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Renal Flashcards

1
Q

UTI

Definitions (6)

A

Bacteriuria: bacteria in the urine, may be asymptomatic or symptomatic
UTI: presence of a pure growth of >10^5 organisms per ml of fresh MSU
Lower UTI: urethra (urethritis), bladder (cystitis), prostate (prostatitis)
Upper UTI: renal pelvis (pyelonephritis)
Pyuria: presence of pus cells in urine, inflammatory response
Sterile pyuria: -ve culture but +ve pus (eg. undeclared antibiotics, renal TB, GU infections, stones/malignancy)

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2
Q

UTI

Aetiology (3)

A

Mostly E.coli
Proteus mirabilis
Klebsiella pneumonia

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3
Q 
UTI 
Risk factors (8)
A

Female: short urethra and close to rectum
Trauma to female urethra in sex/birth
Pregnancy: progesterone dilates ureters and pressure from fetus
Anatomical: VUR, pelvi-ureteric junction obstruction, chronic retention
Pre-existing renal conditions: renal cysts, parenchymal damage, stones
Spermicide activity
Immunosuppression
Foreign body: catheter, cystoscopy, stent

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4
Q

UTI

Uncomplicated (3)

A

Healthy, young, sexually active women
E.coli or Staph saprophyticus
Require no further investigation

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5
Q

UTI

Complicated (8)

A 
In children 
In men 
In patients with abnormal renal tract 
In immunosuppressed 
In patients with foreign body in renal tract 
Bladder tumour 
Chronic retention 
Abnormal bladder outflow tract (BPH, urethral stricture, phimosis)
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6
Q

UTI

Symptoms (9)

A 
Dysuria 
Frequency 
Urgency 
Haematuria 
Suprapubic pain 
Fever
Hesitancy 
Nocturia
Pyelonephritis: fever, rigors, N&V, back and flank pain
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7
Q

UTI

Signs (3)

A

Fever
Abdominal/loin tenderness
Foul-smelling urine

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8
Q

UTI

Investigations (5)

A

Urinalysis: no further investigation if +ve for nitrites and leucocytes (uncomplicated)
Urine MC&S of MSSU: bacteria, WBC, RBC (send immediately if male, child, immunosuppressed)- diagnostic >10^5
Culture for antibiotic sensitivity
Bloods: FBC, U&E, CRP, cultures if systemic unwell
Imaging: USS + referral to urology if child/man/no treatment response/recurrent/pyelonephritis

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9
Q 
UTI 
Dipstick testing (6)
A

Nitrate (metabolic byproduct of bacteria)
Protein (sign of inflammation)
Leucocytes (marker of inflammation)
If all 3 are positive- empirical therapy
If leucocytes only positive- doesn’t diagnose or exclude, urine culture recommended
Blood/protein in absence of nitrate/leucocytes should be further investigated

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10
Q

UTI

Treatment in women (4)

A

Trimethoprim/nitrofurantoin for 3-6 days
2nd line amoxicillin or co-amoxiclav
If no response do urine culture
If upper UTI: co-amoxiclav IV then oral when afebrile

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11
Q

UTI

Treatment in pregnant women (2)

A

Any bacteriuria treat with antibiotic (nitrofurantoin safe)

Dipstick and culture repeated at each antenatal visit

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12
Q

UTI

Treatment in men (2)

A

If fail to respond to antibiotic must refer to urologist as is often due to anomaly in anatomy/function
Quinolone eg. ciprafloxacin

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13
Q

UTI

Treatment of acute pyelonephritis (2)

A

Ciprofloxacin for 7 days

Consider admission for IV co-amoxiclav and gentamicin in 1st 48h if vomiting or septic

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14
Q

AKI

Definition (2)

A

Rise in serum creatinine >26 in 48h or rise in creatinine >1.5x baseline or urine output <0.5ml/kg/h for >6h (consecutive hours)
Leads to a failure to maintain fluid, electrolyte and acid-base homeostasis

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15
Q

AKI

Pre-renal causes (3)

A 
40-70% of cases, due to renal hypoperfusion 
Hypotension (due to hypovolaemia, sepsis, over diuresis) 
Renovascular disease (eg. renal artery stenosis)
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16
Q

AKI

Intrinsic renal causes (5)

A

10-50% of cases, due to direct parenchymal injury and may require renal biopsy for diagnosis
Acute tubular necrosis: commonest, often result of pre-renal damage or nephrotoxins eg. drugs (gentamicin, NSAIDs, ACE-i, lithium), contrast and myoglobinuria in rhabdomyolysis
Glomerular: primary glomerulonephhritis, SLE, drugs, infections
Interstitial: drugs, lymphoma infiltration, tumour lysis syndrome
Vascular: vasculitis, malignant hypertension, cholesterol emboli

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17
Q

AKI

Post-renal causes (4)

A

10-25% of cases, caused by obstruction
Luminal: stones, clots
Mural: malignancy (eg. ureteric, bladder, prostate), BPH, strictures
Extrinsic compression: malignancy, retroperitoneal fibrosis

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18
Q 
AKI 
Risk factors (8)
A 
>75 
CKD 
Heart failure 
Peripheral vascular disease 
Diabetes 
Drugs/other nephrotoxins (especially recently started) 
Sepsis 
Poor fluid intake or increased losses
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19
Q

AKI

Signs + symptoms (10)

A

May be asymptomatic
Systemic: rash, arthralgia, fever
Haemoptysis (vasculitis/anti-GBM disease)
LUTS or anuria (obstruction)
Red-brown urine (rhabdomyolysis)
Fluid overload: hypertension, elevated JVP, lung crackles, peripheral oedema
Fluid deplete: reduced urine volume, non-visible JVP, poor turgor
Palpable percussible bladder or pelvic/abdominal mass (obstruction)
Palpable kidneys (polycystic)
Renal bruits (renovascular disease)

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20
Q

AKI

Investigations (9)

A

U&E + creatinine: assess severity
Urine: urinalysis (nitrites- infection, protein- intrinsic renal, leucocytes- acute interstitial nephritis, blood- glomerulonephritis), Na concentration (low if pre-renal, high in acute tubular necrosis), Bence Jones protein (exclude myeloma)
ECG: exclude hyperkalaemia
VBG: exclude hyperkalaemia
FBC + film: exclude HUS
Anti-dsDNA and ANA: SLE
Urea:creatinine ratio (>100:1= pre renal, <40:1= intrinsic)
Renal USS: obstruction, hydronephrosis, cysts
ABG: acid-base balance

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21
Q

AKI

Classification (3)

A

Stage 1: creatinine increases >1.5x baseline, <0.5ml/kg/h urine output for >6 consecutive hours
Stage 2: serum creatinine rises 2-2.9x baseline, <0.5ml/kg/h urine for >12 hours
Stage 3: serum creatinine >3x baseline or commenced on RRT, <0.3ml/kg/h urine for >24 hours or anuria for 12h

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22
Q

AKI

Treatment (6)

A

Fluid therapy
Stop nephrotoxic drugs
Treat pre-renal causes: correct volume depletion, treat sepsis
Treat intrinsic causes: refer
Treat post-renal causes: catheterise if obstruction, consider retrograde stents or insertion of nephrostomy
RRT if complications or drug overdose

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23
Q

AKI

Indications for RRT (5)

A

Pulmonary oedema
Persistent hyperkalaemia
Severe metabolic acidosis
Uraemic complications eg. encephalopathy or pericarditis
Drug overdose- BLAST (Barbiturates, Lithium, Alcohol, Salicylates, Theophyline)

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24
Q

CKD

Definition (2)

A

Impaired renal function for >3 months based on abnormal structure/function or GFR <60 for >3 months without evidence of kidney damage
End-stage renal failure: GFR <15 or need for RRT

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25
CKD | Aetiology (6)
``` Diabetes Glomerulonephritis: usually IgA Hypertension Renovascular disease Pyelonephritis Polycystic kidney disease ```
26
CKD | Pathology (2)
Renal injury causes kidney to adapt to nephron loss by increasing intraglomerular pressure to maintain filtration Glomerulus becomes more permeable to molecules causing mesangial cell expansion, fibrosis and glomerular scarring
27
CKD | Pathology of complications (5)
Anaemia: low erythropoietin production by kidney interstitial fibroblasts leads to lack of RBC growth Renal osteodystrophy: kidney is site of phosphate excretion and hydroxylation of vit D, low levels of 1,25 dihydroxyvitamin D occurs due to renal scarring and reduced phosphate levels leads to hyperphosphataemia, this causes hypocalcaemia and huge increase in PTH, promoting calcium resorption, changing bones Cardiovascular risk: hypertension, high lipids, high phosphate Hyperlipidaemia: reduced lipoprotein lipase and hepatic triglyceride lipase = less lipid uptake Malnutrition: altered metabolism of protein, water, salt and potassium
28
``` CKD Risk factors (8) ```
``` Nephrotoxins Diabetes Hypertension Cardiovascular disease Structural renal disease, stones or BPH Recurrent UTI/childhood history of vesicoureteric reflux Multisystem disease such as SLE Family history of ESRF or known hereditary disease eg. PKD ```
29
CKD | Signs + symptoms (6)
``` Usually asymptomatic until stage 4/5 Uraemia: anorexia, vomiting, restless legs, fatigue, weakness, pruritus, bone pain Amenorrhoea/impotence Oliguria Dyspnoea Ankle swelling ```
30
CKD | Investigations (4)
Blood: Hb (normochromic normocytic anaemia), U&E, creatinine, glucose, Ca (low), phosphate (high), alk phos (high- renal osteodystrophy), PTH (high if >stage 3) Urine: urinalysis (proteinuria, haematuria), MC&S (exclude UTI), albumin:creatinine ratio Ultrasound: check size and anatomy, usually small (<9cm) in CKD but may be enlarged in amyloid, myeloma, APKD, DM Renal biopsy if rapidly progressive or if unclear cause and normal sized kidneys
31
CKD | Staging (6)
Stage 1: GFR >90 (normal/high GFR but other evidence of renal damage) Stage 2: GFR 60-89 Stage 3A: GFR 45-59 Stage 3B: GFR 30-44 Stage 4: GFR 15-29 Stage 5: GFR <15 (established renal failure)
32
CKD | Treatment of reversible causes (4)
Relieve obstruction Stop nephrotoxins Address cardiovascular risk factors Tight glucose control in diabetes
33
CKD | Treatment to limit progression and complications (3)
BP: target <130/90 use ACE-i or ARB Renal bone disease: check PTH and treat if raised (eg. calcitriol and alfacalcidol), restrict phosphate and give binders (eg. Calcichew) Cardiovascular modification: statins and aspirin
34
CKD | Treatment to control symptoms (5)
Anaemia: replace iron/B12/folate if necessary, consider recombinant human erythropoietin if still anaemic Acidosis: consider sodium bicarbonate supplements if low serum bicarbonate Oedema: high dose loop diuretics and fluid and sodium restriction Restless leg: clonazepam/gabapentin RRT if GFR 8-10
35
``` Haemodialysis Mechanism (4) ```
Blood is passed over a semi-permeable membrane against dialysis fluid flowing in the opposite direction Thus blood is always meeting a less concentrated solution and diffusion of small solutes occurs down the concentration gradient Larger solutes don't clear as effectively Ultrafiltration creates a negative transmembrane pressure to clear excess fluid
36
Haemodialysis | Problems (4)
Disequilibration syndrome Hypotension Time consuming Access problems (AV fistula: thrombosis/stenosis, tunnelled venous access line: infection/blockage/recirculation of blood)
37
``` Haemofiltration Mechanism (3) ```
Blood filtered across a highly permeable membrane Allowing movement of small and large solutes by convection at almost the same rate The ultrafiltrate is replaced with an equal volume of fluid, so there is less haemodynamic instability
38
Haemofiltration | Use (2)
Critically ill patients | Impractical as long-term RRT as it takes much longer than haemodialysis to achieve the same clearance
39
Peritoneal Dialysis | Mechanism (5)
Uses the peritoneum as a semi-permeable membrane Catheter inserted into peritoneal cavity and fluid infused Allows solutes to diffuse slowly across Ultrafiltration by adding osmotic agent eg. glucose Simple to perform, can be carried out continuously and at home, so allows freedom
40
Peritoneal Dialysis | Problems (3)
PD peritonitis Exit site infection Loss of membrane function over time
41
``` Kidney Transplant Absolute contraindications (3) ```
Active infection Cancer Severe comorbidity
42
Kidney Transplant | Types of graft (3)
DCD: donor after cardiac death, high risk of delayed graft function due to long warm ischaemic time DBD: donor after brainstem death, much reduced risk of delayed graft function LD: living donor grafts, planned surgery and minimal ischaemic time, related/unrelated
43
Kidney Transplant | Immunosuppression (2)
Induction: basiliximab/alemtuzumab Maintenance: triple therapy- calcineurin inhibitor (tacrolimus), antimetabolite (mycophenalate) and prednisolone
44
Kidney Transplant | Complications (6)
Delayed graft function (affects approx. 40%) Rejection (acute/chronic) New onset diabetes after transplant Increased infection risk Increased malignancy risk, particularly skin and viral associated Cardiovascular disease (increased bP in >50% of transplant patients)
45
Glomerulonephritis | Pathology (4)
Inflammation of glomerulus and nephrons Damage to the glomerulus restricts blood flow, leading to a compensatory rise in BP Damage to filtration mechanism allows protein and blood to enter the urine Loss of the usual filtration capacity leads to AKI
46
Glomerulonephritis | Presentation (2)
Nephrotic syndrome: BP- normal to mildly high, urine- proteinuria, GFR- normal to mildly low Nephritic syndrome: BP- moderate to severely high, urine- haematuria, GFR- moderately to severely low
47
Glomerulonephritis | Causes (4)
Primary causes of nephrotic syndrome: membranous, minimal change, FSGC, mesangiocapillary Secondary causes of nephrotic syndrome: diabetes, SLE (class V nephritis), amyloid, hep B/C Primary causes of nephritic syndrome: IgA nephropathy, mesangiocapillary Secondary causes of nephritic syndrome: post-Streptococcal, vasculitis, SLE nephritis, anti-GBM
48
Glomerulonephritis | Investigations (10)
Blood: FBC, U&E, LFT, ESR, CRP Immunoglobulines Electrophoresis Complement (C3+C4)- sign of inflammation (SLE) Autoantibodies: ANA, ANCA, anti-dsDNA, anti-GBM HBV & HCV serology Urine: RBC casts, MC&S, Bence Jones protein, ACR CXR Renal ultrasound Renal biopsy: what is affected (mesangial cells, capillaries, basement membrane, endothelium), how much kidney involved (focal vs diffuse), how much glomerulus involved (segmental vs global)
49
``` Nephrotic Syndrome Primary causes (4) ```
Membranous glomerulonephritis Minimal change disease Focal segmental glomerulosclerosis Mesangiocapillary glomerulonephritis
50
``` Nephrotic Syndrome Secondary causes (5) ```
``` Hep B/C SLE (class V lupus nephritis) Diabetic nephropathy Amyloidosis (myeloma) Drug related (NSAIDs, penicillamine, anti-TNF) ```
51
Nephrotic Syndrome | Signs + symptoms (2)
Classic triad: proteinuria, hypoalbuminaemia, oedema Hyperlipidaemia
52
``` Nephrotic Syndrome General treatment (4) ```
Reduce oedema: loop diuretics and fluid restriction and salt restriction Reduce proteinuria: ACE-i or ARB for all patients Reduce risk of complications: anticoagulate if large proteinuria, statin to reduce cholesterol, treat infections promptly and vaccinate Treat underlying cause
53
``` Nephrotic Syndrome Membranous nephropathy (3) ```
20-30% of nephrotic syndrome in adults Mostly idiopathic but can be associated with malignancy, hep B, drugs (penicillamine, NSAIDs) and autoimmunity (thyroid, SLE) On biopsy: diffusely thickened GBM with IgG and C3 deposits
54
Nephrotic Syndrome | Minimal change disease (4)
Commonest cause in children Rapid onset oedema Normal biopsy Treat with steroids
55
Nephrotic Syndrome | Focal segmental glomerulosclerosis (2)
May be primary or secondary (vesicoureteric reflux, IgA nephropathy, Alport's syndrome, vasculitis) Biopsy: glomeruli have scarring at certain segments with IgM and C3 deposits on immunofluorescence
56
``` Nephrotic Syndrome Mesangiocapillary glomerulonephritis (3) ```
Immune complex mediated or complement mediated Biopsy: thickened capillary basement membrane, mesangial and endocapillary proliferation Overlapping nephrotic and nephritic syndromes
57
``` Nephritic Syndrome Primary causes (2) ```
IgA nephropathy | Mesangiocapillary glomerulonephritis
58
``` Nephritic Syndrome Secondary causes (4) ```
Post streptococcal Vasculitis SLE (lupus nephritis- except class V) Anti-GBM disease (Goodpasture's disease)
59
Nephritic Syndrome | Signs + symptoms (1)
Classic triad: hypertension, haematuria, mild proteinuria
60
``` Nephritic Syndrome IgA nephropathy (3) ```
Commonest cause of glomerulonephritis Presentation: macro/microscopic haematuria, occasionally nephritic syndrome, usually young person following a recent URTI Biopsy: mesangial proliferation, IgA + C3 deposits
61
Nephritic Syndrome | Henoch-Schonlein Purpura (2)
Systemic variant of IgA nephropathy causing a small vessel vasculitis Presentation: purpuric rash on extensor surfaces, polyarthritis, nephritic syndrome
62
Nephritic Syndrome | Anti-GBM disease (3)
Caused by autoantibodies to type IV collagen (which is a component of the GBM) AKI may occur within days of symptom onset (it is a type of rapidly progressive glomerulonephritis) Treat with plasma exchange and immunosuppression
63
Nephritic Syndrome | Post-streptococcal glomerulonephritis (3)
Diffuse proliferative glomerulonephritis Occurs 1-12 weeks after a sore throat or skin infection A streptococcal antigen is deposited on the glomerulus, causing a host reaction and formation of immune complex
64
Acute Interstitial Nephritis | Aetiology (5)
Mediated by an immune reaction to drugs, infections or autoimmune disorders Drugs: NSAIDs, antibiotics, diuretics, allopurinol, omeprazole, phenytoin Infections: Staph, Strep, Brucella Autoimmune: SLE, sarcoidosis Idiopathic
65
Acute Interstitial Nephritis | Pathology (1)
Acute inflammation of the renal interstitium, often a hypersensitivity reaction
66
Acute Interstitial Nephritis | Signs + symptoms (4)
Usually just mild renal impairment High BP Oliguria Drugs reactions: often 'allergic' picture with fever, rash and eosinophilia
67
Acute Interstitial Nephritis | Treatment (2)
Stop/treat cause/causative agent | Trial of prednisolone if renal function slow to improve
68
Chronic Interstitial Nephritis | Aetiology (3)
Structural: reflex nephropathy, cystic kidney disease Drugs: NSAIDs Haematological: myeloma, sickle cell disease
69
Chronic Interstitial Nephritis | Pathology (1)
Chronic inflammation of the renal interstitium
70
Chronic Interstitial Nephritis | Signs + symptoms (3)
Often asymptomatic Painless haematuria Signs of CKD
71
``` Rhabdomyolysis Aetiology (9) ```
``` Post ischaemia: embolism, clamped artery Prolonged immobilisation Burns Crush injury Excessive exercise Infection: EBC, influenza Drugs/toxins: statins, alcohol, ecstasy, heroin Metabolic: low K, low phosphate, myositis Duchenne's muscular dystrophy ```
72
``` Rhabdomyolysis Pathology (2) ```
Skeletal muscle breaks down and releases its contents into the circulation (myoglobin, phosphate, potassium, urate and creatinine kinase) Myoglobin is filtered by glomeruli and precipitates into the renal tubule which it obstructs
73
Rhabdomyolysis | Signs + symptoms (4)
Muscle pain Swelling Tenderness Red-brown urine
74
``` Rhabdomyolysis Investigations (6) ```
Plasma CK >10,000 (then have to exclude MI with troponin) Urine +ve for blood on dipstick but without RBC on microscopy U&E + creatinine: AKI occurs 12-24 hours later K (high) Phosphate (very high) Ca (low because it enters muscle)
75
``` Rhabdomyolysis Treatment (4) ```
Treat hyperkalaemia IV fluids to prevent AKI Sometimes need IV sodium bicarbonate to alkalinise urine to stabilise a less toxic form of myoglobin Dialysis may be needed
76
``` Rhabdomyolysis Complications (3) ```
AKI Hyperkalaemia Compartment syndrome from muscle injury
77
Renal Artery Stenosis | Aetiology (3)
Atherosclerosis Fibromuscular dysplasia Thromboembolism
78
Renal Artery Stenosis | Pathology (2)
Narrowing of renal artery leads to reduced renal perfusion Activates renin-angiotensin-aldosterone system leading to hypertension (mediated by angiotensin II) and hypokalaemia and hyponatraemia (secondary hyperaldosteronism)
79
Renal Artery Stenosis | Signs + symptoms (6)
``` Asymptomatic Hypertension resistant to treatment Worsening renal function after ACE-i/ARB 'Flash' pulmonary oedema (sudden onset, without LV impairment on cardiac echo) Abdominal +/- carotid/femoral bruits Weak leg pulses ```
80
Renal Artery Stenosis | Investigations (3)
USS: renal size asymmetry (affected side smaller) MR/CT angiography followed by invasive renal angioplasty U&E + creatinine
81
Renal Artery Stenosis | Treatment (2)
Manage hypertension | Transluminal angioplasty +/- stent placement or revascularisation surgery
82
Renal Tubular Acidosis | Definition (2)
``` Metabolic acidosis (normal anion gap) due to impaired acid secretion by the kidney There are 4 types (but 3 is a rare combination of types 1 +2) ```
83
Renal Tubular Acidosis | Aetiology (3)
``` Type 1 (distal): idiopathic (usually inherited), genetic (Marfan's, Ehlers-Danlos), autoimmune (SLE) Type 2 (proximal): idiopathic, tubulointerstitial disease (myeloma, interstitial nephritis) Type 4 (hyperkalaemia): Addison's disease, diabetic nephropathy, drugs (K-sparing diuretics, NSAIDs) ```
84
Renal Tubular Acidosis | Signs + symptoms (3)
``` Type 1 (distal): rickets/osteomalacia (buffering of H with Ca in bone), nephrocalcinosis with calcium phosphate stones Type 2 (proximal): hypokalaemia (due to osmotic diuretic effect of bicarbonate reabsorption, causing an increased flow rate to distal tubule and therefore increased K excretion) Type 4: hyperkalaemia ```
85
Renal Tubular Acidosis | Investigations (6)
Urine pH U&E + creatinine ABG Type 1: urine pH >5.5 despite metabolic acidosis Type 2: urine pH <5.5 with hypokalaemia and metabolic acidosis, diagnose with IV sodium bicarbonate lead Type 4: urine pH <5.5, hyperkalaemia + metabolic acidosis
86
Renal Tubular Acidosis | Treatment (3)
Type 1: oral sodium bicarbonate or citrate Type 2: high dose sodium bicarbonate Type 4: remove any cause, fludrocortisone/furosemide/calcium resonium to control high K
87
Polycystic Kidney Disease | Epidemiology + genetics (4)
1:1000 Autosomal dominant Almost all have mutations in PKD1 (chromosome 16) and reach ESRF by 50s If mutation is on PKD2 (chromosome 4) reach ESRF by 70s
88
Polycystic Kidney Disease | Signs + symptoms (9)
Renal enlargement with cysts (cysts replace renal tissue) Abdo pain Haematuria if haemorrhage into a cyst Cyst infection Renal calculi Hypertension Progressive renal failure Development of liver cysts/ovarian cysts Intracranial aneurysm which can rupture and cause subarachnoid haemorrhage
89
Polycystic Kidney Disease | Investigations (2)
``` Renal USS (also for screening) Screening for SAH: MR angiography for 1st degree relatives of SAH and APKD ```
90
Polycystic Kidney Disease | Treatment (6)
``` BP control (<130/80 target) with ACE-i Reduce Na intake Increase water intake Treat infections Laparoscopic cyst removal or nephrectomy for painful cysts Dialysis/transplant for ESRF ```

Med Student Finals (23 decks)

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