Deck 7 Flashcards
Renal corpuscle info
Bowman’s capsule, inner (visceral) podyctres), outer (parietal) simple squamous
DCT absorption
Na/K/Ca
AKI
Rapid decline in kidney function (hours/days) as measured by urea and creatinine
AKI RF
65+, hypovolaemia, sepsis, diabetes, chronic liver disease, HF, chronic kidney disease
Pre-renal AKI
Reduced perfusion.
Hypovolaemia, hypotension, fluid overload, reduced CO, vascular causes (renal artery stenosis/occlusion, NSAIDs, ACEi, renal vein thrombosis, AAA)
Gives ATN
Initially get high urine osmolarity (>500), then isotonic urine with high sodium as concentrating power lost
Intrinsic renal damage causes
Glomerular problems (glomerulonephritis, HUS, IgA)
AIN (drug induced, infection, autoimmune or lymphoma)
ATN (most common, ischaemia, rhabdomyolysis, radiocontrast agent)
Vascular (vasculitis, thrombosis/embolii)
HUS (post elcoli or URTI)
Post renal aki causes
luminal (stones, clots, sloughed papillae)
Mural (malignancy, BPH, stricture)
Extrinsic compression (pelvic malignancy, retroperitoneal fibrosis)
AKI S+S
Can be asymptomatic Oliguria, N&V, dehydration, thirst, confusion, fatigue Signs of fluid imbalance. May have vasculitis features. May have palpable abdominal mass
AKI diagnosis
RIFLE (risk, injury, failure, loss, ESRD)
AKIN is like rifle but uses time as well
KDIGO uses serum creatinine and/or urine output
KDIGO 1
1.5-1.9x baseline or >0.3mg/dl increase in sCR
OR <0.5mL/kg/h urine over 6-12 hours (~35mL/ hour)
KDIGO2
2.0-2.9x baseline,
OR <0.5kg/kg/h over 12+h (~35mL/h)
KDIGO3
3+x baseline, or 4mg/dl increase
OR
<0.3mL/kg/h (~21mL/h) for 24h or anuria for over 12 hours
Can also be RRT start or below 18 years with eGFR <35
AKI investigations
FBC (?eosinophilia in acute interstitial nephritis or vasculitis)
Creatinine kinase if ?rhabdomyolysis
Immunology (myeloma screen, lupus screen, vasculitis screen)
Imaging (renal USS to rule out obstruction), CXR is pulmonary oedema), CY KUB in obstruction)
Metformin in AKI
caution. High renal excretion, can lead to lactic acidosis.
AKI complications
Hyperkalaemia Hyperphosphataemia Hyponatraemia Hypermagnesaemia hypocalcaemia Metabolic acidosis Fluid overload Uraemia CKD
Secondary causes of glomerunephritis
N: neoplasm S: SLE A: amyloid I: infection D: diabetes HSP: henoch Schonlein purpura
Features of glomerulonephritis
Immunological attack by Ab or T cell attacking antigen.
Capillary -endothelial proliferation (bigger fenestra) with capillary wall necrosis and mesangial scaring (glomerulosclerosis), thickened BM (more permeable) and cell deposition in Bowman’s space)
Nephrotic basics
BM damaged, allows protein through. Protein loss >3.5g/day Ig loss, hyprecholesterolaemia, oedema (oncotic pressure loss and sodium retention via RAAS), thombosis due to clotting imbalance. May have haematuria Non proliferative histologically.
Nephrotic signs and symptoms
xanthalasma, xanthoma, fatigue, leukonychia, oedema, dyspnoea (can be pleural effusion or pulmonary oedema), may have frothy urine
Nephrotic investigation
MSU, dipstick, FBC, LFT, calcium, U&E, CRP, glucose, Ig (serum, urine), autoimmune screen, hepatitis screen, HIV screen, CXR, renal biopsy
Minimal change
Most common childhood nephrotic
No LM, but podocyte effacement on EM. IF shows IgM in mesangium.
NSAID, allergy and hodgkin lymphoma associations
Membranous glomerulonephritis
30% of adult nephrotic. LM: mesangium expansion and capillary thickening IF shows IgG and C3 EM shows GBM thickening PLA2R antibodies
Penicillin, NSAIDs, malignancy (lung, colon melanoma), SLE, HBV, HVC, syphilis, scistomiasis, malaria
FSGS
Most common adult nephrotic
Often has azotaemia and haematuria
IgM and C3 can be present in sclerotic areas/mesangium
Can be secondary to HIV, heroin, sickle cell
Other nephrotics
Diabetes (most common cause), amyloidosis, HBV,HCV,
Nephrotic management
Diuretics, fluid management, ACEi, anticoagulation, Tx cause
Nephritic basics
Endothelial or mesanglial damage. Proliferative plus GBM thickening.
HTN, haematuria, casts in urine, proteinuria, oliguria, oedema, C3/C4 reduction (overuse)
May have ANA, anti-dsDNA, ANCA, antiGBM
Often abrupt onset
Acute post infectious
Most common nephritic globally.
Group A beta haemolytic streptococcus
IgA disease
Often macroscopic haematuria (often cola coloured). Can occur post URTI or HVB
Most common nephritic.
IgA/C3 deposits
Henoch scholein purpura
Systemic IgA vasculitis.
Typically get cola urine, widespread rash (esp extensors), arthalgia, abdominal pain, haematochezia
Rapidly progressing glomerulonephritis
Crescents, rapid loss of renal function.
Can be anti GBM (goodpastures if lung too)
Immune complex disease (IgA, post strep, SLE)
Pauci immune (very few Igs on staining)
Polyangitis
Churg strauss vasculitis
Poor prognostic indicators in nephritic
Sequalae
Severe renal impairment at presentation, persistent heavy proteinuria, HTN.
Adults often has long term complications
(can be HTN encephalopathy, HF, uraemia (dialysis))
PRGN nephritic screen
ANCA/anti GBM
SLE nephritic screen
ana, DS-dna, COMPLEMENT
myeloma nephritic screen
Igs, serum electrophoresis
RA associated GN screen
Rheumatoid factor
membranoproliferative glomerulonephritis (MCGN)
HBV/HBC screen
Post streptococcal nephritic screen
ASA
SLE associated diseases
Can be mix of nephrotic and nephritis. May see membranous, membranoproliferative and FSFN
CKD
Irreversible progressive renal function decline. Can be diagnosed if EGFR decreases over 3 months
CKD S+S
HTN, proteinuria, anaemia, nocturia (loss of concentrating), fatigue, dyspnoea, ED, oedema (peripheral/pulmonary)
Late shows pruritus, anorexia, N&V
Very late: hiccups, Kussmaul’s resp (met acid), muscle twitch, drowsiness, coma, fits
May have pericardial rub
CKD investigation
- Bloods (U&E - can show hyperkalaemia, increased urea, creatinine)
- FBC (?haemanitinics)
- Calcium, phosphate, PTH
- Lipid profile
- Glucose, HBa1C
- Albumin
- Bicarb
- Myeloma screen
- HIV/HEP serology if transplant needed
- ECG
- Urinalysis (can quantify protein with PCR
Renal US to exclude obstruction ans assess kidney size and any asymmetry (small kidney in CKD, asymmetry suggests renovascular/developmental disease. Polycystic kidney?)
CKD stagings
1 is mild with normal eGFR
2) 60-90
3a) 45-60
3b) 30-45 (anaemia present)
4) 15-30 (electrolytes)
5) <15 (dialysis once <10)
Management of CKD`
ACEi/ARB are key for BP control. Diabetes control.
Referral to nephrologist if young, CK4, rapid deterioration), significant proteinuria/haematuria
CKD complications
anaemia (Target 100-120 with EPO to avoid HTN and thrombosis)
Renal osteodystrophy (lack of 1 alpha hydroxylase, hyperphosphataemia cause lack of calcium) - can get tertiary hyperparathyroidism
Fluid overload (needs water/salt restriction)
Electrolyte disturbances (often hyperkalaemia, acidosis)
Myopathy (poor nutrition, hyperparathyroidism, vit D deficiency, electrolyte derangement)
Peripheral neuropathy
Anorexia
Immunocompromise
N&V
Peptic ulcer disease
Depression
CV issues (pericarditis, atherosclerosis, HTN, hyperlipidaemia)
Dialysis needed if
intractable acidosis, intoxicants (methanol, ethylene glycol, lithium), too much fluid and anuric), uraemic symptoms (N&V, pericarditis, seizures, bleeding, encephalopathy), severe electrolyte derangement
CKD causes
Most common diabetes, then interstitial disease, idiopathic, HTN, systemic inflammation, renal artery stenosis, congenital and drug induced
Diabetic nephropathy
Causes and management
Mediated by HTN, hyperglycaemia (extent and duration) as well as glomerular hyperfiltration, smoking, obesity, physical inactivity, dyslipidaemia, proteinuria, dietary factors, genetic susceptibility
Managed as per CKD (reduce proteinuria, control BP, modify CV risk, BM control)
PCKD
S+S
Investigation
ADPKD more common (autosomal dominant)
ARPKD is recessive and less common - earlier renal failure
Renal cyst, extra renal cyst, IC aneurysm, dolichoectasias, aortic root dilatation/aneurysm, mitral valve prolapse, abdominal wall herniae
HTN, CKD, abdo swelling +/- ruptured IC aneurysm
FHx is key. echo and MRI brain if suspected
Chronic pyelonephritis
interstitial nephritis/reflux nephropathy/chronic atrophic pyelonephritis
Chronic vesico ureteric reflux (congenital) or obstruction related (prostate, retroperitoneal fibrosis, stones)
Chronic tubulointerstitial inflammation, deep segmental cortical renal scarring, calyx clubbing.
Chronic inflammation.
HTN, proteinuria CKD features. Rule out UTI.
Micturating cystogram to diagnose UT abnormalities.
Irreversible, no specific treatment
Obstructive uropathy
RF
S+S
Tx
Urine flow block (kidney(s), or any level).
Commonly stones or BPH
RF are BPH, constipation, medication (anticholinergics, alpha receptor agonist), urolithiasis, advanced age, recurrent UTI
Flank pain, LUT symptoms, distended abdo/bladder, haematuria, Hx of meatal narrowing, pelvic/abdo malignancy, neurological disease, pyrexia, rigors, HTN
Must relieve pressure
.
HTN urological effects
arteriolosclerosis (thickening arterioles, afferent inelastic and rigid causing ischaemia - > glomeruli loss).
Atherosclerosis causes renal artery stenosis
urolithiasis RF
Male 3:1, anatomical abnormalities (horseshoe kidney, stricture), HTN, gout, hyperparathyroidism, immobilisation, dehydration, metabolic disorder
Renal stone composition
Normally calcium (80% calcium oxalate, 20% calcium phosphate). 15% uric acid (purine diet, haematological issue, klebsiella, proteus
4% struvite (ammonium mg, phosph - staghorn)
Cysteine stones are rare (familial cysteine met disorder)
Renal stone constriction sites
PUJ, pelvic brin, VUJ
renal stone symptoms
Urine dip
sudden onset, severe loin to groin pain, N&V, haematuria. if infection too, rigors, fever, lethargy.
Urine dip shows WCC, haematuria, ketone but no glucose (dehydration)
Renal stone management
Abx in infection
Diclofenac/opiates/buscopan for pain
Large stones/hydronephrosis need ECPW, endoscopic removal, percutaneous removal or open surgery
Focus on admission in AKI, uncontrolled pain, ninfection, stones >5mm
May want to fit stent or use nephrostomy (USS guidance)
Renal stone complications
AKI.
Can give CKD and scarring. sepsis in infected
Recurrent stone advice
Avoid dehydrations
In calcium stones, check PTH and avoid excess salt
Oxalate stones - avoid purine and oxalate foods (nuts, rhubarb, sesame)
Urate stones - avoid purine food and consider allopurinol
Cysteine stones need genetic testing
Struvite stones may need UTI treatment
Bladder stone causes
outflow obstruction, prolonged catheterisation, upper UT stone passing down
Infection (e.g. schistosomiasis)
Bladder stone symptoms
UTI symptoms (frequency, pain, haematuria) - pain typically at end of micturation when bladder contracts.
Males may also feel pain at tip of penis.
May get perineal pain
May have anuria or retention if obstructing outflow
Things to exclude in ?ureteric obstruction
acute scrotum (as loin to groin pain), AAA (may be causing obstruction and pregnancy.
Renal cell carcinoma
Adenocarcinoma (can be clear cell, pink cell and papillary renal cell)
Renal cell cancer S+S
60% have haematuria. may have mild loin discomfort and mass. May have pathological fracture (PTH-like protein produced). May have varicoele if left renal vein involved. May have polycythaemia.
Renal vein allows haematological spread to IVC, so may have lung symptoms
RF for renal cancer
smoking, obesity, HTN, renal disease, Fhx, asbestos, heavy metals, oestrogen therapy exposure, CKD, acquired cystic kidney disease, hevy NSAID/aspirin/diuretic use
Peak age is 50+
Diagnosis of renal cell cancer
USS shows solid mass. can do CT scan.
Raised ALP, ESR.
Cannonball lung mets.
Tx of renal cell carcinoma
Radical nephrectomy (can do partial but need to do renal angiography first).
TK inhibitors. Poor prognosis (mets<2 years).
If spread to perinephric fat then already T3
Wilms tumour
Nephroblastoma (primative embyonic tumour). Blood spread. Peak age is 2 years. Excellent prognosis, unless mets
Bladder stone investigation
urine dip, MSU, FBC, U&E, imaging
Bladder stone management
Cytoscopy, stone drainage, lithotripsy
Bladder cancer
S+S
Painless haematuria, recurrent UTI symptoms, pain from local strictures.
Bladder cancer RF
male, smoker, 50+, dye/rubber workers, schistosomiasis infection, chronic cystitis, bladder stones, vesicular diverticulum, leukoplakia
Diagnosis of bladder cancer
Urine MCS/cytology (often shows sterile pyuria), flex cystoscopy with biopsy (GSTD) - CT/MRI can miss if carcinoma in situ.
Bladder cancer types
Generally urothelium (TCC), but can get true squamous cell and squamoid transformation of TCC)
Can also get benign (papillomas, leuimyoma, hemiangiooma, neurofibroma) or malginant non-epithelial tumour (rhabdomyosarcoma)
Bladder cancer Tx
Cytoscopic tumour removal, intravesical BCG (immune response can shrink early stage cancer), radical cystectomy.
BPH
Transitional zone expansion
Very common in 70+
BPH s+S
Hesitancy, UTIs, poor flow, terminal drippling, may have retention, overflow incontinence, haematuria if veins rupture
On PR: sulcus generally palpable. Globally enlarged. Smooth. Non tender
BPH investigation
FBC, U&E, PSA (<4 normal,>10 raised), urnialysis/MCS, uroflowmetry, bladder USS, transrectal USS (rule out carcinoma - may have iopsy)
BPH complications
UTI, overflow incontinence, bladder calculi, bladder diverticulae, bilateral hydronephritis, renal failure
UTI RF
Female, pregnancy (progesterone mediated vesicoureteric reflux, stasis), post menopausal (less lactobacilli), strutural abnormality, sex (first time, long time without), catheter use)
Most common UTI pathogen
E. coli
Most common UTI pathogen in young, sexually active females
Staphylococcus saprophyticus
Pseudomonas UTI
linked to catheterisation
Less common UTI
enterococci, proteus, klebsiella, pseudomonas
UTI found more in hospital
klebsiella, s epidermidis, enterococci and pseudomonas
Boundary for upper UTI
Above VUJ - pyelonephritis
Boundary for lower UTI
below VUJ. cystitis
Cystitis S+S
Dysuria, haematuria, frequency/urgency, suprapubic pain, foul smelling/cloudy urine, strangury (dysuria with small volume only expelled by straining despite urgency), confusion/lethargy/fatigue (urosepsis)
Cystitis investigations
Urine dipstick for women <65. Everyone else gets MSU (all men, pregnant women and over 65 women get one - as well as if persistent symptoms, recurrent UTIs, recent catheterisation, RF for complications, haematuria).
Renal tract imaging (US/CT) if persistent, recurrent, ?obstruction or septic shock
Sterile pyuria
Leukocytes but no organisms grown) then consider recently treated UTI, appendicitis, TB, chlamydia, bladder cancer
UTI Tx
trimethoprim or nitrofurantoin. NSAIDs/paracetamol. Hydration. Hygiene measures
pyelonephritis S+S
Dysuria, frequency, flank pain (or suprapubic pain), haematuria, high grade fever, N&V, rigors. Usually acute onset, systemically unwell. Generally occurs in incompetent vesicoureteric valve
Pyelonephritis investigations
Urine dip/MSU
Bloods (look for AKI)
Blood culture (?sepsis)
USS KUB (often FL - look for obstruction, inflammatory change, hydronephritis)
CT (reserved for cases where not improving. avoid in children/pregnancy)
Dimercaptosuccinic acid (DMSA scan) - detailed imaging of renal cortices to see scarring and poor function. Requires IV dye and monitoring of kidneys to see filtration
DMSA scan
Uses IV dye to look at kidney scarring and function
Pyelonephritis Tx
Abx (ciprofloxacin, trimethroprim, co-amox). If severe then admit for IV abx (cefuroxime or ciprofloxacin). Hydration is key.
FU USS may be needed
pyelonephritis complications
sepsis, AKI, perinephric abscess, renal papillary necrosis
Comparison of pyelonnephritis/cystitis
Both have dysuria, frequency and can have haematuria
LUTI tends to have urgerncy, suprapubic pain, cloudy/smelly urine - can have confusion, lethargy and fatigue if urosepsis
UUTI tends towards flank pain, high grade dever and N&V
Asymptomatic bacteruria
More common in the elderly and with catheters. No Tx unless pregnant or awaiting invasive urological procedure.
Catheters and bacteruria
Catheters always have bacteria, only need to investigate or Tx of symptomatic
Pyuria DDx
Pus in urine
UTI (including TB), interstitial nephropathy (e.g. diabetes), acute glomerulonephritis, tumours, post surery, catheters, contamination from vagina
Diabetic urinary tract complications
Vascular issue (atherosclerosis and hyaline arteriolosclerosis - > ischaemic glomerular damage) Direct flomerular damage via BM thickening (proteinuria) and abnormal mesangium (glomerulosclerosis) - KW lesions Infection risk (pyelonephritis and renal papillary necrosis)
Non blood haematuria
haemolysis, rhabdomyolysis (myoglobin), food dyes, drugs (metronidazole, nitrodurantoin, doxorubicin, rifampicin), porphoryia, tyrosinaemia
Note that haemolysis and rhabdomyolysis would show as “blood” on urine dip
Most common causes of haematuria
Macroscopic - ?malignancy, but can be stones, BPH, UTI etc
microscopic is more commonly UTI, BPH and stones, but can be malignancy
Investigations for haematuria
Urine dip, FBC, U&E, clotting screen, urine red cell morphology (dysmorphic suggests renal origin), cytological examination of urine, imagina (xray, urogram, CT, USS, MRI)
FLT haematuria imaging
USS of kidney and bladder
AXR
Cytoscopy
Hyperkalaemia
Can be pseudohyperkalaemia, AKI, CKD, K sparing diuretics, ACEi, NSAIDs, acidosis, Addison’s disease, tumour lysis syndrome, burns
ECG with hyperkalaemia
Tall T wave, wide QRS, flattened P wave, prolonged PR interval
Can lead to VF/VT
Tx of hyperkalaemia
if >6.5 then 10mL 10% calcium gluconate IV (repeat at 5 minutes until ECG stabilises)
50mL 50% glucose with 10 units Actrapid insulin /30 minutes
Consider 10mg salbutamol neb and sodium bicarb
Phimosis
foreskin wont retract. Can be congenital, chronic balanitis, traumatic). May present as poor stream and ballooning foreskin in children, in adults as pain during sex. Circumcision resolves
paraphimosis
Tight foreskin over glans, obstructing venous return, Can occur following erection or catheterisation. Manually reduce, or circumcision
Penis cancer
Rare. SCC. Associated with HPV 16 and 18. Presents as red patch on penis which then ulcerates. No urethral symptoms or involvement. Diagnosis is punch biopsy. Can be cured if early with radiotherapy, or surgery if late
Priapism
Hours long erection (corpora cavernosa only - spongiosum remains flaccid). Can be idiopathic, trauma induced, sickle cell crisis or intracevernosal infections for impotence. Can treat with ice packs, alpha agonist, selective embolisation, aspiration or surgery.
Peyronies disease
upward curvature. Idiopathic, but scarring following trauma is potential aetiology - Tx may include managing depression and could have surgical intervention).
Transilluminating scrotal mass
hyrocoele, epididymal cyst or varcocoele
Solid scrotal mass
cancer, orchitis, gumma - needs USS
Scrotal lump separate to testes
chronic epidymitis
Can’t get above scrotal swelling
inguinal hernia or proximally extending hydrocoele - check by illuminating
If can get above scrotal swelling
primary scotal swelling
Phren’s sign
Pain relief on lifting testicle, can rule our torsion in favour of epdidymiitis
Testicular torsion
Absent cremasteric reflex, negative phren’s sign
Epidymal cyst
Common, occur due to cystic degeneration of epididymal structures. Associated with PKD and CF. Almost always at the upper pole. Transillulimates. May or may not contain sperm. Can be painful or uncomfortable, may be excised (drainage often doesn’t resolve)
Hydrocoele
Most common cause. Fluctulant, transilluminates. Can be congenital (generally resolves within 1 year), primary (idiopathic - ‘vaginal hydrocoele’) or secondary (due to inflammation/cancer). USS should be undertaken to rule out underlying patohlogy. Excision of hydrocoele sac can be done if problematic
Varicocoele
Paminiform plexus varicosity, generally on the left. Presents as dragging sensation and ache. May only be palpable in standing position. Associated with reduced fertility, but surgical correction often doesn’t correct. Can be valvular incompetence at junction of left renal vein, but can be due to left renal tumour.
