Week 14 Renal Flashcards
3 ways to measure urinary protein excretion
24 hour urine collection
Spot sample (in morning) - protein:creatinine ratio
Albumin:creatinine ratio
3 most important measurements for kidney function
Creatinine
Urea
eGFR
Ideally, substance would be freely filtered at golmerulus, not secreted or absorbed
Creatinine
Muscle breakdown prouduct
More sensitive than urea
However affected by:
Muscle mass (higher with high muscle mass)
Plasma volume (increases when dehydrated)
Diet (increaes in high protein diet)
15% secreted by tubules
Urea
40% reabsorbed
Increased in diet high in protein or if there is GI bleed (as blood is digested to protein to urea)
Increased in dehydration (reabsorbed in proximal tubule)
Increased in tissue breakdown e.g. corticosteroids
Lowers in liver failure (as liver produces urea)
Glomerular filtration rate defintion
Volume of plasma which would be cleared of that substance per unit time
urine conc of substance x urine vol divided by plasma conc of substance
(ml/min)
MDRD4 formula
Estimatation of GFR from plasma creatinine conc (eGFR)
Based on:
Creatinine conc
Age
Sex
Race
(ml/min per 173m2)
Relationship between eGFR and creatinine
As eGFR falls, creatinine increases
However, can lose 50% kidney function before creatinine increases
Why can’t eGFR be used for AKI?
eGFR assumes stable renal function
(so not sutiable for AKI)
Important for drug dosing
Glomerulonephritis
Group of inflammatory diseases involving glomerulus and tubules
Primary: limited to kidney
Secondary: due to underlying cause e.g.
- infections: HIV
- inflammatory conditions: IBD, RA,
- drugs: NSAIDs
- malignancy: lung cancer
Symptoms: Haematuria, oliguria, oedea, HTN
Pathophysiology:
Glomerular injury caused by inflammation due to extrinsic or intrinsic factors:
Extrinsic: antibodies, complement
Intrisnic: cytokines, growth factors
Examples:
IgA Nephropathy
Membranous GN
Minimal change disease
RPGN (rapidly progressing glomerular nephritis)
Clinical presentations of glomerulonephritis
Nephritic: blood and protein in urine, high BP, rising serum creatinine
proliferative/acute inflammation
IgA/lupus nephritis
Nephrotic:
>3.5 proteinuria, low seurum albumin, oedema
Non-proliferative/podocyte damage
Minimal change disease 1, membranous
Rapidly progressing glomerulonephritis
Rapidly increasing serum creatinine, crescentic damage
Vasculitis, lupus nephritis
3 features of nephrotic syndrome
>3.5g proteinuria (per 24hrs)
Low serum albumin <30
Oedema
Also have hyperlipidaemia, risk of venous thromboembolism, hypercoagulable state (due to loss of anti-thrombin III)
IgA nephropathy
Most common primary glomerular disease
Can be precipitated by infection - synpharyngitic (occurs same time as pharyngitis)
May be secondary to ceoliac disease, cirrhosis
Pathophysiology:
Abnormal/overproduction of IgA which deposit in mesangial cells leading to mesangial proliferation
Symptoms:
Haematuria, HTN, proteinuria
1/3 progress to ESRF
Treatment: ACEi
Membranous GN
Presents with nephrotic syndrome
Most common in caucasians
Primary: idiopathic
Secondary: Malignancy (e.g. lung cancer), drugs (e.g. NSAIDs), SLE
Pathophysiology:
Immune complexes deposited into glomerular BM - thickening and damaging BM - increased permeability - proteinuria
70% pts with Anti-phopholipase A2 receptor antibody (PLA2R) (protein on podocytes)
Variable history:
1/3 resolve, 1/3 progress to ESRF, 1/3 persistent proteinuria, maintain GFR
Treatment:
Treat underlying disease if secondary
Non-immunological: ACEi, statins, diuretics, low salk diet
Immunological: Steroids, cyclophosphamide, ciclosporin, rituximab (Anti-CD20 (B cells))
Minimal change disease
Commonest form of GN in children, characterised by minimal histological changes
Causes nephrotic syndrome (proteinuria, oedema, hypoalbuminaemia, hyperlipidaemia)
First presentation: periorbital oedema
GFR normal
Primary: idiopathic
Secondary: malignancy
May occur after URTI
Pathogenesis: T cell mediated. Podocytes fuse/merge together, causes leakiness of protein into urine
Normal glomeruli on H and E stain
Assoc. with Hodgkin’s Lymphoma
Treatment: Prednisolone (as damaged mediated by cytokoines due to T cells)
Rapidly progressing glomerulonephritis
Group of conditions which show golmerular crescents on kidney biopsy
Aggressive - 90% pts progress to ESRF
Causes: ANCA vasculitis (small vessel vasculitis) e.g. granulomatous with polynagiitis, Lupus nephritis, Goodpasture’s syndrome (antibodies to glomerular BM), post-infection, Henoch Schonlein Purpura
Investgiations for Glomerulonephritis
UEs, urine dip, 24- hour urine collection (quantify protein), serum albumin, renal US
Glomerulonephritis screen:
HbA1c/plasma glucose - diabetic nephropathy
ANCA - vasculitis
PLA2R - membranous GN
ANA,complement - lupus
Kidney biopsy: required for clinical diagnosis of glomerulonephritis
- biopsy cortex, examine:
light microscopy: structure
immunofluorescnece: Ig, complement
electron microscopy: BM, deposits
Systemic diseases assoc with renal disease
Diabetes
Atheromatous vascular disease
Amyloidosis
SLE
How do systemic diseases present in kidneys?
AKI (creatinine increases)
CKD
Proteinuria
Nephrotic syndrome (creatinine normal, proteinuria)
Nephritic syndrome (high creatinine, blood/protein in urine)
Risk factors for UTI
Less than 1 yrs old
50% children with UTI have congenital renal tract abnormality (commonly vesico-ureteric reflux)
Females - sex
Men - prostate enlargement
Diabetes
Immunosuppression
UTI in childhood - incidence vs age
Males 50% <1 yrs
Females >80% >1yrs old (more common due to short urethra)
UTI symptoms of upper vs lower
Pyelonephritis (Upper urinary tract infection)
Bacteriuria and fever >38
Bacteriuria and loin pain, fever <38
Symptoms:
Fever, general malaise, loin pain
Cystitis (lower urinary tract infection)
Bacteriuria, symptoms UTI not systemic
Symptoms: Abdo pain, urgency, frequency
Investigations UTI
Urine dip stick
Lecuocyte esterase (LE) - correlates with WBCs
Nitrites (bacteria convert nitrates into nitrites)
Microscopy/flow cytometry
Urine culture - gold standard. Required for all children <3yrs before antibiotics.
> 10^5 CFU (colony forming units)
Most common organisms: E.coli, Klebsiella, proteus (stone former), streptococcus (gram +ve)
UTI management for children
Test urine when infant or child presents with unexplained fever, symptoms/signs suggestive UTI
Oral antibiotcs unless severely ill, vomiting, infants<3 months
Oral: trimethoprim, nitrofurantoin
IV antibiotics:
IV Ceftriaxone
IV Gentamicin
Antibiotic prophylaxis:
Consider for CAKUT (congenital abnormalties of kidney and urinary tract)
- Prophylaxis reduces risk of febrile UTI in vesico-ureteric reflux
UTI in children definition
Bacterial infection of lower uriSavenary tract (cystitis) or upper urinary tract (pyelonephritis), or both.
Cystitis (type of UTI due to infection of lower urinary tract)
Bacteriruria with symptoms of UTi, not systemic:
Symptoms: Dysuria, frequnecy, urgency
Pyelonephritis (type of UTI due to infection upper urinary tract (due to ascending bacteria))
Bacteriruia with fever >38
Symptoms: systemic - fever, malaise, flank pain + symptoms of cystitis
3 complications of UTI in children
Renal scarring
HTN
CKD
3 risk factors renal scarring
Vesico-ureterical reflux
Anatomical obstruction
Dysfunctional voiding
CAKUT
Congenital abnormalities of kidneys and urinary tract
Vesico-ureterical reflux (valve defect)
Obstruction of urinary drainage tracts
Both assoc. with congenital renal dysplasia
Adukt Polcystic Kidney Disease
Disorder characterised by renal cysts and systemic manifestations.
Commonest inherited disorder in kidneys
AD
Causes:
Mutations in PK1 (85%) and PK2 (15%) which are encode polycystin 1 and 2 (present in renal tubule epithelium (and liver/pancreas)
- Leading to overexpression in cyst cells - cyst formation.
PK1 more severe
25% pts no family history
APKD clinical presentation and diagnosis
Presents with family history
Symptoms: HTN, abdo pain, renal cysts
Signs: Palpable renal mass
Diagnosis:
If have family history, US when they are 21yrs, if negative, US at 30 yrs
<30 yrs: 2 cysts
30-59: 2 cysts each kidney
>60: 4 cysts each kidney
If no family history: >10 cysts in both kidneys
CT/MRI pelvis/abdomen
APKD complications
Renal: End stage renal disease, cyst problems e.g. bleeding, pain, replaces normal tissue
Other: HTN, intracranial aneurysms, liver/pancreatic cysts
Management APKD
Supportive
Manage HTN
Tolvaptan (Vasopressin V2 receptor antagonist) - decreaes cyst formation, delays decline in renal function
SE: hypernatraemia (increased Na+) and hepatotoxicity
Alport’s syndrome
X-linked
Mutations in COL4A3, 4, 5, which encodes alpha 3, 4, 5 chains of collagen 4 (main component in GBM). Leads to lamination and splitting of GBM.
Clinical consequences:
Microscopic haematuria, proteinuria, ESRF
Sensorineural deafness (childhood)
Other cystic kidney diseases
AR PKD - children
Von Hippel Lindau (AD) - malignant, benign tumours
Tuberosclerosis (AD) - benign brain tumours, learning difficulties
Medullary cystic disease (AD) - cysts in medulla, gout
Fabry’s disease
X-linked storage disease
Mutation leading to decreased enzyme, alpha galactosidase A which causes increased Gb3 (globotriaosylceramide) in podocytes
Causes proteinuria, ESRF
Symtpoms: cutanoues lesions - angiokeratoma
Diagnosis: alpha-Gal A in leukocytes
Renal biospy: inclusion bodies of Gb3
Treatment: enzyme replacement
Diabetic nephropathy (definition, pathophysiology, structural changes, treatment)
Macroalbuminuria or microalbuminuria, assoc. with retinopathy (TMD1/2)
Pathophysiology:
Hyerpglycaemia - increased pressure in glomerulus - hyperfiltration - proteinuria - HTN and renal failure (20 years)
Structural changes: BM thickening, loss of podocytes, mesangial expansion
Histology: Wilson nodule (areas of mesangial expansion)
Treatment: Glycaemic control, ACEi, SGLT2 inhibitors (as causes glucose excretion, and natriuresis (due to Na+ reabsorption with glucose, leading to activation RAAS)
Atheromatous vascular disease (Renal artery stenosis)
DD: Obstruction, interstitial nephritis
Renal artery stenosis: narrowing of renal artery. Clinical diagnosis.
Pathophysiology:
Atheroma - progressive narrowing - decreased GFR - hypoxia in renal cortex - microvascular damage - parenchyma inflammation - fibrosis
AKI
Decline in renal excretory function over hours/days and increased in serum creatinine and urea
Assessment:
KDIGO
Stage 1: serum creatinine >1.5, <2
Stage 2: serum creatinine >2, <3
Stage 3: serum creatinine > 3
x increase AKI baseline
Management:
Airway
Breathing
Circulation - restore renal perfusion
- correct hyperkalaemia, pulmonary oedema
Remove causes e.g. drugs, sepsis
Exclude obstruction
Hyperkalaemia treatment:
6-6.4: risk of arrythmia
>6.5 is medical emergency
Causes ECG changes: ventricular tacycardia - loss of P wave, peaked T wave
- IV calcium gluconate
- Insulin/dextrose (drives K+ into cells)
Oral calcium resonium (reduce absorption)
Bicarbonate (if high K+, and HCO3 <16)
Dialysis (if refractory hyperkalaemia, pulmonary oedema, acidotic, toxins)
3 types of AKI
Pre-renal (decresaed perfusion)
- Hypotension
- Sepsis (cause vasodilation causing drop in perfusion pressure)
- Cardiac failure
- ACEi
- Renal artery stenosis
Renal
Acute tubular necrosis (most common)
Obstructive
GN
Vasculitis
Gentamicin
Rhabdomyolysis
Post-renal (obstruction)
- Calculi
- Tumours e.g. prostate
- Lymph nodes
ATN (acute tubular necrosis)
Most reversible
Necrosis of tubular cells causing obstruction of tubules
Symptoms: hypotension, tachycardia
Causes:
Ischaemia - hypotension, sepsis
Toxins:
Endogenous - myoglobin (due to rhabdomyolysis. Presents with coca-cola urine), Ca2+
Exogenous - NSAIDs, gentamicin, ACEi, radiocontrast
Complications: polyuric phase (up to 72 hrs), inability to concentrate urine in tubules
CKD: definition, causes, signs/symptoms, investigations
Kidney damage or eGFR <60ml/min for 3 months or more
Causes:
Diabetic nephropathy, chronic glomerulonephritis, APKD, reflux nephropathy
Symptoms: Itch, rotten taste in mouth (due to uraemia), fatigue (due to anaemia), weight loss, SOB, joint/bone pain
Signs: Pulmonary oedema, HTN, increased HR, yellow tinge skin (uraemic frost)
Investigations:
FBC: Anaemia
Ca2+ (decreased), PTH (incresead), phosphate (increased)
- Kidney’s can’t excrete phosphate, and 1a hydroxylate Vit D causing decreased Ca2+. PTH increaesd to compensate (resorbs bone, also increases phosphate)
Serum creatinine (increased)
Urinalysis (proteinuria, haematuria)
eGFR (decreased)
Renal US (kidneys smaller than normal if chronic, and to see if there is obstruction)
Staging:
Stage 1: >90
Stage 2: 60-89
Stage 3: 30-59
Stage 4: 15-29
Stage 5: <15
Stage 1 and 2 normal, unless urine or structural abnormality e.g. proteinuria, APKD
What happens to afferent and efferent arterioles as GFR falls?
Prostaglandins dilate afferent arterioles (to increase flow)
Ang II constricts efferent arteriole
NSAIDs inhibit prostaglandins, ACEi inhibits Ang II, so contra-indicated for AKI
Things to slow progression of AKI
BP control
Glycaemic control
Diet
Smoking
Lowering cholesterol
Treat acidosis
Treatment CKD
1st line treatment ACEi e.g. Ramipril
- Can be used as 25% GFR reduction in first few weeks is a good thing
2nd line: Ca+ channel blockers e.g. verapimil
Activated Vit D (Alfacalcidol)
Phosphate binders e.g. calcium carbonate
Cinalcalcet (calcimimetic) - to decrease production of PTH
4 functions of kidney
Regulates total body water
Regulates electrolytes
Makes EPO
Makes renin
Indication renal replacement therapy
Medically resistant HTN
Medically resistant pulmonary oedema
Medically resistant acidosis
Uraemic pericarditis
Uraemic encephalopathy
No rule for eGFR, but usually 5-10
4 types of renal replacment therapy
Haemodialysis
Peritoneal dialysis
Renal transplant
Conservative treatment
Haemodialysis
Removal of solutes through diffusion
Removal of fluid through pressure: hydrostatic filtration
Uses external semi-permeable membrane
Requires AVF (arterial venous fistula) - artery and vein connected
Pros:
Hospital or home
4h, 3 times a wk
Home based more flexibile, but requires carer, space
Cons:
Acute hypotension “crash”
Access problems
Cramps
Peritoneal dialysis
Diffusion and osmotic filtration
Across peritoneal membrane as filter
Dialysis fluid goes in via catheter (contains high amounts of glucose - hyperosmolality) causing osmotic filtration
Types:
CAPD (continuous ambulatory peritoneal dialysis)
- occurs during day
APD (automated peritoneal dialysis)
- occurs during night
Pros:
Home based
Maintain independence
Cons:
Infection - peritonitis
Glucose load - develop/worsen diabetes
Obese pts, intra-abdominal adhesions not suitiable
Problems not helped by dialysis
EPO, iron supplements needed
Renal bone disease - need phosphate binders, vit D
Neuropathy
When to treat asymptomatic bacteruria
Preschool children
Pregnancy
Immuncompromised
Renal transplant
UTIs causes
90% caused by single organism
E.coli, Klebsiella, Proteus, Enterococcus
Multiple in:
Catheters, recurrent infection
Multi-drug resistant bacteria:
Frequent infections, mutiple antibiotic courses
Renal transplant
Types:
Living or cadaveric (after brainstem, cardiac death)
Average wait 3 years
Pros:
No dialysis
More independence
Better renal function
Cons:
Requires immunosuppressants after e.g. ciclosporin, tacrolimus
Increased cardiovascular risk
Increased infection
Contraindications:
Malignancy
Active infection
Clinical features in adult UTI
Suprapubic discomfort, dysuria, frequency, urgency, low grade fever
Nocturia, incontinece in elderly
Investigations uncomplicated UTI
If first time presenation in non-pregnant women: urine dipstick, culture not mandatory
Children and men require urine culture always
Treatment UTI pregnancy
Amoxillcin or Cefalexin
Treatment recurrent UTI
2 or more episodes in 6 months
3 or more in 1 years
Management:
Oral hydration
Post-coital voiding
oral estrogen
Short course antibiotics
Single post coital antibiotics
Prophylactic abx - if other measure failed
Complicated UTIs
IV Ciprofloxacin
Catheter assoc. UTI
Organisms usually pts flora or healthcare environment
Complications CAUTI:
- chronic renal inflammation
- Risk of bladder Ca
Treatment: IV Gent
Renal pyelonephritis
Upper UTI infection, ascending infection involving pelvis of kidney
Complication: renal abscess (usually gram -ve)
- Can lead to emphysematous pyelonephritis (severe infection that causes gas accumulation in tissue)
Perinephric abscess
Pus in perinephric space
Pts usually septic
Causes:
Untreated lower UTI, anatomical abnormalities
Organisms: E.coli, S. aureus
Management:
FBC, UEs, CRP, urine sample, blood culture, renal US, abx
Acute bacterial prostatitis
Inflammation of prostate due to bacterial infection
Symptoms: Fever, back pain, acute lower UTI symptoms e.g. dysuria, frequency, uregency
Organisms: E.coli, S.aureus, N.gonnorhoea
Complications: Prostate abscess, rupture
Treatment: IV Ciprofloxacin
Chronic prostatitis
Prolonged prostate infection lasting >3 months
Asymptomatic, fever, back pain, UTI symptoms
Organisms: E.coli, Enterococcus, S.aureus
Orchitis and Epididymitis
Orchitis
Inflammation of one/both testicles
Symptoms: testicular pain, fever, dysuria
Causes: bacterial or viral e.g. mumps
Bacterial orchitis: complication of epididymitis
Epididymitis
Inflammation of epididymis
Ascending infection from urethra
Causes: Gram neg, TB
Fournier’s Gangrene
Type of nec fas affecting genital, perineum
Rapid onset, systemic sepsis
Organisms: E.coli, anaerobes
Risk factors: UTI, IBD complications
Treatment: surgical debridement
Urine microscopy interpretation (Epithelial cells, bacteria no WBC, bacteria + WBCs +/- cathether, Pyuria with no bacteria)
Epithelial cells: contamination
Bacteria no WBC: contamination
Bacteria + WBCs, with catheter: assess clinically
Bacteria + WBCs + no catheter: infection
Pyuria (pus in urine) with no bacteria: TB, urethritis (chlamydia), previous antibiotcs
Nephrolithiasis
Colicky pain, haematuria, unilateral flank tenderness
Calcium oxalate/phosphate (most common)
Cause: Idiopathic, hypercalciuria
Infection stones:
struvite (Magneusium, ammonium, phospate) - proteus
Uric acid stone (not seen on XR) - most common seen in gout, hyperuricaemia
Others: cystiene (not seen on CT) - mostly in children
Volume of distribution definition
Volume in which the amount of drug needed to distribute uniformly to produce observed blood conc (tells you how extensively the drug distributes to rest of body compared to plasma)
Vd increased in lipid soluble drugs e.g. diazepam
If Vd near the plasma drug conc, shows drug stays in vascular space e.g. warfarin
PK vs PD
PK: what body does to drug
- Absorption
- Distribution
- Metabolism
- Excretion
PD: what drug does to body
- MOA of drug
- Efficacy
- Safety profile
Clearence
Volume of plasma needed to clear substance per unit time
Half life
Time required for serum plasma conc of the drug to decrease by half
Long half life required loading dose
4-5 half lives to reach steady state
Depends on clearence and Vd
Used to determine:
Time it takes for drug to be eliminated
Time to reach steady state
Dosing interval
Linear vs non-linear pharmacokinetics
Linear: dose proportional to conc of drug e.g. double dose, double conc
Rate of elimiation proportional to conc
Non linear: dose non-proportional to conc
Rate of elimiation constant regardless of drug conc.
What factors influence PK/PD
Age
Renal impairment
Hepatic impairement
Congestive HF
GI disease
How does age influence PK?
Decreased total body water and increased fat - affects Vd
Water soluble drugs e.g. lithium, gentamicin
- Serum levels may increaese due to decreased Vd
Fat soluble drugs e.g. diazepam
- Half life may increase with increaesd body fat
B-blockers effect reduced in age
Cockroft and Gault equation
Creatinine clearence
Depends on age, weight, sex, creatinine conc
Exmaples of drug- disease interactions
PD pts have increased risk of drug induced confusion
NSAIDs can exacerbate CHF
Examples of drug drug interactions in eldery
Statins and erythromycin
Verapamil and B-blockers
Common examples of pescribing cascade in elderly
NSAIDs - HTN - antihypertensives
Ca channel anatagonists - oedema - furosemide
What drugs causes decreased elimiation in renal disease?
Gentamicin
Lithium
Digoxin
Methotrexate
Penicillins
Renal failure and acidic drugs
Renal failure can lead to acidosis
Acidic drugs less bound to albumin (ionised) leading to more free (active) drug in plasma
E.g. phenytoin (acidic)
What do with antibiotics and LMWH, pheytoin, digoxin in renal disease?
Reduce dose
What to do with metformin, NSAIDs?
Avoid
What to do in ACEi in renal disease?
Caution
Renal disease vs heptic disease PD/PK
Renal:
Same/Increased Vd, decreased rate of excretion (t1/2 increased)
Increase dosing interval
Hepatic:
Same/incresed Vd, slower rate of metaoblism (t1/2 and F increases)
Reduce dose, increase dosing interval
Liver disease high vs low extraction drugs
High extraction: metabolised at high rate by liver. Affected by changes in blood flow. E.g. Morphine
Low extraction: metabolised at low rate by liver. Not changed by blood flow. But changes with liver enzyme activity. E.g. theophylline
Effect on pharmacodynamics on liver disease
Increased sensitvity to oral anticoagulants
Fluid retention
Hepatorenal syndrome
Causes of renal stone foramtion?
Abnormal urine (e.g. too much salt)
Urinary obstruction e.g. pelviureteric junction obstriction, medullary sponge kidney
UTI (proteus mirablis splits urea into ammonia, causing alkaline pH leading to struvite stones)
What causes abnormal urine?
Too much salt
- Salt can lead to increaesd acid (metabolic syndrome), hypercalciuria
Not enough water
Lack of inhibitors e.g citrate, magnesium
Type of stones
Calcium oxalate or phosphate (most common)
Struvite
Uric acid
Others e.g. Cysteine
Management of stones
Observation
Medical: NSAIDs (reduces pain, GFR and renal pressure)
Surgical:
ESWL (extracorporeal shockwave lithotripsy)
- shockwaves to break up stones
- proximal utreteric stones <10mm, or renal stones <2cm
Laproscopy/open surgery
- treat huge
ureteric stones, non functioning kidney
Sepsis and osbtructing stone
Medical emergency
Implement sepsis 6
Invstigations:
Bloods, CRP, Coag
USS or CT
Treatment: Nephrostomy (tube placed into kidney to drain urine out) or ureteric stent
Fluids
Maintenance:
0.18% NaCl
5% glucose
Hartmann’s
Replacement:
Hartmann’s
Alternative balanced solutions for resus
Resusication:
Hartmann’s
Alternative balanced solutions for resus
Problems with 0.9% saline
Not physiological
Can cause hyperchloraemia acidosis
Increaesd Cl+ leads to renal vasoconstriction leading to poor UO
Kidney’s can’t excrete Na+ load
So leads to hyperchloraemia, hypernatraemia, acidosis
Rhabdomyolysis
Damaged skeletal muscle breaks down, releasing myoglobin, intracellular ions
Due to trauma, prolonged immobilisation (e.g. due to alcohol, drugs)
Leads to:
- electrolyte imbalance (high K+, Mg, phosphate, low Ca+)
- DIC (increased PT, PTT and INR)
- AKI (increaed urea, creatinine)
Diagnosis: Increased serum creatinine kinase 5x ULN
Differentiating between AKI and chronic kidney disease
Acute:
US: Normal sized kidneys
Electryolyte imbalance e.g. high K+
Chronic:
US – small kidneys
PTH elevated
Phosphate elevated
Anaemic
Causes of bladder obstruction
Posterior urethral valve
- Obstructing membrane at posterior urethra due to abnormal development
- Most common congenital cause of bladder obstruction
- Presents as antenatal hydronephrosis, UTI
Management: valve resection
Prostate hypertrophy
Neurogenic bladder e.g. spinal bifida
PUJO (pelvi-ureteric junction obstruction)
Between renal pelvis and ureter
Common cause of hydronephrosis in children
Commonly found on antenatal US
Abdo mass, haematuria
VUJO (vesico ureteric junction obstruction)
Between ureter and bladder
Anantomical narrowing or obstruction e.g. strictures
Abdo mass, haematuria
Prostate Ca
Adenocarcinoma, usually arises in periphary of prostate
Risk factors: Age, genetics e.g. BRAC2, p53, african american
Signs/symptoms:
Often asymptomatic, UTI, haematuria, bone pain (most common symptom of metastases)
Complications:
SC compression, ureteric obstruction
Diagnosis:
Digital rectal exam
PSA (prostate specific antigen)
TRUS (needle biopsy)
Gleeson Grading (based on how differentiated they are) - provides prognostic information
TNM staging
Treatment
Radiotherapy
Androgen ablation - LHRH analogue, or orchidectomy (surgical castration)
Chemotherapy
Prostatectomy
Bladder Ca
Transitional cell carcinoma
Risk factors: Age, caucasian, chronic inflammtion e.g. stones, long term catheters
Presents: Painless, visible haematuria
Diagnosis: Cystoscopy
Treatment:
TURBT (trans-urethral resection, of bladder tumour)
Cystectomy (bladder and prostate/uterus removed)
Mets: usually pulmonary
M-VAC (Methotrexate, vinblastine, doxorubicin, cisplatin)
Renal carcinoma (risks, investigations, histology, treatment)
Renal cell carcinoma (most common)
Risk factors:
Smoking, obesity, HTN, renal cysts, haemodialysis
Presents: triad: mass, pain, haematuria
lower leg oedema, paraneoplastic syndrome: polycytheamia (increased EPO), HTN, (increased renin),
Investigations:
FBC, CRP, LFTs, bone profile, US, CT kidneys, renal biopsy
Histology:
Clear cell (most common) - vascular, granular and clear (due to lipids)
Papillary - sold, multi-focal
Treatment:
Nephron sparing surgery (part of kidney removed) - if pt ahs one kidney, CKD
Radical nephrectomy (remove kidney)
Mets: Tyrosine kinase inhibitors
Testicular and penile cancer
Germ cell tumours (most common), Stromal tumours
Most curable ca.
Risk factors: Age: 25-40, cryptochordism, HIV
Presentation: painless lump,
Investigation:
Alpha-feta protein (also in HCC)
Beta hCG
LDH
Treatment:
Radical orchidectomy, chemo
Penile cancer:
Risk factors: HPV 16, 18, smoking
Treatment:
Circumcision, penectomy+/-reconstruction
UTI in children investigations
Renal US
Pros: Dilated ducts, no radiation
Cons: Can’t see kindey parenchyma
Micturating cystourethrogram
Dye given through cathether, X rays taken. Shows flow of urine
Pros: GS for VUJ
Cons: radiation
Nuclear:
DMSA
Radiocontrast given, taken up by healthy tissues
Pros: Scarring
Cons: GS Radiation
MAG3 indirect cystogram
Radiocontrast injected, passed out into urine
Pros: VUJ, no catheter required
Cons: Continence and co-operation required
MAG3 diuresis renogram
Pros: GS for obstruction
Cons: continence and co-operation
