Renal Flashcards
Benign renal tumours?
Angiomyolipoma
Oncocytoma
Malignant renal tumours?
Clear Cell RCC (75%)
Papillary RCC (15%)
Chromophobe RCC (5%)
Collecting Duct RCC (<1%) v aggressive
What is the most common benign renal tumour?
Angiomyolipoma
Why may angiomyolipomas get removed even though they are benign?
Because there is a risk of severe haemorrhage when they are large
What should be considered if there are bilateral angiomyolipomas?
Tuberous Sclerosis
Genes TSC1 and TSC2
Features of oncocytoma?
1/3 cases have central scar
microscopically solid nests of eosinophilic cells
Bilateral or multifocal oncocytoma should make you consider?
Birt-Hogg-Dube syndrome
What accounts for 90% of primary renal malignancies?
RCC (90%)
Risk factors for RCCs?
smoking obesity HTN acquired cystic kidney disease (from dialysis) genetic factors
Classic presentation of RCCs?
Classic triad (flank pain, mass, haematuria) - only 10% Incidental CT finding- 50%
What occurs in 30% of patients with RCC?
Paraneoplastic Syndromes
Treatment of RCC?
If localised- partial or radical nephrectomy
If mets- surgical metastasectomy (if low volume), cytoreductive nephrectomy (? benefit)
How many patients who undergo ‘curative’ resection for RCC still develop mets?
30-40%
Inheritance pattern of Von Hippel Lindau Disease?
Autosomal Dominant
What carcinomas are associated with Von Hippel Lindau disease?
Clear cell RCC and clear cell cysts
Retinal/ cerebellar hemangioblastomas
Pheochromocytoma
What type of transformation is associated with a very bad prognosis?
Sarcomatoid transformation
What is the name given to a nephroblastoma?
Wilm’s tumour
When does Wilm’s tumour occur?
In childhood
98% in under 10s
Genes associated with Wilm’s tumour?
WT1 and WT2 on chromosome 11
How are Wilm’s tumours detected?
Often as a palpable mass
Can be very large in size
Prognosis of Wilm’s tumour?
Good- over 90% long term survival
Benign tumours of the urinary tract?
Urothelial papillomas
Inverted urothelial papilloma
leiomyoma
Malignant tumours of the urinary tract?
Urothelial carcinoma (>90%)
SCC
Adenocarcinoma
Epidemiology of bladder cancer?
Risk increases with age
50s-80s
M>W
Causes of haematuria?
Cancer (RCC, upper urothelial carcinoma, bladder cancer, advanced prostate cancer) Stones Infection Inflammation BPH (large)
Risk factors for bladder cancer?
smoking occupation pelvic radiotherapy immunosuppression with cyclophosphamide stones Schistosoma haematobium infection genetics (rarely)
Clinical features of bladder cancer?
haematuria (gross or microscopic) painful micturition urgency frequency weight loss, bone pain, pelvic mass
Diagnosis of bladder cancer?
USS, CT, MRI
Histology Gold Standard
Urothelial Carcinoma in Situ Features?
high grade flat urothelial lesion
reddening or granularity of mucosa
diagnosed by urine cytology as cells are readily shed
Risk of urothelial carcinoma in situ progression?
High risk
50% become invasive carcinoma within 5 years
Treatment of urothelial carcinoma in situ?
Intravesical BCG
Treatment of urothelial carcinoma?
high grade superficial tumours- intravesical BCG
detrusor muscles invasive tumours- radical cystectomy or external beam radiotherapy
high risk of recurrence
Secondary malignant tumours of the bladder usually come from?
Prostate
Rectum
Cervix
What percentage of malignant bladder tumours are secondary?
15%
Acute pyelonephritis causative organisms?
E coli proteus Klebsiella Enterobacter Pseudomonas
Clinical features of acute pyelonephritis?
loin pain, fever, rigors, malaise
Predisposing factors for acute pyelonephritis?
urinary tract obstruction, DM, VUR, pregnancy, instrumentation
2 paths for pyelonephritis?
Lower urinary tract (ascending)
Haematogenous (endocarditis)
Characteristics of chronic pyelonephritis?
interstitial inflammation and scarring
Causes of chronic pyelonephritis?
Chronic obstructive (unilateral or bilateral) Reflux associated
What is hydronephrosis?
dilatation of the renal pelvis and calyces
atrophy of the renal parenchyma
caused by obstruction to urine outflow
Causes of obstruction that causes hydronephrosis?
Congenital
Acquired (foreign body, tumour, BPH, inflammation)
When does bilateral hydronephrosis occur?
Only when obstruction occurs below the level of the ureters (e.g., BPH)
What occurs if hydronephrosis is left untreated?
irreversible damage and ESRF
Renal failure definition?
renal dysfunction resulting in elevated blood urea and creatinine and reduction in GFR with metabolic and endocrine disturbances
Types of renal failure?
Acute (AKI)
Chronic (CKD)
Causes of renal failure?
Pre-renal - circulatory failure
Renal - Glomerular (GN, DM, amyloid), Tubular (ATN, tubulointerstitial nephritis), vascular (HTN, vasculitis)
Post-renal- obstruction
Acute Renal Failure Onset?
develops over days/weeks
potentially reversible
Acute Renal Failure Clinical Features?
oliguria, fluid retention, symptoms of uraemia, arrhythmias, metabolic acidosis, bleeding tendency, retention of drugs, lower response to infection, lower wound healing
Metabolic disturbances of AKI?
Inc. urea Inc. creatinine Inc. H+ Inc. K+ Inc. PO4 Inc. Na and water retention
What is acute tubular necrosis (ATN)?
often referred to as acute tubular injury
occurs in 3 main contexts: ischaemia, following nephrotoxic agents, damage from pigments
3 phases of ATN?
initiating, maintenance, recovery
Macroscopic appearance of ATN?
cortical pallor and swelling, medullary congestion
Microscopic features of ATN?
loss of brush border of proximal tubular epithelial cells epithelial flattening granular casts tubular mitoses interstitial oedema
minimal interstitial inflammation
CRF timeline?
Over months/years
Irreversible
Main causes of CKD?
chronic GN, chronic pyelonephritis, DM, polycystic kidney disease, HTN, drugs, hereditary
Histological feature of CKD?
interstitial fibrosis
tubular atrophy
global glomerulosclerosis
Presentation of CKD?
Picked up incidentally
Follow up of known illnesses
Symptoms of uraemia
What causes renal osteodystrophy?
CRF -> phosphate retention and hypocalcaemia
- > secondary hyperparathyroidism
- > inc. osteoclast activity and bone resorption
Electrolyte change in CKD?
Dec. Ca, Inc. PO4, Inc. PTH
Characteristics of nephritic syndrome?
RBCs and red cell casts in urine renal dysfunction oliguria oedema HTN
Characteristics of nephrotic syndrome?
proteinuria (3.5g/24hrs)
hypo-albuminemia
oedema
hyperlipidaemia
Glomerular changes in renal disease?
Hypercellularity
Thickening of GBM
Crescent formation
Who is Minimal Change Disease common in?
Children
Clinical features of Minimal Change Disease?
selective proteinuria (nephrotic levels) normal BP and renal function no RBCs
Pathophysiology of Minimal Change Disease?
direct injury to podocytes due to abnormal cytokine response
Treatment of Minimal Change Disease?
90% respond to steroids
Detection of Minimal Change Disease?
Light microscopy- normal glomeruli
Immunofluorescence- negative
Electron microscopy- extensive food process effacement
Clinical features of Focal Segmental Glomerulosclerosis (FSGS)?
usually nephrotic levels of proteinuria (>3.5mg/24 hours)
Treatment of FSGS?
no cure
doesn’t usually respond to steroids
recurs even post-transplant
Detection of FSGS?
Light microscopy- FSGS
IF- negative
EM- extensive foot process effacement
What is the commonest cause of nephrotic syndrome in adults?
Membranous glomerulonephritis
What is the pattern of progression in membranous glomerulonephritis?
1/3 remit
1/3 continue
1/3 progress to renal failure
Detection of membranous glomerulonephritis?
LM- thickening of glomerular capillary walls, silver stain- BM ‘spikes’
IF- IgG and complement, granular along capillaries
EM- subepithelial immune-complex deposits
When does post-infectious glomerulonephritis occur?
4 weeks after Group A streptococcus infection classically
Presentation of post-infectious glomerulonephritis?
Majority are nephritic presentation
5-10% with nephrotic range proteinuria
Prognosis of post-infectious glomerulonephritis?
in children good- 95% full recovery
in adults more variable
Bad prognostic factors in post-infectious glomerulonephritis?
nephrotic presentation
crescents
Detection of post-infectious glomerulonephritis?
LM- diffuse global proliferative GN with neutrophils ++
IF- granular capillary walls and lesser mesangial IgG and C3
EM- scattered subepithelial ‘hump shaped’ deposits +/- mesangial deposits
What is the clinical presentation of crescentic GN?
Rapidly progressive GN
Microscopy of Crescentic GN?
proliferation of extra capillary and inflammatory cells
Causes of RPGN?
Pauci-immune GN
Anti-GBM disease (Goodpasture syndrome)
Immune-complex mediated
What is Pauci-immune vasculitis?
systemic disorder
characterised by inflammation of blood vessels
What is Pauci-immune GN usually associated with?
Anti-neutrophil circulating antibodies (ANCA)
How does Pauci-immune GN usually present?
Usually nephritic
treatable if caught early
What is anti-GBM disease/ Goodpasture syndrome?
production of auto-antibodies against alpha 3 chain of type IV collagen which if found in glomerular BM and in the lung
What are the 2 major features of Goodpasture syndrome?
haemoptysis
acute renal failure (rapidly progressive esp. in young males)
Treatment of anti-GBM/ GP syndrome?
plasmapheresis and immunosuppression
Detection of anti-GBM GN?
LM- segmental necrotising GN with crescents
IF- global linear IgG along capillary walls
EM- nothing
What is membranoproliferative GN?
combined nephritic/nephrotic presentation often with hypocomplementemia and progressive renal failure
How many types of membranoproliferative GN are there?
2
Type I
Type II- dense deposit disease
What percentage of membranoproliferative GN progress to ESRF?
40%
Detection of membranoproliferative GN?
LM- diffuse global endocapillary hypercellularity with thickening of capillary walls
IF- IgG and IgM complement, granular capillary wall and mesangium
EM- subendothelial and mesangial complexes with reduplication of the GBM
What disease is related to IgA nephropathy?
Henoch-Scholein purpura (HSP)
Detection of IgA nephropathy?
LM- variable, usually mesangial hypercellularity
IF- mesangial IgA deposition
EM- mesangial immune deposits
Detection of diabetic nephropathy?
LM- mesangial expansion, capillary wall thickening and arteriolar hyalinosis
IF- none
EM- diffuse BM thickening +/- foot process effacement
Renal amyloidosis typically presents as?
Nephrotic range proteinuria
In children, who are UTIs most common in?
Uncircumcised boys
2 paths of UTIs?
ascent of bacteria (more common)
haematogenous (S. aureus)
When are asymptomatic UTIs significant?
During pregnancy
In what patients would a suprapubic aspirate be most appropriate?
Neonates
2 media for bacterial cultures?
MacConkey’s medium
CLED medium
Organisms in UTI?
E Coli (95%) Staph saprophyticus (2%) (sexually active young women) Enterobacter Pseudomonas aeruginosa Streptococci Enterococci
Resistant organisms?
MRSA
ESBL
CPE
VRE
Prevention of re-infection?
Good hygiene
fluids
frequent micturition
*******Not prophylaxis with antibiotics- only promotes resistant strains
Causes of relapsing UTIs?
Stones
Anatomical Abnormalities
No cause (most cases)
Risk factors for UTIs?
Mechanical factors
Host factors
Bacteria factors
Mechanical risk factors for UTIs?
females obstruction catheter VUR pregnancy sexual activity DM neurological
Host factors for UTIs?
host antibacterial mechanisms impaired
Bacteria factors for UTIs?
Fimbriae
Haemolysins
Urease
Why should early morning urine samples be collected?
Tuberculosis
