cardiac failure refractory to treatment. • Uncontrolled hypertension. • Hyperkalemia (≥7mmol/L) unresponsive to conservative treatment, or serum urea greater than 150 mg/dl. • Serum bicarbonate < 12mmol/L. • Clinical deterioration with convulsions and coma. • Multiple organ failure. 35 ACUTE KIDNEY INJURY Prognosis: Determined by • Type of precipitating cause. • Promptness and adequacy of management. • Most patients recover if properly managed. 36 CHRONIC KIDNEY DISEASE DEFINITIONS: • The term CHRONIC KIDNEY DISEASE (CKD) is used to describe patients with kidney damage or decreased level of renal function for three months or more irrespective of the underlying aetiology. • Chronic renal failure is defined as a progressive and irreversible reduction in GFR accompanied by increasing biochemical and clinical manifestations as the renal function CHRONIC KIDNEY DISEASE DEFINITIONS: • Chronic kidney disease (CKD) is Kidney damage for ≥3 months, as defined by structural or functional abnormalities of the kidney, with or without decreased GFR OR GFR <60 mL/min/1.73m2 for ≥3 months, with or without kidney damage. CHRONIC KIDNEY DISEASE DEFINITION: • Once established, CKD progresses and becomes irreversible because the adaptive hyperfiltration of the remaining nephrons leads to the vicious cycle of nephron loss. • Screening for stages I and II (Identifying those with microalbuminuria/overt proteinuria) and treating them can slow or prevent the progression of the kidney disease. CHRONIC KIDNEY DISEASE HOW TO CALCULATE GFR: SCHWARTZ FORMULAGFR (ml/min/1.73m 2) = K x Height(cm) serum creatinine(mg/dl) Where K is: 0.3 for LBW < 1 year 0.45 for infants 0.55 for children and adolescent females 0.7 for adolescent males 0.413 (CKD patients irrespective of age). CHRONIC KIDNEY DISEASE CLASSIFICATION: CKD is divided into 5 stages, based on the level of the GFR. This has resulted in standardized definitions and categorization of the disease • Stage I Slight kidney damage with normal or increased filtration GFR > 90 ml/min/1.73 m 2 • Stage II Mild decrease in kidney function GFR = 60-89 ml/min/1.73 m 2 CHRONIC KIDNEY DISEASE CLASSIFICATION: • Stage III Moderate decrease in kidney function GFR = 30-59ml/min/1.73m 2 • Stage IV Severe decrease in kidney function GFR = 15-29ml/min/1.73m 2 • Stage V Kidney failure: requiring dialysis or transplantation. GFR < 15ml/min/1.73m 2 CHRONIC KIDNEY DISEASE CLASSIFICATION: K/DOQI Stage Description 1 2 3 4 5 GFR(ml/min/m2 Kidney damage/normal ≥90 Mild renal insufficiency 60-89 Moderate renal insufficiency 30-59 Severe renal insufficiency 15-29 End Stage Kidney Failure <15 CHRONIC KIDNEY DISEASE CLASSIFICATION: • It may also be is categorised into; -Mild chronic renal insufficiency – GFR 50 – 75 ml/min/1.73m2 -Moderate renal insufficiency – GFR 25-50ml/min/1.73m2 -Chronic renal failure – GFR 10-25ml/min/1.73m2 -End stage renal disease (ESRD) - GFR < 10ml/min/1.73m2 CHRONIC KIDNEY DISEASE AETIOLOGY: It may be the result of -congenital, -acquired, inherited or metabolic renal disease. under the age of 5 years • Bilateral renal hypoplasia • Dysplasic kidneys • Obstruction of the urinary tract e.g. PUV, PUJ • Congenital single kidney • Reflux nephropathy CHRONIC KIDNEY DISEASE AETIOLOGY: Whereas after 5 years of age • Glomerulonephritis (FSGN, MPGN, PSGN) • Haemolytic-uraemic syndrome • Pyelonephritis (acute and chronic) • Nephrotic syndrome • HIVAN • Bilateral Wilm’s tumour • Systemic Lupus Erythematosus • Alport’s syndrome • Cystic disease CHRONIC KIDNEY DISEASE AETIOLOGY: common causes in our environment include 1. Glomerulonephtitis – FSGN,CGN 2. Obstructive Uropathy e.g. PUV, PUJ obstruction, renal stones 3. Nephrotic Syndrome 4. Chronic Pyelonephritis 5. Reflux nephropathy 6. Developmental anomalies e.g. Bilateral renal CHRONIC KIDNEY DISEASE • PATHOGENESIS: Once a critical level of renal functional deterioration is reached, progression to end-stage renal failure is inevitable. The precise mechanism resulting in progressive functional deterioration is unclear, but factors that may play important roles include: • 1. Ongoing immunologic injury • 2. Haemodynamic mediated hyperfiltration in some glomeruli • 3. Dietary protein and phosphorus intake • 4. Persistent proteinuria • 5. Hypertension • 6. Hyperlipidaemia CHRONIC KIDNEY DISEASE • PATHOGENESIS: Ongoing deposition of immune complexes or antiglomerular basement antibodies in the glomerulus may result in persistent and chronic glomerular inflammation that eventually results in scarring. CHRONIC KIDNEY DISEASE • PATHOGENESIS: Hyperfiltration mediated partly by an increase in glomerular blood flow. The increased blood flow increases the driving force for glomerular filtration in the surviving nephrons, damage these glomeruli through the direct effect of the elevated hydrostatic pressure on the integrity of the capillary wall resulting in increase in passage of protein across the capillary wall. This ultimately leads to changes in the mesangium and epithelial cells with the development of glomerular sclerosis. CHRONIC KIDNEY DISEASE PATHOGENESIS: • Persistent proteinuria and/or systemic hypertension from any cause may directly damage the glomerular capillary wall resulting in glomerular sclerosis and initiation of hyperfiltration. • Hyperlipidaemia may adversely affect glomerular function through oxidant mediated injury. CHRONIC KIDNEY DISEASE CLINICAL FEATURES: • Oedema • Oliguria • Stunting from growth retardation • Sallow complexion(from anaemia) • Brown skin pigments associated with pruritus and purpura • Vomiting and diarrhoea • Renal osteodystrophy CHRONIC KIDNEY DISEASE CLINICAL FEATURES : Poor concentration at school Lethargy Anorexia Hypertension In infants • Dribbling of urine • Poor feeding • Failure to thrive • • • • Easy fatigueability CHRONIC KIDNEY DISEASE INVESTIGATIONS: Urinalysis, MCS – Proteinuria, haematuria, bacteriuria Hb level (normocytic, normochromic anaemia) Electrolytes (hyponatraemia, hyperkalaemia, metabolic acidosis) BUN (increased creatinine and urea levels) Ca, PO4 levels (hypocalcaemia, hyperphosphataemia) CHRONIC KIDNEY DISEASE INVESTIGATIONS: Alkaline phosphatase activity - Increased Parathyroid hormone levels - Elevated Chest X-ray (Cardiomegaly) and Echocardiography to assess cardiac function MCUG in cases of PUV Serum albumin, Zinc, transferrin, folic acid, & iron levels CHRONIC KIDNEY DISEASE COMPLICATIONS: • Urinary concentrating defect -Solute diuresis -Tubular damage • Hyperkalemia -Metabolic acidosis -Excessive potassium intake. CHRONIC KIDNEY DISEASE COMPLICATIONS: • Hyporeninemic hypoaldosteronism • Renal osteodystrophy -Impaired renal production of 1, 25dihydroxycholecalciferol -Hyperphosphatemia -Hypocalcemia -Secondary hyperparathyroidism CHRONIC KIDNEY DISEASE COMPLICATIONS: • Growth retardation -Inadequate caloric intake -Renal osteodystrophy -Metabolic acidosis -Anemia -Growth hormone resistance CHRONIC KIDNEY DISEASE COMPLICATIONS: • Anemia -decreased erythropoietin production -iron deficiency -folate deficiency -vitamin B12 deficiency -decreased erythrocyte survival CHRONIC KIDNEY DISEASE COMPLICATIONS: • Bleeding tendency Infection -defective platelet function • Increased susceptibility to infections -defective granulocyte function -impaired cellular immune functions -indwelling dialysis catheters CHRONIC KIDNEY DISEASE COMPLICATIONS: • Neurologic symptoms ( uremic encephalopathy: coma, poor concentration, headache, drowsiness, memory loss, seizures, peripheral neuropathy) • Gastrointestinal symptoms (feeding intolerance, anorexia, abdominal pain, gastroesophageal reflux, gastritis, upper GI bleeding, constipation) CHRONIC KIDNEY DISEASE COMPLICATIONS: • Hypertension (CVA, volume overload). • Pulmonary Oedema. • Hyperlipidemia (decreased plasma lipoprotein lipase activity). • Pericarditis/cardiomyopathy (Uraemia). • Glucose intolerance (tissue insulin resistance). CHRONIC KIDNEY DISEASE MANAGEMENT: This is a multidisciplinary approach and requires team management. • In developing countries like ours this may be difficult as a result of lack of adequate manpower and personnel. Specialist nurses Dietician Pharmacist Teacher Social worker Psychologist Play therapist Ward nurses Doctors (Paediatric nephrologist, surgeon) CHRONIC KIDNEY DISEASE MANAGEMENT: The treatment of CKD is aimed at: 1. Replacing absent/diminished renal function. 2. Slowing the progression of renal dysfunction by optimal control of hypertension and BP maintenance at <75th centile for age & sex. 3.Minimize renal CaPO4 deposition by CHRONIC KIDNEY DISEASE MANAGEMENT: 4. Prompt treatment of infections, complications and episodes of dehydration can minimize additional loss of renal parenchyma 5. Correct anaemia 6. Control hyperlipidaemia 7. Nutritional support CHRONIC KIDNEY DISEASE MANAGEMENT: Fluid and electrolyte Restrict fluids according to output (Intake = Insensible Loss +previous 24hrs urine output) Remove excess fluid by administration of diuretics or dialysis Limit salt NaHCO3 if serum bicarbonate is 15mmol/L or less CHRONIC KIDNEY DISEASE MANAGEMENT: Anemia and growth retardation • Use of synthetic recombinant human erythropoietin (rHuEpo) and recombinant human growth hormone (rHuGH), beginning early in the course of renal failure treatment and continuing to end stage. • Intravenous or subcutaneous injections of CHRONIC KIDNEY DISEASE MANAGEMENT: Renal Osteodystrophy • Adhere to dietary restrictions for phosphorus and calcium. • Administer phosphate binders eg Tum’s tablet with food (but at least 30 min. apart from iron supplementation) • vitamin D and calcium supplements NB: -avoid use of aluminum-based phosphate binders in children to prevent aluminum toxicity. CHRONIC KIDNEY DISEASE MANAGEMENT: Nutrition Moderate restriction of cow milk is advised because it contains a lot of phosphate. supply any deficiency in water soluble vitamins (which may occur due to inadequate intake). Restrict dietary protein if BUN exceeds 80mg/dL, as the patient may develop nausea, vomiting and anorexia due to accumulation of nitrogenous waste products. CHRONIC KIDNEY DISEASE MANAGEMENT: Nutrition Caloric intake can be enhanced by adding to diet: • unrestricted amounts of carbohydrates, fats and • proteins of high biologic value-that are metabolized primarily to usable amino acids rather than to nitrogenous wastes. E.g. Eggs, milk, meat, fish, and chicken in that order. • Protein is provided at the level of 1.5 g/kg/24 CHRONIC KIDNEY DISEASE MANAGEMENT: Renal replacement therapy • Renal replacement therapy (RRT) is a treatment option to take over function of a failing kidney with the removal of wastes and fluids. • Employed in ESRD, in which renal dysfunction has progressed such that homeostasis and survival can no longer be sustained with native kidney function and medical management. CHRONIC KIDNEY DISEASE MANAGEMENT: Renal replacement therapy(RRT). Types include; • Dialysis • Peritoneal dialysis (PD) • Haemodialysis (HD) • Renal transplant (RT) CHRONIC KIDNEY DISEASE MANAGEMENT: Renal replacement therapy(RRT). • However, RRT is still inaccessible to children in Nigeria due to financial restrictions and inadequate dialysis facilities. • Hospitals offering renal care in Nigeria include St. Nicholas- Lagos, MUTH, OAUTH- Ife, AMKTHKano, UPTH- PH, UCH- Ibadan, LUTH- Lagos, UNTH- Enugu, UNILORINTH, UBTH- Benin, JUTH, BMSH- PH Private hospitals. CHRONIC KIDNEY DISEASE MANAGEMENT: Dialysis- indications • Severe Hyperkalaemia >6.5 mmol/L. • Metabolic acidosis (in a situation where fluid overload prevents NaHCO3 administration) HCO3 < 10mmol/L, pH >7.2 • Creatinine >500umol/L in infants and >300umol/L in older children • Seizures from hypo or hypernatraemia CHRONIC KIDNEY DISEASE MANAGEMENT: Dialysis- indications • Symptoms of uraemia – CNS depression, seizures • Fluid overload with or without severe hypertension or CCF • Calcium/ phosphate imbalance with hypocalcaemic tetany • Recalcitrant pulmonary oedema which does not resolve with lasix • Hypertensive pericarditis CHRONIC KIDNEY DISEASE MANAGEMENT: Peritoneal Dialysis Peritoneal dialysis: uses the body's peritoneum as a semi-permeable filter for toxin and fluid removal. A permanent curled or straight silastic catheter is implanted into the peritoneal cavity. Sterile dialysis solution is instilled through the catheter, allowed to dwell for a prescribed period of time while solutes and excess fluid move indirectly from the serum into the dialysis solution, then CHRONIC KIDNEY DISEASE MANAGEMENT: Peritoneal Dialysis There are two variations of peritoneal dialysis: (a) continuous ambulatory (CAPD), which employs several manual exchanges or cycles during the day with a longer overnight dwell, without use of a machine. (b) continuous cycling (CCPD), which allows a programmed cycling machine to deliver the desired exchanges automatically at night while the child and family sleep, allowing for more CHRONIC KIDNEY DISEASE MANAGEMENT: Peritoneal Dialysis Advantages • Easy to perform and tolerate especially in children and infants. • Better haemodynamic stability and metabolic control. • Less expensive. • Freedom to attend school. CHRONIC KIDNEY DISEASE MANAGEMENT: Peritoneal Dialysis Complications • The most common complication of peritoneal dialysis is peritonitis, which can be mild to severe and ultimately result in loss of membrane integrity prohibiting further use of the peritoneum as a filter. • Other complications include catheter problems of exit site. • Infections. CHRONIC KIDNEY DISEASE MANAGEMENT: Peritoneal Dialysis Complications • The most common complication of peritoneal dialysis is peritonitis, which can be mild to severe and ultimately result in loss of membrane integrity prohibiting further use of the peritoneum as a filter. • Other complications include catheter problems of exit site. • Infections. • Discuss appetite/diet • Review medication • Discuss compliance • Psychosocial issues • Discuss schooling Home Visits Acute PD-6 year old CHRONIC KIDNEY DISEASE MANAGEMENT: Haemodialysis This method provides direct filtration of blood, by osmosis and diffusion across an artificial membrane, for solute and fluid removal. Substances that need to be retained in the blood are contained in a balanced electrolyte dialysate solution or "bath" to be returned to the blood. Through a surgically created vascular access, haemodialysis is performed 2 to 4 times a week CHRONIC KIDNEY DISEASE MANAGEMENT: Haemodialysis Special dialyzers (filtering membrane or "artificial kidney") and blood lines are selected based on the weight and body surface area of the child. Blood flow modeling calculations for clearance are individualized according to the size and status of the child. CHRONIC KIDNEY DISEASE MANAGEMENT: Haemodialysis Advantages Some advantages of haemodialysis include • Immediate improvement in fluid and chemical status. • Short treatment time. • Less demand on the family and child for performing procedures at home. CHRONIC KIDNEY DISEASE MANAGEMENT: Haemodialysis Complications • Greater dietary and fluid compliance. Vascular access difficulties. Other related life-threatening complications of clotting, air embolism, infections, shock, disequilibrium syndrome, hypoglycemia, hypo/hypervolemia or bleeding. • Less independence than with peritoneal dialysis.  CHRONIC KIDNEY DISEASE MANAGEMENT: Renal Transplant Kidney transplantation is universally accepted as the treatment of choice for children with ESRD. Successful transplantation in children with ESRD not only ameliorates uraemic symptoms but also allows for significant improvement of delayed skeletal growth, sexual maturation, cognitive performance and psychosocial functioning. The child with a well functioning kidney transplant can enjoy a quality of life that cannot be achieved by any form of dialysis therapy. CHRONIC KIDNEY DISEASE MANAGEMENT: Renal Transplant • Transplantation result in better survival than dialysis for paediatric patients of all ages. • Five year survival rates in transplant patients are close to 95% whereas in dialyzed patients the survival rates are about 80%. First Transplant done 6/3/2000 (on an adult!) 12/4/23 Nigerian Association of Nephrology 12/4/23 Nigerian Association of Nephrology

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