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 Mr Gangfløt – 50-year-old male 1. No treatment Mr Hukkelberg – 50-year-old male 2. Dialysis Mr Mokkelbost – 50-year-old male 3. Kidney transplant 3
Case-based discussion: 1 History You are a medical student on your elective in a developing country. Your next patient is Mr Gangfløt, a 50-year-old gentleman who visits the local doctor to complain about his swollen ankles. He says that this has been bothering him for many months. Past medical history includes HTN and T2DM. On examination, you note pitting oedema up to his knee level, as well as conjunctival pallor. Observations HR 64, BP 174/102, RR 11, SpO2 98%, Temp 37.3 4
Case-based discussion: 1 History Peripheral oedema Causes of bilateral : You are a medical student on your elective in a developing country. Your next patient is Mr Heart • Gangfløt, a 50-year-old gentleman who visits Heart failure • the local doctor to complain about his swollen ankles. He says that this has been bothering Kidney • him for many months. CKD • Nephrotic syndrome • Past medical history includes HTN and T2DM. Liver • On examination, you note pitting oedema up Liver failure • to his knee level, as well as conjunctival pallor. Venous/lymphatic obstruction • Observations Pelvic tumour • HR 64, BP 174/102, RR 11, SpO2 98%, Temp Not your first thought! • 37.3 5
Case-based discussion: 1 eGFR calculation [1] Clerking cont. Serum pro-NT-BNP - normal • Calculated using the MDRD (modification of Serum liver function test • diet in renal disease), which uses the Albumin – 36 (35-50) • following parameters: Bilirubin – 4 (1-17) • 1. C reatinine ALT - 25 (<50) • 2. A ge Serum urea and electrolytes • 3. G ender Urea - 6.9 (2-7) 4. E thnicity • Creatinine - 200 (50-120) • Urine dipstick • eGFR (ml/min/1.73 m 2 ) = Protein ++ • 175 × (S cr ) -1.154 × (Age) -0.203 × (0.742 if Glucose ++ • female) × (1.212 if African American) 6
Chronic Kidney Disease (CKD) Definition Epidemiology Progressive deterioration in renal function • It is estimated that 10% of the general population are thought to have CKD The KDIGO guidelines [2] : • Risk factors: Age • Present for >3 months • Ethnicity: Afro-Caribbean • With implications for health • Co-morbidities: HTN, T2DM, renal disease • Abnormalities of kidney structure or function • Medications • 1. This means ALL patients with an eGFR <60 or; Congenital abnormalities • 2. ANY patient with markers of kidney damage: Urinary tract pathology • Proteinuria • Haematuria • CKD mortality is difficult to assess due to • ACR >3 mg/mmol • the fact that patients with CKD will often Structural abnormalities (e.g. PKD) • die from linked cardiovascular disease Abnormalities on renal biopsy • prior to reaching end-stage renal failure. History of renal transplant • 7
Staging CKD grade GFR range G1 >90 ml/min , with some sign of kidney damage on other tests (if all the kidney tests are normal, there is no CKD) G2 60-89 ml/min with some sign of kidney damage (if kidney tests are normal, there is no CKD) G3a 45-59 ml/min with a mild-moderate reduction in kidney function G3b 30-44 ml/min with a moderate reduction in kidney function G4 15-29 ml/min with a severe reduction in kidney function G5 <15 ml/min , established kidney failure - dialysis or a kidney transplant may be needed 8
Staging Urinary albumin : creatinine ratio (ACR) In addition, CKD is staged by urinary ACR to measure how leaky the glomerulus is to protein • A1 – ACR <3 (mg/mmol) A2 – ACR 3-30 (mg/mmol) • • A3 – ACR >30 (mg/mmol) The higher the A grade in CKD, the poorer the prognosis, as proteinuria is considered a poor prognostic factor. 9
Aetiology 2 1 3 Diabetes Hypertension Glomerulonephritis Other: mellitus PKD • Renal artery • stenosis SLE • Amyloidosis • RA • HIV •
Pathophysiology (Diabetes) Mechanism of kidney damage: 1. Excessive glucose in the blood results in glycosylation of proteins 2. In particular, the efferent arteriolar surface proteins are prone to this 3. This leads to hyaline arteriole sclerosis , creating a stiff and narrow arteriole 4. This raises the pressure in the glomerulus and causes hyperfiltration and mesangial cell expansion 5. Over many years , this leads to reduced filtration and leakiness of the glomerulus 11
Pathophysiology (Hypertension) Mechanism of kidney damage: 1. In hypertensive states, the renal arteries become stenosed 2. Reduced blood supply to the glomerular arterioles means the glomeruli undergo ischaemic injury 3. This results in deposition of macrophages 4. These release growth factors, which cause mesangial cell regression to mesangioblasts 5. These precursor cells produce excess extracellular matrix, causing glomerulosclerosis and lowered eGFR 12
[3] Pathophysiology (Glomerulonephritis) Definition: Collective term for any condition that causes • inflammation of the glomerulus Can present as AKI, CKD or nephrotic/nephritic • syndrome Nephrotic Nephritic Minimal change IgA nephropathy • • FSGS Post-infectious GN • • Membranous Anti-GBM disease • • nephropathy MPGN • 13
Pathophysiology (other causes) Other: PKD • SLE • RA • Amyloidosis • HIV • NSAIDs • Toxins • Etc. • Regardless of the aetiology, the end result is glomerular scarring and resultant kidney failure 14
Clinical features Symptoms Signs Lethargy Hypertension Pruritis Peripheral oedema Nausea Pulmonary oedema Anorexia Uraemic sallow: yellow/brown colour to skin Frothy urine (secondary to proteinuria) Evidence of a specific underlying cause, e.g. butterfly rash in lupus More features to come when we introduced dialysis and transplant* 15
Investigations Bloods FBC • U&Es • HbA1c • Bone profile • Urine Dipstick • ACR • Imaging Renal US • CT KUB • Specialist tests Renal biopsy • The “renal workup” • 16
Management Why ACE-inhibitors? Lifestyle Encourage regular exercise, achieve a healthy • “Stop them in AKI, start them in CKD” weight and stop smoking Offer dietary advice about potassium, phosphate, • 1) They reduce the intraglomerular calorie and salt intake (keep these low) pressure and thus reduces hyperfiltration à less proteinuria Low protein diets are NOT required • 2) They reduce the blood pressure Pharmacological à a cause of CKD ACE-inhibitor or ARB if: • 3) Other – poorly studied, e.g. ATII Diabetic + ACR of 3mg/mmol or more • causes renal injury Hypertensive + ACR of 3mg/mmol or more • An ACR of 7mg/mmol or more • Offer statin and anti-platelet • Renal replacement therapy (RRT) Dialysis – haemodialysis vs peritoneal dialysis • Kidney transplant 17 •
Complications [3] System Description Cardiovascular Cardiovascular disease is the leading cause of death in CKD, e.g. IHD or heart failure Musculoskeletal CKD-metabolic bone disease (CKD-MBD) Endocrine Secondary hyperparathyroidism à Tertiary hyperparathyroidism Haematological Anaemia (usually normocytic and normochromic). Caused by: 1) Low EPO production; 2) Reduced iron absorption; 3) Uraemia causing anorexia / reduced erythropoiesis Metabolic Metabolic acidosis, hyperkalaemia, uraemic encephalopathy/pericarditis 18
CKD-MBD Mechanism 1. Active vitamin D = 1,25- dihydroxycholecalciferol Definition 2. Reduced 1-alpha hydroxylase activity in CKD Also known as renal osteodystrophy , this is a bone disorder that results in: 3. Leads to reduced vitamin D activation Bone and joint pain • Bone deformation • 4. Less vitamin D means: Bone fractures • Reduced mobility • A. Reduced renal excretion of phosphate (rises) B. Reduced absorption of calcium in gut C. Reduced release of calcium from bone Expected laboratory results Serum calcium ↓ 5. Results in hypocalcaemia and Serum phosphate ↑ hyperphosphataemia Serum vitamin D ↓ 6. Low calcium à raised PTH Serum PTH ↑ Alkaline phosphatase (ALP) ↑ Manage with phosphate binders & vitamin D analogues 19
Recap CKD is a progressive deterioration in renal function 1. >3 months and; 2. eGFR <60 or markers of kidney damage (e.g. haematuria, ACR >3) Staging: G1 to G5 – based on eGFR • A1 to A3 – based on ACR • Management: Lifestyle • ACE-inhibitors / ARBs • Renal replacement therapy (RRT) – when the time comes • Complications: Cardiovascular disease • CKD-MBD • Hyperparathyroidism (2º or 3º) • Anaemia • 20
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