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Summary

t s 80 GA, days M a 60 660 n i 40 480 a l 20 360

P 0

0 7 10 15 21 28 Age, days Versmold HT et al (1981) Pediatrics 67:607 This on-demand teaching session will cover a comprehensive overview of Chronic Kidney Disease and Renal Transplantation, with case presentation and detailed information regarding factors predictive of long-term prognosis. Led by Dr. Stephen Marks, a leading Consultant Paediatric Nephologists with Great Ormond Street Hospital for Children NHS Foundation Trust and UCL GOS Institute of Child Health, London, UK, medical professionals will explore the specific functions of the kidney, normal age-related renal function, and neonatal renal failure and management. Assessment of renal function, prognosis of PUV, and neonatal vulnerability to renal failure will also be discussed. Don't miss this informative session!

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Description

This sessions is UKMLA geared to aid with revision on Nephrology and Renal System.

Speaker: Professor Stephen Marks

45 minutes lecture with 15 minutes question time in the end.

Learning objectives

a % n t y 50 m 0 < 1000 1045 1123 1366 1548 1772 >2500

            Birth weight (g)  Estimate of GFR (ml/min/1.73m2)

          Derived from Calcagno A et al (1993) Pediatrics 92:574 Learning Objectives:

1.Identify the functions and normal age-related renal function of the kidney 2.Distinguish between AKI, CKD, AKI on CKD and ESKD 3.Evaluate factors predictive of patient long-term prognosis 4.Calculate and illustrate neonatal renal function with plasma creatinine 5.Implement an appropriate assessment of renal function for neonates using Cockcroft-Gault equation, Schwartz formula or clearance of a substance.

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Chronic kidney disease and renal transplantation Stephen Marks Consultant Paediatric Nephrologist Great Ormond Street Hospital for Children NHS Foundation Trust and UCL GOS Institute of Child Health, London, UK Medic Learn, UKMLA Tuesday 14 November 2023 Introduction • Case presentation • Functions of kidney • Normal age-related renal function • Renal dysfunction – AKI, CKD, AKI on CKD and ESKD • Neonatal renal failure and management Case presentation - 1 • Premature male infant – 34 + 6 weeks gestation, birth weight 3.35kg • Maternal multigravida • Normal antenatal ultrasounds – at 6 and 12 weeks gestation • Antenatal diagnosis of right hydronephrosis – detected at 20 weeks gestation – contralateral kidney is bright Case presentation - 2 • Bilateral hydronephrosis with increased echogenic kidneys, distended bladder and oligohydramnios – at 34 weeks gestation, so induction of labour at 34+6w • Respiratory distress syndrome (no pneumothorax) – requiring ventilation for 5 days and NICU for 8 days • Neonatal interventions – including insertion of suprapubic catheter for 5 weeks – insertion of bilateral nephrostomies for 2 weeks – maximum plasma creatinine of 288µmol/l – received blood transfusionMCUG - valve Progress notes • MCUG confirms posterior urethral valves • No evidence of vesicoureteric junction obstruction on nephrostogram – > resection of posterior urethral valves • Cystoscopy and re-do resection of left sided remaining posterior urethral valve leaflet at 1m • What factors are predictive of this patient’s long term prognosis ? Prognosis of PUV • Important factors – bilateral renal dysplasia, VUR and bladder function – episodes of UTI, hypotension, dehydration – development of proteinuria and hypertension • Follow-up at 17 months – growing and developing normally • weight = 10.8kg (above 25 centile) • height = 81.9cm (on 50 centile) • head circumference 47.5cm (9 centile) – normotensive at 88/58mmHg without proteinuria – on NaHCO3, sytron and trimethoprim prophylaxis 2 – GFR = 97ml/min/1.73m (when PCr = 33µmol/l) at 15m Functions of kidney • Remove waste and foreign materials, at the least cost in useful materials and energy • Regulate (homeostasis) body’s water, electrolyte levels, and the acid-base balance • To do the above over a wide range of water, salt and protein dietary intakes and degrees of muscular activity • Allow cells to act on blood and an ultrafiltrate of blood • Otherwise assist body’s functions Neonatal vulnerability to renal failure • The newborn infant is at special risk of developing renal failure because of ‘state of chronic insufficiency’ – low blood pressure – elevated renal vascular resistance – low renal blood flow – low glomerular filtration rateAortic Blood Pressure in VLBW infants BW 750 g 1000 g Mean BP 33 (24 - 42)35 (25 - 44) Systolic BP 44 (34 - 54)49 (39 - 59) Diastolic BP 24 (14 - 34)26 (16 - 36) Values (mmHg) measured during the first hours of life Versmold HT et al (1981) Pediatrics 67:607 Assessment of neonatal renal function • Where do you start ? Assessment of renal function - 1 • Plasma creatinine – initial values reflection of maternal creatinine – rises progressively throughout childhood – according to height and muscle bulk – normal newborn 20+ rising to 100µmol/l after pubertal development in adolescence – does not rise until renal function has halved – creatinine may not be raised in a child who is small and thin due to CKD Relation between foetal and m2.0rnal plasma creatinine e e i n t1.6 a e r c1.2 c m r e1.0 s l0.8 a n e t F a0.4 M 0 20 25 30 35 40 Weeks of gestation Guignard JP, DrukkerA (1999) Pediatrics 103(4):e49 Plasma creatinine in premature neonates GA< 27 weeks 140 ) GA27-28 weeks l 120 GA29-30 weeks o GA31-32 weeks ( 100 e n 80 t r 60 c 40 u e 20 S 0 0 1 2 3 4 5 6 7 10 1724 31 38 45 52 Days of life Adapted from Gallini F et al (2000) Pediatr Nephrol 15:119-124 200 Neonatal plasma 180 creatinine 160 / o 140 m ( 120 n i 100 a r 80 a m 60 l 40 P 20 0 0 5 10 15 20 25 30 35 Age (days) Feldman H, Guignard JP (1982)Arch Dis Child 57:123-126 Plasma creatinine during the first 4 weeks of life l m 90 1000 -1500 g µ 1501 - 2000 g l 80 2001 - 2500 g v 70 term l i 60 i 50 a c 40 a 30 s 20 l P 10 0 - 1 2 3 4 Age, weeks Bueva A, Guignard J-P (1994) Pediatr Res 36: 572. Assessment of renal function - 2 2 • Estimated glomerular filtration rate (ml/min/1.73m ) – can be estimated by Cockcroft-Gault equation in adults CrCl (mls/min) = K x (140 – Age (yrs)) x Weight (kg) Plasma creatinine (µmol/l) • where K = 1.04 for females (n = 95) and K = 1.23 for males (n = 120) • assumes no confounding factors (eg. catabolic states) • must use lean body weight (?weight at 18 years !) – Cockcroft DW, Gault MH(1976) Nephron; 16(1): 31 - 41 Assessment of renal function - 3 • Estimated glomerular filtration rate (ml/min/1.73m ) 2 – can be estimated from Schwartz formula in children as eGFR (mls/min/1.73m ) = K x height (cm) Plasma creatinine (µmol/l) • where K is constant but varies from sources - GOSH: K = 33 - 34 - Age dependent: K = 30 -> 40 -> 45 ->48 -> 62 prem, term, <10kg, <12y / F, adult M K = 29 -> 33 -> 40 -> 45 -> 49 -> 60 prem, LBW, term, <10kg, F, M Assessment of renal function - 4 • Formal glomerular filtration rate (ml/min/1.73m ) 2 – measured by calculating the clearance of a substance 51 (e.g. Cr-EDTA, iohexol, inulin, cystatin C) • after 12 months corrected age – from a timed urine collection for creatinine clearance GFR in neonates e a 100 n 2 t m 80 r 7 i 1*60 r i u / 40 e m 20 m l 0 G 0 1 2 3 4 Age (weeks) Preterm neonate Term neonate adapted from J. Pediatr. 87: 268-272, 1975 What is normal GFR ? Wt BSA GFR Age (kg) (m ) (mls/min; mls/min/1.73m ) Premature 1.0 0.1 0.2 3.5 infants 2.0 0.15 0.5 6 Neonates 3.2 0.2 1.5 13 1 month 4.0 0.25 7.5 52 3 months 6.0 0.35 11 54 1 year 9.2 0.45 30 115 10 years 30.0 1.0 70 120 Adults 70.0 1.73 120 120 - Fawer CL et al (1979) Helv Paediatr Acta 34: 11 - 21 Neonatal renal failure • Acute renal failure / acute kidney injury • Acute on chronic renal failure / kidney disease • Chronic renal failure / kidney disease • End-stage renal failure / kidney disease – requiring dialysis as renal replacement therapy Neonatal acute kidney injury - 1 • Acute kidney injury is defined as rapid, reversible deterioration of GFR associated with nitrogenous waste product accumulation • In a prospective study, 8% of babies in NICU experienced AKI – Stapleton FB et al (1987) Pediatr Nephrol 1:314 • Pre-renal failure (so-called vasomotor nephropathy), is the most common type of AKI in 72% of all neonatal cases – Norman ME, Asadi FK (1979) Pediatrics 63:475 Neonatal acute kidney injury - 2 • Severe AKI occurs when increase in creatinine > 50 µmol/l/day = 5.65 mg/l/day • Oliguria is defined as – reduction in urine output to < 0.5mls/kg/hour in children but < 1ml/kg/hour in neonates (cf. anuria < 1ml/kg/day) • AKI associated with asphyxia is predominantly non-oliguric – Karlowicz MG et al (1995) Pediatr Nephrol 9:718-722 Acute kidney injury • Prerenal • Renal • Postrenal Aetiology - 1 • Pre-renal failure – Decreased true intravascular volume • DEHYDRATION or GASTROINTESTINAL LOSSES • SALT-WASTING or DIABETES INSIPIDUS • THIRD SPACE LOSSES OF SEPSIS AND NS – Circulatory failure • CCF • PERICARDITIS • CARDIAC TAMPONADE – Barratt, Aver and Harmon (1999) Aetiology - 2 • Intrinsic renal disease – Acute tubular necrosis • ISCHAEMIC-HYPOXIC INJURY, DRUG/TOXIN-MEDIATED – Uric acid nephropathy / tumour lysis syndrome – Interstitial nephritis • DRUG-INDUCED OR IDIOPATHIC – Glomerulonephritis (GN) – Vascular lesions • HUS, DRUG-INDUCED • CORTICAL NECROSIS • RENAL ARTERY/VENOUS THROMBOSIS – Infectious causes • SEPSIS AND PYELONEPHRITIS Aetiology - 3 • Obstructive uropathy – Obstruction in a solitary kidney – Bilateral ureteric obstruction – Urethral obstruction Acute kidney injury Prerenal failure Organic failure Hypoxia - anoxia Hyploplasia Dehydration Dysplasia Hypovolaemia Vascular disorders Hypotension ATN Congestive Nephrotoxic agents cardiac failure Pyelonephritis 1 2 Postrenal failure 3 Urethral obstruction or diverticulum Ureterocoele Neurogenic bladder 6179 Complications of neonatal AKI • Fluid, electrolyte and acid-base imbalance – fluid overload, acidosis, hyponatremia – hyperkalemia, hypocalcemia • Convulsions • Sepsis • Renal vascular thrombosis • Arterial hypertensionPresentation of chronic kidney disease • Acute on chronic renal failure / kidney disease – precipitated by infection or dehydration • Antenatal diagnosis of bilateral renal anomalies • Anorexia and lethargy • Polydipsia and polyuria • Failure to grow normally • Bony abnormalities from renal osteodystrophy • Hypertension • Incidental finding of proteinuria When to suspect CKD ? • Creatinine above the normal range -> ?eGFR • Haematological and biochemical abnormalities – anaemia, hyperkalaemia, hypocalcaemia, – hyperphosphataemia, secondary hyperparathyroidism • Bilateral renal anomalies on antenatal scans • Bilateral renal defects on scans – eg. for UTI • Family history of CKD • Persistent proteinuria • After an episode of acute renal failure Causes of childhood CKD • Structural malformati40% • Glomerulonephritis 25% • Hereditary nephropath20% • Systemic diseases 10% • Miscellaneous/unknown5% 11 Annual UK Renal Registry paediatric ESKD data 3%2%2%1% 5% Dysplasia +/- VUR Glomerular diseases 4% 36% Obstructive uropathy 7% Tubulo-interstitial disease Congenital nephrosis Metabolic diseases 7% Renovascular disease Polycystic kidney disease Unknown Malignancy 17% Drug nephrotoxicity 16% Causes of renal dysplasia • Renal dysplasia 83% • MCDK 6% • “Prune belly” 4% • Renal hypoplasia 4% • BOR syndrome 2% • Bardet-Biedl syndrome 2% • Megacystis megaureter 1% APPEARANCE OF KIDNEYS ON RENAL ULTRASOUND Cystic Small Normal sized obstruction Calculi Dysplasia Dysplasia ± Glomerulo- Dysplasia Recurrent UTIs vesico-ureteric nephritides with posterior ± obstruction / reflux urethral reflux valves Autosomal Vascular insults Familial Dysplasia Calcium recessive (venous or nephropathies with VUJ disorders polycystic arterial) obstruction kidney disease Autosomal All causes may Nephrotic Dysplasia Hyperoxaluria dominant result in small syndromes with PUJ polycystic kidneys at obstruction kidney disease ESRF Tuberous Nephronophthisis Neuropathic Purine sclerosis (may be cystic) bladder disorders Glomerulocystic Tubulopathies Cystine diseasesWhich is the most frequent genetic cause for ESKD in the first two decades of life ? Which is the most frequent genetic cause for ESKD in the first two decades of life ? • Juvenile nephronophthisis – recessive cystic kidney disease caused by genetic mutations – including NPHP1, 2, 3 and 4 – positive genetic tests in children presenting in ESRF Gradation of CKD Grade GFR Features 2 ml/min/1.73m 1 > 90 Renal parenchymal disease present 2 60-90 Usually no symptoms but may develop biochemical abnormalities at the lower end of the GFR range 3 30-60 Biochemical abnormalities and in addition may develop poor growth and appetite 4 15-30 Symptoms more severe 5 <15, ESKD Kidney replacement therapy required Clinical features - History • Presenting complaint – hypovolaemia, fever, diarrhoea, vomiting, burns – urinary symptoms; flow; polydipsia; haemorrhage • Drug history • Neonatal, medical and surgical history – including UTIs, growth, failure to thrive • Family history – renal problems, hypertension, RRT and transplant Clinical features - Examination • State of patient • Routine observations – temperature, HR, SBP, RR, SaO , AVPU (GCS) – core-peripheral temperature 2 • Serial plot of weights, heights and OFC • State of hydration – peripheral perfusion, oedema • Signs of cardiac failure • Clinical clues of multi-system disease • Palpable kidneys or bladder or masses Investigations - Blood tests • Full blood count, blood film • Coagulation screen • Cross-match • Serum electrolytes – U&Es, Cl, CO2, urea, creatinine, glucose – LFTs, CK, urate, bone profile – Ca, Mg, PO4, ALP, albumin • Blood culture and CRP • Ionised calcium, PTH and ferritin • Reticulocyte count • Specific investigations as suggested by cause Investigations - Urine tests • Urine dipstick • Urine albumin : creatinine ratio • Urine microscopy and culture • Urine electrolytes • Fractional excretion of sodium (FE Na = U Na x PCr ————— P Na x UCr Investigations - Other tests • ECG • CXR • Echocardiogram • Urgent renal ultrasound scan – principally to exclude obstruction but will also pick up large bright kidneys of an acute process or small kidneys of CKD / dysplasia • Further investigations to consider when older – percutaneous renal biopsy – x-ray of left wrist and hand Investigations - Ongoing tests • U&Es, CO and2creatinine – frequency determined by clinical picture and may be appropriate to perform up to every 6 hours • Ca, PO ,4Mg, albumin, ALP (at least daily) • FBC daily • Urinalysis daily • Urine electrolytes daily (unless on diuretics) • Renal ultrasound scan – if initial images suggest follow-up indicated Fluid balance HYDRATION CLINICAL INITIAL STATUS FEATURES MANAGEMENT * Dehydrated Tachycardic, cool peripheries, Fluid challenge 10-20 ml/kg prolonged CRT, dry mucous normal saline over 1 hour membranes, sunken eyes, UNa <10 (<20 in neonates), FE Na< 1% (< 2.5% in neonates) Euvolaemic Fluid challenge 10-20 ml/kg normal saline over 1 hour, consider furosemide up to 5 mg/kg if no urine response Overloaded Tachycardic, gallop rhythm, Furosemide 5 mg/kg if fluid elevated JVP, oedema, overload is severe; dialysis if hypertension no response to furosemide Patient Progress - 1 • Further fluid boluses of crystalloid or colloid +/- furosemide as indicated by clinical state of hydration and urine output • Monitoring – daily or twice daily weights – accurate input-output recording – at least 4 hourly BP – at least 4 hourly monitoring of peripheral-core temperature gradient Patient Progress - 2 • On going fluid management – initially simplest plan is to give insensible losses (400 ml/m /d or 30 ml/kg/d) and replace UO • GIVE 100% URINE OUTPUT (UO) IF EUVOLAEMIC • RESTRICT TO 50-75% UO IF OVERLOADED • MODIFIED TO FLUID RESTRICTION IF ON DIALYSIS OR URINE OUTPUT ESTABLISHED • In polyuric recovery phase – replace urine output with insensible losses for 24 hours, then set fluid target if renal function continuing to improve Clinical problems • How would you manage 1. Hyperkalaemia 2. Hyponatraemia 3. Hypernatraemia 4. Hypocalcaemia 5. Hyperphosphataemia 6. Acidosis 7. Hypertension ? Treatment - 1 • Hyperkalaemia – cardiac monitor; salbutamol; NaHCO3; – furosemide; Ca resonium and insulin:dextrose • Hyponatraemia 2y to fluid overload – fluid restriction; RRT; hypertonic saline (Na<120) • Hypernatraemia 2y to sodium retention – furosemide; dialysis (if oliguria) • Hypocalcaemia is mulitfactorial – 1-alphahydroxycholecalciferol – calcium supplements Treatment - 2 • Hyperphosphataemia – dietary phosphate restriction – phosphate binders • Acidosis – sodium bicarbonate therapy • Hypertension 2y to fluid overload or alteration in vascular tone – diuretics; medical management; – dialysis if failure to respond to diuretics – dialysis if pulmonary oedema and oliguria Nutritional aspects of neonatal renal failure • AKI associated with catabolic state and malnutrition can develop rapidly • Malnutrition delays AKI recovery and anecdotal evidence that good nutrition improves outcome • Dietetic review for ALL neonates with AKI to prescribe low K, low PO d4et • Aim for at least maintenance calorie intake and protein intake of 0.6g/kg • Start nutritional feeds orally or via NG tube to minimise catabolism & uraemia: IF NOT TPNDrug dosages in renal dysfunction • For the purposes of correcting drug doses according to GFR – assume GFR < 20mls/min/1.73m before recovery – change of GFR is important and drug doses may need to be revised regularly • Many drugs require decreased doses or prolonged dosage interval in renal failure – consult formulary and pharmacist for advice • Best to avoid known nephrotoxic drugs Prognosis • Various reports as various definitions – definition of AKI (rise in Cr vs. PD or HD) – definition of outcome (death vs. off dialysis) – centre reporting, quality of basic care – prevention is better than cure – patients included (inc premature neonates) – depend on facilities (eg. CICU)End-stage kidney disease management Renal transplant ESRF management Peritoneal Haemo dialysis -dialysisEnd-stage kidney disease management Renal transplant ESRF management Peritoneal Haemo HOSPITAL dialysis -dialysis or HOMEEnd-stage kidney disease management Renal transplant ESRF management HOSPITAL Peritoneal Haemo HOSPITAL dialysis -dialysis or HOME or HOMEEnd-stage kidney disease management PRE-EMPTIVE vs ON DIALYSIS DECEASED DONOR Renal - en bloc; DBD and DCD kidneys transplant LIVING RELATED / UNRELATED - altruistic - antibody removal - paired / pooled exchange ESRF management HOSPITAL Peritoneal Haemo HOSPITAL dialysis -dialysis or HOME or HOME Individual patient GFR at 2y GFR results 0 10 20 30 40 50 60 70 80 90 100 110 Present at 2 years with acute illness Individual patient GFR at 3y GFR results 0 10 20 30 40 50 60 70 80 90 100 110 One year follow-up Individual patient GFR at 4y GFR results 0 10 20 30 40 50 60 70 80 90 100 110 Two year follow-up Individual patient GFR at 5y GFR results 0 10 20 30 40 50 60 70 80 90 100 110 Three year follow-up - start planning for live-related renal Tx Individual patient GFR at 5.5y GFR results 0 10 20 30 40 50 60 70 80 90 100 110 3.5 year follow-up - intercurrent infection so needs dialysis Individual patient GFR at 6y GFR results 0 10 20 30 40 50 60 70 80 90 100 110 4 year follow-up - received kidney transplant from mum Individual patient GFR at 7y GFR results 0 10 20 30 40 50 60 70 80 90 100 110 5 year follow-up (1y post-Tx) - rejection & infection episodes - worse kidney function Individual patient GFR at 8y GFR results 0 10 20 30 40 50 60 70 80 90 100 110 6 year follow-up (2y post-Tx) - worsening kidney function Individual patient GFR at 9y GFR results 0 10 20 30 40 50 60 70 80 90 100 110 7 year follow-up (3y post-Tx) - worsening kidney function - planning for next kidney transplant Individual patient GFR at 10y GFR results 0 10 20 30 40 50 60 70 80 90 100 110 8 year follow-up (4y post-Tx) - worsening kidney function - requires dialysis Individual patient GFR at 11y GFR results 0 10 20 30 40 50 60 70 80 90 100 110 9 year follow-up (5y post-Tx) - receives second transplant Individual patient GFR at 14y GFR results 0 10 20 30 40 50 60 70 80 90 100 110 12 year follow-up (8y/3y post-Tx) Individual patient GFR at 17y GFR results 0 10 20 30 40 50 60 70 80 90 100 110 15 year follow-up (11y/6y post-Tx) - transferred to adult nephrologists Circular model of ESKD management Normal renal function Pre-ESKD B Transplant x1,2… HD/PD dialysis A Pre-ESKD Summary • Monitoring changes in clinical status is paramount in renal failure – observations – blood and urine test results • Most crucial element to management is fluid balance • Check if clinically acute on chronic renal failure / kidney diseaseQuestions Question 1 • What is the estimated glomerular filtration rate of patient with Stage I chronic kidney disease ? A. >90mls/min/1.73m 2 2 B. 60 to 90mls/min/1.73m C. 30 to 60mls/min/1.73m 2 D. 15 to 30mls/min/1.73m 2 2 E. <15mls/min/1.73m Question 2 • What is the estimated glomerular filtration rate of patient with Stage II chronic kidney disease ? A. >90mls/min/1.73m 2 2 B. 60 to 90mls/min/1.73m C. 30 to 60mls/min/1.73m 2 D. 15 to 30mls/min/1.73m 2 2 E. <15mls/min/1.73m Question 3 • What is the estimated glomerular filtration rate of patient with Stage III chronic kidney disease ? A. >90mls/min/1.73m 2 2 B. 60 to 90mls/min/1.73m C. 30 to 60mls/min/1.73m 2 D. 15 to 30mls/min/1.73m 2 2 E. <15mls/min/1.73m Question 4 • What is the estimated glomerular filtration rate of patient with Stage IV chronic kidney disease ? A. >90mls/min/1.73m 2 2 B. 60 to 90mls/min/1.73m C. 30 to 60mls/min/1.73m 2 D. 15 to 30mls/min/1.73m 2 2 E. <15mls/min/1.73m Question 5 • What is the estimated glomerular filtration rate of patient with Stage V chronic kidney disease ? A. >90mls/min/1.73m 2 2 B. 60 to 90mls/min/1.73m C. 30 to 60mls/min/1.73m 2 D. 15 to 30mls/min/1.73m 2 2 E. <15mls/min/1.73m Question 6 • Which of the following would not be part of an effective management plan for hyperkalaemia ? A. Calcium carbonate B. Calcium gluconate C. Calcium resonium D. Cardiac monitor E. Furosemide F. Insulin and dextrose infusion G. Salbutamol H. Sodium bicarbonate Question 1 • What is the estimated glomerular filtration rate of patient with Stage I chronic kidney disease ? A. >90mls/min/1.73m 2 2 B. 60 to 90mls/min/1.73m C. 30 to 60mls/min/1.73m 2 D. 15 to 30mls/min/1.73m 2 2 E. <15mls/min/1.73m Question 1 • What is the estimated glomerular filtration rate of patient with Stage I chronic kidney disease ? A. >90mls/min/1.73m 2 2 B. 60 to 90mls/min/1.73m C. 30 to 60mls/min/1.73m 2 D. 15 to 30mls/min/1.73m 2 2 E. <15mls/min/1.73m Question 2 • What is the estimated glomerular filtration rate of patient with Stage II chronic kidney disease ? A. >90mls/min/1.73m 2 2 B. 60 to 90mls/min/1.73m C. 30 to 60mls/min/1.73m 2 D. 15 to 30mls/min/1.73m 2 2 E. <15mls/min/1.73m Question 2 • What is the estimated glomerular filtration rate of patient with Stage II chronic kidney disease ? A. >90mls/min/1.73m 2 2 B. 60 to 90mls/min/1.73m C. 30 to 60mls/min/1.73m 2 D. 15 to 30mls/min/1.73m 2 2 E. <15mls/min/1.73m Question 3 • What is the estimated glomerular filtration rate of patient with Stage III chronic kidney disease ? A. >90mls/min/1.73m 2 2 B. 60 to 90mls/min/1.73m C. 30 to 60mls/min/1.73m 2 D. 15 to 30mls/min/1.73m 2 2 E. <15mls/min/1.73m Question 3 • What is the estimated glomerular filtration rate of patient with Stage III chronic kidney disease ? A. >90mls/min/1.73m 2 2 B. 60 to 90mls/min/1.73m C. 30 to 60mls/min/1.73m 2 D. 15 to 30mls/min/1.73m 2 2 E. <15mls/min/1.73m Question 4 • What is the estimated glomerular filtration rate of patient with Stage IV chronic kidney disease ? A. >90mls/min/1.73m 2 2 B. 60 to 90mls/min/1.73m C. 30 to 60mls/min/1.73m 2 D. 15 to 30mls/min/1.73m 2 2 E. <15mls/min/1.73m Question 4 • What is the estimated glomerular filtration rate of patient with Stage IV chronic kidney disease ? A. >90mls/min/1.73m 2 2 B. 60 to 90mls/min/1.73m C. 30 to 60mls/min/1.73m 2 D. 15 to 30mls/min/1.73m 2 2 E. <15mls/min/1.73m Question 5 • What is the estimated glomerular filtration rate of patient with Stage V chronic kidney disease ? A. >90mls/min/1.73m 2 2 B. 60 to 90mls/min/1.73m C. 30 to 60mls/min/1.73m 2 D. 15 to 30mls/min/1.73m 2 2 E. <15mls/min/1.73m Question 5 • What is the estimated glomerular filtration rate of patient with Stage V chronic kidney disease ? A. >90mls/min/1.73m 2 2 B. 60 to 90mls/min/1.73m C. 30 to 60mls/min/1.73m 2 D. 15 to 30mls/min/1.73m 2 2 E. <15mls/min/1.73m Question 6 • Which of the following would not be part of an effective management plan for hyperkalaemia ? A. Calcium carbonate B. Calcium gluconate C. Calcium resonium D. Cardiac monitor E. Furosemide F. Insulin and dextrose infusion G. Salbutamol H. Sodium bicarbonate Question 6 • Which of the following would not be part of an effective management plan for hyperkalaemia ? A. Calcium carbonate B. Calcium gluconate C. Calcium resonium D. Cardiac monitor E. Furosemide F. Insulin and dextrose infusion G. Salbutamol H. Sodium bicarbonateAny questions ?