Anatomy/Physiology
Nephritic/Nephrotic
Tubular/interstitial
Other
100
Describe the flow of blood through renal vessels
Aorta > renal artery > segmental > interlobar > arcuate > cortical radiate (interlobular) > afferent arteriole > glomerulus > efferent arteriole > peritubular capillaries or vasa recta
100
Patient with previous URTI now presents with haematuria and oedema. What is your DDx and why? Can you explain the pathophysiology?
IgA nephropathy
URTI = overproduction of IgA = form immune complexes that deposit in renal mesangium = activate complement in type 3 HSR
Haematuria, proteinuria, RBC casts = nephritic syndrome
Microscopy = granular staining (immune complexes), mesangial proliferation
100
What is the most common type of kidney stone?
Can you list some other types?
Ca oxalate most common
Others: uric acid, cystine, triple/struvite stones
100
What must you consider in a patient with painless haematuria? What investigation will you order?
Bladder cancer (transitional cracinoma)
Must do a cystoscopy to visualise bladder lesions with possible transurethral resection of the tumour
Other tests: urinalysis to determine origin of haematuria, UEC
200
List solutes that are reabsorbed at the PCT and the mechanism by which they are reabsorbed
Na via primary transport (Na/K basolateral pump) and secondary (alongside glucose or H)
Nutrients - glucose, amino acids - via secondary transport with Na
HCO3- via secondary transport
Paracellular passive diffusion of Cl, K, Mg, Ca
200
Most common nephrotic syndrome in children? Most common nephrotic syndrome in adults?
Briefly explain their mechanisms
Adults = Membranous (immune complexes activate complement and injure podocytes)
Children = Minimal Change (podocyte damage by T cells)
200
What are the aetiologies of Acute Tubular Necrosis? Where is it more likely to occur and why?
Ischaemia (distal part of PCT further from perfusion) = hypovolaemia, embolism
Nephrotoxins (PCT closest to toxin) = contrast, aminoglycosides, myoglobin
200
What does a 'granular' or 'linear' staining pattern mean on immunofluorescence? Give examples
Granular = immune complex deposition e.g. membranous (nephrotic), IgA nephropathy (nephritic), streptococcal (nephritic)
Linear = immunoglobulin deposition e.g. Goodpasture's (nephritic)
300
Explain the intrinsic mechanisms that regulate GFR
Myogenic response - high GFR = stretching of afferent arteriole opens Ca channels, Ca influx promotes vasoconstriction, reducing GFR
Tubuloglomerular feedback via Macula Densa cells detecting high [NaCl] in filtrate (suggesting low GFR) = release vasoconstrictor ATP = constriction of afferent = reduced GFR
300
Describe the pathophysiology of nephritic syndrome? Compare it to nephrotic. What might you see in their urine?
Nephritic = glomerular inflammation with haematuria (acanthocytes, RBC casts)
Nephrotic = injury to podocytes, causes massive proteinuria (frothy urine), loss of proteins (= hypoalbuminemia, hypercoagulability, increased synthesis of lipids with fatty casts/lipiduria)
300
Which RTA involves a mutated H/K pump? Explain the consequences of this (serum findings).
RTA type 1 involving the distal tubules
Damaged H/K pump = no H excretion or K reabsorption
Metabolic acidosis (high H remaining in serum) and hypokalaemia (no K reabsorption)
300
Go around the group and each give 1 suggestion on how you would manage a patient with CKD and why
Na, K, protein, fluid restriction
Avoid nephrotoxic medications
Control their risk factors - BP, BGL, lipids
Manage anaemia
Manage acid/base balance
Manage CKD-MBD, give calcitriol (active vitamin D)
Consider dialysis
Renal transplant
400
How is HCO3- reabsorbed in the distal nephron?
Intercalated cells with carbonic anhydrase - α intercalated cells secrete H and reabsorb HCO3
400
Pathophysiology/aetiology of streptococcal GMN?
Clinical features?
Infection with GAS = immune complexes deposit within the glomerular basement membrane via molecular mimicry = complement and inflammation destroys glomeruli
Haematuria, oedema
400
Compare the clinical signs of someone with Pyelonephritis vs Renal Calculi
Pyelonephritis = costovertebral tenderness and flank pain, nausea, vomiting, chills, fever, dysuria
Renal Calculi = COLICKY pain loin to groin, dysuria, haematuria (macro or micro), dysuria, frequency and urgency
400
What are the 3 types of AKI? Give an example of each.
Pre-renal from reduced perfusion e.g. hypovolaemic shock
Intrinsic from direct kidney damage e.g. glomerulonephritis (vascular) or tubular necrosis
Post-renal from obstruction of urinary flow e.g. BPH, tumours
500
Can you list 3 things that would trigger the kidneys to release renin?
Afferent arteriolar stretch mechanism (reduced MAP = reduced stretch = less Ca influx = reduced release of renin)
Macula densa detect low NaCl in filtrate = release PGE2 to afferent to release renin
Sympathetic = activation of JG cells to release renin
Anything that activates RAAS!
500
This nephritic syndrome has 3 subtypes based on their aetiology. Patients often present with haemoptysis along with deranged renal function tests. What is the DDx? What are the subtypes?
Crescenteric GMN
Type 1 = Goodpasture's due to anti-GBM
Type 2 = immune complexes (e.g. IgA nephropathy, lupus, streptococcal)
Type 3 = pauci-immune (neither anti-GBM or immune complexes), usually ANCA positive e.g. granulomatosis with polyangiitis, eosinophilic GPA, microscopic polyangiitis
Rapid destruction of glomeruli (inflammatory cells infiltrate into Bowman space and compress glomerulus)
500
What do you expect to see in the urine of someone with Fanconi Syndrome? Why?
High glucose, AA, phosphate due to inability to reabsorb in PCT
Urine pH will be alkaline initially (as HCO3- is lost) but since DCT is unaffected, more H will be excreted to compensate and so urine pH will then decrease
Negative urine anion gap (kidneys try to regenerate more HCO3- and excrete H as NH4)
High NH4 in urine = negative urine anion gap
500
A 60-year-old man with haematuria, flank pain, and a palpable renal mass. What is the likely diagnosis?
What are the risk factors?
What is the histological classification? Which one is more common?
Renal cell carcinoma
Risks = smoking, obesity, Von Hippel-Lindau, Tuberous Sclerosis, but mostly idiopathic cause
CLear cell renal cell carcinoma (most common) arising from the PCT renal tubular cells
Or non-clear cell (papillary, chromophobe)