Renal Flashcards
Define ACUTE KIDNEY INJURY (AKI).
AKI is defined as reduction in renal function over a 48 hour period, as defined by ONE or more of the following:
- increase in serum creatinine by 26.4 umol / L (absolute)
- increase in serum creatinine by 1.5 times baseline level
- reduced urine output < 0.5mL / kg / hour for > 6 hours
AKI can be classified as:
✔️ STAGE I –> urine output < 0.5 mL / kg / hour for > 6 hours
✔️ STAGE II –> urine output < 0.5mL / kg / hour for > 12 hours
✔️ STAGE III –> urine output < 0.3mL / kg / hour for > 12 hours
PRE-RENAL AKI
✔️ causes
✔️ key findings
CAUSES ✔️ dehydration ✔️ hypovolemia (e.g. haemorrhage) ✔️ sepsis ✔️ congestive cardiac failure ✔️ liver failure ✔️ thrombosis / renal artery occlusions
KEY FINDINGS
✔️ urine MCS –> hyaline casts
✔️ urine osmolality –> greater than 500 mOsm
✔️ UCR > 100 (increased)
INTRA-RENAL AKI
✔️ causes
✔️ key findings
CAUSES: ✔️ acute tubular necrosis (ATN) ✔️ glomerulonephritis ✔️ vasculitis ✔️ nephrotoxic substances
KEY FINDINGS
✔️ urine MCS –> muddy brown casts (ATN) or red cell casts (glomerulonephritis)
✔️ urine osmolality –> less than 350 mOsm
✔️ UCR normal or decreased (40 to 100)
POST-RENAL AKI
✔️ causes
✔️ key findings
CAUSES: ✔️ renal stone obstruction ✔️ BPH ✔️ prostate cancer ✔️ ovarian cancer ✔️ any abdominal mass leading to obstruction of urinary outlet ✔️ urethral stricture
KEY FINDINGS
✔️ KUB USS
✔️ gross haematuria
What are some common casts that might be seen on URINE MCS and what pathologies do these correlate to?
Hyaline casts --> dehydration (pre-renal AKI) Muddy brown casts --> ATN Waxy casts --> CKD Fatty casts --> nephrotic syndrome Red cell casts --> nephritic syndrome White cell casts --> pyelonephritis
Identify indications for RENAL BIOPSY.
NATIVE KIDNEY ✔️ glomerulonephritis ✔️ suspected SLE ✔️ rapidly progressing GN (RPGN) ✔️ atypical diabetes mellitus ✔️ AKI not of a pre- or post- renal cause ✔️ suspected interstitial nephritis ✔️ new or known nephrotoxicity
DONOR KIDNEY ✔️ acute rejection ✔️ chronic rejection ✔️ infection ✔️ recurrent underlying disease
Identify CONTRAINDICATIONS to renal biopsy.
ABSOLUTE CONTRAINDICATIONS
✔️ uncontrolled hypertension
✔️ bleeding diathesis
RELATIVE CONTRAINDICATIONS ✔️ malignancy ✔️ single kidney ✔️ polycystic kidney disease ✔️ small, fibrotic kidney ✔️ coagulopathy
Outline appropriate management of HYPERKALAEMIA.
Acute management:
✔️ salbutamol (nebulised)
✔️ insulin dextrose (IV)
Membrane stabilisation:
✔️ calcium glyconate
Binding agents:
✔️ resonium
Other:
✔️ telemetry
✔️ ABG monitoring
Outline appropriate management of ACIDEMIA.
The aim for acidosis management includes maintaining pH > 7.2 plus bicarb between 20 to 22 mmol / L.
IV or oral sodium bicarbonate is first-line management.
Renal dialysis may be required if electrolyte balance cannot be achieved through medical management.
Outline appropriate indications or RENAL DIALYSIS.
A –> acidosis (pH < 7.2)
E –> electrolyte imbalances refractory to medical therapy (K+ > 6.5 mmol / L)
I –> intoxication of nephrotoxic drugs (e.g. salicylic acids, lithium, dabagatrene)
O –> overload (fluid) refractory to diuretics
U –> uremic pericarditis, encephalopathy etc.
Define CHRONIC KIDNEY DISEASE (CKD).
CKD is defined as a reduction in renal function over a three month period, as defined by either: 1. eGFR < 60 2. existing renal damage / dysfunction ✔️ polycystic kidney disease ✔️ renal transplant recipient ✔️ proteinuria ✔️ pathological disorders ✔️ functional disorders
Outline the classification of CKD stages.
STAGE I: eGFR > 90 STAGE II: eGFR 60 to 89 STAGE IIIa: eGFR 45 to 59 STAGE IIIb: eGFR 30 to 44 STAGE IV: eGFR 15 to 29 STAGE V: eGFR < 15
Identify risk factors for CKD.
The three main causes of CKD are:
- diabetic nephropathy
- hypertension nephropathy
- glomerulonephritis
Risk factors for CKD include : ✔️ increasing age ✔️ diabetes mellitus ✔️ hypertension ✔️ family history of kidney disease ✔️ family or personal history of CD ✔️ ATSI
Outline clinical presentation for CKD.
Most patients with CKD are asymptomatic. Symptoms tend not to develop until 90% of renal function has been lost.
Symptoms include: ✔️ fatigue, lethargy ✔️ malaise and anorexia ✔️ nausea and vomiting ✔️ loss of lean muscle mass ✔️ oedema ✔️ pleural and pericardial effusions ✔️ uremic encephalopathy ✔️ sallow, yellow skin ✔️ polyuria, nocturia
Identify appropriate investigations for CKD.
✔️ urine dipstick + MCS ✔️ blood glucose level ✔️ ABG (metabolic acidosis, lactate and bicarb levels) ✔️ FBC + WCC ✔️ Inflammatory markers ✔️ UECs ✔️ urine ACR ✔️ urea creatinine ratio ✔️ Iron studies ✔️ Vitamin B12 + folate ✔️ EPO levels ✔️ Inflammatory screen (HepB, HepC, HIV) ✔️ Autoimmunity screen (ANA, ANCA, anti-GBM, dsDNA) ✔️ Myeloma screen (urine Bence Joyce protein, protein electrophoresis, serum light chain analysis) ✔️ KUB doppler USS
Outline the goals of management for CKD.
✔️ early and appropriate referral to nephrologist
✔️ plan for RRT (dialysis) when eGFR < 30
✔️ appropriate end of life discussions (eg. AHD, EPOA, will) when renal dialysis not appropriate
✔️ multi-disciplinary team involvement
✔️ adjust medications when eGFR < 30
✔️ avoid nephrotoxic agents
✔️ early detection and management of complications
✔️ reduce CVD risk
Discuss management of HYPERTENSION in patients with CKD.
Hypertension should be managed aggressively to prevent the development of both CVD and CKD.
In patients with PROTEINURIA, aim for BP < 130 / 80mmHg.
In patients without proteinuria, aim for BP < 140 / 90 mmHg (given that no other cardiovascular risk factors co-exist).
Lifestyle options include: ✔️ smoking cessation ✔️ alcohol reduction ✔️ adequate physical activity ✔️ appropriate nutrition (suggest referral to dietician) ✔️ reduce salt intake
Medical management includes:
✔️ ACE-I or ARB (adjust when eGFR < 30; hypokalaemia risk)
✔️ loop diuretics
✔️ CCB
Discuss management of PROTEINURIA in patients with CKD.
✔️ ACE-I / ARB
✔️ loop diuretic
✔️ CCB
✔️ appropriate diet (e.g. reduce protein consumption to < 0.8g / kg / day)
Discuss management of ANAEMIA in patients with CKD.
Anaemia in CKD patients can arise due to one, or both of the following mechanisms:
- anaemia of chronic disease, whereby chronic inflammatory markers stimulate HEPCIDIN, which blocks the transport of FERRITIN across the ferroportin transported
- reduced EPO synthesis and production from the kidneys
CKD-related anaemia should be treated first with oral iron therapy (high dose).
When Hb is persistently < 100, EPO may be considered.
Aim for Hb between 110 to 150.
Discuss management of BONE AND MINERAL DISORDERS in patients with CKD.
CKD is characterised by: ✔️ low calcium ✔️ low Vitamin D ✔️ high parathyroid hormone ✔️ high phosphate ✔️ high ALP
Appropriate Vitamin D and calcium supplementation should be considered (oral is usually appropriate).
Define NEPHROTIC SYNDROME.
Nephrotic syndrome is a type of glomerulonephritis characterised by:
- proteinuria > 3g per day
- hypoalbuminemia
- oedema
- dyslipidemia
Hypertension and hypercoaguability are also key components of the disease.
Identify common causes of PRIMARY versus SECONDARY nephrotic syndrome.
PRIMARY CAUSES
- minimal change disease (90% of cases in children, 10% of cases in adults)
- focal segmental glomerulosclerosis (more common in adults)
- membraneous nephropathy
SECONDAY CAUSES
- diabetes nephropathy
- pre-eclampsia
- amyloidosis
Outline the pathophysiology of NEPHROTIC SYNDROME.
Nephrotic syndrome most commonly is precipitating by a viral infection, systemic illness, drugs or toxins.
Dysregulated T Lymphocytes promote increased permeability of the podocyte foot processes within the basement membrane of the glomerulus. This facilitates increase loss of protein (particularly albumin) into urine.
Hypoalbuminemia causes fluid shift in the body due to reduced serum oncotic pressure. This leads to peripheral and periorbital oedema.
As a result of low plasma albumin levels, the liver stimulates increased albumin production. This is accompanied by increased production of LDL-C, leading to dyslipidemia.
Increased podocye permeability also facilities the loss of anti-coagulation factors, including AT-III. Consequently, nephrotic syndrome is characterised as being a pro-thrombotic state.
Identify appropriate investigations for NEPHROTIC SYNDROME.
Bedside Ix
✔️ 24-hour urine protein levels
✔️ urine dipstick
✔️ urine ACR, MCS etc.
Laboratory Ix ✔️ FBC + WCC ✔️ Inflammatory markers ✔️ UECs ✔️ urea and creatinine levels; UCR ✔️ serum albumin levels ✔️ fasting lipids ✔️ LFTs ✔️ coags ✔️ Infective screen (HepB, HepC, HIV) ✔️ Auto-immune screen (ANA, ANCA, dsDNA, anti-GBM)
Imaging Ix
✔️ CXR (pleural and pericardial effusions)
✔️ KUB doppler USS
✔️ Renal biopsy
Discuss appropriate management of a patient with NEPHROTIC SYNDROME.
- Investigate and identify the underlying cause. Treat if possible.
- IV corticosteroids (e.g. prednisolone)
- IV frusemide for oedema management
- IV albumin for oedema management and hypo-albuminemia
- Appropriate anti-coagulation (e.g. LMWH)
- Statin therapy for dyslipidemia
- Management of hypertension with ACE-i or ARBs
Define NEPHRITIC SYNDROME.
Nephritic syndrome is a type of glomerulonephritis characterised by: ✔️ P - proteinuria (variable) ✔️ H - haematuria (gross) ✔️ A - azotaemia (increased BUN) ✔️ R - red cell casts on urine MCS ✔️ A - anti ASO antibodies (in PSGN) ✔️ O - oliguria ✔️ H - hypertension
Outline the most common causes for NEPHRITIC SYNDROME.
ACUTE CAUSES
✔️ post-streptococcal glomerulonephritis (PSGN)
✔️ rapidly progressive glomerulonephritis (RPGN)
CHRONIC CAUSES ✔️ IgA nephropathy ✔️ anti-GBM (Good Pasteur's Syndrome) ✔️ thin basement membrane disease ✔️ hereditary nephritis
POST-STREPTOCOCCAL GN (PSGN) ✔️ pathophysiology ✔️ clinical features ✔️ investigations ✔️ appropriate management
PATHOPHYSIOLOGY
PSGN occurs following infection with Group A beta-haemolytic strep (GAS), such as impetigo or pharyngitis.
Antigens bind to basement membrane and cause local or systemic inflammation.
Disease onset is typically acute.
CLINICAL FEATURES ✔️ preceding GAS infection (e.g. impetigo, pharyngitis) ✔️ gross haematuria ✔️ oedema ✔️ hypertension
INVESTIGATIONS
✔️ red casts on urine MCS
✔️ proteinuria, haematuria on urine dipstick
✔️ anti-ASO titre positive OR positive throat / skin culture
✔️ increased inflammatory markers
✔️ reduced C3 and C4 levels
✔️ renal biopsy
MANAGEMENT
- Identify and treat underlying cause (antibiotics may be required in GAS infection is still present).
- Blood pressure management (e.g. ACE-I or ARBs).
- Odema management (e.g. IV frusemide)
- Fluid and salt restriction
RAPIDLY PROGRESSIVE GN (RPGN) ✔️ pathophysiology ✔️ clinical features ✔️ investigations ✔️ appropriate management
PATHOPHYSIOLOGY RPGN can occur after any type of inflammation / damage to the glomerulus. This includes: ✔️ PSGN ✔️ IgA nephropathy ✔️ lupus nephropathy ✔️ ANCA vasculitis ✔️ anti-GBM disease RPGN is characterised by progressive kidney disease over a relatively short period of time, such as a few weeks.
CLINICAL FEATURES ✔️ macroscopic haematura ✔️ oliguria ✔️ hypertension ✔️ significant oedema
INVESTIGATIONS ✔️ urine MCS ✔️ urine dipstick ✔️ anti-ASO antibiotics, anti-GBM antibodies, anti-dsDNA levels, ANA, ANCA antibiotics ✔️ complement levels ✔️ renal biopsy will show CRESCENT shape
MANAGEMENT
Spontaneous remission is rare. Between 80 to 90% of patients will go on to develop ESKD within 6 months.
✔️ IV prednisolone
✔️ IV cyclophosphamide
✔️ plasma exchange
✔️ rituximab
IgA NEPHROPATHY ✔️ pathophysiology ✔️ clinical features ✔️ investigations ✔️ appropriate management
PATHOPHYSIOLOGY
IgA nephropathy is a chronic cause of nephritic syndrome. Increased IgA deposition within the glomerular basement membrane promotes chronic inflammation and associated inflammatory changes.
The exact mechanism of IgA deposition is unknown, however, may be explained by:
✔️ increased IgA production
✔️ reduced IgA clearance
✔️ defective mucosal immune system
✔️ increased inflammatory cytokines
CLINICAL FEATURES
✔️ progressive haematuria, hypertension and oedema (over 10 to 15 years)
✔️ progression to CKD is common
MANAGEMENT
✔️hypertension management with ACE-I or ARBs
✔️ diuretics for fluid overload
✔️ corticosteroids for inflammation
✔️ cyclophosphamide for acute exacerbations
✔️ renal transplant as a final option
