Download as PDF, PPTX
aki_vs_ckd2015.pdf the differences between aki and ckd
- 1. AKI VS CKD FRACPcourse 2015 OVERVIEW How to tell the difference between acute and chronic kidney disease for exam purposes How to work out whether is it glomerular or tubular and what the cause is Some background info time permitting SOME DEFINITIONS Chronic Kidney Disease ( chronic renal failure) Loss of renal function over a prolonged time This means that there is time for impact on growth, bones ( aka CKD – MBD or renal osteodystrophy) and anaemia. So look for words like short, pale, bones as clues WHAT’S A GFR
- 2. CKD STAGES Stage GFR (ml/min/1.73m 2) DescriptionImpact 1 90+ Normal function but known structural or persistent urine abnormalities Little 2 60‐89 Mildly reduced function As above + estimate rate progression – start to monitor for biochemical abnormalities and growth 3 30‐59 Moderately reduced function Monitor CKD‐ MBD, growth, anaemia, appetite, cardiovascular 4 15‐29 Severely reduced function Symptoms become more severe 5 <15 or dialysis ESKD RRT required MECHANISM OF PROGRESSIVE CKD CAUSES OF PAEDIATRIC CKD NON‐GLOMERULAR Hypoplasia/dysplasia Ciliopathies Nephronopthisis Obstructive uropathy PUV Prune Belly Neurogenic bladder Cystic PKD Tubulopathies Cystinosis GLOMERULAR FSGS Congenital Nephrotic Syndrome Chronic GNs – SLE, MPGN, HSP, IgA, membranous Alport HUS Cortical necrosis DIAGNOSTIC CLUES FOR TYPES OF CKD Glomerular disease – loss of ( sclerosis) and damage to glomeruli lead to retention of salt and water, raised renin and loss of blood and protein in the urine So words that should make you think of a glomerular cause include oliguria, haematuria/proteinuria, hypertension (increased extra cellular fluid and and increased renin) Chronic tubular/tubulointerstitial diseases – concentrating defect so loss of salt and water May have proteinuria ( not all protein is albumin but much less likely to have haematuria) May be resistance to ADH, may also have other electrolyte losses So words that suggest a non glomerular cause include polyuria& polydipsia enuresis / nocturia Always thirsty Loss of other electrolytes in the urine
- 3. CAUSES OF PAEDIATRICCKD NON‐GLOMERULAR Hypoplasia/dysplasia Ciliopathies Nephronopthisis Obstructive uropathy PUV Prune Belly Neurogenic bladder Cystic PKD Tubulopathies Cystinosis Clues CAUSES OF PAEDIATRIC CKD Clues GLOMERULAR FSGS Congenital Nephrotic Syndrome Chronic GNs – SLE, MPGN, HSP, IgA, membranous Alport HUS Cortical necrosis ON THE OTHER HAND ‐ AKI Acute Kidney Injury – previously known as acute renal failure, acute kidney failure etc Sudden onset of loss of kidney function May be presented with exactly the same numbers for renal function but… No time for impact on growth, bone CLINICAL CONTINUUM OF AKI Devarajan, Biomarkers Med 4:265‐80, 2010
- 4. ALSO STAGED –RIFLE CRITERIA WHO GETS AKI FOR EXAM PURPOSES HUS Glomerulonephritis ATN Interstitial nephritis Rhabdomyolysis CLINICAL FEATURES Uraemia Hypervolaemia ( glomerular) /hypovolaemia ( tubular) Hypertension/ hypotension due in part to the above High Potassium, High P04, low Ca, high magnesium or low if tubular Metabolic acidosis Oliguria/anuria ( glomerular), Polyuria (nephrotoxic injury) & electrolyte loss Increased anion gap (Na – (Chl+HCO3))
- 5. AKI VS CKD FRACPcourse 2015 Tonya Kara PRERENAL AKI Decreased perfusion to the kidneys, and as a consequence a reduction in GFR: True volume depletion :bleeding, intestinal/cutaneous loss Effective renal hypoperfusion :decreased arterial pressure ‐ heart failure or septic shock or cirrhosis RENAL Affects renal parenchyma Vascular e.g. RVT, TTP, HUS Glomerular e.g. Post infectious GN, HSP, anti GBM. Interstitial e.g. pyelonephritis, NSAIDs, diuretics Tubular e.g. ATN, aminoglycosides. Aciclovir, tumour lysis POST RENAL Affects the drainage of the kidney: Stones Bladder outlet obstruction Trauma/clots Tumours Sometimes comes up as a question about post obstructive polyuria
- 6. ACUTE Urine osmolality Urine Na(mmol/l) Urinalysis Urea/creat ratio Fractional excretion of Na (%) U Na x P Cr x 100 U Cr x P Na Pre renal ATN > 500 < 350 < 20 > 40 Bland Casts >100 <40 < 1 > 1 HUS Triad: haemolytic anaemia, thrombocytopenia and AKI Categories: Typical: usually diarrhoea positive Atypical: usually diarrhoea negative Pneumococcal Complement disorders ( low C3) TYPICAL HUS Represents 90% HUS childhood Mainly <3 yo Serotype ecoli 0157:h7 most frequent Bloody diarrhea can be complicated by rectal prolapse intussusception, colitis, perforation Extrarenal: CNS 20% Seizures Cranial nerve palsy cerebral oedema coma Aki 1‐14 days after diarrhea Diabetes 5%
- 7. Spontaneous Resolution (85-90%) HUS (~15%) -3 -2 -10 1 2 3 4 5 6 7 Diarrhea Bloody diarrhea HUS FOR THE FRACP History of bloody diarrhoea Full blood count – Hb low, WCC up(Neutrophilia – predictor of disease severity) Plt low Haemolysis screen‐ reticulocyte count, ‐ up LDH, ‐ up Bilirubin, ‐ up haptoglobin ‐ down PT/APTT/ ‐ normal Fibrinogen ‐ up U&Es – UP!! Blood film – fragments, schistocytes ACUTE GLOMERULONEPHRITIS Retention of salt and water leading to hypertension, doe and oliguria Urine contains blood and protein Frequently have low Hb due to fluid retention, high urea in relation to creatinine My quick and dirty guide to telling them apart for exam purposes C3 ANA ANCA Anti GBM C4 FH Other Biopsy Infection IgA ‐ ‐ ‐ ‐ ‐ occ Often boys recurrent IgA At time ANCA associated vasculitis ‐ ‐ High ‐ ‐ ‐ Systemic Multiple causes ‐ SLE low high low systemic “Full house” ‐ Anti GBM ‐ ‐ ‐ present ‐ ‐ May have pulmonary haenorrhag e Linear staining on IF ‐ Alports ‐ ‐ ‐ ‐ ‐ yes Deafness Male relative in ESKD “basket weave” ‐ PIGN low ‐ ‐ ‐ In real life low, in exam normal ‐ Should not be recurrent Few weeks preceding – skin or throat HSP ‐ ‐ ‐ ‐ ‐ ‐ Skin, GI IgA Sometime precipitates MPGN/ C3 glomerulopath y low ‐ ‐ ‐ ‐ occ May have HUS features C3 HUS features without the diarrhoea history
- 8. THINKING RHABDOMAYOLYSIS? Typicalhistory of exercise followed by bright red urine +/ ‐ minus muscle pain Tests to confirm: The dipstick tests +ve for blood but no haematuria on microscopy Urine and serum myoglobin up Very high CK INTERSTITIAL NEPHRITIS Often drug related, can also be autoimmune with associated uveitis Polyuria Tired, generally not right Generalised tubular dysfunction including glycosuria, loss of electrolytes, tubular proteinuria Important differential is nephropthisis – remember growth RECAP ‐CLUES TO ACUTE V CHRONIC Think about things associated with renal disease Growth parameters Anaemia Bones With little blood or protein in the urine think about tubular disease You can usually work out a GN from the story Imaging Small kidneys usually chronic structural disease. Large echogenic kidneys – acute disease – GNs or ARF. PHYSIOLOGIC CONSEQUENCES OF HYPERTENSION AND PROTEINURIA ON CKD
- 9. TIME Haematuria microalbuminuria Proteinuria No Intervention……. Intervention? Albuminuria Proteinuria CKD ESKD Haematuria CKD‐MBD – METABOLIC BONE DISEASE Reduced PO4 excretion, decreased 1,25‐OH VitD3 production n and often low 25‐OH Vit D contribute to raised PTH Abnormal osteoblast and clast activity subperiosteal bone resorption, rickets, slipped epiphyses OTHER ISSUES Anaemia Reduced erythropoietin production by kidney Fe deficiency, ineffective utilisation of Fe Hyperparathyroidism can suppress RBC production Shortened RBC lifespan Significant anaemia occurs when GFR<25ml/min/1.73m2 but EPO production is already reduced at 35‐40ml/min/1.73m2 Tx anaemia reduces progression ‐ ? via decr oxidative stress causing tubular damage and interstitial fibrosis ESAs improve cardiac fn, physical exercise tolerance, school attendance, appetite, cognitive function Acidosis d/t retained anions, tubular dysfunction Increases protein catabolism, impairs GH release, accelerates CKD progression Tx if persistently <20mmol/L
- 11. Figure. Risk‐stratification andtreatment algorithm for high‐risk pediatric populations.Directions: Step 1: Risk stratification by disease process (Table 1). Kavey R W et al. Circulation 2006;114:2710-2738 Copyright © American Heart Association
- 12. TAKE HOME NONEXAM MESSAGE AKI can result in chronic proteinuria Proteinuria is CKD, and untreated will progress CKD affects much more than the kidney Advanced disease is under recognised Overall mortality higher than ALL Good luck for your exam