Renal Revision Summary General Specific • AKI • Glomerulonephritis Causes Minimal change disease • • Investigation and management FSGS • • Complications Membranous nephropathy • • • CKD MPGN • IgA nephropathy Causes • • Post-streptococcal glomerulonephritis Investigation and management • • Amyloidosis Complications • • • Polycystic kidney disease • Nephrotic vs nephritic syndrome Beware urology • Causes • • SLE (lupus) Investigation and management • Complications • ANCA-associated vasculitides • • Anti-GBM disease 2
Layout for today’s session Renal Mrs Lowe – 86 year-old female Pre-renal 1. Pre-renal Mrs Bridney – 57 year-old female 2. Renal / Intrinsic Mrs Post – 74 year-old female 3. Post-renal Post- renal 4. Complications of all AKI 3
Case-based discussion: 1 History Mrs Lowe is an 86-year-old female who lives in a nursing home. Half of the residents have been suffering from a norovirus outbreak, including Mrs Lowe. She has been vomiting multiple times a day and the staff have noted that she seems more confused than usual. N.B. We will use Mrs Lowe to cover some general points about AKI, as Past medical history includes T2DM, HTN and well as one of the 3 types of AKI. AF. Observations HR 110, BP 89/72, RR 17, SpO2 96%, Temp 37.3 4
Question: 1 5
Case-based discussion: 1 History Mrs Lowe is an 86 year-old female who lives in a nursing home. Half of the residents have been suffering from a norovirus outbreak, including Mrs Lowe. She has been vomiting multiple times a day and the staff have noted that she seems more confused than usual. Past medical history includes T2DM, HTN and AF. Observations HR 110, BP 89/72, RR 17, SpO2 96%, Temp 37.3 6
Case-based discussion: 1 Clerking continued. Observations stabilise and the patient undergoes the following basic investigations over the next 6 hours: Bloods: Urea • 20 mmol/L (2 – 7) Creatinine 200 µmol/L (55-120) • Serum U : Cr • 100 Urine output Hour 1 20ml • Hour 2 20ml • Hour 6 15ml • Weight 50kg • 7
Acute Kidney Injury (AKI) Epidemiology Definition Incidence: 13-18% of hospital admissions Abrupt and sustained decrease in kidney • have AKI [2] function Risk factors: • The KDIGO guidelines [1] : Age • Co-morbidities: HTN, T2DM, CKD • 1. Rise in serum creatinine >26 μ mol/L within 48h Medications • Hypovolaemia • OR Sepsis • High rates of morbidity and mortality (up 2. Rise in serum creatinine >1.5x baseline • to 40%) (before AKI) within 7 days OR 3. Urine output <0.5ml/kg/h for >6 consecutive hours 8
Staging Multiple • Beyond the scope of medical school • To be aware: • 1. RIFLE – risk, injury, loss, failure, ESRD* 2. AKIN – stage 1, stage 2, stage 3 What does a higher stage mean? • Increased length of stay in hospital • Increased length of stay in ICU • Increased mortality • Reduced likelihood of renal recovery • *ESRD = end-stage renal disease 9
Aetiology (pre-renal) Reduce d Renal Volum Systemic cardiac vasculature e loss vasodilatati output on Inflammation Decreased blood flow to glomerulus
Pathophysiology Decreased blood flow to glomerulus Decreased blood filtration Reduced Raised Raised urine output urea creatinine 11
Clinical features (all AKIs) Symptoms Signs Oliguria Peripheral oedema Anuria Chest crackles (pulmonary oedema) Confusion Raised JVP Nausea Haematuria Shortness of breath Proteinuria 12
Question: 2 13
Management First line IV fluid bolus: treat hypovolaemia with 250-500ml boluses of crystalloid (e.g. saline or Hartmann’s) • Serial VBGs: monitor lactate for tissue hypoperfusion • Maintenance fluids: 1L of saline (+20mM K + ) + 2L of 5% dextrose (+20mM K + ) • Suspend common medications that will worsen AKI ACE-inhibitors (e.g. ramipril): dilates efferent arteriole • Diuretics (e.g. bendroflumethiazide): reduce flow through tubular capillaries • NSAIDs (e.g. naproxen): constricts afferent arteriole • Second line KDIGO recommend the use of vasopressors in patients with vasomotor shock • KDIGO do NOT recommend using low-dose dopamine • KDIGO do NOT recommend using diuretics to treat AKI, except in the management of volume • overload 14
Recap AKI is an abrupt and sustained decrease in kidney function • Divided into pre-renal, renal and post-renal causes • Pre-renal causes: • Volume loss • Reduced cardiac output • Systemic vasodilatation • Excessive constriction of afferent arteriole • Distinguishing features: • History • High urea : creatinine ratio • Low urine sodium – kidney can still reabsorb • Management: • Fluid responsive • ICU – if features of vasomotor shock • Stop exacerbating medication, e.g. diuretics, NSAIDs, ACE-i/ARB • 15
Case-based discussion: 2 History Mrs Bridney is a 57-year-old female who is being treated in hospital for sepsis of unknown origin. • Metformin • Enoxaparin Past medical history includes T2DM. • Amoxicillin • Metronidazole In the last 12 hours, she has been noted to have a urinary output of 0.4ml/kg/hour. • Amikacin Despite regular IV fluids and catheterisation this has not improved. Observations HR 104, BP 100/77, SpO2 96%, temp 37.6 16
Question: 3 17
Case-based discussion: 2 History Mrs Bridney is a 57 year-old female who is being treated in hospital for sepsis of unknown origin. • Metformin • Enoxaparin Past medical history includes T2DM. • Amoxicillin • Metronidazole In the last 12 hours, she has been noted to have a urinary output of 0.4ml/kg/hour. • Amikacin Despite regular IV fluids and catheterisation this has not improved. Observations HR 104, BP 100/77, SpO2 96%, temp 37.6 18
Aetiology (renal/intrinsic) 1. Glomerular 2. Interstitial 3. Tubular 4. Kidney vascular supply
Pathophysiology Glomerular Interstitium Acute interstitial nephritis (AIN) • Glomerulonephritis conditions • Neutrophils/eosinophils infiltrate • IgA nephropathy • the interstitium of the kidney FSGS • NSAIDs • MPGN Penicillin • • Diuretics • SLE (lupus nephritis) • May present as acute kidney injury • • Amyloidosis More commonly will present with: • • May present as acute kidney injury Rash • • More commonly will present with Joint pain • nephrotic or nephritic syndrome Eosinophilia • • Beyond the scope of a single lecture on AKI 20
Pathophysiology (cont.) Tubular Renal vascular supply Acute tubular necrosis (ATN) NOT to be confused with glomerular • • blood supply (for ultrafiltration) Death of the tubular cells results in a • clogged tubule and loss of pressure Blood supply to kidney tissue • gradient Can be compromised à infarct • Causes: • E.g. TTP, HUS • Ischaemia • Rhabdomyolysis (e.g. myoglobin) • Aminoglycoside antibiotics • (e.g. amikacin , gentamicin) Lead • Ethylene glycol (anti-freeze) • Good prognosis as tubular cells • continually replace within 1-3 weeks 21
Question: 4 22
Investigations (“the renal workup”) Bloods [3] Type Urea : Creatinine ratio Serum urea : creatinine ratio • Serum free light chains (FLCs) • Pre-renal > 100 : 1 Serum complement (C3, C4) • ANCA, ENA, anti-dsDNA Renal < 40 : 1 • Blood-borne virus serology • Post-renal 40-100 : 1 Urine Dipstick • Worked example: Microscopy: 400x magnification reveals muddy • Urea = 10mmol/L brown casts Creatinine = 250µmol/L Sodium • 10,000 : 250 Imaging 40 : 1 Renal US • Specialist tests Renal biopsy • 23
Management [4] One size does not fit all! Specific to the underlying cause • Some general tips: • Glomerulonephritis will likely require • various immunosuppressive medications à à à ATN will likely recover with suspension of • toxic agent, e.g. suspend amikacin Call the renal team and get help! • 24
Recap AKI is an abrupt and sustained decrease in kidney function • Divided into pre-renal, renal and post-renal causes • Renal causes: • Glomerular • Interstitial • Tubular • Vascular • Distinguishing features: • Unresponsive to fluids or catheterization • Complex medical history • Nephrotoxic agent use • Low urea : creatinine ratio • High urine sodium • Management: • Varying • 25
Case-based discussion: 3 History Mrs Post is a 74-year-old female who is admitted to hospital with suprapubic pain and is passing very little urine in the past 24 hours. She denies dysuria or haematuria. Past medical history includes osteoarthritis and HTN. She takes amlodipine and amitriptyline. Examination reveals suprapubic tenderness. A catheter is easily inserted and Mrs Post cries with immediate relief. 26
Question: 5 27
Aetiology (post-renal) General: Urinary tract infection • Kidney stones • Malignancy • Strictures • Specific: Enlarged prostate (BPH) • Phimosis • Occluded indwelling catheter (common) • Pharmacological • Anti-cholinergics, e.g. amitriptyline • α -adrenergic agonists • Calcium channel blockers •
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