renal Flashcards
classification of CKD

proteinuria?

earliest expression of diabetic nephropathy?
microalbuminuria
how to differentiate between pre-renal failure and intrinsic renal damage

functions of kindey
maintain water + electoclyte balance
acid-base balance
excrete waste products (urea + creatinine)
produces erythropoetin adn renin
function of proximal covoluted tubule?
loop of henle?
distal convoluted tubule?
PCT = reabsorbs 100% glucose, proteins, carbohydrates
* 70% Na+ and H2O
Loop of Henle = creates hypeosmotic environment in medulla
DCT = reabsorbs water, Na+ and bicarbnate, excretes K+ and H+
epithelial cells lining glomerular capallaries?
glomerular filter?
podocytes
glomerular filter = enodthelium of capillary + basement membrane + pedicels of podocytes
blood supply to renal medulla?
vasa recta
hormone that acts on DCT?
ALDOSTERONE
increases reabsorption of Na+ thus water, increasing BP
what hormone acts on collecting ducts?
ADH - increases water reabsoprtion
structures lined by transitional epihtelium (urothelium)?
features
mior calyx, major calyx, ureter, bladder
cells of luminal surface called umbrella cells because domed

urethra of female vs male
female 3-5cm
* lined by trnasitional epithelium which transitions to stratified squamous
male 20cm
* prostatic urethra (from bladder through prostate) - transitional epithelium
* membranous (from prostate to bulb of penis) - transitional changes to straified columnar
* penile urethra - changes to stratified squamous
osmolarity of body fluids
300 mosmol/l

body water components
ICF = 70%
ECF = 30%
* ECF = plasma (20%), interstitial fluid (80%), lymph
how to calculate body fluid compartments
TBW = ICF + ECF
tracer for ECF = inulin
TBW = H2O
ICF = TBW - ECF
ionic concentrations of ICF vs ECF

osmotic concentratiosn of ECF vs ICF
IDENTICAL 300 mosmol/l
extracellular K+?
>95% of K+ is intracellular
leakages can cause
* muscle weakness + paralysis
* arrhythmias and cardaic arrest
regulation of renal blood flow thus GFR
extrinsic = sympathetic via baroreceptor reflex
intrinsic = myogenic + tubuloglomerular feedback

if capillary blood pressure falls…
GFR will decrease

kidney response to haemorrhage

mucula densa cell function?
sense NaCl content of tubular fluid
high levels = constriction of afferent arterioles
other determinants of glomerular filtration rate

plasma clearance of inulin? - what is used instead
glucose?
what is used to calculate renal plasma flow?
inulin = GFR (creatinine used clinically)
glucose = 0
para-amino hippuric acid (PAH) used to calculate renal plasma flow
accelerated hypertension?
medical emergency
diastolic BP >120 mmHg
papilloedema
encephalopathy, fits, cardiac failure, acute renal failure
leukonychia?
splinter haemorrhages?
leukonychia seen in nephrotic syndrome - low albumin
splinter haemorrhages - CKD, vasculitis
UTI urinalysis
leukocytes + nitrites
normal 24 hour urine?
normal P:CR
grading proteinuria
normal 24 hour = <150mg/24 hours
urine protein:creatinine = 0.5g/24 hours
asymptomatic low grade = PCR <1g/day
heavy proteinuria = PCR 1-3 g/day
nephrotic = PCR >3g/day
ACR >30 = proteinuria
what does this show?

LVH!!
(probably severe hypertension)
what does this show?

hyperkalaemia - tall teneted T waves
Acute kidney injury?
classifcation?
An abrupt (<48 hrs) reduction in kidney function defined as:
- Increase in serum creatinine by >26.4umol/l (50%)
- Reduction in UO

nephrotic syndrome triad?
proteinuria >3g/day
hypoaluminaemia
oedema

nephritic syndrome symptoms?
AKI
oliguria
oedema/fluid retention
hypertension
active urinary sediment - RBCs (haematuria), leukocytes
risk factors AKI?
older age
CKD
Diabetes
Cardiac failure
Liver disease
PVD
Previous AKI
Also – hypotension, hypovolaemia, sepsis, deteriorating NEWS, recent contrast, exposure to certain medications
Ax pre-renal AKI?
Tx?
pre-renal AKI (commonest cause of AKI in hopsital - sepsis + severe dehydration)
- hypovolaemia = haemorrhage, burns
- hypotension = cardiogenic shock, sepsis, anapylaxis
- renal hypoperfusion = NSAIDs, ACEI, hepatorenal syndrome, rhadbomyolysis
Tx = fluid challenge for hypovolaemia (NaCL, NOT dextrose)
Ax AKI?
pre-renal
renal
post-renal
untreated pre-renal AKI?
leads to tubular necrosis
Ax renal AKI?
Vascular
- Vasculitis, renovascular disease
Glomerular
- Glomerulonephritis
Interstitial nephritis
- Drugs - antibiotics e.g. penicillin
- Infection (TB)
- Systemic (sarcoid)
Tubular injury
- Ischaemia
- Drugs (gentamicin)
- Contrast
- Rhabdomyolysis
s/s renal AKI?
Anorexia, weight loss, fatigue
N + V
Itch
Fluid overload – oedema, SOB
Signs
- Fluid overload – hypertension, oedema, pul oedema, effusions
- Uraemia – itch, pericarditis
- Oliguria
clues to cause of renal AKI?
History e.g. sore throat (antibiotics), rash (vasculitis), joint pains, D + V, haemoptysis
Recent contrast
Drugs
Bloods – eosinophilia, CK
Vascular bruits
Dx renal AKI?
obviously increase in serum creatinine >26.4 (50%)
+ reduction in UO
in addition:
- U + Es (hyperkalaemia)
- FBC + coagulation (abnormal clotting, anaemia, CK)
- urinalysis (haematoproteinuria)
- USS (?obstruction)
- immunology - ANA, ANCA, GBM
Tx renal AKI?
Stop nephrotoxics
Establish good perfusion pressure – fluid resuscitiate (if no improvement = inotropes, vasopressors)
Treat underlying cause
Dialysis if no urine passage
life threatening complications AKI?
Hyperkalaemia
Fluid overload (pulmonary oedema)
Severe acidosis (pH <7.15)
uraemic pericardial effusion
severe uraemia (>40)
post-renal AKI Ax?
Tx?
Obstruction of urine flow leading to back pressure (hydronephrosis)
Ax = Stones, cancer, strictures, BPH
Tx = relieve obstruction, catheter/nephrostomy
life threatening hyperkalaemia?
signs?
Tx?
Life threatening hyperkalemia = >6.5
signs = muscle weakness, T waves on ECG
Tx = calicum gluconate (to protect myocardium), then insulin with 50% dextrose (move K+ back into cells), then calcium resonium (to stop GI absoprtion)
urgent indications for dialysis?
Hyperkalaemia >7 ( or >6.5 unresponsive to therapy)
Sever acidosis pH <7.15
Fluid overload
Urea >40, pericardial rub/effusion
ECG changes hyperkalaemia?

medicines to stop on sick days?
ACE-I and ARBS
NSAIDs
diuretics
metformin + empagliflozin

1 = goodpasture’s syndrome
2 = rhabdomyolysis?
3 = acute tubular necrosis?
4 = obstructive uropathy

furosemide

calcium gluconate

elevated creatinine
kidneys reabsorb….
99% of fluid
99% of salt
100% of glucose
100% of amino acids
50% of urea
0% creatinine
proximal tubule absoprtion + secretion?
fluid is?
Reabsorbed in PT
- 70% Na (via K+ATPase) + water
- 100% glucose + amino acid
- phosphate, sulphate, lactate
Secreted in PT
- H+, neurotransmitters, bile pigments, uric acid, drugs, toxins
fluid is iso-osmitic (~300) in PT
Loop of Henle function?
physiology
formation of hypertonic urine
entire loop functions as countercurrent multiplier
together the loop and vasa recta establish a hyper-osmotic medullary interstitial fluid
ascending vs descending limb loop of henle?

CKD Dx?
complications?
CKD requires 2 samples at least 90 days apart
comps = AKI, falls, fragility
stages CKD?

ACR CKD?

golden rules of CKD?
Monitor people for development/progression of CKD for at least 2-3 years after AKI, EVEN IF serum creatinine has returned to baseline
Advise people who have had AKI that they are at increased risk of CKD
accelerated progression CKD?
risk factors associated wtih CKD progression?
Sustained decrease in GFR of >25% within 12 months
OR
Sustained decrease in GFR of 15/ml/min per year
risk factors = CVD, AKI, hypertension, diabetes, smoking, chronic use of NSAIDs, untreated urinary outflow obstruction, African/Asian origin
people with CKD who should be referred for specialist assessment?
GFR <30 (G4 + 5)
ACR >70
ACR >30 with haematuria
sustained decrease of GFR by 25% in 12 months
poorly controlled hypertension
suspected renal artery stenosis
blood pressure targets CKD?
In people with CKD, aim to keep <140/90
In people with CKD and diabetes, keep <130/80
CKD Tx?
ACE-I/ARB
atorvastatin 20mg
alfacalcidol, phosphate binders, calcimimetic for CKD-MBD
iron therapy for anaemia
Ax CKD?

clinical signs CKD?
Anaemia – conjunctival + palmar pallor
Weight loss
Advanced uraemia
- Lemon yellow
- Uraemic frost
- Twitching
- Encephalopathic flap
- Confusion
- Pericardial rub/effusion
- Kussmaul breathing (metabolic acidosis)
symptoms CKD?
Uraemic
- N + V
- Anorexia
- Weight loss
- Fatigue
- Itch
- Altered taste
- Restless legs
- Muscle twitching
- Difficulties concentrating
- Confusion
Thirst
Anaemia = fatigue, muscle weakness
Pain = bony, neuropathic, ischaemic, visceral
consequences CKD?
Renal
- Pain, haemorrhage, infection
- Haematuria, proteinuria
- Impaired salt and water handling
- Hypertension
- Electrolyte abnormalities
- Acid-base disturbance (metabolic acidosis)
- ESRD
Extra-renal
- CVD
- Mineral and bone disease (extra PTH, calcium moved from inside bones)
- Anaemia
- Malnutrition
ESRD Tx?
dialysis
transplant
CVD in CKD?
Starts early – eGFR <50
Risk increases with microalbuminuria even if eGFR normal
Tx CKD-mineral bone disease
Phosphate restriction
Salt reduction
Potassium restriction
Fluid restriction
meds = alfacalcidol, phosphate binders (aluminium), calcimimetic (Cinacalcet)
renal anaemia?
Target?
renal anemia = HB <100 despite no iron deficiencies
target Hb = 100-120g/l
autosomal dominant polycystic renal disease Ax?
significance?
S/s?
extra-renal features?
Mutation in PKD1 gene
Important cause of ESRD!!
s/s = chronic pain (back), hypertension, haematuria (cyst rupture etc), cyst infection, renal failure
extra-renal:
- hepatic cysts
- intra-cranial aneurysms!!
- cardiac valvular disease
- abdominal/inguinal hernias
Dx ADPKD?
USS = cysts + renal enlargement
CT/MRI
genetics - PKD1

ADPKD genetic counselling?
Offspring of affected individual 50% risk of having disease
Tx ADPKD?
Tolvaptan!
control BP
if progressed to renal failure = dialysis + transplant
autosomal recessive PKD affects?
gene?
cysts where?
S/s?
children - associated with hepatic lesions
gene = PKDH1 on chromosome 6
cysts bilateral + symmetrical, collecting ducts!
S/s
- kidneys always palpable
- hypertension
- recurrent UTI
Alport’s syndrome?
S/s?
Dx?
Tx?
X-linked herediatary nephritis
S/s = haematuria, sensorineural deafness, anterior lenticonus, leiomyoma of oesophagus/genitalia
Dx = suspect in haematuria + hearing loss
renal biopsy characteristic feature = variable GMB thickness
Tx = no specific treatment, treat BP, maybe dialysis/transplant
Anderson Farby’s disease clinical features?
Dx?
Tx?
features = renal failure, angiokeratomas, cardiomyopathy + valve disease, stroke, acroparaesthesia
Dx = plasma a-GAL, renal biopsy
Tx = enzyme replacement - fabryzyme
medullary cystic kidney?
difference from ADPKD?
Dx?
Tx?
autosomal dominant
difference from ADPKD = normal sized/small kindeys (in ARPKD and ADPKD kidneys are enlarged + palpable)
Dx = family history + CT scan
Tx = renal transplant
medullary sponge kidney?
sporadic inheritance - medulla looks like a sponge
fluid in loop of henle?
Tubular fluid leaving loop of Henle entering distal convoluted tubule is hypo-osmotic to plasma
hormones controlling fluid + electolyte balance?
ADH = increased water reabsorption (collecting duct)
Aldosterone = increased Na reabsorption, increased H+/K+ secretion (DCT)
Atrial natriuretic hormone = decreased Na reabsorption
Parathyroid hormone (PTH) = increased calcium reabsorption, decreased phosphate reabsorption
distal tubule fluid?
permeability?
segments?
Tubular fluid is hypo-osmotic to plasma
Distal tubule has LOW permeability to water and urea
Distal tubule can be described as 2 segments (early + late)
- Early = NaCl reabsorption
- Late = Ca, Na, K reabsorption (except K+ is secreted in presence of aldosterone) + H+ secretion
high ADH?
low ADH?
High ADH = high water permability + hypertonic urine
Low ADH = low water permeability + hypotonic urine
diabetes insipidus s/s?
Tx?
s/s = large volumes of dilute urine + constant thirst
Tx = ADH replacement
ADH release?
hypothalamic osmoreceptors!!! = most important
also stimulated by decreased left atrial pressure = increased ADH
GI stretch receptors = inhibits ADH
nicotine stimulates ADH, alcohol inhibits
aldosterone released by?
when?
function?
aldosterone secreted by adrenal cortex
secreted in response to rising K+ or falling Na+ in the blood
OR activation of RAAS
stimulates Na+ reabsorption and K+ secretion in DCT
effect of aldosterone?
Normally 90% of K+ is reabsorbed in proximal tubule
When aldosterone absent, the rest is reabsorbed in the distal tubule (therefore, no K+ excreted in urine)
An increase in [k+] directly stimulates adrenal cortex
Aldosterone stimulates secretion of K+ in distal tubule
A decrease in plasma [Na+] promotes indirect secretion of aldosterone
triggers for renin release from JGA?
reduced pressure in afferent arteriole
macula densa cells (decreased NaCl)
reduced arterial blood pressure
what is responsible for fluid retention in congestive heart failure?
Tx?
RAAS
Tx = low salt diet, loop diuretics + ACE-I

Atrial natriuretic peptide?
Heart produces ANP which is stored in atrial muscle cells
ANP released when cells mechanically stretched due to increase in circulating plasma volume
ANP promotes excretion of Na+ and diuresis
Lowers BP :))
micturation controlled by?
Micturition reflex
- Stretch receptors in bladder wall initiate micturition reflex
- Bladder contraction and opening of internal and external urethral sphincters
Voluntary control
- Tightening of external sphincter and surrounding pelvic diaphragm

aldosterone summary

pH of artrial vs venous blood?
increase in [H+]?
pH of arterial blood = 7.45
pH of venous blood = 7.35
An increase in H+ REDUCES pH
complication of acidosis?
alkalosis?
acidosis = depression of CNS
alkalosis = overexcitability of PNS and then CNS
most important physiological buffer

what is the most common cause of ESRD?
2nd most common?
most common = diabetes
2nd most common = chronic glomerulonephritis
what is glomerulonephritis?
Immune-mediated disease affecting glomeruli
clinical presentation glomerulonephritis?
Damage to endothelial or mesangial cells leads to proliferative lesion + red cells in urine
Damage to podocytes leads to non-proliferative lesion and protein in urine
Ix glomerulonephritis?
Clinical presentation
Blood tests
Urinalysis – haematuria, proteinuria
Urine protein:creatinine ratio
Kidney biopsy
S/s glomerulonephritis?
nephritic syndrome/nephrotic syndrome/mixed
impaired renal function (can lead to ESRD)
hypertension
s/s nephritic syndrome?
indicative of?
Acute renal failure
Oliguria
Oedema/fluid retention
Hypertension
RBCs, RBC and granular casts in urine
Indicative of a proliferative process affecting endothelial cells
nephrotic syndrome s/s?
indicative of?
Proteinuria >3g/day
Hypoalbuminemia (<30)
Oedema
Hypercholesterolaemia
Usually normal renal function
Indicative of a non-proliferative process affecting podocytes
nephrotic syndrome complications?
Infections – loss of antibodies
Renal vein thrombosis - loss of anticoagulants
Pulmonary emboli
Volume depletion – overuse of diuretics may lead to ARF (pre-renal)
Vit D deficiency - also lost in urine
Subclinical hypothyroidism - urinary loss protein-bound thyroid hormones
Ax glomerulonephritis?
idiopathic GN (types discussed later)
secondary = infections, drugs, malignancy, systemic disease (ANCA, lupus, goodpastures, HSP)
crescenteric glomerulonephritis?
Crescentic = presence of crescents in e.g. RPGN in vasculitis
Tx glomerulonephritis?
immunosuppression - corticosteroids, azathioprine, cyclophosphamide/chlorambucil
anti-hypertensives (target <130/80 or <120/75 if proteinuria)
ACE-I/ARBs
statins
?anticoagulants
Tx nephrotic patients?
remission?
Fluid + salt restriction
Diuretics
ACEI/ARBS
Anticoagulation
IV albumin (only if volume depletion)
Immunosuppression
- Complete remission = proteinuria <300mg/day
- Partial remission = proteinuria <3g/day
idiopathic GN main types?
Minimal change
Focal segmental glomerulosclerosis (FSGS)
Membranous
Membranoproliferative
IgA nephropathy
minimal change nephropathy?
Dx?
Tx?
ESRD?
COMMONEST cause of nephrotic syndrome in children!!
Dx = normal renal biopsy!!
Tx = 94% complete remission with oral steroids
- second-line drugs = cyclophosphamide
does NOT cause progressive renal failure
focal segmental glomerulosclerosis?
Ax?
Dx?
Tx?
Complication?
COMMONEST cause of nephrotic syndrome in adults!!
1* or 2* (HIV, heroin use, obesity, reflux nephropathy)
Dx renal biopsy = minimal immune deposition
Tx = steroids (60% remission)
50% progress to ESRF after 10 years

membranous nephropathy?
Ax?
Dx?
Tx?
Complication?
2nd commonest cause of nephrotic syndrome in adults
1* or 2* - important secondary causes:
- infections (hep B/parasites)
- connective tissue disease (lupus)
- malignancies!!! (lung, colon + melanoma)
- drugs (gold/penicillamine, NSAIDs)
Dx renal biopsy = subepithelial immune complexes in basement membrane
Tx = steroids, alkylating agents (cyclophosphamide + chlorambucil), monoclonal Ab
30% progress to ESRF in 10 years
PLA2r antibody?
present in >70% of primary membranous nephropathy
IgA nephropathy clinical features?
Ax?
Associated with?
Dx?
Tx?
complication?
Asymptomatic microhaematuria + non-nephrotic proteinuria
Classic presentation = macroscopic haematuria after resp/GI infection
Associated with HSP
Dx renal biopsy = mesangial cell proliferation and IgA deposits
Tx = ACEI/ARB + fish oil
25% lead to ESRF in 10-30 years
rapidly progressive glomerulonephritis?
Clinical features?
Ax?
characteristic feature?
rapid deterioration in renal function over days/weeks
clinical features = RBCs, red blood cell clasts + granular clasts in urine
Ax = pic
characteristic feature = glomerulr crescents on biopsy

goodpasture’s syndrome can cause?
Dx?
Tx?
goodpasture’s syndrome can cause rapidly progressive glomerulonephritis (pulmonary-renal syndrome)
Dx = anti-GBM antibody (IgG)
Tx = steroids, cyclophosphamide, plasmapheresis
Ax nephritis?
infective = pyelonephritis
non-infective = glomerulonephritis
acute urinary retention?
Ax?
S/s?
triggering events?
Tx?
renal emergency!!
Ax = BPH, prostatitis, anticholinergic medication
S/s = inability to urinate resulting in increasing pain
triggering events = surgery, catheter, anaesthesia
Tx = catheter, alpha blocker, 5-alpha reductase inhibitor
Acute loin pain DDx?
Tx?
if stone hasn’t passed within a month?
ureteric colic secondary to calculus (renal stone)
DDx = AAA
Tx renal stone = NSAIDs + opiate, tamsulosin (alpha-blocker) for small stones that are expected to pass
if stone hasn’t passed in a month = ureteric stent, stone fragmentation
for infected hydroneprhosis = nephrostomy
indications to treat renal stone urgently?
Tx?
pain unrelieved
pyrexia
persistent nausea/vom
high-grade obstruction
Tx
- Ureteric stent
- Stone fragmentation
- Nephrostomy for infected hydronephrosis
Causes of frank haematuria?
Ix?
Ax
- cystitis/pyelonephritis
- Stones
- bladder cancer
- BPH
- Polycystic kidneys
- Trauma
- Coagulation/platelet deficiencies
Ix = CT urogram + cystoscopy
acute scrotum Ax
Torsion of spermatic cord
Epididymitis
Inguinal hernia
Hydrocele
Trauma/insect bite
Inflammatory vasculitis
Tumour
Torsion of spermatic cord epidemiology?
S/s?
O/E?
Ix?
Tx?
teenage boys - puberty
S/s = severe pain (often woken from sleep), nausea + vomiting, sometimes referal of pain to lower abdomen
O/E = testis high in scrotum, absence of cremasteric reflex
Ix = doppler USS
Tx = emergency surgery (within 4 hours)!!!!
NB - fix contralteral side otherwise bell-clapper deformity
torsion of appendage symptoms?
clinical features?
dinstinguish from testicular torsion?
Tx?
s/s = variable, may be same as spermatic cord torsion
clinical features = localised tenderness at upper pole + blue dot sign
difference from cord torsion = testis mobile + cremasteric reflex present
Tx = resolves on its own

epididymitis s/s?
Ax?
when to suspect?
Dx?
Tx?
(how to diff. from testicular torsion)
s/s = dysuria + pyrexia
Ax = UTI, urethritis, catheterisation
suspect if pyuria (pus in urine)
Dx = doppler (swollen epididymis) + urine culture
Tx = ofloxacin 400mg for 14 days
(NB - can differentiate from TT = cremasteric reflex is present)

idiopathic scrotal oedema?
self-limiting, unknown cause, usually associated with scrotal erythema
no fever, minimal tenderness, may be pruritus

paraphimosis?
Ax?
Tx?
Painful swelling of foreskin distal to a phimotic ring
Often happens after foreskin retracted for catheterisation and staff member forgets to replace it in natural position
Tx
- Iced glove, granulated sugar 1-2hrs, multiple punctures in oedematous skin
- Manual compression of glans with distal traction on oedematous foreskin
- Dorsal slit

Fournier’s gangrene?
Ax?
S/s?
Dx?
Tx?
Form of necrotising fasciitis occurring around male genitalia
Ax = diabetes, local trauma, urinary extravasation, perianal infection
S/s
- Starts as cellulitis – swollen, erythematous, tender, marked pain, fever, systemic toxicity
- swelling + crepitus of scrotum, dark purple areas
- marked toxicity out of proportion to local findings
Dx = x-ray or USS may confirm gas in tissues
Tx = antibiotics + surgical debridement

nephritic vs nephrotic syndrome
how to distinguish cause of glomerulonephritis?
Nephritic = haematuria, hypertension
Nephrotic = heavy proteinuria, non-dependent oedema, hyperlipidaemia
distinguish cause = renal biopsy
- Light microscopy
- Electron microscopy
- Immunofluorescence (goodpasture’s = linear IgG)
s/s minimal change disease?
FSGS?
Membranous?
IgA?
minimal change = nephritic (haematuria + HTN)
FSGS = nephritic
membranous = nephrotic (proteinuria, oedema, hyperlipidaemia)
IgA = nephritic
membranoproliferative GN Ax?
Dx?
idiopathic primary or 2* (infection, lupus, malignancy)
Dx = tram tracks on microscopy

diabetes kidney?
Nodules = kimmelstiel Wilson lesion
bosniak score?
predicts cancer risk in renal cysts
Xanthogranulomatous pyelonephritis?
infection creates kidney mass
renal tumours staging?
benign tumours?
malignant?
paediatric tumour?
1 = benign
4 = malignant
benign - oncocytoma
malignant = chromophobe, clear cell, papillary and collecting duct
paediatric = Wilm’s tumour
oncoytoma features?
BENIGN
small, oval, well-circumscribed
brown with stellate star

chromophobe features?
Difficulty is histological similarity to oncocytomas (benign vs malignant)
Oncocytotic but with raison-like nuclei and perinuclear haloes

papillary tumour kindey features?
2nd most common malignant tumour
papillary = finger-like projections

collecting duct tumour kidney?
least common malignant tumour
very poor survival
clear cell tumour kidney?
risk factors?
s/s?
features?
most common malignant tumour
when people say renal cancer they normally mean clear cell
risk factors = obesity + genetics
S/s
- heamaturia
- mass
- hypertension
BRIGHT YELLOW TUMOUR SURFACE (histologically clear)

significance of clear cell renal cancer?
has potential for renal vein involvement and can even extend into vena cava and grow towards the heart!!!
genetics renal cancer?
Von Hippel Lindau
Von Hippel Lindau increases risk of?
Renal cell carcinoma
Cerebellar hemangioblastoma
Pancreatic tumours
Epididymal tumours
systemic causes of CKD?
Diabetes (most common)
Myeloma
Amyloidosis
Vasculitis
SLE
multiple myeloma?
S/s?
classic presentation?
Cancer of plasma cells
symptoms
- Bone pain
- Weakness + fatigue
- Weight loss
- Recurrent infections
Signs
- Anaemia
- Hypercalcaemia
- Renal failure
- Lytic bone lesions
classic presentation = back pain and renal failure!!

Dx multiple myeloma?
Tx?
Bloods = serum protein electrophoresis, serum free light chains
Urine = bence jones protein
Bone marrow biopsy
Skeletal survey (lytic lesions)
Renal biopsy
Tx = manage hypercalcaemia (saline + bisphosphonates), chemo, stem cell transplant, plasma exchange to remove light chains, dialysis (supportive)
amyloidosis?
types?
Deposition of amyloid in tissues or organs
Types:
primary/light chain amyloidosis (AL)
secondary/systemic/inflammatory (AA)
dialysis-related amyloidosis (DRA)
hereditary and old age amyloidosis
primary AL amyloidosis pathophys?
affects?
prognosis?
Production of abnormal immunoglobulin light chains from plasma cells
Light chains enter bloodstream and cause amyloid deposits
affects heart, bowel, skin, nerves + kidneys
prognosis = 6 months - 4 years untreated
AA amyloidosis associated with?
e.g.?
Dx?
Associated with systemic inflammation from either chronic inflammatory conditions (RA, IBD, psoriasis) or chronic infections (TB, osteomyelitis, bronchiectasis)
Dx = production of acute phase protein – serum amyloid A protein (SAA)
presentation amyloidosis?
Depends on organs or tissues involved:
- Renal (nephrotic) = proteinuria + impaired renal function
- Cardiac – cardiomyopathy
- Nerves – peripheral or autonomic neuropathy
- Hepatomegaly/splenomegaly
- GI – malabsorption
S/s renal amyloidosis?
Ix renal amyloidosis?
s/s = nephrotic syndrome (proteinuria + impaired renal function)
Ix
- urinalysis (protein)
- bloods - U+E, CRP, protein electrophoresis, serum free light chain assay
- renal biopsy (congo red, apple green under polarised light)
- SAP scan i.e. scintigraphy with radiolabelled serum amyloid, shows extent of disease

Tx amyloidosis?
no cure
AA – treat underlying condition
AL – immunosuppression (steroids, chemo, stem cell transplant)
summary amyloidosis

ANCA associated vasculitis general s/s?
Dx?
Fever, arthralgia, weight loss, anorexia, malaise
Dx
- Urinalysis – blood, protein
- Bloods – raised CRP, AKI i.e creatinine, anaemia
- Immunology – ANCA, MPO, PR3
- Renal biopsy

p-ANCA vs c-ANCA
p-ANCA = MPO
c-ANCA = PR3
tx vasculitis?
Steroids!
- Also cyclophosphamide + ritixumab
- plasma exchange
- dialysis (supportive)

malar rash of SLE
lupus diagnostic criteria
(MD SOAP BRAIN)

SLE kidney disease s/s?
Dx?
- Nephrotic!!! – proteinuria
- Red-cell clasts!!
- Microhaematuria
- Reduced renal function
- Hypertension
- Hyperkalaemia
Dx
- bloods - raised CRP, ANA + anti-dsDNA, complement proteins
- urinalysis - proteins + microhaematuria
most frequently observed abnormality in lupus nephritis?
proteinuria
most common cancer in men in UK?
Dx?
Tx?
prostate cancer
Dx
- bloods (PSA) + biopsy
Tx
- Surgery
- Radiotherapy
- Brachytherapy
- Anti-androgens
- LHRH-agonists
staging prostate cancer
gleasons plus…

most common bladder cancer?
presentation?
Dx?
transitional cell carcinoma
presentation = 80% with visible haematuria
Dx = CT urogram + cystoscopy!!
Tx bladder cancer?
Surgery
If muscle invasion = radiotherapy
If metastatic = cisplatin based chemotherapy
urothelium lines?
Bladder, ureters and collecting ducts
also significant proportion of urethra
cystitis important subtypes?
- bacterial
- parasites and mycotic (fungal) infection
- aseptic
- reactive to catheters
parasitic Ax cystitis?
where?
complication?
Schistosomiasis – swims up urethra
found in lake Malawi
if untreated = persistent inflammation = squamous metaplasia = squamous cell carcinoma
aseptic cystitis?
presents with?
Tx?
Used to be called interstitial cystitis (painful bladder syndrome)
presents with dysuria but with persistently negative cultures + urinalysis
Tx = NSAIDs + tricyclics
urothelial neoplasia risk factors?
SMOKING+++ (almost as strong an association as lung cancer)
beta-napthylamine (dye industry) - regulated now
transitional cell carcinoma appearance?
papillary - finger-like projections
other types of bladder cancer?
Adenocarcinoma (can occur due to metaplasia - difficult to distinguish from colon cancer that has metastasised)
Squamous cell carcinoma – catheters + schistosomiasis
prostate cancer usually occurs where?
risk factors?
Usually occurs in periphery of gland
Risk factors = cadmium battery workers
when is PSA unreliable for diagnosing prostate cancer?
unreliable in:
- big prostates
- prostatitis
- immediately following PR exam
- bike-riding
- spironolactone
Ax bladder outflow obstruction (BOO)?
Benign prostatic hyperplasia (BPH)
Urethral stricture
Prostate cancer
Bladder stones
Extrinsic – cystocele, cancers
drugs like anticholinergics and nasal decongestants - ASK ABOUT MEDICATIONS
symptoms of BOO
storage – when bladder is filling with urine
- frequency
- urgency
- nocturia
voiding – when patient is trying to pass urine
- hesitancy
- poor flow
- intermittent flow
- sensation of incomplete emptying
- post-micturition dribbling
red flag signs bladder cancer?
Haematuria
Suprapubic pain
Recurrent urinary tract infections
Ix BOO?
Ix
- Frequency-volume chart
- Urinalysis
- Serum creatinine
- PSA
- renal USS if - loin pain, haematuria
- cystoscopy if - haematuria, pain, recurrent UTIs
Tx for LUTS (storage vs voiding)
alpha blocker = tamsulosin
5-alpha reducstase inhibitor = finasteride

benign renal tumours?
malignant?
Benign
- Simple cysts
- Angiomyolipoma
- Oncocytoma
Malignant
- Renal cell carcinoma
- Transitional cell carcinoma
- Lymphoma
s/s oncocytoma?
difficulty?
Dx?
Tx?
S/s = asymptomatic (85%), loin pain, haematuria
radiologically very difficult to distinguish from renal cell carcinoma
Dx
- CT scan - spoke wheel pattern
- biopsy
Tx - depends on size
- <3cm = surveillance (unfit) or ablation (fit)
- >3cm = partial nephrectomy
- large tumours = laparoscopic (gold standard) radical nephrectomy

angiomyolipoma?
Ax?
s/s?
Dx?
Tx?
most common benign renal tumor
Ax = 80% sporadic in middle ages females, 20% associated with tuberous sclerosis
s/s = asymptomatic, loin pain, haematuria, mass
10% Wunderlich’s syndrome - massive retroperitoneal bleed
Dx
- USS + CT (fatty tumour of low density)
Tx
- elective = embolisation + partial nephroctomy
- emergency = embolisation + emergency nephrectomy
Wunderlich’s syndrome?
associated with?
emergency - massive retroperitoneal bleed
associated with angiomyolipoma of the kidney
renal cell carcinoma?
types?
Adenocarcinoma of renal cortex
types
- clear cell (80%)
- papillary
- chromophobe
- collecting duct (rare - young patients, v poor prognosis)
- medullary cell = sickle cell patients
medullary cell renal carcinoma associated with?
SICKLE CELL
staging renal cancer?
T1 - <7cm
T2 - >7cm confined to kidney
T3 – extends beyond kidney into renal vein, perinephric fat, renal sinus, IVC
T4 – beyond Gerota’s fascia into surrounding structures
s/s renal cancer?
Dx?
Haematuria, loin pain, mass
Pyrexia of unknown origin
Varicocele (appears suddenly)
Paraneoplastic syndrome (30%)
Dx
- USS
- CT chest, abdomen, pelvis for staging
- FBC
- renal and liver functions
Tx renal cell carcinoma?
follow-up?
Small tumours <3cm = surveillance (unfit) + ablation (fit)
>3cm = partial nephrectomy
large tumours
- radical nephrectomy
- laparoscopic approach gold standard
Followup
- FBC/renal and liver functions
- CT/USS + CXR
- 5-10 years
testicular cancer epidemiology?
risk factors?
Epidemiology
- Men 20-45
- Seminomatous 35-45 y/o
- Non-seminomatous <35 y/o
risk factors = previous TC (increased risk in contralateral testi), cryptochordism, HIV, family history
types testicular cancer?
seminoma is same as dysgerminoma in females

clinical presentation testicular cancer?
O/E?
s/s
- Scrotal lump!!!
- 5% acute pain due to bleeding
- 10% symptoms of advanced disease: weight loss, neck lumps, chest symptoms or bone pain
O/E
- Asymmetry or slight scrotal discolouration
- Hard, non-tender, irregular mass
- Secondary hydrocele
- Abdominal mass = advanced disease
Ix testicular cancer?
Imaging – USS testicle, CT abdomen + chest for staging
Bloods – serum tumour markers
- Alpha fetoprotein - yolk sac
- B-HCG - choriocarcinoma
- LDH - seminoma
FBC
LFTs + renal function tests
Tx testicular cancer?
Radical inguinal orchidectomy – offer sperm preservation
- re-check tumour markers 1 week post-op
Chemo as adjuvant even in non-metastatic cases
penile cancer types?
Squamous cell carcinoma (95%) – i.e. skin cancer
Kaposi’s sarcoma
BCC, malignant melanoma, sarcoma
risk factors penile cancer?
Age (50-60)
Phimosis – chronic inflammation
Geography – Asia, Africa, South America
HPV types 16 + 18
Smoking
Immunocompromised patients
most common site of penile cancer?
glans
presentation penile cancer?
Ix?
Hard painless lump
Ix
- MRI to assess tumour depth
- CT scan abdomen, pelvis, chest in advanced disease
Tx penile cancer?
Prepucal lesions = circumcision
Glans lesions
- Superficial = glans resurfacing
- Deep = glansectomy
More advanced disease
- total penile amputation with formation of perineal urethrostomy
Inguinal lymphadenectomy if involved
micturation reflex?
S2-S3 – pelvic parasympathetic nerves (pudendal)
overflow incontinence s/s?
Huge palpable bladder
Chronic retention
Often wet at night
Renal impairment
detrusor overactivity?
Ax?
can be a cause of urge incontinence
Ax
- irritation of bladder - afferent overstimulation
- paraplegia (loss of central inhibition)
- idiopathic
extraurethral causes of incontinence?
ectopic ureter (rare, congenital)
vesico-vaginal fistula
BXO?
Balantitis xerotic obliterans i.e. lichen sclerosis of the penis
testicular lumps differential?
Hernia
Cystocele
Hydrocele
Spermatocele
testicular cancer
hydrocele?
features?
Accumulation of fluid around testes
- between 2 layers of tunica vaginalis
Unicystic, smooth and fluid filled - transilluminates!!

spermatocele?
Ax?
presentation?
Cystic change within vas deferens (epididymis)
Unknown cause and usually asymptomatic
(normally present after self-examination)
Varicocele?
Varicose venous plexus that drains testis
May present having felt a lump “bag of worms”
remember sudden variocele can be symptom of RCC
potato tumour?
prognosis?
seminoma
excellent cure rate
respiratory alkalosis Ax?
excessive removal of CO2 from body
- Altitude hypoxia
- Hyperventilation (fever, brainstem damage)
- Hysterical overbreathing
urine alkaline when?
metabolic compensation for respiratory alkalosis
metabolic acidosis Ax?
ingestion of acids
excessive metabolic production of H+ (lactic acid during exercise or ketoacidosis)
excessive loss of base from the body (e.g. diarrhoea – loss of HCO3-)
metabolic alkalosis Ax?
Loss of HCL from stomach (vomiting)
Ingestion of alkali or alkali-producing foods (used to be a problem with old antacids!!)
Aldosterone hypersecretion (causes stimulation of Na+/H+ exchange at apical membrane of tubule = acid secretion)

….
loop diuretics e.g.?
mechanism?
used for?
containdications?
furosemide + bumetanide
mechanism = inhibit Na/K/2Cl- co-transporter in loop of henle
used in = acute pulmonary oedema, heart failure, CKD, ascites, nephrotic syndrome, to reduce acute hypercalcaemia
containdications
- severe hypovolaemia or dehydration
- severe hypokalaemia/hyponatraemia
- hepatic encephalopathy
- GOUT
adverse effects loop diuretics?
hypokalaemia
metabolic alkalosis – increased H+ secretion
hypocalcaemia/hypomagnesaemia
hypovolemia and hypotension (especially in the elderly)
hyperuricemia – may precipitate acute gout attack!!
Dose-related loss of hearing
thiazide + thiazide-like diuretics e.g.?
mechanism?
benefits?
thiazide = bendroflumethiazide
thiazide-like = chlorthalidone, indapamide and metolazone (thiazide-like)
mechanism = inhibits Na/Cl co-transporter in DCT
benefit = has vasodilator action which is effective for hypertension
- also no hypocalcaemia like loop diuretics (advantage in elderly patients with osteoporosis)
clinical uses thiazide diuretics?
contraindications?
uses:
- heart failure
- Hypertension
- Severe resistant oedema
- Renal stone disease (nephrolithiasis) – reduced urinary excretion of Ca++ discourages Ca++ stone formation
- Nephrogenic diabetes insipidus (mechanism not clearly understood)
Contraindications
- Hypokalaemia
- Hyponatraemia
- Gout
adverse effects thiazide diuretics?
Hypokalaemia
Metabolic alkalosis
Hypovolemia and hypotension (esp in elderly)
Hypomagnaesmia (not hypocalcaemia – advantage in elderly patients with osteoporosis)
Hyperuricemia – may precipitate gout
Erectile dysfunction
Impaired glucose tolerance in diabetics
potassium sparing diuretics?
mechanism?
Spironolactone and eplerenone
mechanism = aldosterone antagonists
drugs to avoid with potassium-sparing diuretics?
clinical uses?
containdications
do not use with ace-inhibitors = SEVERE HYPERKALAAEMIA
clinical uses of aldosterone antagonists:
- Heart failure
- Primary hyperaldosteronism (conn’s syndrome)
- Resistant essential hypertension
- Secondary hyperaldosteronism (due to hepatic cirrhosis with ascites)
contraindications
- severe renal impairment
- hyperkalaemia
- Addison’s disease
carbonic anhydrase inhibitor e.g.?
clinical use
acetazolamide
use:
- glaucoma
- altitude sickness prophylaxis
diabetes insipidus Ax?
Tx?
neurogenic (lack of ADH from post. pituitary)
- Tx = desmopressin
nephrogenic (inability of kidney to respond to ADH)
- genetic
- drugs - lithium, demecloclycine, vaptans
- Tx = thiazides + NSAIDs
what drugs are of use in hypervolaemic hyponatraemia (i.e. SIADH)?
vaptans e.g. Tolvaptan
complicated UTI?
complicated UTI = a UTI complicated by systemic symptoms OR urinary structural abnormality/stones
does bacteriuria mean UTI?
no - esp in elderly patients or patients with catheter
bacteria Ax UTI?
E.Coli
Klebsiella
enterobacter
proteus
pseudomonas aeruginosa

what makes E.coli dangerous?
endotoxin in LPS layer
proetus UTI?
produces urease which breaks down urea to form amonia
increases urinary pH which causes formation of phosphate stones

pseudomonas aeruginosa?
Ax UTI?
Tx?
Gram negative bacillus but not a coliform
Associated with catheters
Tx = ciprofloxacin
staph aureus UTI?
uncommon - usually from bacteraemia rather than urinary tract
s/s UTI?
Dx?
S/s
- Dysuria (pain passing urine)
- Frequency
- Nocturia
- Haematuria
- Fever
- Loin pain (suggests involvement of kidneys, complicated)
- Rigors (complicated)
Dx = MSU sample
- can also do dipstick but NOT in elderly or catheter patients
- nitrites + leukocytes indicate UTI
Kass’s criteria?
>10^5 organisms/ml = probable UTI (significant bacteriuria)
<10^3 organisms/ml = not significant bacteriuria
10^4 organisms/ml – contaminated? Infection? Repeat specimen
asymptomatic bacteriuria?
Significant bacteriuria (>10^5 orgs/ml)
No pus cells in urine
Antibiotic treatment often not required EXCEPT in pregnancy
asymptomatic bacteriuria in pregnancy?
Tx?
MUST TREAT
if untreated can cause sepsis, IUGR
Tx = nitrofurantoin 7 days
UTI catheterised patients?
Catheterised patients with >10^5 orgs/ml should ONLY be given antibiotics if there is supporting evidence of UTI (fever, symptoms)
UTI Tx?
female uncomplicated = nitrofurantoin or trimethoprim 3 days
male UTI = nitrofurantoin or trimethoprim 7 days
complicated UTI/pyelonephritis = co-amoxiclav or co-trimoxazole 7 days
- hospital = IV gentamicin + amoxicillin 7 days
- if penicillin allergic = co-trimox + gentamicin
complicated UTI pregnancy?
AVOID gentamicin !!!!
ESBL bacteria?
Tx?
resistant to ALL cephalosporins and to almost all penicillins
Tx
- Nitrofurantoin (oral), pivmecillinam (oral)
- Fosfomycin (oral), temocillin (IV)
- Meropenem (IV), ertapenem (IV)
trimethoprim pregnancy?
forms?
avoid in 1st trimester (3 months) of pregnancy
can be given on its own or as co-trimoxazole
nitrofurantoin pregnancy?
Avoid in late pregnancy (can cause neonatal haemolysis), breastfeeding and children <3 months old
so 1st and 2nd trimester = nitrfurantoin
3rd trimester = trimethoprim
drugs implicated in AKI?
1 – pre-renal failure – hypotension, hypovolemia
- e.g. diuretics, ACEI/ARBs
2 – renal – AIN/tubular necrosis (ATN)
- e.g. gentamicin, sulphonamides (trimethoprim), aspirin (NSAIDs)
3 – post renal – retroperitoneal fibrosis, crystalluria, urinary calculi
- e.g. methysergide or chemotherapy
drug reactions to know about
Theophylline and macrolide antibiotics
Statins and macrolides/fibrates
Warfarin and multiple drugs (aspirin, antibiotics)
ACE and sulphonylureas (hypoglycaemia)
Clopidogrel and PPIs
drug-disease interactions
Urinary retention in BPH patients on decongestants or anticholinergics
Constipation worsened by calcium, anticholinergics, CCB
Neuroleptics, tramadol and quinolones = worsen epilepsy
Beta blockers and asthma
drug-food interactions
Bananas, oranges, green leafy vegetables (K+ rich) interact with ACEI, ARBS, K-sparing diuretics
Apples, chickpeas, spinach, nuts, broccoli, cranberry juice interact with warfarin
Chicken, turkey, milk, soy, cheese, yoghurt = antibiotics, thyroid meds, digoxin, diuretics
Grapefruit, apple, orange and cranberry = statins + antihistamines
type B drug reaction examples?
drug rashes
bone marrow aplasia (chloramphenicol)
hepatic necrosis (halothane)
HIGH MORTALITY
long term effect of steriods?
B-blockers?
NSAIDs?
steroids = cushings
b-blockers = diabetes
NSAIDs = hypertension
type E (end of treatment) drug reaction examples?
Beta-blocker withdrawal and angina
steroid withdrawal and Addison crisis
anticonvulsant withdrawal and changes in epilepsy frequency
haematuria?
regarded as urologic malignancy until proven otherwise
inflammatory causes of haematuria?
Urethritis
Prostatitis
Cystitis
Ureteritis
Pyelonephritis
Glomerulonephritis
jogger’s haematuria?
Tx?
due to renal/bladder trauma
Tx = self-limiting (lasts 7 days)
red diaper syndrome?
serratia marcescens infection
referal to urology vs nephrology
urology
- all patients with visible haematuria
- all patients with symptomatic miscroscopic haematuria
- >40 years with asymptomatic microscopic haematuria
nephrology
- evidence of declining renal function
- CKD eGFR <30
- significant proteinuria
- isolated haematuria with hypertension in <40 y/o
- visible haematuria coinciding with infection