Renal I Flashcards
raised urinary WCC and eosinophils, alongside impaired renal function indicates what pathology? [1]
Acute interstitial nephritis
A patient reports haematuria following a TURP.
Describe what is occurring and how to fix x
This patient presents with clot retention after transurethral resection of prostate (TURP).
It is a common complication following the procedure, hence most patients are advised to refrain from walking and lifting heavy weights for at least one week post-surgery. In the event of clot retention, an emergency clot evacuation and diathermy to the bleeding point is the definitive management.
A patient is suffering from a kidney stone.
After taking a history from them you learn their mother also has a history of kidney stones.
What is the most likely type of kidney stone found and why? [2]
Cystine
- result from inherited recessive inborn errors of metabolism causing disruption in cystine transport and decreased absorption from the renal tubule.
A patient has renal tubular acidosis. What is the most likely cause of their stone? [1]
Calcium phosphate stones
A patient has a renal stone. As part of the work up you perform an urinalysis and obtain the pH. This is identified as being 7.5
What is the most likely cause of the stone?
Calcium phosphate
Calcium oxalate
Uric acid
Struvate
Cystine
A patient has a renal stone. As part of the work up you perform an urinalysis and obtain the pH. This is identified as being 7.5
What is the most likely cause of the stone?
Calcium phosphate
Calcium oxalate
Uric acid
Struvate
Cystine
Dialysis disequilibrium syndrome is a rare complication of dialysis.
How long after dialysis starting does it usually occur? [1]
What is the pathological consequence of this syndrome? [1]
Dialysis disequilibrium syndrome is a rare complication and usually affects those who have recently started renal replacement therapy. It is caused by cerebral oedema, but the exact mechanism is unclear.
Describe what is meant by Alport’s syndrome [1]
State a mneumonic for Alport’s syndrome features [3]
Alport’s syndrome:
- due to a defect in the gene which codes for type IV collagen resulting in an abnormal glomerular-basement membrane (GBM). The disease is more severe in males with females rarely developing renal failure.
- A favourite question is an Alport’s patient with a failing renal transplant. This may be caused by the presence of anti-GBM antibodies leading to a Goodpasture’s syndrome like picture.
Helpful mnemonic:
Can’t see - Lenticonus
Can’t pee - CKD, hematuria
Can’t hear a high C - sensorineural deafness
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)
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
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
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
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 are the diseases that cause glomerulonephritis? [5]
- Membranous nephropathy
- Post streptococcus nephropathy
- Focal segmental glomerulosclerosis
- IgA nephropathy
- Goodpasture’s disease
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.
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
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.
