Nephrology Flashcards

(117 cards)

1
Q

Describe the structure of the glomerular filtration barrier

A

Constriction of afferent arteriole is controlled by SNS

Constriction of efferent arteriole is controlled by angiotensin II

Layers of filtration

Fenestrated capillary endothelium (endothelial cells covered by glycocalyx)

Negatively charged glomerular basement membrane

Foot processes of podocytes
> Wrap around capillaries and leave slits between them for blood to filter through

> Podocytes secrete the basement membrane

> . Filtration slits (slit diaphragm)

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2
Q

Describe how urea is processed and how its levels may change

A

Byproduct of amino acid metabolism in liver

Reabsorbed in inner medullary collecting ducts (passively)

Changes in urea

Diet
> High protein or GI bleed leads to high urea

Tissue breakdown e.g. corticosteroid
> High urea

Liver failure
> Lowers urea

Dehydration
> Passive reabsorption in proximal tubule - high urea

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3
Q

Explain why creatinine is used to measure renal function

A

Normal product of muscle metabolism

Provides good estimate of GFR because
> Daily production is constant
> (almost) fully filtered at the glomerulus
> Neither reabsorbed nor secreted (almost) in the tubule

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4
Q

Describe the limitations of eGFR

A

Only accurate in steady state and assumes average muscle mass
> Overestimation of function those with lower muscle mass e.g. amputees, para/quadriplegics, rheumatoid arthritis

eGFR not accurate >60ml/min and <18 years of age

Inverse relationship between GFR and serum creatinine leads to
> Slow recognition of loss of the first 70% of kidney function
> Surprise at the sudden rise in creatinine

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5
Q

Desribe the formulae used to calculate eGFR

A

Cockgroft and Gault formula for estimating creatinine clearance
> Attempts to correct for muscle mass

MDRD 4-variable formula for estimated GFR
> Based on serum creatinine, age, sex

eGFR < 60ml/min/1.73m2 or raised serum creatinine means reduced kidney function (adults)

CKD-EPI equation for patients with high levels of eGFR

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6
Q

Describe acute interstitial nephritis

A

May have raised eosinophil count and rash

  • Haematuria, fever, oliguria
  • Swelling, nausea, vomiting

Caused by autoimmune disorders, systemic disorders, infections, allergic reaction to antibiotics, anticonvulsants, diuretics…

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7
Q

Describe the staging of CKD

A

Stage 1:
Normal
GFR >90ml/min

Stage 2:
Early CKD
GFR 60-89ml/min

Stage 3:
Moderate CKD
GFR 30-59ml/min

Stage 4:
Severe CKD
GFR 15-29ml/min

Stage 5:
End-stage renal disease
GFR <15ml/min

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8
Q

Describe the measurement of urinary protein excretion

A

24h urine collection (g/24h)

Protein:creatinine ratio (PCR) on morning spot sample (mg/mmol)

Albumin:creatinine ratio (mg/mmol)

If excess proteinuria, the balance changes

30% other proteins
> Immunoglobulin
> Tamm Horsfall

70% albumin

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9
Q

Which cells and pathophysiological mechanisms are involved in glomerulonephritis?

A

Cells
- Parietal epithelial cells
- Podocytes
- Mesangial cells
- Endothelial cells
- Basement membrane

Pathophysiological mechanisms
- Antibodies, immune complexes, complement
- Cell-mediated mechanisms: cytokines, growth factors, proteinuria
- Metabolic / genetic / vascular causes

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10
Q

Describe the spectrum of presentations of glomerulonephritis

A

Incidental finding of urinary abnormalities +/- impaired kidney function

Visible haematuria

Synpharyngitic – sore throat and visible haematuria

Nephritic syndrome

Nephrotic syndrome

Acutely unwell with rapidly progressive glomerulonephritis

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11
Q

Describe nephrotic syndrome

A

Cause
> Damage to podocytes
> Scarring and deposits

Triad
> 3.5g proteinuria per 24h (urine PCR >300)
> Serum albumin <30
> Oedema

> (hyperlipidaemia)

Complications
> Venous thromboembolism
> Infection

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12
Q

Describe nephritic syndrome

A

More acute and inflammatory than nephrotic syndrome

Triad
> Hypertension
> Blood and protein in urine
> Declining kidney function (oliguria)

Berger’s disease (IgA nephropathy) is the most common cause of nephritic syndrome

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13
Q

Describe IgA nephropathy

A

Most common primary glomerular disease
> Precipitated by infection, can be synpharingitic
> May be secondary to HSP, cirrhosis, coeliac disease

Pathophysiology
> Abnormal overproduction of IgA1, IgA I/C
> Mesangial IgA, C3 deposition
> Mesangial proliferation

Clinical signs
> Haematuria
> Hypertension
> Proteinuria (varies with prognosis)

Complications
> End-stage renal failure (ESRF)

Treatment
> No specific therapy
> Antihypertensives
> ACE inhibitors
> SGLT2 inhibitors

Spectrum of disease
> Minor urinary abnormalities
> Hypertension
> Renal impairment and heavy proteinuria
> Rapidly progressive glomerulonephritis

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14
Q

Describe membranous glomerulonephritis

A

Presents with nephrotic syndrome
> Commonest primary cause
> Often chronic

Anti-phospholipase A2 receptor antibody – found in podocytes

IC in basement membrane / sub-epithelial space

Secondary causes
> Malignancy
> Connective tissue disease (CTD)
> Drugs

Variable natural history
> 1/3 spontaneously remit
> 1/3 progress to ESRF over 1-2 years
> 1/3 persistent proteinuria, maintain GFR

Treatment
> Treat underlying cause if secondary

> Supportive non-immunological
> ACEi
> Statin
> Diuretics
> Salt restriction

Specific immunotherapy
> Steroids
> Alkylating agents – cyclophosphamide

Alternative agents
> Rituximab: anti-CD20 MAb
> Cyclosporin
> Tacrolimus

Outcomes
> Complete or partial remission
> ESRD
> Relapse
> Death

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15
Q

Describe minimal change disease

A

Commonest form of glomerulonephritis in children
> 90% of GN <10 years, 20% of adults of all ages

Causes nephrotic syndrome

EM – foot process fusion

Causes
> Idiopathic
> Secondary to malignancy

Pathogenesis
> T cell and cytokine mediated
> Target podocytes, alter glomerular basement membrane charge

Clinical features
> Acute presentation
> May follow URTI
> GFR is normal or reduced due to intravascular depletion
> Rarely causes renal failure
> Not usually biopsied in children

Relapsing course – 50% will relapse

Treatment
> High dose steroids
> Prednisolone 1mg/kg for up to 8 weeks

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16
Q

Describe crescentic disease

A

Aka rapidly progressive GN

Group of conditions which demonstrate glomerular crescents on kidney biopsy

Nephritic presentation

Kidney biopsy
> Crescent-shaped collection of fibrin and matrix in Bowman’s space
> Can break through into surrounding cortex

Course of disease
> Aggressive disease – progress to ESRF quickly

Causes
> ANCA vasculitis – MPO/PR3
> Goodpasture’s syndrome: anti-GBM
> Lupus nephritis
> Infection-associated
> HSP nephritis

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17
Q

Describe diabetic nephropathy

A

Glomerulus
> Kimmelstiel Wilson lesions - nodules characteristic of DM
> Thickened basement membrane
> Associated with proteinuria

Pathophysiology
> Hyperglycaemia
> Volume expansion
> Intra-glomerular hypertension
> Hyperfiltration
> Proteinuria
> Hypertension and renal failure

Natural course
> After 20 years of diabetes
> Associated with other complications such as retinopathy
> Always with proteinuria
» Microalbuminuria
» Proteinuria
» Rise in serum creatinine

Management
> Treat hypertension
» ACEi or ARB
» Low sodium diet
» Weight loss
» Exercise

> Improve blood glucose control
> Education – DAFNE course
> Drugs
» Insulin
» Oral hypoglycaemia drugs including SGLT2 inhibitors
>Technology
» Glucose sensors and pumps

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18
Q

Describe renal artery stenosis

A

Clinical diagnosis
> No angiogram/CT angiogram/ MRI

Angioplasty/stenting is rarely effective

Pathophysiology
> Progressive narrowing of renal arteries with atheroma
> Perfusion falls by 20%

> GFR falls but tissue oxygenation of cortex and medulla maintained

> RA stenosis

> Cortical hypoxia causes microvascular damage and activation of inflammatory and oxidative pathways

> Parenchymal inflammation and fibrosis progresses and becomes irreversible

> Restoration of blood flow provides no benefit

Management
> Medical
» BP control (avoid ACEi and ARBs)
» Statin
» If diabetic – good glycaemic control

> Lifestyle
> Smoking cessation
> Exercise
> Low sodium diet

> Angioplasty
> Rapidly deteriorating renal failure
> Uncontrolled BP on multiple agents
> Flash pulmonary oedema

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19
Q

Describe amyloidosis

A

Deposition of highly stable insoluble proteinous material (amyloid) in extracellular space (felt-like substance made of beta pleated sheets)

Amyloid deposits in liver, heart, kidneys, gut

8-10mm fibrils sticking to wall

Test – Congo Red stain

Apple green birefringence – pathognomic

Electron microscopy
> Amyloid fibrils 9-11nm cause mesangial expansion

AA amyloid
> Inflammatory diseases e.g. chronic pyogenic or granulomatous infections, familial mediterranean fever (FMF)
> Causes systemic amyloidosis

AL amyloid
> Immunological fragments from haematological condition e.g. myeloma

Treatment
> AA amyloid
» Optimise treatment for underlying condition

> AL amyloid
> Optimise treatment for underlying condition

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20
Q

Describe lupus nephritis

A

Pathophysiology
> Autoimmune disease: intravascular immune complex-mediated glomerular disease

> Auto-antibodies produced against dsDNA, nucleosomes, snRNPs (anti-dsDNA, anti-histone)

> Auto-antibodies attach to basement membrane

> Activate complement (consumes C4)

> Renal damage

Investigations
> ANCA
> Anti-GBM antibody
> ANA
> Complement – C3 & C4
> Anti-dsDNA antibodies
> Serum immunoglobulin

Kidney biopsy

Confirm diagnosis and stage disease

Poor prognosis

Treatment

Treat underlying disease

Immunosuppression

Steroids

MMF

Rituximab

Cyclophosphamide

Hydroxychloroquine

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21
Q

Describe lupus nephritis

A

Pathophysiology
> Autoimmune disease: intravascular immune complex-mediated glomerular disease

> Auto-antibodies produced against dsDNA, nucleosomes, snRNPs (anti-dsDNA, anti-histone)

> Auto-antibodies attach to basement membrane

> Activate complement (consumes C4)

> Renal damage

Investigations
> ANCA
> Anti-GBM antibody
> ANA
> Complement – C3 & C4
> Anti-dsDNA antibodies
> Serum immunoglobulin

Kidney biopsy
> Confirm diagnosis and stage disease
> Poor prognosis

Treatment
> Treat underlying disease

> Immunosuppression
> Steroids
> MMF
> Rituximab
> Cyclophosphamide
> Hydroxychloroquine

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22
Q

Describe myeloma renal disease

A

Cast nephropathy

Hypercalcaemia / dehydration

Amyloid

Light chain deposition disease

Acquired Fanconi syndrome (proximal tubule dysfunction)

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23
Q

Describe the inheritance and clinical presentation of Adult Polycystic Kidney Disease (ADPKD)

A

Autosomal dominant pattern of inheritance

PKD 1 gene mutation in chromosome 16
> More common and aggressive, reach ESRF before 50
> Codes for polycystin 1

PKD2 gene mutation in chromosome 4
> Less common, less aggressive, may never reach ESRF)
> Code for polycystin 2

Clinical presentation
> Incidental finding on USS
> Hypertension
> Impaired renal function
> Loin pain
> Haematuria

Cysts gradually enlarge, normal kidney tissue replaced

Kidney volumes increased and eGFR falls

Complications
> Cyst infection, cyst rupture, haematuria and pain

Extra-renal manifestations
> Intra-cranial aneurysms
> Hypertension, LVH, valve abnormalities e.g. mitral valve prolapse
> Liver cysts
> Bronchiectasis
> Diverticular disease and abdominal hernias (due to size and pressure effect of enlarged kidneys)

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24
Q

Describe the function of polycystins

A

Polycystins are located in renal tubular epithelia & liver and pancreas ducts

Overexpressed in cyst cells

Membrane proteins involved in intracellular calcium regulation

Mechanism of cyst formation poorly understood

Genetic testing not routine but increasing

Vasopressin drives cyst development

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25
Describe the diagnosis and management of ADPKD
Diagnosis - Family history > Age 15-30: 2 unilateral or bilateral cysts > Age 30-59: 2 cysts in each kidney > Over age 60: 4 cysts in each kidney - No family history > 10 or more cysts in both kidneys > Renal enlargement > Liver cysts - Ultrasound > Differentiate between simple renal cysts - CT or MRI more sensitive - Genetic testing Management > Supportive > Early detection and management of blood pressure > Treat complications > Manage extra-renal associations > Prepare for renal replacement therapy Tolvaptan > Vasopressor antagonist, acts at V2 receptor - counteracts vasopressin > Delays onset of RRT by 4-5 years > Side-effects: hepatotoxicity, hypernatraemia
26
Describe Alport's syndrome
Inherited progressive glomerular disease Second most common inherited kidney disease Caused by an inherited defect in type IV collagen (basement membrane) - found in ears, eyes and kidney Usually X-linked - more severe presentation in males Collagen IV abnormalities > Alpha 3 gene mutation > Alpha 4 gene (COL3A4) mutation > Alpha 5 (COL3A5) mutation Deafness and renal failure – can affect other organs including eyes Presentation > Asymptomatic persistent non-visible haematuria from early childhood > Proteinuria, hypertension and progressive renal impairment > ESRD – 90% on dialysis or transplanted by age 40 > Sensorineural hearing loss in late childhood > Ocular defects >> Lens – anterior lenticonus >> Retina – bilateral white or yellow granulations >> Cornea – posterior polymorphous dystrophy, recurrent corneal erosion Management > Supportive – BP control > Prepare for dialysis or transplant
27
Describe Fabry disease
Rare X-linked lysosomal storage disorder Alpha galactosidase A deficiency resulting in accumulation of globotriaosylceramide (Gb3) Also causes neuropathy, cardiac and skin features GB3 accumulates in glomeruli, particularly in podocytes causing proteinuria and ESRF > Pro-inflammatory and pro-fibrotic Clinical presentation > Intermittent episodes of burning pain in extremities > Cutaneous vascular lesions – angiokeratomas > Diminished perspiration > Characteristic corneal and lenticular opacities > Abdominal pain, nausea and/or diarrhoea > Left ventricular hypertrophy > Arrythmia > Stroke > CKD and proteinuria Diagnosis > Measure alpha-Gal A activity in leukocytes (unreliable in females) > Renal biopsy >> Inclusion bodies of G3b aka zebra bodies Management > Enzyme replacement therapy; prevents progression to irreversible tissue damage
28
Describe the embryological development of the kidney
Pronephros Mesonephros Metanephros Nephrogenesis commences in week 10 No new nephrons after 36 weeks Approximately 1 million nephrons per kidney GFR > 120mls/min/1.73m2 > At birth: 40-65 mls/min/1.73m2
29
Describe the embryological development of the kidney
Pronephros Mesonephros Metanephros Nephrogenesis commences in week 10 No new nephrons after 36 weeks Approximately 1 million nephrons per kidney GFR > 120mls/min/1.73m2 > At birth: 40-65 mls/min/1.73m2
30
Describe renal hypodysplasia
Renal hypoplasia – reduction in number of nephrons but normal architecture Renal dysplasia – malformed renal tissue Renal hypodysplasia – congenital small kidneys with dysplastic features Presentation > Antenatal:US growth > Neonate: >> Lung issues >> IUGR >> Acidosis >> Raised creatinine > Children >> FTT >> Anorexia >> Vomiting >> Proteinuria Management - supportive
31
Describe renal agenesis
Congenital absence of renal parenchymal tissue: metanephric stage Male:female preponderance Unilateral or bilateral (mostly sporadic) Associated with increased risk of other anomalies
32
List renal cystic diseases
- Multicystic dysplastic kidney (MCDK) - ADPKD - ARPKD
33
Describe multicystic dysplastic kidney (MCDK)
Abdominal mass detected antenatally or neonatally Involution: 35-65% Risks > Hypertension > Malignancy
34
Which anomaly is associated with ARPKD?
Congenital hepatic fibrosis: subclinical to liver disease > Portal hypertension > Ascending cholangitis
35
Describe the childhood presentation of ADPKD and its associated anomalies
Presentation > Haematuria > Hypertension > Flank pain > UTIs Associated anomalies > Mitral valve prolapse > Cerebral aneurysm > AVM > Hepatic / pancreatic cysts > Colonic diverticula / hernia
36
Describe hydronephrosis and list its causes in children
Male preponderance Bilateral in some cases Associated with renal injury and renal impairment Postnatal US – renal pelvic diameter >10mm Causes > Vesico-ureteric reflux > Obstruction of urinary tract
37
Describe vesico-ureteric reflux
38
Describe obstruction of the urinary tract in children
Level of obstruction - Pelvis/ureter (PUJ) > Partial/total blockage of urine at ureter junction with kidney > Males > females > Bilateral in some > Antenatal diagnosis >> Abdominal mass, UTI, failure to thrive (FTT) >> Abdominal or flank pain >> Ureter - Ureter/bladder (VUJ) > Vesico-ureteric junction obstruction > Functional or anatomical abnormality >> Megaureter >>> Primary: reflux / obstruction >>> Secondary: bladder issues >> Ureteric dilation >7mm - Bladder > Posterior urethral valves >> Most common obstructive uropathy >> Antenatal detection >> Investigations: US, MCUG >> Bilateral hydronephrosis; UTI >> Management – cystoscopy, ablation of valve >> Risk of CKD and bladder dysfunction - Urethra
39
Describe the staging of AKI
Decline of renal excretory function over hours or days > Avoid eGFR – not reliable in AKI > Serum creatinine more reliable Severity of AKI – KDIGO - Stage 1 > Serum creatinine >1.5 and <2x AKI baseline or >26 micromol/l increase above AKI baseline - Stage 2 > Serum creatinine >2.0 and <3x AKI baseline - Stage 3 > Serum creatinine 3x AKI baseline or > >354 micromol/l increase above AKI baseline Oliguria <1mL/kg/h in infants <0.5mL/kg/h in children <400-500mL/24h in adults
40
Describe the classification of the causes of AKI
Pre-renal > Hypovolaemia + hypotension > Reduced effective circulating volume > Drugs > Renal artery stenosis Renal > Glomerular >> Glomerulonephritis > Tubular >> Ischaemic ATN >> Nephrotoxic ATN >> Myeloma cast nephropathy > Tubulointerstitial >> Drugs >> Myeloma >> Sarcoid Post-renal > Renal papillary necrosis > Kidney stones > Retroperitoneal fibrosis > Carcinoma of the cervix > Prostatic hypertrophy/malignancy > Urethral strictures
41
Describe the pre-renal causes of AKI
Hypotension Hypovolaemia > Blood loss > Diarrhoea/vomiting > Burns Reduced effective circulating volume - hypoperfusion > Cardiac failure > Septic shock > Cirrhosis Hypoxia Drugs > ACEi > NSAIDs Toxins Renal artery stenosis
42
Describe the renal causes of AKI
Large blood vessels > Polyarthritis nodosa Glomeruli and small blood vessels > Glomerulonephritis > Vasculitis Tubular > Ischaemic acute tubular necrosis (ATN) >> Unresolved pre-renal causes: >>> hypoperfusion or direct toxicity >>> Hypotension >>> Sepsis Toxins Exogenous > Drugs > NSAIDS, gentamicin, ACEi > Contrast > Poisons (metals, antifreeze) Endogenous > Myoglobin (rhabdomyolysis) > Haemoglobin > Immunoglobulins (myeloma) > Calcium > Urate Nephrotoxic ATN > Toxins (ethylene glycol, lithium), contrast, gentamicin > Myeloma cast nephropathy Tubulointerstitial > Acute tubulointerstitial nephritis > Rhabdomyolysis > Drugs > Myeloma > Sarcoid
43
Describe post-renal causes of AKI
44
Describe glomerular haemodynamic regulation
Hypovolaemia leads to a fall in glomerular filtration pressure Prostaglandins dilate afferent arteriole to increase flow as MAP falls towards 80 mmHg > Blocked by NSAIDs Efferent arteriole can vasoconstrict, increasing glomerular pressure > Blocked by ACEi
45
Describe the investigations used in AKI
Acute or chronic Bloods – both urea and creatinine elevated Potassium must be controlled as it can cause heart problems > <6.0 is abnormal but no immediate concern > 6.0-6.4 risk of arrhythmia > >6.5 is a medical emergency Urine output Clinical assessment of fluid status > BP, JVP, oedema, heart sounds Underlying diagnosis – history, exam, meds
46
Briefly summarise the treatment of AKI
- Circulation - restore renal perfusion - Treat hyperkalaemia - Treat pulmonary oedema if present - Remove causes: drugs, sepsis... - Exclude obstruction and consider renal causes - Refer to ICU or renal unit
47
Describe the treatment of hyperkalaemia
Protect the heart > IV calcium gluconate 10ml 10% as cardiac membrane stabiliser Drive K+ into cells > Insulin 10-15 units actrapid + 50ml dextrose – moves potassium into cells > If raised potassium and low bicarb, supplementation of bicarb – IV NaBicarb 1.26% > Beta agonists – nebulised salbutamol Remove K+ from body > Acute >> Haemodialysis >>> Refractory potassium >6.5 mmol/l >>> Refractory pulmonary oedema >>> May be considered for >>>> Acidosis (pH < 7.1) >>>> Uraemia (pericarditis, encephalopathy) >>>> Toxins (lithium, ethylene glycol...) >> Loop diuretic - furosemide > Long-term >> Reduce absorption from gut – calcium resonium 15g/day orally or enema
48
Describe the recovery from ATN
Polyuric phase 48-72h Up to 6L urine/day Often subsequent low K, Ca, Mg Tubules fail to concentrate urine
49
Define CKD and list causes
Kidney damage or GFR <60ml/min per 1.73m2 for 3 months or more Aetiology - Diabetic nephropathy - Glomerular sclerosis - Nodular lesions - Proteinuria and deterioration of renal function - Renovascular disease / ischaemic nephropathy - Chronic glomerulonephritis - Membranous glomerulonephritis - IgA nephropathy - Reflux nephropathy / chronic pyelonephritis - ADPKD - Obstructive uropathy
50
Describe symptoms of CKD
- Pruritus - Nausea, anorexia, weight loss - Fatigue - Leg swelling - Breathlessness - Nocturia - Joint/bone pain - Confusion Advanced CKD - Peripheral and pulmonary oedema - Pericardial rub - Rash/excoriation - Hypertension - Tachypnoea - Cachexia - Pallor & lemon yellow tinge
51
Describe the treatment for anaemia as a consequence of renal failure
eGFR <30 Iron absorption and utilisation are suboptimal Replace iron, B12 and folate if low Treatment > ESA (erythropoiesis stimulating agent) e.g. darbepoietin alfa 30 micrograms every 2 weeks > Trigger usually Hb < 100g/L > Target Hb is 100-120g/L
52
Describe the pathophysiology and treatment of secondary hyperparathyroidism due to renal failure
Reduced 1-alpha hydroxylation of 25-hydroxycholecalciferol - low vitamin D, low calcium Reduced phosphate excretion - high phosphate High PTH – can lead to osteitis fibrosa cystica, left ventricular hypertrophy... Treatment > Activated vitamin D: alfacalcidol > Mg supplements > Phosphate binders > Calcium-based: calcium carbonate/acetate > Non-calcium: sevelamer, lanthanum, aluminium > Calcimimetic: cinacalcet > Parathyroidectomy
53
Describe the management of CKD
Slowing progression > Aggressive BP control - ACEi/ARB > Good diabetic control > Diet > Smoking cessation > Lowering cholesterol > Treating acidosis Renal replacement therapy (RRT) > Conservative care > Home-based therapies >> Home haemodialysis >>> Most start with eGFR 6-8ml/min >>> Side-effects >>>> Weight loss and persistent nausea >>>> Persistent hyperkalaemia >>>> Acidosis >>>> Severe hyperphosphataemia >>>> Pruritus >>>> Problematic fluid overload >> Peritoneal dialysis > Hospital-based therapies >> Hospital haemodialysis >> Self-care unit > Transplant
54
List the indications for renal replacement therapy
Medically resistant hyperkalaemia Medically resistant pulmonary oedema Medically resistant acidosis Uraemic pericarditis Uraemic encephalopathy
55
List the symptoms a clinically uraemic patient would experience
Anorexia Vomiting Itch Restless legs Weight loss Metallic taste
56
Describe the mechanisms behind haemodialysis
> Hospital or home > Daily or nocturnal Mechanism > Blood is removed using a blood pump > Passed through arterial circuit into dialysis filter > Blood flows countercurrent to dialysis fluid > Dialysis fluid is lower in concentration of solutes such as potassium, phosphate... > Removal of solutes from blood e.g. potassium, urea occurs via diffusion down a concentration gradient > Removal of fluid or "ultrafiltration" occurs through hydrostatic filtration > Filtration removes fluid and dialysate is discarded > Passes through dialysis filter into an air detector and back into patient > Continuous loop for 4 hours Access > AVF access >> Arteriovenous fistula – connection between artery and vein If veins not suitable for procedure, graft can be used > TCVC (tunneled central venous catheter)
57
Describe peritoneal dialysis
CAPD (continuous ambulatory peritoneal dialysis) or APD (automated peritoneal dialysis) Daily or nocturnal
58
Describe the process of kidney transplantation
Donor kidney placed in right or left iliac fossa Ureter is shorter Stent placed from donor kidney to bladder, removed a few weeks after transplantation Native kidneys are left in body unless causing infection
59
List the disadvantages of dialysis
Fatigue Fluid restriction Restricted diet – potassium, phosphate Women are infertile Reduced life expectancy
60
Describe contraindications for transplant
Reduced life expectancy > Older age > Comorbidity Surgical contraindications > No bladder > Calcified blood vessels Medical contraindications > Hypertension > Hypotension > Diseases that will recur in the transplant
61
Describe the pathogenesis of transplant rejection
> Body recognises cell surface proteins as "non-self" > Blood group or HLA incompatibility Pathogenesis of transplant rejection > Foreign antigenic peptide recognised and bound by APC > APC presents foreign antigenic peptide to T cell receptor and binds > T cell activated, produces IL-2 > Leads to cascade of events and results in activation of T and B cells, as well as antibody production Cell-mediated rejection > Interstitial inflammation and tubulitis > Treated with steroids > Diagnosis – biopsy > Does not present with proteinuria Antibody-mediated rejection > Endothelial swelling, glomerulitis and peritubular capillaritis > Donor specific antibodies > May present with proteinuria
62
Describe the immunosuppressive agents used after transplantation
Basiliximab > Chimeric mouse-human monoclonal antibody directed against IL-2 receptor Tacrolimus > Calcineurin inhibitor Mycophenolate mofetil > Inhibitor of inosine-5'-monophosphate dehydrogenase – depletes guanosine nucleotides in T and B lymphocytes, inhibits proliferation Steroids
63
Describe the complications associated with immunosuppression
Rejection Infection Common organisms in common sites > Chest infection > Skin/wound infections > Urine infection Re-activation infections > CMV disease – pneumonitis, colitis, hepatitis, renal disease > BK nephropathy Uncommon organisms > Pneumocystis jirovecii Malignancy > Kaposi sarcoma > Skin: non-melanoma, non-epithelial; melanoma > Non-Hodgkin & Hodgkin lymphoma > Lung > Kidney > Colon and rectum > Pancreas
64
Define bacteriuria, giving risk factors and management plan
Bacteria in urine Asymptomatic Affects preschool age (girls > boys), adults (females > boys) Other risk factors > Urinary catheterisation > Diabetes > Anatomical abnormalities of urinary tract > Pregnancy Management > Treat asymptomatic bacteriuria only in >> Preschool children >> Pregnancy >> Renal transplant >> Immunocompromised > Treatment in other asymptomatic patients not indicated
65
Describe the causes of UTI
>95% caused by single organism > Gram negative bacilli >> E. coli >> Klebsiella species >> Proteus species >> Pseudomonas species > Gram positive bacteria >> Streptococcus species >>> Enterococcus species >>> S. Agalactiae (Group B streptococcus) >> Staphylococcus species >>> S. saprophyticus >>> S. aureus > Candida species >> Fungal balls >> Renal / peri-nephric abscesses > Anaerobes >> Associated with bladder malignancies Multiple organisms in > Long-term catheteres > Recurrent infections > Structural / neurological abnormalities Multi-drug resistant organisms > Anatomical/neurological abnormalities > Frequent infections > Multiple antibiotic courses > Prophylactic antibiotic use
66
List the clinical features of a UTI
Suprapubic discomfort Dysuria Urgency Frequency Cloudy, blood-stained, smelly urine Low-grade fever Sepsis Failure to thrive or jaundice in neonates Abdominal pain and vomiting in children Nocturia, incontinence and delirium in the elderly
67
Describe the management of UTIs
Non-pregnant women > First presentation, culture not mandatory > Dipstick – high false positive rate > Check previous culture results Empirical antibiotic > Amoxicillin, trimethoprim, nitrofurantoin > Pivmecillinam, fosfomycin No response to treatment > Urine culture > Change antibiotic Children and men > Send urine for every presentation > Treat appropriately (empirical > targeted) Pregnancy > Send urine and treat each episode > Check previous sensitivities > Amoxicillin and cefalexin relatively safe > Avoid trimethoprim 1st trimester; avoid nitrofurantoin near term Recurrent UTI > Send sample from each episode > Encourage hydration, urge-initiated and post-coital voiding > Urology investigation > Intravaginal/ oral oestrogen > Antibiotic therapy as per symptoms Catheter-associated UTI > Colonisation common > Biofilm production by bacteria > Send CSU > Start antibiotic – initially empirical based on previous microbiology > Drug resistant and polymicrobial infections > Remove / replace catheter
68
Describe the symptoms of acute pyelonephritis as well as its management
Upper urinary tract infection > Moderate to severe infection > Flank pain +/- systemic infection > Enlarged kidney > Abscesses on surface of kidney (severe) Management > Urine > Blood culture > Imaging Community > Co-amoxiclav > Ciprofloxacin > Trimethoprim Hospital > IV antibiotics >> Amoxicillin / vancomycin >> Gentamicin / aztreonam / temocillin > Uncomplicated pyelonephritis > 7 day antibiotic course Complicated pyelonephritis > At least 2 weeks of antibiotics +/- radiological/surgical intervention (drainage of abscesses)
69
Describe the complications of pyelonephritis
Renal abscess > Complication of pyelonephritis – similar symptoms > Positive urine and blood culture > Usually gram negative bacilli Can become life-threatening > Emphysematous pyelonephritis > Bubblewrap appearance > Poor response to antibiotic therapy alone Perinephric abscess > Uncommon > Often from haematogenous spread > Common organisms >> Gram negative bacilli – E. coli, proteus species >> Gram positive cocci – S. aureus, streptococci >> Candida species > Symptoms >> Similar to pyelonephritis >> Localised signs, local invasion > Investigations >> Urine and blood cultures usually positive >> Pyuria +/- bacterial growth > Poor response to antibiotic therapy – surgical management
70
Describe acute bacterial prostatitis, including causes, signs and symptoms, complications, investigations and management
Usually spontaneous; may follow urethral instrumentation Signs and symptoms > Diffuse oedema > Microabscesses > Perineal / back pain > UTI symptoms > Urinary retention > Pyrexia Complications > Prostatic abscess > Spontaneous rupture – urethra, rectum > Epididymitis > Ascending infection > Systemic sepsis Investigations > Urine and blood culture > Transrectal US > CT/MRI > Do not obtain prostatic secretions Likely organisms > Gram negative bacilli – E. coli, proteus species > S. aureus – MSSA, MRSA > Neisseria gonnorhoea Management > Empirically ciprofloxacin / ofloxacin
71
Describe chronic prostatitis
Rarely associated with acute prostatitis > May follow Chlamydia urethritis Signs and symptoms > Recurrent UTI symptoms > Perineal discomfort > Back pain > Low grade fever Relapse common Common organisms > Gram negative bacilli – E. coli, proteus species > Enterococcus species > S. aureus – MSSA, MRSA
72
Describe epidiymitis
Inflammatory reaction of the epididymis Cause > Ascending infection from urethra > Urethral instrumentation Symptoms > Symptoms of UTI / urethritis > Pain > Fever > Swelling > Penile discharge Common organisms > GNB, enterococci, staphylococci > TB in high risk areas and individuals > Rule out Chlamydia and N. gonorrhoea in sexually active men
73
Describe orchitis, including aetiology & signs and symptoms
Inflammation of one or both testicles Signs and symptoms > Testicular pain and swelling > Dysuria > Fever > Penile discharge Aetiology > Usually viral – mumps > Bacterial >> Pyogenic >> Complication of epididymitis >> IV antibiotics as per complicated UTI + surgical drainage Complications > Testicular infarction > Abscess formation
74
Describe Fournier's gangrene including risk factors, investigations and management
Form of necrotising fasciitis Usually >50 years of age Rapid onset and spreading infection Systemic sepsis Risk factors > UTI > Complications of IBD > Trauma > Recent surgery Common organisms > Mixed infections – mainly GNB and anaerobes Investigations > Blood cultures > Urine > Tissue / pus Management > Surgical debridement > Broad spectrum / combination antibiotics > Piperacillin-tazobactam + gentamicin + metronidazole +/- clindamycin
75
Describe the risk factors for prostate cancer
Age >65 Familial and genetic risk factors > Especially first degree relatives > Abnormalities on chromosomes 1q, 8p and Xp > BRCA2 gene mutations > PTEN and TP53 TSGs mutations Hormones Racial factors - increased risk in black population Geographic variation - highest incidence in westernised nations
76
What are the signs and symptoms of prostate cancer
Often asymptomatic Painful or slow micturition Urinary tract infection Haematuria – blood in urine Urinary retention – may cause anuria, uraemia Lymphoedema
77
Describe the metastatic complications of prostate cancer
Bone pain – most common symptom of metastases Renal failure – ureteric obstruction > Anorexia > Weight loss > Raised creatinine > Stent or nephrostomy Spinal cord compression > Urological emergency – urgent MRI > Severe pain > Off legs > Retention > Constipation > Radiotherapy v spinal decompression surgery
78
Describe PSA and how it changes throughout life
PSA is a serine protease (33kD) secreted into seminal fluid Responsible for liquefaction of seminal coagulation Efficiently hydrolyses semenogelins causing release of sperm Small proportion leaks into circulation > Tends to rise with age > Depends on prostate size > Is influenced by inflammation and infection
79
Describe the diagnosis and screening of prostate cancer
Digital rectal examination PSA – prostate specific antigen TRUS (trans-rectal ultrasound) – guided needle biopsy
80
Describe the pathophysiology and grading of prostate cancer
Majority is primary adenocarcinoma Usually arises in peripheral zone of prostate Gleason grading 6 – well-differentiated, 25% likelihood of local progression 7– moderately differentiated, 50% likelihood of local progression >7 – poorly differentiated, 75% likelihood of local progression
81
Describe the staging and treatment of prostate cancer
TNM classification > T1 – within prostate > T2 – felt on DRE > T3 – cancer invades wall into seminal vesicles > T4 – cancer invades adjacent organ i.e. bladder, bowel, pelvic floor Localised prostate cancer > Watchful waiting > Active surveillance > Radiotherapy (with or without LHRH analogue) >> External beam >> Conformal >> Brachytherapy > Radical prostatectomy > Cryotherapy / HIFU > TURP if symptomatic Advanced prostate cancer > Androgen ablation therapy >> Medical castration – LHRH analogue >> Surgical castration – orchidectomy Chemotherapy TURP for relief of symptoms (transurethral resection of the prostate) Radiotherapy
82
List risk factors for bladder cancer
Age >50 Race – more common in Caucasians Environmental carcinogens Chronic inflammation > Stones > Infection – schistosomiasis > Long-term catheters Drugs – phenacitin, cyclophosphamide Pelvic radiotherapy Occupation Smoking – especially from 4-ABP and naphythylamines
83
Describe the presentation and investigations used in bladder cancer
Presentation / diagnosis > Classically painless frank haematuria Investigations > Cystoscopy > Renal US > CT KUB
84
List the different types of bladder cancer
Transitional cell carcinoma (90%) > Superficial – 75% > Invasive – 25% Squamous carcinoma (5%) Adenocarcinoma (2%) Other secondaries Muscle invasive bladder cancer is highly aggressive
85
Describe the treatment of bladder cancer
> Diagnosed at flexible cystoscopy > Urgent TURBT (trans-urethral resection of bladder tumour) > CT IVU > Bimanual examination carried out at TURBT > Intravesical mitomycin reduces risk of recurrence Low-grade superficial TCC > Flexible check cystoscopy 3 months > 30% chance of recurrence > Course of 6 weekly mitomycin treatment given for persistent Ta tumours High-grade non-muscle-invasive bladder cancer (HG NMIBC) > 80% recurrence risk; 50% chance of progressing to muscle invasive disease > Do early check cystoscopy and rebiopsy > Treat with intravesical BCG immunotherapy – effective in 50% > Course of 6 weekly instillations then further cystoscopy/biopsy > Cystectomy if treatment fails MIBC > Requires radical therapy > Radical cystectomy or radiotherapy > Bladder and prostate/uterus removed > Urine diverted into an ileal conduit or rarely an orthotopic neobladder > Neo-adjuvant chemotherapy Metastatic disease > Often pulmonary > Treat with chemotherapy > Classic M-VAC >> Methotrexate >> Vinblastine >> Doxorubicin >> Cisplatin > Gemicitobine / docetaxel
86
Describe the types of renal cell carcinoma and associated risk factors
85% of all renal tumours Others > Transitional cell carcinoma > Sarcoma > Metastases Risk factors > Smoking > Obesity > Hypertension > Acquired renal cystic disease > Haemodialysis Genetics > VHL (Von Hippel Lindau) > HPRCC – hereditary papillary renal carcinoma > HLRCC – hereditary leiomyomatosis and renal cell cancer > Birt-Hogg-Dube > Tuberous sclerosis
87
Describe the presentation of renal cell carcinoma
Incidental Systemic symptoms > Night sweats > Fever > Fatigue > Weight loss > Haemoptysis Classic triad > Mass > Pain > Haematuria > Varicocoele > Lower limb oedema > Paraneoplastic syndrome >> Polycythaemia due to increased EPO >> Hypercalcaemia due to PTHrP or from osteolytic hypercalcaemia >> Hypertension due to renin secretion >> Deranged LFTs – Stauffer's syndrome – due to hepatotoxic tumour products
88
Describe the histology and staging of renal cell carcinoma
Histology > Clear cell (80%) >> Vascular, granular and clear (lipids) > Papillary > Chromophobe – large polygonal > Collecting duct – rare > Medullary cell – rare Staging - TNM staging > T3a – invasion into renal vein > T3B – IVC below diaphragm > T3c – IVC above diaphragm > T4 – beyond Gerota's and adrenal gland
89
Describe the treatment of renal cell carcinoma
Radical nephrectomy (includes Gerota's fascia, spares adrenal gland) > Large renal mass > If no absolute indication for nephron-sparing surgery (NSS) Indications for NSS > Single kidney > CKD > CV risk factors > pT1a tumours Small renal mass > Biopsy > Treatment >> NSS >>> Partial nephrectomy >>> Cryotherapy >> Radical nephrectomy >> Surveillance > Metastatic disease - tyrosine kinase inhibitors
90
Describe the risk factors and presentation of testicular cancer
Most common solid cancer in younger men (20-45) Most curable cancer Risk factors > Age 20-45 > Cryptorchidism > HIV > Caucasian population Clinical presentation > Painless lump
91
Describe the investigations and classification of testicular cancer
Scrotal ultrasound Tumour markers > Alpha-fetoprotein – teratomas and yolk sac tumours > Beta hCG – teratoma, seminoma > LDH – seminoma Classification > Germ cell tumours > Seminoma > Teratoma > Mixed > Yolk sac Stromal tumours > Leydig > Sertoli Other > Lymphoma > Metastasis
92
Describe the treatment of testicular cancer
Radical orchidectomy Chemotherapy Para-aortic nodal radiotherapy Retroperitoneal lymph node dissection
93
Describe penile cancer and its treatment
Rare Associated with HPV infection (16, 18, 21) and smoking Premalignant lesions – chronic changes Even rarer in males circumcised at birth Treatment > Circumcision > Topical treatment CO2/5FU > Penectomy +/- reconstruction > Lymphadenectomy > Chemo-radiotherapy
94
Describe the position, size and surrounding fascia of the kidneys
Paired retroperitoneal organs (T12-L3)) Right lies lower than left; normally 10-12cm in length, 5-7cm wide and 3cm thick Surrounded by Gerota's fascia Clinically important > For PCNL (percutaneous nephrolithotomy) >> Upper pole more posterior and medial >> Medial surface more anterior > Gerota's fascia deficient inferiorly >> Often where haemorrhage or haematoma can appear after trauma
95
Describe the anatomy of the ureters including layers and physiological narrowings
25-30cm long, 4-5mm calibre 3 segments > Proximal: PUJ-pelvic brim > Mid: segment over sacral bone > Distal: lower sacral border to UO 4 layers > Urothelial mucosa > Lamina propria > Muscular layer > Adventitial layer 3 physiological narrowings > Pelviureteric junction (PUJ) > Ureters cross iliac vessels at pelvic brim (midureter) > Vesicoureteric junction (VUJ) >> Ureter joins bladder
96
Describe the risk factors for urolithiasis
Intrinsic > Sex (male:female 2:1) >> Testosterone increases production of oxalate >> Females produce more citrate (productive) > Age: peak 20-50 years > Family history >> More common in Caucasian, Asian >> Familial renal tubular acidosis >> Cystinuria > Comorbid factors Extrinsic > Fluid intake > Diet >> High animal protein >>> High oxalate, low pH, low citrate >> High salt – hypercalciuria >>Low calcium diets > Sedentary lifestyle > High incidence in hot climates > Country of residence
97
Describe the different types of kidney stones
Calcium oxalate stones most common > Radio-opaque: seen on X-ray Uric acid > Form due to chronic dehydration > Increased risk with gout, genetic tendency, diet with excess protein Calcium phosphate + calcium oxalate Pure calcium phosphate > Rare > May be seen in renal tubular acidosis Struvite > Seen in UTIs > Consist of magnesium, ammonium and phosphate > Require aggressive treatment of UTI Cysteine > Rare, predominantly associated with cysteinuria (genetically inherited condition) Xanthine > Enzyme deficiency causes buildup of xanthine deposits Silica > Rare > Caused by medications or herbal supplements
98
Describe the pathogenesis of urolithiasis
Undersaturated Supersaturated but stable – metastable Supersaturated with spontaneous precipitation – unstable Saturation product > level at which no more solute will dissolve in a solution without a change in pH, temperature Formation product – level at which spontaneous formation occurs Free particle model of stone formation > Crystals growing and agglomerating > Critical particle trapped in tubule Fixed particle model of stone formation > Crystals growing and agglomerating > Particle adheres to a damaged site on the tubule wall and other crystals agglomerate with it
99
Describe the presentation of kidney stones
Incidental Pain > Colic > Radiates from loin to groin > In males can be testicular or penile pain > Cannot settle > Unable to stay still Haematuria > Visible or non-visible Sepsis/infection > Unknown source until imaged DDX > AAA > Appendicitis > Gynae pathology
100
Describe the investigations used for kidney stones
History and examination Bloods > U&Es, CRP, FBC Urine > Dipstick MSSU > Calcium > Urate > Sodium nitroprusside – cystine Stone analysis Imaging > Gold standard – CT KUB >> Stone diameter >> Skin to stone distance > Ultrasound >> Especially young females > X-ray >> Better for follow-up of known radioopaque stone
101
Describe the treatment of
Analgesia > NSAIDs – reduce pain due to reduced glomerular filtration, renal pressure and ureteric peristalsis Tamsulosin > Alpha blocker which blocks muscle contraction > Relaxes ureter and encourages stone passage Surgical options > Ureteroscopy and basket > Ureteroscopy and fragmentation > FURS – flexible ureteroscopy > ESWL – extracorporeal shockwave lithotripsy > PCNL – percutaneous nephrolithotomy Evidence of sepsis > Retrograde ureteric stent >> Inserted by urology under anaesthetic >> Connects bladder to kidney >Nephrostomy >> Inserted percutaneously by interventional radiology in an antegrade fashion
102
Describe ESWL
Produces a shockwave > Electrohydraulic > Electromagnetic > Piezoelectric Direct effect > Shearing > Spalling Cavitation effect > Shockwave in fluid causes a microbubble > Dissolved gas in fluid around bubble expands into bubble > Bubble collapses > Microjets enter stone causing fragmentation
103
Describe staghorn calculi and how they are formed
Branched stones that fill all or a part of the renal pelvis and branch into several or all of the calyces Most often composed of struvite > Bacteria produce urease, breaks down urea into ammonia > Causes alkalinisation of urine and formation of magnesium ammonium phosphate crystals
104
Describe percutaneous nephrolithotomy (PCNL)
Creates a percutaneous tract from skin to kidney Able to clear larger volumes of stone e.g. struvite Increased risk as it is an invasive procedure
105
Describe the fluid compartments of the body
Intracellular > 2/3 of fluid > Composition: potassium Extracellular > 1/3 of fluid > Composition >> Interstitium: sodium, chloride >> Plasma (intravascular)
106
Describe third space losses and risks associated with osmolar problems
Third space losses > More fluid in extracellular compartment than there should be e.g. low albumin in intravascular space – fluid taken into interstitium > Interstitial space becomes overexpanded Risk of osmolar problems > Cerebral oedema >> Acute hyponatraemia > Osmotic demyelination syndrome >> Sodium corrected too quickly
107
Describe signs and symptoms associated with fluid depletion and fluid overload
Relevant history > Fluid depletion – diuretics, abnormal losses > Fluid overload - heart failure, renal failure Symptoms > Fluid depletion – postural hypotension, thirst, dry mouth > Fluid overload – breathlessness, swollen ankles Signs > Fluid depletion – reduced skin turgor, CRT >2 secs, tachycardia > Fluid overload – hypertension, increased JVP, 3rd heart sound, pulmonary oedema Lab tests > Fluid depletion - U&Es, especially high urea > Fluid overload – serum albumin
108
Describe the NICE guidelines's 5 R's
Resuscitation > Restore circulation to vital organs following loss of intravascular volume Clinical signs of hypovolaemia > Hypotension > Tachycardia > Peripherally cool > CRT > 2 secs > NEWS > 5 Passive leg raising suggests fluid responsiveness Fluid bolus, usually saline or Hartmann's Routine maintenance > Patients not drinking / unable to drink / having to fast for over 8-12h > Calculate requirement based on >> Projected losses >> Intake e.g. IV drug volumes / NG feed Replacement > Treat deficits or ongoing losses not needed urgently for resus Redistribution Reassessment > Daily U&Es and fluid balance > Consider daily bicarbonate or magnesium if abnormal GI or renal losses
109
Describe the different types of IV fluids
Crystalloids > Saline (various, 0.9% is standard) >> Distributes between extracellular compartments > Dextrose (various, 5% is standard) >> goes straight into intracellular compartments > Balanced solutions e.g. Hartmann's or Ringer's lactate >> Distributes between extracellular compartments > Sodium bicarbonate (1.26%) - expert advice only Colloids > E.g. Gelofusion or starch-based fluid > Stay in intravascular space Blood products > Packed red cells > Platelets or fresh frozen plasma (clotting factors) > Human albumin solution
110
Describe the KDIGO criteria for AKI
Severity of AKI – KDIGO Stage 1 > Serum creatinine >1.5 and <2x AKI baseline or >26 micromol/l increase above AKI baseline Stage 2 > Serum creatinine >2.0 and <3x AKI baseline Stage 3 > Serum creatinine 3x AKI baseline or >354 micromol/l increase above AKI baseline
111
State why peritoneal dialysis can cause hyperglycaemia
The dialysate contains dextrose. Absorbing some of the dialysate might cause the consumption of hundreds of extra calories daily, leading to hyperglycaemia and weight gain.
112
Discuss why nephrotic syndrome can increase risk of DVT
Antithrombin II deficiency can be inherited or acquired. The patient has nephrotic syndrome, which is associated with a loss of antithrombin III from the kidneys resulting in an acquired deficiency and a hypercoagulable state and thus puts this patient at risk of the development of deep vein thrombosis.
113
Discuss presentation and management of renal carcinoma
Painless flank mass, haematuria, and paraneoplastic features including hypertension, polycythaemia, hypercalcaemia, and Cushing's syndrome Localised renal cancer (that is 7 cm or larger) is definitively treated with a radical nephrectomy. Adjuvant treatment does not help completely resected disease
114
List characteristics of Wegener granulomatosis
elevated serum creatinine level sinusitis hematuria pleural effusions positive result of antineutrophil cytoplasmic antibody test
115
What bacteria infection is commonly associated with peritoneal dialysis
staphylococcus epidermis
116
State the difference in onset after respiratory infection in PSGN and IgA nephropathy
IgA nephropathy would occur a few days after the respiratory infection rather than weeks.
117
State the first line analgesia in renal colic
IM diclofena