Acute Kidney Injury (AKI) 1 - PDF

ACUTE KIDNEY INJURY - 1 Dr Andrew Miller ACKNOWLEDGEMENT OF COUNTRY I’d like to begin today by acknowledging and paying respect to the Komumberri people and the Yugembah speaking people, the Minjungbal and Nandawul people, all Elders past, present and emerging on whose land this lecture was prepared...

ACUTE KIDNEY INJURY - 1 Dr Andrew Miller ACKNOWLEDGEMENT OF COUNTRY I’d like to begin today by acknowledging and paying respect to the Komumberri people and the Yugembah speaking people, the Minjungbal and Nandawul people, all Elders past, present and emerging on whose land this lecture was prepared and presented. I’d like to specifically acknowledge the ongoing work that Australian First Nations health workers contribute to our workplace and improvement in health outcomes for all First Nations People. LEARNING OBJECTIVES Describe the aetiology, epidemiology, pathophysiology, clinical features and natural history of AKI Select, justify and interpret appropriate investigations for management of AKI Outline the basic therapeutic principals (pharmacological and non-pharmacological) in the management of AKI LECTURE OUTLINE -1 Epidemiology Definition Physiology Classification Pathophysiology EPIDEMIOLOGY 5000/ million/ year 1.9% of hospital inpatients ~5% of these require dialysis 60% of ICU patients DEFINITION risk criteria understand the best criteria GFR and urine output proteinuria significance Source: P. Kumar & M. Clark: Kumar and Clark’s Clinical Medicine, Eighth Edition Copyright Elsevier. Source: KDIGO (2012). KDIGO 2012 Clinical Practice Guideline for Acute Kidney Injury. https:// kdigo.org/guidelines/ PROGRESSION Source: KDIGO (2012). KDIGO 2012 Clinical Practice Guideline for Acute Kidney Injury. https:// kdigo.org/guidelines/ measuring filtering, not just damage death - from progressing through all stages most are reversible but to a degree to developing kidney injury CREATININE & GFR cellular break down tells how much you are filtering produced a steady state dehydration and diet can influence consider age and body mass creatine is less affected by variables estimate GFR through this Source: P. Kumar & M. Clark: Kumar and Clark’s Clinical Medicine, Eighth Edition Copyright Elsevier. BIOMARKERS Source: S.D Gumbert, F. Kork et al. Perioperative Acute Kidney Injury, Anaesthesiology. 2020; 132:180-204. expensive and not change how we treat patients RISK FACTORS Source: KDIGO (2012). KDIGO 2012 Clinical Practice Guideline for Acute Kidney Injury. https://kdigo.org/ guidelines/ lead to susceptibility DRUG EFFECTS Source: R. Bellomo, J. Kellum, C. Ronco. Acute Kidney Injury, The Lancet. 2012; 380:756-766. medications can cause kideny injury affects nephron, kidney parenchyma Source: J. Kellum & J. Prowle. Paradigms of acute kidney injury in the intensive care setting, Nature Reviews Nephrology. 2018; 14: 217-230. CLASSIFICATION pre-renal injury proximal to afferent arteriole before glomerus post - after renal duct Source: P. Kumar & M. Clark: Kumar and Clark’s Clinical Medicine, Eighth Edition Copyright Elsevier. CLASSIFICATION PRE Hypovolaemia Hypotension Poor Cardiac Output Vascular disease catastrophe Raised Intra-abdominal Pressure INTRA POST Glomerular IE Glomerulonephritis Parenchymal IE Acute Tubular Obstruction (ureters, bladder, Necrosis prostate, urethra or extra Interstitium IE Interstitial renal IE retroperitoneal Nephritis fibrosis, lymph nodes, uterus, etc) Vascular IE vasculitis, microangiopathy, hypertensive crisis microvasculature raised intra-abdominal pressure interruption PRE Is a pre-renal injury really an AKI?? Is the oliguria seen reflective of renal damage?? PHYSIOLOGICAL RESPONSE Source: S.D Gumbert, F. Kork et al. Perioperative Acute Kidney Injury, Anaesthesiology. 2020; 132:180-204. ABNORMAL PHYSIOLOGICAL RESPONSE Source: S.D Gumbert, F. Kork et al. Perioperative Acute Kidney Injury, Anaesthesiology. 2020; 132:180-204. GLOMERULONEPHRITIS Immunological injury to glomeruli Many aetiologies Classification based on syndrome of presentation immunological injury Management principles immunosuppression and managing complications (IE nephrotic syndrome) suppress immune system that causes problem Source: J.L. Jameson, A.S. Fauci, D.L.Kasper, S.L. Hauser, D.L. Longo, J. Loscalzo: Harrison’s Principles of Internal Medicine, 20th Edition Copyright McGraw-Hill Education IGA NEPHROPATHY Incidence? Most common GN Pathophysiology? Mesangial deposits IgA -> response to antigen Associations? Respiratory/ viral illness; CLD/ HSP/ Malignancy Age? Children and young men Treatment? Steroids and ACEi Progression? If proteinuria can lead to ESKD (~25%) Presentation Haematuria, 5% proteinuria POST STREPTOCOCCAL GN Incidence? Used to be most common, less in developed world Pathophysiology? Immune complex deposition, inflammation without necrosis Associations? 1-3 weeks post strep (GAS) infection Age? Children Treatment? Anti-htn, diuretics, salt restriction, ?steroids if slow recovery Progression? Good prognosis, some adults may develop Htn or CKD Presentation Nephritic syndrome MINIMAL CHANGE NEPHROPATHY Incidence? Most common cause nephrotic syndrome Pathophysiology? Immune response ?trigger. Podocytes fuse but otherwise NAD Associations? Atopy, some drugs (NSAID’s, B Lactams, lithium) Age? Children and young men Treatment? Steroids +/- cyclophosphamide Progression? Typically self limited Presentation Nephrotic syndrome FOCAL SEGMENTAL GLOMERULOSCLEROSIS Incidence? Less common Pathophysiology? Circulating factor causes protein leak. Focal -> global sclerosis Associations? Minimal change disease Age? All age groups Treatment? Steroids, cyclosporin, cyclophosphamide Progression? 50% to ESKD in 10 years. Will affect transplanted kidney. Presentation Nephrotic syndrome; massive proteinuria MEMBRANOUS GLOMERULOPATHY Incidence? Less common Pathophysiology? IgG and complement deposits in BM Associations? 75% idiopathic, otherwise drugs/ AI/ neoplasm/ infections Age? Adult males Treatment? Steroids and ACEi Progression? If Htn, renal impairment or older worse prognosis. 40% CKD Presentation Nephrotic syndrome ATN CAUSES Broadly divided into 2 categories Ischaemic Inflammatory/ toxin induced pre-renal injury - to tubules other causes e.g. snake bite toxic response Source: P. Kumar & M. Clark: Kumar and Clark’s Clinical Medicine, Eighth Edition Copyright Elsevier. ATN PHASES Distinct phases of ATN Can overlap Oliguric/ polyuric depending stables and goes back to normal Source: J.L. Jameson, A.S. Fauci, D.L.Kasper, S.L. Hauser, D.L. Longo, J. Loscalzo: Harrison’s Principles of Internal Medicine, 20th Edition Copyright McGraw-Hill Education INTERSTITIAL NEPHRITIS Usually drug related Present with fever, arthralgia and rash Or just AKI in context of new drug May respond to steroids Usually no long term complications Source: P. Kumar & M. Clark: Kumar and Clark’s Clinical Medicine, Eighth Edition Copyright Elsevier. most commonly associated with drugs PYELONEPHRITIS Acute interstitial nephritis Wedge shaped areas of inflammation in renal cortex leads to kidney injury Complicated UTI Host reasons for complication If AKI + UTI then by definition complicated Source: P. Kumar & M. Clark: Kumar and Clark’s Clinical Medicine, Eighth Edition Copyright Elsevier. SEPSIS? Multifactorial kidney injury More than just pre-renal cause kidney injury in multiple ways toxins, microvascular Source: R. Bellomo, J. Kellum, C. Ronco. Acute Kidney Injury, The Lancet. 2012; 380:756-766. Source: J. Kellum & J. Prowle. Paradigms of acute kidney injury in the intensive care setting, Nature Reviews Nephrology. 2018; 14: 217-230. POST RENAL Urinary obstruction leads to AKI From renal pelvis to urethral meatus Intra, luminal, extra obstruction to kidney injury very susceptible back pressure through collecting duct will affect GFR aggressively Hoàng, T. Large ureteric calculus causing severe hydronephrosis. Case study, Radiopaedia.org. (accessed on 10 Oct 2021) https://radiopaedia.org/cases/49032 LECTURE SUMMARY Common problem that will be encountered often Categorise based on anatomical location of lesion Investigations and management all flow from understanding of renal physiology and pathophysiology