Renal Flashcards
Acute Kidney Injury (AKI) - state the following:
- Pathophysiology (outline causes later)
- Presentation
- Investigations
- Management
Pathophysiology:
- Defined as an acute reduction in renal function
- Pre-renal, renal and post-renal causes
- Classification based on serum creatinine vs baseline OR urine output
Presentation:
- Reduced renal function
- Measured by increased serum creatinine OR reduced renal output
- Suspect in unwell patients with declining renal function or urine output
Investigations:
- Routine bloods including FBC, U&Es, LFTs, CRP, creatinine kinase
- Blood pressure
- Bladder scan
- Urine dipstick and MC&S
- ECG
- USS KUB
- CT / Chest x-ray
Management:
Treat the underlying cause!!
- IV fluids if hypovolaemic
- Refer to specialist if renal/intrinsic cause, if there is no clear cause or if complications develop
- Stop any nephrotoxic medications e.g. NSAIDs or antihypertensives
- Relieve obstructions if possible e.g. catheter
List some potential causes of raised urea
Usually a sign of poor kidney function
- AKI (including dehydration)
- CKD
- GI haemorrhage
- Medications
Outline the causes of acute kidney injury
Pre-renal (reduced perfusion):
- Hypotension: hypovolaemia / dehydration / anaphylaxis / sepsis
- Congestive heart failure
- Anti-hypertensives e.g. ACEi
- NSAIDs
- Renal artery stenosis
Renal (intrinsic):
- Acute tubular necrosis
- Glomerulonephritis
- Interstitial nephritis
- Vasculitis
Post-renal (obstructive):
- Ureteric strictures
- Masses leading to obstruction
- BPH
- Renal calculi (bilateral)
- Retro-peritoneal fibrosis
Outline the classification for AKI
Classification:
- Assessed by measuring serum creatinine compared to baseline or by urine output
- Chose the worst one
Serum creatinine:
Stage 1: serum creatinine 1.5 - 2 X baseline
Stage 2: serum creatinine 2 - 3 X baseline
Stage 3: serum creatinine > 3 X baseline
OR
Urine output:
Stage 1: urine output < 0.5mls/kg/hr (35ml/hr) for 6-12 hrs
Stage 2: urine output < 0.5mls/kg/hr (35ml/hr) for > 12 hrs
Stage 3: urine output < 0.3mls/kg/hr (20ml/hr) for > 24 hrs OR anuria for > 12 hrs
Outline the risk factors for AKI
- Increased age
- Cognitive impairment
- Chronic kidney disease
- Heart failure
- Diabetes
- Liver disease
Use of nephrotoxic medications:
- Anti-hypertensives
- NSAIDs
- Contrast medium (for CT scans)
Outline the 4 biochemical complications of an AKI
- Hyperkalaemia (can’t secrete K via ROMK)
- Metabolic acidosis (can’t produce sufficient HCO3)
- Fluid overload (can’t fluid balance)
- Uraemia (can’t be cleared from blood)
Chronic Kidney Disease (CKD) - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management principles
Pathophysiology:
- Chronic deterioration in renal function
- Deterioration is permanent and progressive
- Classification based on eGFR (G SCORE) OR urine albumin:creatinine ratio (A SCORE)
Presentation:
May be asymptomatic and diagnosed on routine testing
- Pruritus
- Pallor
- Oedema
- Hypertension
- Nausea / loss of appetite
- Muscle cramps
- Peripheral neuropathy
Investigations:
- Measure eGFR and calculate urine albumin:creatinine ratio
- Urine dipstick to check for haematuria
- Ultrasound to check for causes including haematuria, CKD, obstruction
Management principles:
- Slow progression
- Reduce complications and treat complications
- Reduce risk of cardiovascular disease
Outline some ways to reduce the progression of chronic kidney disease and to reduce the risk of complications
Reduce CKD progression:
- Good diabetes control
- Good hypertension control
- Manage glomerulonephritis
Reduce risk of complications:
- Be healthy (no smoking, reduce alcohol, exercise)
- Diet modifications: sodium, potassium, fluid intake and phosphate
- Statins for primary prevention of cardiovascular disease (Atorvastatin 20mg)
Outline some long term complications of CKD and how they are treated
Anaemia of chronic disease:
Treatment: exogenous erythropoietin and iron supplements
Renal bone disease:
Treatment: active forms of vitamin D and low phosphate diet
Cardiovascular disease:
Treatment: primary prevention (Atorvastatin 20mg) and control risk factors e.g. hypertension, diabetes
End-stage renal failure (ESRF)
Treatment: dialysis or renal transplantation
Metabolic acidosis:
Treatment: oral sodium bicarbonate
Peripheral neuropathy (uraemic neuropathy):
Treatment: neuropathic pain relief
Outline the pathophysiology of renal bone disease
Key issue = reduced functioning of kidneys
(1) High phosphate levels due to reduced clearance
(2) Reduced vitamin D activation at the kidneys
(3) Low Ca (due to reduced vitamin D)
Results in:
- Low Ca and high phosphate detected by the parathyroid glands
- Increased PTH production
- Bone resorption = renal bone disease
Describe the 2 main types of dialysis, including subtypes
Peritoneal dialysis:
- Uses peritoneal membrane as a filtration membrane
- Requires a Tenckhoff catheter to insert and remove the dialysis solution
- Can be done at home
1) Continuous ambulatory - fluid in all the time, replaced at regular intervals (manual exchange)
2) Automated - fluid in overnight replaced continuously by a machine (automated exchange)
Haemolysis dialysis:
- Filtered by a haemodialysis machine at the hospital
- Generally 3 days a week, for approx. 4 hrs each time
- Can use either an arterio-venous fistula or a tunneled cuffed catheter
Outline the indications for acute dialysis
Basically if the patient is symptomatic (matters less about the eGFR)
Suffering from complications of severe AKI (AEIOU):
- (Acidosis) Metabolic acidosis
- (Electrolytes) Hyperkalemia
- (Intoxication) Overdose of certain medications
- (Oedema) Fluid overload
- (U) Uraemia
Outline the indications for long term dialysis
- End stage renal failure / stage 5 CKD
- Complications of severe AKI continuing long term
List some complications of peritoneal dialysis
- Infection (bacterial peritonitis) due to glucose solution
- Sclerosis / fibrosis
- Ultrafiltration failure (due to absorbing Dextrose solution and reducing gradient)
- Weight gain (due to absorbing Dextrose solution)
- Psychological effects
Outline 2 veins commonly used for tunneled cuffed catheter (in haemodialysis)
Subclavian vein
Jugular vein
Despite which entry, catheter ends up in the SVC or right atrium
Outline some complications of haemodialysis, in relation to catheters and AV fistulas
Tunneled cuffed catheter:
- Infection
- Thrombosis
- Pneumothorax
AV fistula:
- Infection
- Bleeding risk
- Thrombosis
- Aneurysm
- STEAL syndrome
- High output heart failure
Outline which arteries and veins are typically connected in an AV fistula for haemodialysis (2)
Brachio-cephalic (brachial artery and cephalic vein)
Radio-cephalic (radial artery and cephalic vein)
List some complications associated with renal transplantation and associated immunosuppression
Related to organ:
- Infection
- Transplant failure
- Transplant rejection
- Electrolyte imbalances
Related to immunosuppression:
- Malignancy (non-Hodgkin’s lymphoma and squamous cell carcinoma imparticular)
- More frequent or severe infections
- Atypical infections e.g. PCP, CMV, TB
- Steroid-induced T2DM
- Ischaemic heart disease
Diabetic nephropathy - state the following:
- Pathophysiology
- Presentation and screening
- Management
Pathophysiology:
- Scarring of the glomerulus, due to high flow of glucose (uncontrolled diabetes)
- Leads to damage of the glomerulus, allowing proteins to leak through the glomerulus, into the urine
- Most common cause of glomerular pathology and CKD in UK
Presentation and screening:
- Frothy urine (proteinuria)
- Signs of uncontrolled diabetes e.g. high HbA1C, peripheral neuropathy, vision changes
- Regular screening for diabetic nephropathy using albumin:creatinine ratio and U&Es
Management:
- Control of diabetes (good blood sugar control)
- BP control with ACEi
Outline Nephrotic Syndrome and it’s pathophysiology
Nephrotic syndrome:
- A clinical syndrome characterised by: proteinuria, hypoalbuminaemia and oedema + hyperlipidaemia
- Caused by damage to the basement membrane in the glomerulus leading to increased permeability and leakage of protein
Pathophysiology:
- Cytokines damage podocytes causing them to fuse together and destroy charge of the glomerular basement membrane.
- Increased permeability and massive protein loss
- Also leeds to low serum albumin (beyond the ability of the liver to replace them)
- Due to the loss of albumin, disruption to oncotic pressure with fluid leaking into interstitial = oedema
- As an attempt to maintain oncotic pressure, the liver tries to compensate by increased synthesis of lipids
- Also in a hypercoagulable state due to urinary loss of antithrombin 3
- Also in an immunosuppressed state due to urinary loss of immunoglobulins
Outline the most common causes of Nephrotic Syndrome (in children and adults) as well as a couple of other common causes
Most common cause in children: Minimal change disease
Most common cause in adults: Membranous glomerulonephritis
Other common causes:
- Systemic diseases: SLE and amyloidosis
- Diabetes mellitus
- Focal segmental glomerulosclerosis (FSGS)
Outline the presentation, investigations and management for Nephrotic Syndrome
Presentation:
- Oedema (peripheral and periorbital)
- (Proteinuria, hypoalbuminaemia and hyperlipidaemia)
Investigations:
- Urine dipstick / urinalysis
- Serum albumin
- Blood pressure
- Creatinine
- Renal biopsy only if unresponsive to treatment or diagnosis is unclear
Management:
- High dose steroids for 12 weeks (treat underlying cause, which is damage by cytokines)
- Diuretics, may need large doses
- Fluid and salt restriction
- ACEi (vasodilate EA, helps to reduce pressure which reduces loss of protein)
- Statins (hyperlipidaemia)
- Anticoagulants (hypercoagulable state)
- May need to manage underlying cause if clear e.g. SLE
List the complications of Nephrotic Syndrome
- Thromboembolism (hypercoagulable state due to urinary loss of antithrombin 3)
- Infection (immunosuppressed state due to urinary loss of immunoglobulins)
- Hyperlipidaemia (overcompensation of liver to replace albumin)
- Hypocalcaemia (loss of vit D in urine)
- Acute renal failure (acute tubular necrosis)
Outline the 2 main types of interstitial kidney disease and key causes, including brief outline of management
- Acute interstitial nephritis
- Acute inflammation of the interstitium and tubules
- Mainly a hypersensitivity reaction to a trigger
Key causes:
- Hypersensitivity reaction to drugs e.g. NSAIDs and Antibiotics
- Hypersensitivity reaction to infection
Management:
- TREAT UNDERLYING CAUSE
- Steroids may have some role - Chronic tubulo-interstitial nephritis
- Chronic inflammation of the interstitium and tubules
- Presents with CKD
Key causes:
- Many causes including: infection, autoimmune, iatrogenic, granulomatous disease
Management:
- TREAT UNDERLYING CAUSE
- Steroids may have some role
Outline the presenting triad of symptoms for acute interstitial nephritis
Interstitial hypersensitivity reaction causes:
- Erythematous rash
- Fever
- Eosinophilia
Outline some drugs that can cause acute interstitial nephritis
- NSAIDs
- Diuretics
- PPI
- Antibiotics (e.g. penicillins, sulfa drugs, cephalosporins and quinolones)
- Allopurinol
- Rifampicin
Acute tubular necrosis - state the following:
- Pathophysiology
- Common causes
- Investigations
- Management
Pathophysiology:
- Damage and death of the epithelial cells of the renal tubules
- Most common cause of AKI
- However is reversible (recovery in 1-3 weeks)
Common causes
1. Ischaemia secondary to hypoperfusion e.g. sepsis, hypovolaemia, shock
2. Toxins e.g. contrast dye, NSAIDs, Gentamicin, Heroin, Lithium
Investigations:
Urinalysis - shows ‘muddy brown casts’ (pathognomonic for ATN)
Management:
Similar management to AKI
- Treat underlying cause
- Supportive management
- IV fluids
- Stop any nephrotoxic medications
Briefly outline the 4 types of renal tubular acidosis (type 1 and 4 are likely to be examined)
Type 1:
- Distal tubule unable to excrete H+
- Leads to build up of H+ in the blood = metabolic acidosis
Type 2:
- Proximal tubule unable to reabsorb HCO3-
- Leads to excessive HCO3- in urine, reduced HCO3- in the blood = metabolic acidosis
Type 3:
- Mix of type 1 and type 2
- Pathology in both the distal tubule and proximal tubule
Type 4:
- Reduced aldosterone (normally Na reabsorption and K+ / H+ excretion)
- So low aldosterone = Na loss and K+ / H+ retaining
- Hyperkalaemia suppresses ammonia production; low ammonia levels leads to more acidic urine
Type 1 renal tubular acidosis - state the following:
- Pathophysiology
- Common causes
- Clinical findings (blood, urine)
- Management
Pathophysiology:
- Distal tubule unable to excrete H+
- Leads to buildup of H+ in the blood = metabolic acidosis
Common causes:
- Genetic
- SLE / Sjogren’s / PBC
- Hyperthyroidism
- Marfan’s syndrome
- Sickle cell anaemia
Clinical findings (blood, urine):
- Metabolic acidosis
- Alkaline urine
- Hypokalaemia
Management:
- Oral bicarbonate (correct hypokalamia as well)
Type 4 renal tubular acidosis - state the following:
- Pathophysiology
- Common causes
- Clinical findings (blood, urine)
- Management
Pathophysiology:
- Reduced aldosterone (normally Na reabsorption and K+ / H+ excretion)
- So low aldosterone = Na loss and K+ / H+ retaining
- Hyperkalaemia suppresses ammonia production; low ammonia levels leads to more acidic urine
Common causes:
- Adrenal insufficiency
- Medications e.g. ACEi or Spironolactone
- SLE
- Diabetes
- HIV
Clinical findings (blood, urine):
- Metabolic acidosis
- Acidic urine
- Hyperkalaemia
- High Cl-
Management:
- Fludrocortisone (Aldosterone replacement)
- Sodium bicarbonate
- May require treatment of hyperkalaemia
Haemolytic uraemic syndrome - state the following:
- Pathophysiology
- Presentation (classic triad)
- Management
Pathophysiology:
- Occurs when there is thrombosis in small blood vessels throughout the body
- Triggered by the shiga toxin
Presentation (classic triad):
- Haemolytic anaemia
- AKI
- Thrombocytopenia (low platelets)
Management:
- Supportive management
- Antihypertensives
- Blood transfusions
- Dialysis
List things that are released during muscle cell breakdown (in rhabdomolysis)
- K+
- Creatine kinase
- Myoglobin
- Phosphate
List some causes of rhabdomyolysis
- Extremely vigorous exercise (beyond the capabilities of the individual)
- Falls in long lie / prolonged immobility
- Compartment syndrome
- Crush injuries
- Seizures
List some symptoms and signs of rhabdomyolysis
- Red-brown urine
- Muscle aches/pain
- Oedema
- Confusion
- Fatigue
Outline the key management of rhabdomyolysis
IV fluids = encourage filtration and hydrates
IV Sodium Bicarbonate = more alkaline urine, less toxic to kidneys
IV Mannitol = increase GFR to encourage filtration and reduce oedema
Treat any complications e.g. hyperkalaemia
List some causes of hyperkalaemia
Conditions:
- Rhabdomyolysis
- AKI
- CKD
- Adrenal insufficiency
- Tumour lysis syndrome
Medications:
- Aldosterone antagonists (diuretics e.g. Spironolactone)
- ACEi / ARB
- NSAIDs
- K+ supplements
Outline the management for hyperkalaemia
< 6 mmol/L and stable renal function
> 6 mmol/L and ECG changes
> 6.5 mmol/L
< 6 mmol/L and stable renal function = mild changes e.g. stopping hyperkalaemic drugs or modifying diet
> 6 mmol/L and ECG changes = urgent treatment
> 6.5 mmol/L = urgent treatment, regardless of other signs
Management:
- Insulin + Dextrose fluid = drives glucose into cells, takes K+ with it
- IV Calcium Gluconate = stabilise cardiac muscle cells
- IV Calcium Resonium = draws K+ into stool
- IV fluids = increase urine output and K+ excretion in urine
List some common causes of CKD
2 most common:
- Diabetes
- Hypertension
+
- Glomerulonephritis
- Polycystic kidney disease
- Chronic use of nephrotoxic medications e.g. NSAIDs, Lithium, PPIs
- Age-related decline
What is the best blood test to detect rhabdomyolysis
Serum creatine kinase (CK)
List some drugs that should be stopped in AKI (nephrotoxic and renally excreted drugs)
Nephrotoxic drugs:
- NSAIDs
- Aminoglycosides e.g. gentamicin
- ACE inhibitors/ARBs
- Diuretics
Renally excreted drugs:
- Metformin
- Lithium
- Digoxin
List 3 absolute contraindication for renal transplant
- Metastatic cancer
- Active infections
- Severe comorbidity
Alport’s syndrome - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Rare X-linked inherited nephropathy due to abnormal glomerular basement membrane (defective type 4 collagen)
- Problems with the eyes, ears and kidneys
Presentation:
- Gross haematuria
- Sensorineural hearing loss
- Vision changes
Investigations:
Quite general!
- Routine bloods e.g. FBC, U&Es
- Audiometry and ophthalmoscopy
- Renal biopsy
- Genetic testing
Management:
- Ongoing annual monitoring e.g. U&Es
- Manage comorbidities or manifestations e.g. HTN
- ACEi if proteinuria
- May eventually need dialysis
What drugs should be stopped in AKI? (DAMN)
DAMN
D- Diuretics
A - ACEi and aminoglycosides
M - Metformin
N - NSAIDS
Outline some clinical signs of a patient with CKD
- Coarse crackles or reduced breath sounds (pulmonary oedema)
- Peripheral pitting oedema
- Excoriation marks from pruritus
- Evidence of CKD replacement therapy e.g. AV fistula or permacath
Outline 2 pros and 2 cons for both live kidney donation and decreased kidney donation
Live kidney donation:
+ planned surgery (elective)
+ generally a better match / better quality kidney, reduced risk of failure
- hard to find a donor
- emotional turmoil if it fails
Decreased kidney donation:
+ don’t have to find the donor
+ no connection to donor
- not always the best match, increased risk of failure
- surgery can be at short notice and longer waiting times
