Renal Flashcards
1
Q
What are the functions of the kidneys?
A
Endocrine release - epo, renin, prostaglandins
Removal of waste products - urea, drugs
Metabolism - proteins, vit D
Fluid regulation
2
Q
What are the 3U’s that must always be remembered in investigation for renal disease?
A
U&E, urinalysis, USS
3
Q
How is proteinuria measured?
A
Albumin:creatinine ratio (<2.5 men, <3.5 women)
24 hr collection albumin
If they have proteinuria do culture of urine
4
Q
What is the main cause of haematuria? What are some other causes?
A
- Glomerular disease (>1g)
- Transient causes - orthostatic, exercise, fever (<1g)
- Tubulointerstitial disease (<1g)
- Upper/lower UTI (<1g)
- Diabetes (30-300mg)
- Minimal change disease (30-300mg)
5
Q
In terms of proteinuria, what are the indications for biopsy?
A
Persisent (>3g) or alongside haematuria
6
Q
How much blood is usually lost in the urine?
A
<1uL/day
7
Q
What is the main cause of proteinuria? What are some other causes?
A
- Glomerular disease (IgA nephropathy, thin basement membrane disease)
- Transient causes (UTI, exercise, menstruation)
- Neoplasia (painless, bladder/renal)
- Drugs
8
Q
Which drugs may cause haematuria?
A
Cephalosporins
Ciprofloxacin
Furosemide
NSAIDS
9
Q
What is the 2WW criteria for haematuria?
A
Visible >45 yers
Non-visible >60yrs
Do renal USS and cystography
10
Q
What are the normal values for glucose in the urine?
A
0-0.8mmol/L
11
Q
What causes glycosuria?
A
DM
Pregnancy
Sepsis
Renal tubular damage
12
Q
What causes nitrites/leucocytes in the urine?
A
UTI, high protein meal
13
Q
What causes ketones in the urine?
A
Starvation, ketoacidosis
14
Q
What does urine microscopy look for? What do they show?
A
CASTS
white cell casts - UTI, acute interstitial nephritis
red cell casts - glomerular bleeding, vasculitis, nephritis
epithelial casts - acute tubular necrosis
15
Q
What factors influence creatinine levels?
A
Muscle mass
Muscle catabolism
Liver function
16
Q
What causes high creatinine levels?
A
- Kidney dysfunction
- Hypertension
- Drugs (statins)
- Rhabdomyolysis
- Large muscle mass
17
Q
What are the problems associated with measuring creatinine levels?
A
- Muscle mass
- Log relationship to GFR ( as GFR decreases lots, creatinine only increases a little)
- Tubular and gut secretion
- Variability of assay
18
Q
How is eGFR calculated?
A
Takes into account creatinine, age, gender and ethnicity
19
Q
What is the definition of AKI?
A
A rapid reduction in kidney function over hours to days, as measured by serum urea and creatinine and leading to a failure to maintain fluid, electrolyte and acid-base homeostasis
20
Q
How is AKI diagnosed?
A
- Rise in creatinine >26umol/L in 48hours
- Rise in creatinine >1.5 x the baseline
- Urine output <0.5ml/kg/h for 6 consecutive hours
1st line investigations - U&Es and creatinine
21
Q
What are the symptoms of AKI?
A
Urinary - dysuria, oliguria, anuria, haematuria,
Systemic - fever, vomiting, myalgia, diarrhoea
Kidney dysfunction - oedema, bruising
22
Q
What are the risk factors for AKI?
A
- Age>75
- CKD
- Cardiac failure
- Sepsis/infection
- PVD
- Chronic liver disease
- Diabetes
- Drugs
- Poor fluid intake
23
Q
Which investigations results would raise your index of suspicion for AKI secondary to CKD?
A
- Small kidneys
- Anaemia
- Low calcium
- High phosphate
- Previous bloods
24
Q
What investigations should be done in AKI?
A
BEDSIDE - urinalysis, BP, ECG
BLOODS - FBC, U&E, CRP, LFTs, bone profile, CK, clotting, ESR, cultures, immunoglobulins, complement, autoantibodies
IMAGING - renal USS, CXR
SPECIAL - kidney biopsy
25
What are the indications for kidney biopsy for AKI?
Intrinsic cause other than ATN is suspected, such as glomerulonephritis
26
How can you tell it is a pre-renal cause of AKI?
Restoration of blood flow will resolve the problem with no cell injury
27
What are some pre-renal causes of AKI?
Volume depletion - GI bleed, diarrhoea, vomiting, burns
Low CO - tamponade, massive PE, MI
Distributive - sepsis, anaphylaxis, hepatorenal, pancreatitis
Drugs - NSAIDS, contrast, antihypertensives
28
How do NSAIDs cause kidney injury?
Vasoconstriction of the afferent arteriole (supplying the kidney) and therefore decreased GFR
29
How do antihypertensives cause kidney injury?
Cause vasodilation of efferent arteriole, causing a decrease in filtration pressure, causing decreased GFR
30
What are some renal causes of AKI?
1. Tubulointerstitial disease - ATN, cast obstruction, acute allergic interstitial nephritis (no haematuria/proteinuria)
2. Glomerular disease - glomerulonephritis (haematuria, proteinuria)
3. Microvascular - HUS, MAHA, vasculitis, microemboli
4. Infection
31
What is the main cause of renal AKI?
Acute tubular necrosis - this is when ischaemia to tubular cells or exposure to a toxin causes cell death.
Patients will be oliguric first as a compensatory mechanism, but then become polyuric, as the tubules grow back.
Recovery may take weeks
32
What causes ATN?
Ischaemia - can progress from pre-renal AKI involving hypo perfusion
Toxins - aminoglycosides, cisplastin, contrast
33
What kind of casts can obstruct the tubules causing renal AKI?
Paraprotein - myeloma
Myoglobin - rhabdomyolysis
Urate - tumour lysis syndrome
Crystals - drugs, alcohol
34
What is acute interstitial nephritis?
Abnormal inflammatory response, often accompanied by a fever, painful joints and a rash - can cause renal AKI.
35
How is acute interstitial nephritis diagnosed?
White cell casts, eosinophils
36
How is acute tubular necrosis diagnosed?
Epithelial casts
37
What causes allergic acute interstitial nephritis?
NSAIDS, pencilllins, PPIs
38
What can cause glomerulonephritis?
Immune, drugs, infection
39
What can cause microvascular damage in intrinsic AKI?
- Haemolytic uraemia syndrome - post-viral
- MAHA - anaemia, shistocytes
- Vasculitis - ANCA
- Microemboli of cholesterol post angiography, causing distal necrosis
40
What are the post-renal causes of AKI?
Luminal - stones, clots
Mural - malignancy, BPH, strictures, fibrosis
Extrinsic compression - malignancy, retroperitoneal fibrosis
Retention - UTI, constipation
41
How is AKI managed?
1. IV fluids - give boluses then assess
2. Stop nephrotoxic drugs
3. Monitor (fluid status, U&E)
4. Treat sepsis
5. Give inotropes if low BP
6. Treat cause
7. Manage complications
8. Dialysis
42
Which nephrotoxic drugs need to be stopped in AKI?
NSAIDS, antihypertensives, gentamicin, metformin, morphine
43
How do you treat a pre-renal cause of AKI?
IV fluids, abx, inotropes
44
How do you treat an intrinsic cause of AKI?
Refer to nephrology
45
How do you treat a post-renal cause of AKI?
DO USS, catheterize, CTKUB, relieve obstruction
46
What complications might arise secondary to AKI, and how can they be managed?
Hyperkalaemia - IV calcium gluconate, salbutamol, dextrose and insulin, sodium bicarb, fluids
Pulmonary oedema secondary to fluid retention - MONA
Uraemia - dialysis
Metabolic acidosis - sodium bicarb, dialysis
NB any of these complications could be an indication for dialysis
47
What is the pathophysiology of glomerulonephritis, and how does this lead to AKI?
1. Damage to the glomerulus restricts blood flow, leading to compensatory rise in BP
2. Damage to the filtration mechanisms from rise in BP, allows protein and blood to enter the urine
3. Loss of usual filtration capacity, leading to AKI
48
How do patients with glomerulonephritis present?
- Hypertension
- Proteinuira/haematuria
- AKI or other renal impairment
49
What is a nephritic picture?
- Inflammatory
- Blood + protein on urine
- Very high BP and low eGFR
- Implies immune pathology
- Rarely pain
50
What are the primary cause of nephritis?
- IgA nephropathy
| - Mesangiocapillary glomerulonephritis
51
What are the secondary causes of nephritis?
- Goodpastures syndrome
- SLE
- Vasculitis
- Post-strep infection
- HSP
52
What is a nephrotic picture?
- Disturbance of permeability barrier
- Triad of proteinuria, hypo albumin and oedema
- Protein ++++ on urine
- Rarely pain
53
What are the primary causes of nephrotic syndrome?
- Minimal change disease
- Focal and segmental glomerulosclerosis
- Membranous
54
What are the secondary causes of nephrotic syndrome?
- Diabetes
- SLE
- Amyloidosis
- HepB/C
- Drugs
55
Describe the normal structure of the glomerular filtration barrier
3 layers of filtration, all negatively charged to repel plasma proteins:
1. Fenestrated capillary endothelium, made from podocalyxin (50-100nm holes)
2. Thick basement membrane, made from heparan sulphate proteoglycans
3. Filtration slits in between the interdigitating processes of the podocytes (4-14nm)
These ensure that large molecules are not filtered out
56
What is the pathophysiology of IgA nephropathy, and how is it diagnosed??
At times of infection, IgA deposits in the kidney and attacks the glomeruli.
Diagnosis
- Increased IgA and C3 on immunofluorescnece
- Mesangial proliferation on renal biopsy
57
What are the clinical features of IgA nephropathy?
Typically young patient with episodic macroscopic haematuria and rapid recover, at times of illness
58
How is IgA nephropathy managed?
Good BP control with ACEis
| Immunosuppression
59
What is the pathophysiology of HSP and how is it diagnosed?
Small vessel vasculitis due to deposition of IgA complexes, post infection (type of IgA nephropathy)
Diagnosis
- Usually clinical
- Increased IgA and C3 on IF
60
What are the clinical features of HSP?
Post-viral, abdo pain, purpuric rash on extensor surfaces and buttocks, polyarthritis
61
How is HSP managed?
Usually self-limiting
62
What is the pathophysiology of SLE and how is it diagnosed?
Autoantibodies cause tissue damage via immune complex formation and complement activation
Diagnosis
- Anti-dsDNA, ANA, anti-Sm antibodies
- Low C3/4 on IF
- Presence of cellular casts on microscopy
63
What are the clinical features of SLE?
Varied - malar rash, photosensitivity, alopecia, oral ulcers, malaise, arthritis, raynauds, nephritis, relapsing/remitting course etc
64
How is SLE managed?
- Steroids
- Immunosuppresion
- Dialysis/transplant
65
What is the pathophysiology of Anti-GBM disease (good pastures) and how is it diagnosed?
Type II hypersensitivity reaction in which IgG is formed against against type IV collagen, found in the BM of the kidneys and the lungs
Diagnosis
- Anti-GBM antibodies
- Kidney biopsy - shows crescents (this is more of a prognostic investigation)
- Also do CXR to look for lung involvement
66
What are the clinical features of Anti-GBM disease?
AKI, haematuria and lung haemorrhage
67
How is Anti-GBM disease managed?
- Immunosuppresion
- Steroids
- Plasmaphoresis to remove antibodies
68
What are crescents?
They are a marker of severity of renal damage, representing infiltration of the Bowmans space with cells and inflammatory mediators
They indicate rapidly progressive nephritis
69
Which small vessel vasculitis can cause glomerulonephritis? How are they diagnosed?
- Wegeners (granulomatous polyangitis ) - cANCA, RP3
- Microscopic polyangitis - pANCA, MPO
- Eosinophilic polyangitis (Churg Strauss) - pANCA, MPO
70
Which small vessel vasculitis is associated with:
a) ENT/URTI problems
b) rapidly deteriorating kidney function
c) asthma
a) Wegeners (granulomatous)
b) Microscopic
c) Eosinophilic (churg strauss)
71
What is the pathophysiology of post-strep glomerulonephritis and how is it diagnosed?
Generally self-limiting immune complex deposition in the kidney 1-4 weeks after a pharyngeal infection (typically with strep pyogenes)
Diagnosis
- Antistreptolysin O antibodies
72
What are the clinical features of post-strep glomerulonephritis?
Slight fever, nausea, smoky-brown urine
73
What is the diagnostic criteria for nephrotic syndrome?
1. Proteinuria (>3.5g/24h or ACR>250)
2. Hypoalbuminuria (<25)
3. Oedema
You also often get severe hyperlipidemia (TC>10mmol/L) due to overproduction of the liver to compensate for low protein
74
What are the signs and symptoms of nephrotic syndrome?
Severe oedema
Frothy urine
Wight gain
75
What is the pathology of minimal change disease and how is it diagnosed?
T cells release a cytokine that injures the processes of podocytes
Diagnosis
- Nothing seen at microscopy ('minimal change') so need to do electron microscopy which would show foot effacement
76
What are the causes of minimal change disease?
Idiopathic, drug associated, lymphoma
77
What is the pathology of membranous nephropathy and how is it diagnosed?
Immune deposition and spike formation due to autoantibodies against epithelial cell receptor PHOSPHOLIPASE A2
Diagnosis
- Diffusely thick GBM without hyper proliferation of cells
- IgG and C3 increased on IF
78
What is the pathology of membranous nephropathy and how is it diagnosed?
Immune deposition and spike formation due to autoantibodies against epithelial cell receptor PHOSPHOLIPASE A2
Diagnosis
- Diffusely thick GBM without hyper proliferation of cells
- IgG and C3 increased on IF
79
What is the pathology of FSGS and how is it diagnosed?
Sclerosis of certain areas of the glomerulus
Diagnosis
- Increase in hyalin, collagen and fat cells on biopsy (segmental pattern)
- IgM, C3 increased in certain areas
80
What are the causes of FSGS?
Idiopathic, malignancy, obesity, HIV (poor prognosis), alport syndrome, heroine use
81
What are the complications of nephrotic syndrome?
- Increased susceptibility to infection
- Thromboembolsim due to increased production of clotting factors
- Hyperlipidemia
NB - renal function may be normal in bloods
82
How is nephrotic syndrome managed?
1st line - Reduce oedema - diuretics
2. Reduce proteinuria - ACEi/ARB
3. Reduce complication risk - anticoagulants, statins
4. Treat cause - immunosuppression, steroids
Dont recommend bed rest as patients are already in a hyperthrombotic state
83
What is the main cause of CKD? What else causes it?
1. Diabetes
2. Hypertension
3. Glomerular disease
4. Other - urinary obstruction, inherited disease
84
How does diabetes cause CKD?
- Mesangial expansion due to hyperglycaemia
- GBM thickening
- Sclerosis due to intraglomerular hypertension
85
How does hypertension cause CKD? (and vice versa)
Thick vessels encroach on the lumen, leading to decreased renal perfusion. This has numerous effects:
- activates the RAAS system which further increases BP
- decreases GFR causing sodium retention, which increases BP
ie. it is a cycle!!
86
What is the pathophysiology of CKD?
- Various causes lead to expansion, proliferation and eventual fibrosis and scarring of nephrons
- This causes irreversible loss of nephrons
- Remaining nephrons have to work harder to maintain renal function
- This leads to up regulation of the RAAS and further damange and fibrosis
- The end result is widespread GLOMERULOSCLEROSIS and TUBULOINTERSTITIAL FIBROSIS
87
What are the symptoms of CKD?
Often asymptomatic
| May present stage 4/5 with weight loss, oedema, SOB, fatigue, itch, neuropathy, pallor, uraemia etc
88
What investigations should be done if you suspect CKD?
FIRST CHECK PREVIOUS KIDNEY RESULTS - NEED TO COMPARE
1. Bedside - urinalysis (ACR, mc&s)
2. Bloods - FBC, glucose, U&E, ESR, calcium (low), phosphate (high) , PTH (high)
3. Imaging - USS (<9cm kidneys), APKD, MRangiogram
4. Special - histology
89
What are the indications for kidney biopsy?
Unclear cause and normal sized kidneys on USS
90
How is kidney disease staged?
```
According to GFR
1 >90
2 >60
3a >45
3b >30
4 >15
5 - 0-15
```
Stage 4/5 - refer to nephrologist
91
How can you stop progression of CKD?
1. Treat underlying cause
2. BP control
3. ACEis for proteinuria
4. Glycaemic control
5. Low salt diet
6. Lifestyle
7. Reduce CVS risk (aspirin, statins)
92
What BP should you aim for in CKD?
<140/90 (or<130/80 if ACR>30mg/mol)
Higher ACR indicates worse disease
93
What are the symptoms of uraemia and how can it be treated?
Fatigue, appetite loss, itch, nausea (non-specific)
Treat with dialysis
94
What are the symptoms of oedema and how can it be treated?
Breathlessness, hypertension
Treat with diuretics, ACEis/ARBs
95
What are the symptoms of hyperkalemia and how can it be treated?
Arrhythmia, sudden death
Treat with IV calcium gluconate, salbutamol, dextrose and insulin, sodium bicarbonate and fluids
96
What are the symptoms of acidaemia and how can it be treated?
Fatigue
Treat with sodium bicarbonate, dialysis
97
What are the symptoms of hyperphosphataemia and how can it be treated?
Itch, bone disease
Treat with phosphate binders, diet restriction (no milk, dairy, eggs) and vit D analogues
98
What are the symptoms of anaemia and how can it be treated?
Fatigue, pallor etc (this is due to decreased epo production)
Treat with epo replacement and iron
99
What are the symptoms of hyperparathyroidism and how can it be treated?
Osteoporosis, bone disease
Treat with hydroxylated vit D (can't be normal form as kidney can't metabolise it)
100
What is the biggest cause of mortality in CKD?
Cardiovascular complications
101
What are the indications for dialysis?
```
Chronic - GFR<10ml/min
ACUTE - AEIOU
Acidosis
Electrolyte imbalance
Intoxicants
Overload/oedema
Uraemic symptoms
```
102
What are the symptoms of uraemia?
Fatigue, pericarditis, bleeding, nausea and vomiting
103
How does dialysis work?
Filters out toxin urea and electrolytes by maintaining a diffusion gradient, allowing solutes to diffuse across a semi-permeable membrane.
Essentially acts as an artificial glomerular basement membrane??
104
How does haemodialysis work?
Blood is circulated outside the body - 4 hours, 3 times a week
Risk of infection at entry site
105
How do you access circulation in haemodialysis?
Artifical AV fistula (permanent)
| Central venous catheter (temp)
106
How does peritoneal dialysis work?
Uses the peritoneum as a semi-permeable membrane - continuous or overnight
Risk of peritonitis
107
How do you access circulation in peritoneal dialysis?
Use a Tenckhoff catheter
108
What is the gold standard treatment for kidney failure and why?
Kidney transplant - improves survival, corrects metabolic acidosis and is cost-effective
109
What are the requirements for transplant?
Patient must be fit (no chronic infection, malignancy, CVS disease)
110
What is the diagnostic criteria of haemolytic uraemic syndrome?
Triad of:
- Haemolytic anaemia
- AKI
- Thrombocytopenia
111
What are the features of HUS?
- Commonly affects children (most common cause of AKI in kids)
- Usually preceded by E.coli infection (diarrhoea)
- Thrombotic microangiopathy (thrombosis in small vessels)
112
What is the definition for UTI?
>10^5 organisms per mL of fresh MSU
113
What are the symptoms of UTI?
Lower - dysuria, lower back pain, frequency
| Upper - fever, rigors, vomiting, loin pain
114
What is lower and upper UTI?
Lower - cystitis urethritis, prostatitis
| Upper - pyelonephritis
115
What is the difference between a complicated and uncomplicated UTI?
Complicated - abnormal renal tract, virulent organism, pregnant, obstruction, abnormal function
Uncomplicated - normal renal tract
116
How is UTI diagnosed?
Leucocytes and nitrites on urine dip
117
What organisms most commonly cause UTI?
E.coli
| Proteus mirabilis
118
What are the RF for UTI?
- Sex
- Pregnancy
- Catheter
- Condom use
- Menopause
- Kidney stones
119
How is UTI treated?
Uncomplicated - 3 days trimethoprim/nitrofurantoin
Complicated - 7 day course
Only treat if symptomatic!!
120
How is UTI treated in pregnancy?
1st trim - can't give trimethoprim
3rd trim - can't give nitrofurantoin
Amoxicillin fine always, always treat, even if asymptomatic
121
How is UTI treated in men?
Quinolone, will need imaging as it could indicate structural problem
122
How is UTI treated in pregnancy?
1st trim - can't give trimethoprim
3rd trim - can't give nitrofurantoin
Cephalexin/amoxicillin fine always (although growing resistance to amoxicillin)
Always treat, even if asymptomatic
123
What would haematuria from bladder pathology be like?
Through voiding
124
What would haematuria from prostate pathology be like?
End of voiding
125
What would haematuria from urethral pathology be like?
Beginning of voiding
126
Which investigation is best for detecting kidney stones?
Renal USS
127
What investigations is best for detecting renal artery stenosis?
MRI
128
What are some signs of diabetic nephropathy?
Normocytic anaemia
Proteinuria
High ESR
129
What is the classic presentation of bladder cancer?
Painless, gross haematuria throughout voiding
130
What is the classic presentation of renal cell carcinoma?
Triad of:
- Haematuria
- Flank pain
- Abdo/flank mass
Non specific symptoms
131
What is the best
a)initial
b)diagnostic
investigation for PCKD?
a) Abdo USS
| b) MRI??
132
What is Alport syndrome?
A genetic defect in synthesis of type IV collagen causing:
- hereditary nephritis
- sensorineural deafness
- ocular abnormalities - 'retinal fleeks' and cataracts
133
What is the best investigation for renal artery stenosis?
Renal arteriography - can show the exact location of the occlusion
Uses radiological dyes which are then detected using xray
134
What is a common complication of bladder cancer?
Bilateral hydronephrosis - due to obstruction to urine-outflow, creating a back pressure upon the kidneys
135
What is the best way to monitor renal function following a diagnosis of diabetes?
Microalbuminuria
136
What is the best management for minimal change disease?
Steroids eg. oral prednisolone
137
What are the characteristic biopsy changes in diabetic nephropathy?
Kimmel-Stiel nodules
138
What HbA1c should you aim for in CKD?
<53 mmol
139
What are the 2 most useful tests for looking for the cause of AKI?
Urinalysis
| Urine microscopy
140
Positive MBO?
Microscopic polyangitis
| COCAINE
141
In CKD how should you measure iron stores?
Transferrin
142
How should you usually measure iron stores?
Ferritin
