MED: Renal Flashcards
What are the causes of AKI?
Prerenal:
- Volume Depletion - haemorrhage, GIlosses (V/D), excessive diuresis
- Reduced CO - heart failure, shock (septic, hypovolaemic, cardiogenic), large vessel occlusion
- Systemic Vasodilation - septic shock, anaphylaxis
- Drugs -NSAIDs and ACE inhibitors can interfere with renal autoregulation
Intrinsic Renal Causes:
- Acute Tubular Necrosis (ATN): Caused by ischaemia (sustained prerenal factors) or toxins (drugs, contrast, rhabdomyolysis).
- Acute Interstitial Nephritis (AIN): Typically drug-induced, but can also be caused by infections or autoimmune diseases.
- Vascular: Includes conditions like renal artery or vein thrombosis, malignant hypertension, and vasculitides.
- Glomerular: Rapidly progressive glomerulonephritis or other glomerulopathies.
Postrenal Causes:
- Obstruction: Obstruction can occur at any level from the renal pelvis to the urethra due to stones, tumours, strictures, or prostatic hypertrophy.
What are the investigations for an AKI?
Urine analysis:
- Urine dip - UTI (leucocytes +/- nitrites), glomerulonephritis (haematuria + leucocytes), AIN (leucocytes)
- MC&S - if evidence of UTI on dip
- Protein:creatinine ratio - if glomerulonephritis suspected
Bloods:
- U&Es - detect hyperkalaemia
- FBC, CRP and bone profile as minimum
- If cause not known further tests should be considered including: CK, ANA, ANCA, anti-GBM, complement levels, immunoglobulin levels, antistreptolysin O titre, HIV
Ultrasound:
- Performed in new cases of AKI
- If obstructive uropathy or pyelonephritis is suspected should be performed urgently (<24hrs)
What is the diagnostic criteria for an AKI?
- Rise in serum creatinine of 26 or greater within 48 hours
- 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
- Fall in UO to less than 0.5 ml/kg/hour for more than 6 hours in adults
How is an AKI staged?
AKI can be staged using the KDIGO classification
Stage 1:
- Creatinine 1.5-1.9x baseline or >26umol/L within 24 hours
- UO <0.5 mL/kg/hour for 6 hours
Stage 2:
- Creatinine 2-2.9x baseline
- UO <0.5 mL/kg/hour for 12 hours
Stage 3:
- Creatinine >3x baseline or >353.6 umol/L or initiation of renal replacement therapy or decrease of eGFR to <35 mL/min
- UO <0.3 mL/kg/hour for 24 hours or anuria for 12 hours
What medications should be stopped in AKI as may worsen renal function?
- NSAIDs
- Aminoglycosides
- ACE inhibitors
- Angiotensin II receptor antagonists
- Diuretics
What medications may have to be stopped in AKI as increased risk of toxicity (but doesn’t usually worsen AKI itself)?
- Metformin
- Lithium
- Digoxin
What is the management of an AKI?
Supportive:
- Careful fluid balance - ensure kidneys are properly perfused but not fluid overloaded
- RV medications
- Role for loop diuretics in patients who experience significant fluid overload
Specialist input:
- Nephrologist input required when cause not known or severe AKI
- All patients with suspected AKI secondary to urinary obstruction require prompt review by a urologist.
Renal replacement therapy:
- e.g. haemodialysis
- Used when patient not responding to medical treatment of complications, for example hyperkalaemia, acidosis or uraemia.
What is the cause of PKD?
Autosomal dominant mutation in PKD1 or PKD2 gene
What is the classification of PKD?
Type 1 ADPKD: 85% of cases
- Caused by a mutation in PKD1 on chromosome 16
- Symptoms tend to be more severe in this type
Type 2 ADPKD: 15% of cases
- Caused by a mutation in PKD2 on chromosome 4
- Symptoms tend to be less severe in this type
What are the clinical features of PKD?
- Haematuria - both microscopic and macroscopic are common
- Loin pain - chronic loin pain may be due to distension of the renal capsule, traction of the renal pedicle, and/or hepatic enlargement. Acute loin pain may be caused by kidney stones, cyst haemorrhage and/or infection.
- Hypertension
- Recurrent UTIs
- Kidney stones
- Headache - may be a sign of a ruptured berry aneurysm and subsequent SAH
What are the signs O/E of PKD?
- Palpable kidneys/abdominal mass
- Hepatomegaly due to hepatic cysts
- Abdominal wall hernias
- Cardiac murmur - increased incidence of mitral valve prolapse, mitral regurgitation, aortic regurgitation and dilated aortic root
What are the symptoms of renal failure?
Peripheral oedema
Shortness of breath
Poor appetite and weight loss
Polyuria
Pruritus
Nausea
What are the investigations for PKD?
Renal ultrasound scan:
- First investigation when ADPKD is suspected
MRI/CT:
- If renal ultrasound is equivocal, MRI or CT scan may be considered
- > 10 renal cysts is diagnostic.
- An MRI scan of the head may be performed to identify intracranial berry aneurysms which occur in up to 40% of cases of ADPKD.
Genetic testing:
- Not routinely performed for diagnosis
- May be used to assess potential living related kidney donors with equivocal or negative scan results.
What criteria is used to diagnose PKD?
Ravine’s criteria: With positive family history
- 15-29 years: presence of 3 or more renal cysts (unilateral or bilateral)
- 30-39 years: presence of 2 or more renal cysts (unilateral or bilateral)
- 40-59 years: presence of 2 or more cysts in each kidney
In patients with no family history, ultrasound criteria for diagnosis is >10 cysts in each kidney
What is the management of PKD?
- All patients newly diagnosed with ADPKD should be referred to a nephrologist
- Blood pressure control - antihypertensive medications and lifestyle modifications
- Management of renal pain - underlying causes excluded before starting analgesia
- Treatment of UTIs - 7-14 day course of antibiotics is recommended
- Treatment of kidney stones
- Tolvaptan to slow progression of cyst formation and renal insufficiency if they don’t have CKD stage 2 or 3 at the start of treatment and there is evidence of rapidly progressive disease
What is the management of ESRD?
Renal transplantation is the management of choice for ESRD caused by ADPKD; a living donor is preferable to a cadaveric donor
Dialysis is the second-line management of ESRD caused by ADPKD; haemodialysis is preferred to peritoneal dialysis in this group
What are the complications of PKD?
Hepatic cysts:
- Majority are asymptomatic and do not require treatment
- Some patients may experience heartburn, nausea, early satiety and an increased abdominal circumference due to hepatomegaly caused by hepatic cysts
Cardiovascular disease:
- Hypertension > increases risk of coronary heart disease, stroke and MI
- Mitral valve prolapse, mitral regurgitation, aortic regurgitation and dilated aortic root are also associated with ADPKD
Intracranial aneurysms and subarachnoid haemorrhage:
- Patients with ADPKD and a FHx of SAH are offered an MRA scan at intervals of 1 to 5 years to screen for intracranial aneurysms
- If aneurysms are detected they may be treated surgically using a clip or coil to prevent rupture
What are the causes of CKD?
- diabetic nephropathy
- chronic glomerulonephritis
- chronic pyelonephritis
- hypertension
- adult polycystic kidney disease
What are the clinical features of CKD?
Early:
- Fatigue
- Polyuria / nocturia
- Hypertension
- Puffiness / swelling
Late:
- Decreased UO - oliguria / anuria
- Fluid overload - SOB, peripheral oedema, hypertension.
- Uraemic Symptoms - nausea, vomiting, anorexia, metallic taste in the mouth, hiccups, and pruritus
- Neurological Symptoms - difficulty concentrating / fatigue, seizures /coma (uraemic encephalopathy)
- Cardiovascular Symptoms - chest pain or SOB due to CKD-related cardiovascular disease, including coronary artery disease and pericarditis.
- Anaemia Symptoms
- Bone and Mineral Disease - CKD can disrupt calcium and phosphate balance, leading to bone pain, fractures, and other symptoms of renal osteodystrophy.
- Metabolic Acidosis Symptoms - rapid breathing, confusion, and lethargy.
Describe the stages of CKD
Stage 1:
- GFR >90 ml/min
- Some sign of kidney damage on other tests (i.e. abnormal U&Es / proteinuria)
Stage 2:
- GFR 60-90 ml/min
- Some sign of kidney damage on other tests
Stage 3a:
- GFR 45-59 ml/min
- Moderate reduction in kidney function
Stage 3b:
- GFR 30-44 ml/min
- Moderate reduction in kidney function
Stage 4:
- GFR 15-29 ml/min
- Severe reduction in kidney function
Stage 5:
- GFR < 15 ml/min
- Established kidney failure - dialysis or a kidney transplant may be needed
What are the complications of CKD?
- Anaemia
- Hypertension
- Mineral bone disease
What are the causes of DI?
Central DI:
Acquired - idiopathic, tumours (germ cell tumours, Langerhans cell histiocytosis, pituitary tumours, craniopharyngioma), trauma (most commonly following pituitary surgery), infections (encephalitis, cryptococcal meningitis, TB meningitis), vascular damage
- Congenital - mutation in Arginine vasopressin-neurophysin II gene (AVP-NPII) (AD), Wolfram syndrome (AR)
Nephrogenic DI:
- Congenital (85%) - mutation in vasopressin-2-receptor (X-linked mutation - 90% cases), mutation in aquaporin 2 gene (AR)
- Acquired - drug induced (most commonly lithium), hypercalcaemia, hypokalaemia, kidney disease
Gestational DI:
- Increased production of vasopressinase from the placenta decreases the amount of ADH
- Increased prostaglandins may reduce the sensitivity of the kidney to ADH.
Dipsogenic DI:
- Due to an impairment of the thirst mechanism
- Causes may include chronic meningitis, multiple sclerosis
What are the clinical features of DI?
- Excessive thirst
- Copious dilute urine
- Nocturia
- Symptoms associated with dehydration - fatigue, dizziness, weakness
- Symptoms associated with a SOL causing central DI - headache, visual changes, seizures
In children, features may also include:
- Nocturnal enuresis after continence has been gained
- Failure to thrive
- Irritability
O/E:
- Signs of dehydration
- Palpable distended bladder
- A neurological exam may show focal neurology such as altered visual fields if DI has been caused by a space-occupying lesion.
What are the investigations for DI?
24-hour urine collection:
- If <3L/24hr - DI unlikely
Urine and serum osmolality to calculate the urine to plasma (U:P) osmolality ratio:
- If U:P ratio > 2:1 (urine twice as concentrated as plasma), DI unlikely
- If U:P is <2:1 it confirms dilute urine.
Bloods:
- Glucose - to rule out diabetes mellitus.
- Calcium - to rule out hypercalcaemia.
- U&Es - sodium may be raised if inadequate water is consumed and other electrolyte abnormalities may be present.
Water deprivation test:
Serum copeptin:
- can suggest the levels of ADH present in the blood
- Nephrogenic DI = Random serum copeptin >21.4pmol/L
- Central DI = Stimulated serum copeptin <4.9pmol/L
- Dipsogenic DI = Stimulated serum copeptin >4.9pmol/L
If a diagnosis of central DI is made, the patient will undergo an MRI to identify any lesions or pathology that may be causing the condition.
What is the management of DI?
Conservative:
- Treat underlying cause
- Easy access to water and adequate fluid intake.
- Patient education including what to do if they become unwell.
- Low solute diet to reduce osmotic load.
Medical:
- Central DI = desmopressin (sublingual, intranasal, SC, IV or IM)
- Nephrogenic DI = focused on treating underlying cause and conservative measure however some medications can be considered to help with symptoms. These include: Thiazide diuretics, Prostaglandin synthesis inhibitors
Managing an inpatient with DI:
- Fluid status assessment.
- Monitor serum Na+ and urine output.
- Appropriate fluid replacement.
- Strict adherence to patient’s desmopressin requirement.
- Avoidance of rapid overcorrection of hypernatraemia.
What is Fibromuscular dysplasia?
An idiopathic non-atherosclerotic, non-inflammatory disorder of arteries encompassing two subtypes, focal and non-focal FMD
What arteries are most commonly affected by FMD?
Renal artery FMD
Cerebrovascular (carotid/vertebral artery) FMD
What are the key features of renal artery FMD?
- Hypertension (74%), resistant to medical management.
- Abdominal bruit in the absence of atherosclerotic risk factors
- Unilateral small kidney on imaging, with no urological cause
What are the key features of symptomatic cervical artery FMD?
- Severe or chronic migraines (70%)
- Pulsatile tinnitus (22%)
- Cervical bruit
- Unilateral head/neck pain
- Focal neurology suggesting cervical artery dissection (ipsilateral ptosis, miosis)
What are the investigations for FMD?
Bloods:
- Lipid profile - hyperlipidaemia modifiable risk factor for atherosclerosis, not typically present in FMD
- ESR and auto-antibody screen - arteriopathies such as GCA, Takayasu’s arteritis have elevated ESR and/or presence of serum auto-antibodies
Imaging:
- First line imaging = CT-angiography (CTA) local to the suspected site e.g. renal artery
- MR-angiography second line if CT is contraindicated.
- Intra-cranial CT- or MR-angiography is recommended at least once (regardless of disease site) to screen for intracranial aneurysm.
Gold standard:
- If CTA is negative and significant clinical suspicion remains, catheter-based angiography is the gold standard diagnostic technique
- Also used in CTA -confirmed FMD where it can offer further clinically valuable information
What is the management of FMD?
- Oral Anti-platelet therapy
- Management of hypertension - ACE-Is or ARBs first line renovascular hypertension (BBs may be protective following coronary artery dissection if it occurs)
- Surgical management of critical stenosis
- Smoking cessation
What are the complications of FMD?
- Spontaneous coronary artery dissection (SCAD)
- Renal infarction
- Cervical artery dissection (CeAD)
What is Goodpasture’s disease?
Autoimmune disease where antibodies attack the alpha-3 subunit of type IV collagen found in the basement membrane of the lungs and kidneys.
This anti-glomerular basement membrane (anti-GBM) disease leads to small vessel vasculitis in the kidneys and lungs causing bleeding in the lungs and renal failure.
What are the clinical features of Goodpasture’s?
- Haemoptysis
- Cough
- Shortness of breath
- Nausea and vomiting
- Chest pain
- Decreased urine output
- Fatigue and malaise
- Haematuria
- Lung crackles
- Fever
- Lower extremity oedema
