MET3 Revision: Renal I Flashcards
Define the term ‘acute kidney injury’ [3]
- Rise in serum creatinine of > or equal to 26 μmol/L within 48 hours
- or 1.5x increase in serum creatinine known or presumed to have occurred in the last 7 days
- or 6 hours oliguria (urine output < 0.5ml/kg/hour)
Which populations are at risk of AKI? [6]
- · Elderly
- · CKD patients (eGFR < 60ml/min/1.73m2)
- · Cardiac failure
- · Liver disease
- · Vascular disease
- · Taking potentially nephrotoxic medications (ARBS, ACEIs, NSAIDs)
What is diabetic kidney disease? [1]
How does it present:
urine findings? [2]
US? [1]
This typically presents with:
- proteinuria and albuminuria
- reduced estimated glomerular filtration rate (eGFR) in the absence of signs or symptoms of other primary causes of kidney damage.
On ultrasound, the kidneys may be enlarged if diabetes is poorly controlled
Describe how you manage AKIs
IV fluids for dehydration and hypovolaemia
- If hypovolameic: give bolus fluids (250-500mls)
- (Assess BP (lying/standard), JVP, HR, Cap. refill, Conscious level, Lactate, Weight (important if on dialysis))
- If >2 L given & remains hypoperfused: give further circulatory support (+ve inotropes)
- If euvolaemic & passing urine: give maintenence fluids (est. daily output + 500ml)
Withhold medications that may worsen the condition
- NSAIDs
- ACE inhibitors
Withhold/adjust medications that may accumulate with reduced renal function:
- metformin
- opiates
Relieve the obstruction in a post-renal AKI:
- insert a catheter in a patient with prostatic hyperplasia
Dialysis may be required in severe cases
How do you monitor patients with AKI? [5]
- Urine catheter: monitor hourly input/output
- U&Es, bone profile, venous bicarbonate at least once a day whilst creatitine rising
- Blood gases & lactate: if septic & underperfused
- Daily weights (measurement of daily body weight change can provide a more accurate method of monitoring body fluid status)
- Regular fluid management
Describe how you would investigate AKI [3]
Urine dipstick:
- UTI (leukocytes & nitrates)
- Glomerulonephritis (haematuria & leuocytes)
- Acute interstitial nephritis (leucocytes by themselves)
- Glucose suggests diabetes
Bloods:
- U&E: important to ID hyperkalaemia
- FBC, CRP & bone profile
- ANA & ANCA: ID vasculitis
- anti-GBM (formation of anti-GBM antibodiescan be directed against collagen in the kidneys and lungs)
- complement levels (C3, C4)
- RF
- immuglobulins
- creatine kinase (evidence of rhabdomyolysis)
- LFTs
- HIV, HCV, IgG and Hep B Surface antigen
Ultrasound (within 24hrs; within 6hrs if due to sepsis obstruction)
- should be performed in new cases of AKI
Explain why each of the following may worsen AKIs: [3]
ACE inhibitors
NSAIDs;
Aminoglycoside antibiotics
ACE Inhibitors:
- depress A-II and thus inhibit A-II-mediated vasoconstriction of the efferent arteriole (efferent arteriole dilates)
- This lowers glomerular filtration pressure and decreases the glomerular filtration rate
NSAIDS:
- Reduced renal plasma flow caused by a decrease in prostaglandins, which regulate vasodilation at the glomerular level.
Aminoglycosides:
- have a preferential accumulation in the kidney cortex
How can you manage hyperkalamia (if have AKI), if:
ECG changes [1]
If K > 6.5mmol/L [1]
ECG changes:
* Calcium gluconate (stabilises cardiac membrane)
If K > 6.5mmol/L:
* Insulin dextrose (causes intracellular movement of AKI)
How do you treat AKI complicated pulmonary oedema [3]
GTN infusion
Furosemide > 80 mg bolus
Recovery requires functioning renal system
Refer adults, children and young people immediately for renal replacement therapy if any of the following are not responding to medical management
Describe three differential diagnoses for AKI [3]
:Chronic kidney disease:
- Reduced kidney function with elevation of creatinine is chronic (>3 months), although there may be acute on chronic kidney disease.
Increased muscle mass:
- Any elevation of creatinine is minor and typically non-acute.
Drug AEs
- Certain medicines such as cimetidine or trimethoprim may lead to an elevation of creatinine that is minor and non-acute.
Define uraemia [1]
State 4 pathological consequences of uraemia [4]
Uraemia: build up of urea in your blood. It occurs when the kidneys stop filtering toxins out through your urine.
Causes:
- nausea and vomiting
- altered mental state & confusion by causing encephalopathy
- acute pericardititis
- asterixis
How can microscopy be used to help distinguish between causes of AKI [3]
It is not widely used in the UK but is more commonly performed in other countries (e.g., USA, China). * It may reveal:
- Granular casts in acute tubular injury
- Red cell casts in glomerulonephritis/vasculitis
- Oxalate crystals - suggestive of ethylene glycol poisoning}}
What is the difference between crystalloid & colloid fluids for resuscitation of AKI? [2]
Crystalloids have small molecules, are cheap, easy to use, and provide immediate fluid resuscitation, but may increase oedema
Colloids have larger molecules, cost more, and may provide swifter volume expansion in the intravascular space, but may induce allergic reactions, blood clotting disorders, and kidney failure.
Cyrstalloids are preffered in AKI
A patient is suspected to have AKI and after testing their bloods, is found positive for ANA and ANCA. What is their likely cause of AKI? [1]
Antineutrophil cytoplasmic antibodies (ANCAs) cause ANCA and ANA associated vasculitis
Acute interstitial nephritis accounts for 25% of drug-induced acute kidney injury.
Name 5 drugs / classes that can cause this [5]
penicillin
rifampicin
NSAIDs
allopurinol
furosemide
Name 3 systemic diseases and 2 infections that cause acute interstitial nephritis [5]
systemic disease: SLE, sarcoidosis, and Sjögren’s syndrome
infection: Hanta virus , staphylococci
What are features of acute interstitial nephritis? [5]
Features:
* fever, rash, arthralgia
* eosinophilia
* mild renal impairment
* hypertension
* sterile pyuria
* white cell casts
One of the best ways to differentiate between acute kidney injury (AKI) and chronic kidney disease (CKD) is what type of imaging? [1]
Explain your answer [4]
One of the best ways to differentiate between acute kidney injury (AKI) and chronic kidney disease (CKD) is renal ultrasound
most patients with CKD have bilateral small kidneys. Exceptions to this rule include:
* autosomal dominant polycystic kidney disease
* diabetic nephropathy (early stages)
* amyloidosis
* HIV-associated nephropathy
What mineral serum level would indicate chronic kidney diseae? [1]
Hypocalcaemia
How can you distinguish between AKI and dehydration? [1]
Urea:Creatitine Ratio:
In dehydration: urea that is proportionally higher than the rise in creatinine
Given the likely diagnosis of haemolytic uraemic syndrome, what are likely expected investigational findings? [3]
acute kidney injury
microangiopathic haemolytic anaemia
thrombocytopenia
Which form of GN has an overlap with IgA nephropathy? [1]
How does this commonly present? [3]
Henoch-Schonlein purpura: IgA mediated samlled vessel vasculitis
- palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs
- abdominal pain
- polyarthritis
Which drugs should be stopped in cases of AKI? [5]
DIANA:
D: diuretics
I: Ionated contrasts
A: ace inhibitors / ARBs
N: NSAIDs
A: aminoglycosides
Define what the triad of nephrotic syndrome are [3]
A triad of the following:
1. Proteinuria (> 3g/24hr) causing
2. Hypoalbuminaemia (< 30g/L) and
3. Oedema
Which are the diseases that cause glomerulonephritis? [5]
- Membranous nephropathy
- Post streptococcus nephropathy
- Focal segmental glomerulosclerosis
- IgA nephropathy
- Goodpasture’s disease
What symptoms are usually seen in glomerulonephritis? [4]
Haematuria (blood in the urine), which can be microscopic (not visible) or macroscopic (visible)
Oliguria (significantly reduced urine output)
Proteinuria (protein in the urine), but less than 3g per 24 hours (higher protein suggests nephrotic syndrome)
Fluid retention
Describe the pathophysiology of primary and secondary FSGS [2]
Primary FSGS: Idiopathic
- A circulating factor that damages podocytes in the glomeruli leading to foot process effacement
- Proteins and lipids pass through BUT ALSO get stuck inside th glomerulus causing hyalinosis and eventually sclerosis.
Secondary FSGS: SCA, post- HIV / Herion / Lithium
- represents an adaptive response to renal injury that is usually associated with less significant proteinuria and renal impairment.
What does renal biopsy depict in FSGS? [1]
Renal biopsy shows focal and segmental sclerosis and hyalinosis on light microscopy, and effacement of foot processes on electron microscopy. Sclerosis is seen in this light microscopy image next to the bowmans capsule.
Define membranous nephropathy [1]
Membranous nephropathy (MN) is an immunologically mediated disease characterised by glomerular basement membrane thickening in the absence of significant cellular proliferation on histology
Describe the pathophysiology of membranous nephropathy [3]
Autoimmune reaction against important antigens in the filtration barrier.
This causes development of autoantibodies: directed against the phospholipase A2 receptor (PLA2R) that are highly expressed on podocytes are a major cause of primary MN seen in up to 80% of case
Causes the formation of immune deposits and subsequent thickening of the glomerular basement membrane.
Histology shows IgA deposits and mesangial proliferation.
Describe the biospy freatures of MN [3]
A thickened GBM with subepithelial electron-dense droplets.
This creates a ‘spike and dome’ appearance.
It is thought these subepithelial deposits are immunoglobulins, as it is primarily an autoimmune disease.
There will also be thickened capillary loops
Investigations for IgA nephropathy:
A diagnosis of IgAN can only be made by WHAT investigation? [1]
What are the results for this investigation? [1]
Kidney biopsy:
* Mesangial IgA deposition either by immunofluorescence or immunoperoxidase studies.
What does biopsy of kidneys of a patient with post-streptococcal glomerulonephritis depict? [2]
Subendothelial deposits activate complement, leading to the infiltration of inflammatory cells: neutrophils! and proliferative glomerulonephritits
Subepithelial ‘humps’ of deposits trigger inflammation, leading to epithelial cell damage, which allows the protein to filter more freely into the urine.
Describe what rapidly progressive glomerulonephritis is? [1]
How does it appear histologically ? [1]
Any aggressive GN, rapidly progressing to renal failure over days or weeks.
presents with an acute severe illness but tends to respond well to treatment.Histology shows glomerular crescents.
Describe what rapidly progressive glomerulonephritis is? [1]
How does it appear histologically ? [1]
