Renal 2.77-84 Flashcards
1
Q
What composes the glomerular barrier?
A
- Fenestrated capillary endothelium
- Trilaminar glomerular basement membrane
- Foot processes of podocyte cells forming filtration slits
(Barrier is size selective and charge selective; all component are negatively charged, as are plasma proteins)
2
Q
Symptoms of advanced kidney disease?
A
Tiredness, peripheral oedema, SOB (pulmonary oedema and anaemia), nausea, fatigue, haematuria (visible or non visible)
3
Q
Features of acute glomerulonephritis?
A
May be oedematous, hypertensive; may have cola/smoky urine, may be oliguric/anuric, may have systemic features (rash, eye symptoms, arthralgia, haemoptysis, hair/skin changes)
4
Q
Features of nephrotic syndrome?
A
Swelling (over days/weeks); urine frothy (massive protein leak), creatinine may be normal (hence why PCR/ACR is helpful), BP can be normal/low/high if very overloaded (oncotic pressure falls).
5
Q
Nephrotic vs nephritic?
A
- Nephrotic is podocyte injury, changed architecture to get scarring and deposition of matrix or other elements i.e. altered permability. Leaky, with low serum albumin, high urine protein, oedema and hypercholesterolaemia. Heavy proteinuria!
- Nephritic is inflammation, with reactive cell proliferation, breaks in GBM, crescent formation. Less leaky, but may see red cell casts. e.g. small vessel vasculitis. More “AKI” like. Haematuria. Still often have proteinuria but not nephrotic range. Usually immune, rapidly deteriorating
6
Q
Which diseases are more “nephrotic” than “nephritic”?
A
MOST: Minimal change nephropathy, FSGS, membranous nephropathy, diabetic nephropathy, amyloidosis. SLE is either
7
Q
Which diseases are more “nephritic” than “nephrotic”?
A
MOST: anti-GBM, small vessel vasculitis, post-streptococcal glomerulonephritis, MCGN. IgA nephropathy! SLE is either
8
Q
Clues in history for kidney disease?
A
- FHx (dialysis, transplant, ADPKD)
- Personal history (HTN, DM (if have retinopathy then will have microvascular disease everywhere), gout, CVA/PVD
- Childhood UTI (some may cause renal scarring)
- Drug history!!! (NSAIDS, antibiotics, recreational)
- Problems in pregnancy (PET)
- Previous kidney stones, cystitis, LUTS, loin pain
- Systemic signs (suggesting inflammationa)
- Swollen ankles!
- Urinary abnormalities
- Occupational (heavy metals, toxins etc.), smoking!!!!!!
9
Q
Features on exam for kidney disease?
A
Anaemia (low epo, pulmonary haemorrhage), rash/vasculitic lesions, fevers, arthral/myalgia, eye changes, oedmea, pulses and bruits for renovascular disease, fluid status (BP l+s), palpable kidneys, transplant kidneys, palpable bladder, AAA.
10
Q
Causes of hyaline casts?
A
Precipitated Tamm-Horsfall protein; low flow/concentrated urine/acid can cause this; so seen in dehydration/heavy exercise in normal patients.
11
Q
Categorising CKD?
A
G1/2/3a/3b/4/5 with ACR <3, 3-30 and >30 for A1/2/3. Corresponds to risk of adverse outcomes.
12
Q
ACR interpretation?
A
Done in diabetics. Normal range 0-3.5; microalbuminuria >2.5 (M) or >3.5 (F); proteinuria >30. (A1/2/3). Nephrotic range >220.
13
Q
Total urinary protein loss interpretation?
A
Nephrotic is >3.5g/24 hours. Normal loss is <150mg (T-HP and albumin). Sticks only detect albumin.
14
Q
Tamm-Horsfall protein and hyaline casts?
A
Precipitates in tubules, according to flow, pH; get casts. In immune damage/inflammation, RBC/WBC pass through damaged GBM/tubules and stick to tubular cast to give cellular casts.
15
Q
Light microscopy of fresh MSU re casts etc.
A
Red cell casts diagnostic of glomerular disease, white cell casts of interstitial nephritis, tubular debris in acute tubular necrosis.
16
Q
Investigations in renal disease?
A
- U+E, FBC, LFTs, BG, CRP, coag, CK, bone.
- Urinalysis + MCS + PCR
- Renal US
- ECG (K+)
- CXR (systemic/cardiac/overload)
- ABG, MSSU, virology, urate, lactate, KUB (xray), urine biochemistry
- BIOPSY
17
Q
Renal screen?
A
Looks for intrinsic causes of disease.
- GN screen: ANCA (MPO + PR3), anti-GBM, complement, ANA/ENA/Igs, ASO/cryoglobulins/RhF
- Myeloma screen: serum (+urine) free light chains/electrophoresis
- Virology (HBV/HIV/HCV)
18
Q
Imaging of kidneys?
A
USS + Doppler first line, AXR-KUB for calcification , stones. IVU, CT, MR, nuclear medicine (GFR, excretion, scarring), angiography (RA stenosis). Remember to be wary of contrast! + BIOPSY
19
Q
What to do if someone presents with very high potassium?
A
ECG, repeat bloods.
20
Q
Findings in membranoproliferative glomerulonephritis?
A
Gives mixed nephrotic/nephritic syndrome. Low C3. C3 nephritic factor usually +ve (i.e. antibody to C3 convertase).
21
Q
IgA nephropathy?
A
Most common cause of GN. IgA deposits in glomerulus, increased by concurrent URT infection; occurs in 2-3 days rather than weeks with post-streptococcal GN. Raised serum IgA; can do IgA/G/M electrophoresis
22
Q
What is pulmonary-renal syndrome?
A
Bleeding in lungs and GN; usually Wegener’s (GPA) or Goodpasture’s. May be SLE or microscopic polyangitis.
23
Q
What is crescentic GN?
A
A form of rapidly progressive GN (along with focal necrotising). Glomerular tuft compressed by surrounding hypercellular (macrophages, epithelial cells) in Bowman’s space. Crescents are not diagnostic of ANCA vasculitis, but do indicate severe glomerular injury
24
Q
What is rapidly progressive GN?
A
Syndrome of glomerular haematuria (dysmorphic red cells or red cell casts), rapidly developing kidney failure, and glomerular necrosis with or without crescent development. Causes include IgA nephropathy, ANCA, HSP, SLE, post-infectious etc.
25
Which renal functions are principally affected in AKI?
Excretion of nitrogenous waste (raised urea) and fluid/salt homeostasis (overload, electrolyte disturbance)
26
Consequences of sudden loss of renal function?
1. K+ rises; death/arrhythmia/muscle weakness
2. Uraemic toxins accumulate. N+v, malaise, pericarditis/pleurisy, fits, coma. (and bleeding risk)
3. Salt and H20 accumulate; get fluid overload and rapid death with pulmonary oedema
4. Metabolic acidosis (kidney normally secretes H+). Get haemodynamic instability, cellular function disrupted. Can be fatal.
27
Stage 1 AKI?
Cr 1.5-1.9* baseline in 7 days, or increase of >26.4 in 48 hours. UO <0.5ml/kg for 6-12 hours
28
Stage 2 AKI?
Cr 2-2.9* baseline in 7 days; UO <0.5ml/kg for >12 hours.
29
Stage 3 AKI?
Cr >3* baseline in 7 days, reaching >354, dialysis. Or UO <0.3ml/kg for >24 hours or anuria for >12 hours.
30
Causes of pre-renal azotaemia?
1. Volume depletion
2. Low cardiac output (tamponade, massive PE, MI)
3. Distributive (sepsis, ana, pancreatitis, hepatorenal)
4. Vasoconstrictors (NSAIDs)
31
Effect of NSAIDs and ACEI on kidneys?
NSAIDs constrict aa; get reduced perfusion AND GFR; ACEI dilate efferent so perfusion normal but GFR drops. Neither are nephrotoxic as such but do decrease GFR, particularly if given together.
32
Tubulo-interstitial AKI?
Less likely to have protein and blood than in glomerular disease (as this is where they would be filtered)
33
Types of tubulointerstitial AKI?
1. ATN (cells lining tubules)
2. Tubular obstruction by casts (myoglobin, paraprotein, urate)
3. Acute allergic interstitial nephritis. May get rash!
34
What is ATN?
Acute tubular necrosis. Proximal tubule cells work hardest (as with hepatocytes) (ie 'return' most of GFR) and are most vulnerable to ischaemia. Get cell death, blocked tubules, lower GFR, oligo/anuria. Recovery may take weeks or be incomplete
35
Causes of ATN?
1. Ischaemia/hypotension (i.e. progression from persistent pre-renal azotaemia, renal artery stenosis.
2. Toxins (aminoglycosides, cisplatin, contrast
36
Diagnosing ATN?
FENa >3% (fractional excretion of sodium) and presence of muddy casts (type of granular cast) on urinalysis. Can confirm with biopsy; necrosis and tubular obstruction.
37
Tubular obstruction by casts (a type of tubulointerstitial AKI)?
Can be paraprotein (free light chains clump with Tamm-Horsfall), myoglobinin from rhabdomyolysis, urate from TLS. If myoglobin, see DARK URINE and haematuria dipstick may be positive! Low flow favours precipitation so give IVT
38
Three types of rapidly progressve/crescentic glomerulonephritis?
1. Immune complex GN (lupus, IgA, post-infectious)
2. Anti GBM (if involves lung and kidney = Goodpasture's syndrome).
3. ANCA-associated vasculitis
39
HUS?
A microvascular cause of intrinsic AKI. Damage to endothelium by 0157 Shiga toxin/complement dysregulation; get microthrombi in response to damage, which 'cut' RBCs so see fragments (MAHA) and thrombocytopenia +/- anaemia. May have diarrhoea as precipitant
40
Cholesterol embolisation syndrome?
Another microvascular cause of intrinsic AKI; occlusion of microvasculature by atherosclerotic plaques; can be spontaneous or following arterial instrumentation!
41
Oliguria in AKI?
A feature of hypoperfusion and ATN specifically, but not oliguria reflects hypoperfusion (may be instrinsic/post) so IVT may not resolve it. Also, not all AKI oliguric. Recovering ATN often polyuric phase, relief of chronic obstruction can be polyuric. Means must push fluids or become volume deplete again!
42
AKI Ix?
Pre = fluids, post = USS etc. Intrinsic = CK, ANCA, electrophoresis, blood film, complement, DS DNA, biopsy (if suspect intrinsic,GN/interstitial nephritis cause other than ATN).
43
Indications for dialysis in AKI?
Refractory hyperkalaemia, pulmonary oedema, symptoms and signs of uraemia, acidosis. Also, removal of some toxic substances in OD.
44
How to give fluids in AKI?
If deplete, give bolus/challenge and reassess. Be cautious if overloaded/pulmonary oedema. Match input to output of previous hour. Do not just give according to creatinine; give according to fluid status.
45
What does/doesn't get filtered in glomerulus?
Creatnine, glucose, inulin, K etc. all freely filtered; 75% myoglobin filtered (hence why rhabdomyoloysis causes cast formation and ruins kidneys); Hb and albumin <0.1%.
46
What is thin BM disease?
Inherited collagen defect; only diagnosed biopsy. Common cause of (asymptomatic) haematuria, along with IgA nephropathy.
47
Referring haematuria?
2 week wait if:
1. Visible, >45, no UTI
2. Invisible, >60. All relates to cancer risk.
48
Normal protein loss?
<150mg/day (Tamm-Horsfall and albumin); urine only detects albumin; microalbuminuria is by definition dipstick -ve so needs urinalysis.
49
Using ACEI in CKD?
More of a place in early diabetic nephropathy, when main pathology is proteinuria and glomerular hypertension. In severe CKD, when all of glomerulus is fibrosed etc, tinkering with EA won't really help, and may have dual pathology ie renal artery stenosis and ACEI could cause renal function to collapse. Hard to know when to stop ACEI. CKD also causes hyperkalaemia (reduced excretion) and ACEI/ARB cause K+ rise so can be dangerous.
50
Definition of microalbuminuria (per 24 hours?)
30-300mg
51
Causes of modest proteinuria (<1g)?
Common. Can be tubulointerstitial, upper and lower UTI, stones, benign. Tubulointerstitial dysfucntion gives proteinuria because some protein is filtered at the glomerulus in health e.g. myoglobin but will not be resorbed.
52
Causes of proteinuria?
```
Glomerular disease (heavy)
Tubulointerstitial disease (modest)
Orthostatic (benign, do morning sample), physical exercise, fever, heart failure.
```
53
What constitutes nephrotic syndrome?
1. Proteinuria (>3.5g in 24 hours)
2. Hypoalbuminaemia
3. Oedema
4. (Hypercholesterolaemia)
5. (Hypercoagulability)
54
Why is nephrotic syndrome important?
Indicates severe disease and possibly rapid loss of renal function, prothrombotic and hypercholesterolaemiic (abnormal reactive protein synthesis by liver; risk of vascular disease), risk of infection (lose immunoglobulin).
55
Why is recent infection important in proteinura?
Can cause IgA nephropathy (i.e. mucosal response to URTI) or post-strep GN.
56
Investigating proteinuria?
Quantify (ACR), presence of haematuria, renal function normal, blood pressure, kidney size, likely aetiology.
57
ACR values?
A1 = 0-3, A2 = 3-30 (microalbuminuria), A3 = 30+ (including nephrotic range i.e. >220).
58
Problem with just measuring creatinine?
Relationship with GFR is non-linear i.e. can have substantial change in GFR before creatinine rises. Also differences in muscle mass, plus tubular and gut secretion. Means need validated formula instead
59
Causes of nephrotic syndrome?
1. GN. Minimal change disease, membranous GN, FSGS, SLE, others e.g. IgA nephropathy (usually causes haematuria)
2. DM, amyloidosis.
60
Membranous glomerulonephropathy?
A cause of nephrotic syndrome. Mostly primary ie idiopathic, can be secondary to AI disease, malignancy, drugs e.g. NSAIDs
61
Focal segmental glomerulosclerosis?
A cause of nephrotic syndrome. Primary, or secondary to obesity/heroin/HIV
62
Renal causes of secondary HTN?
ADPKD, renal artery stenosis/FMD, pyelonephritis, chronic glomerulonephritis
63
Four scenarios where may suspect secondary HTN?
1. Young (<30)
2. HTN with physical signs of underlying cause
3. Refractory HTN despite good compliance
4. Patient with sudden worsening of essential HTN
64
Why do adrenal vein sampling in Conn's?
Make sure you don't remove incidental adrenal mass
65
Three things that trigger renin release by juxtaglomerular cells?
Decreased salt to macula densa cells, decreased pressure in AA, SNS drive.
66
What happens if macula densa cells detect raised/low Na+ delivery?
Constrict aa to decrease glomerular filtration pressure and GFR; if low then macula densa cells release NO and prostaglandins to dilate afferent
67
Effects of angiotensin II?
1. Aldosterone release
2. Vasoconstriction
3. ADH release
4. Potentiates SNS response
5. Renal role more complex; increases Na+ resorption, and acts on EA and AA (usually to constrict); even though this restricts inwards flow, EA constricted more and so GFR rises
68
Where do spironolactone and amiloride act?
Spiro on MR receptor on tubular cells (aldosterone antagonist); amiloride on ENaC on luminal side (decrease Na+ resorption so no K+ exchanged out, hence they are both K+ sparing)
69
What is the consequence of aldosterone binding to MR receptor?
ENaC inserted into luminal membrane, Na+ in, K+/H+ out into urine to maintain polarity. For this reason, spironolactone can cause metabolic acidosis as H+ is not excreted.
70
What does mutation in 11bHSD/liquorice mean for BP?
Means that cortisol (active on MR) not converted to cortisone (inactive) so BP up due to increased salt and water retention. And become hypokalaemic!
71
Investigating renovascular disease?
U+E, dip, USS, renal artery doppler, MR angio/renal angiogram. Look for end-organ damage too!
72
What is it called when HTN directly damages kidney?
Hypertensive nephrosclerosis
73
Kidneys, parathyroids and BP?
Kidney failure leads to decreased vit D hydroxylation and therefore hypocalcaemia; this leads to secondary hyperparathyroidism which increases IC calcium, causing vasoconstriction and HTN.
74
Epo and HTN?
Treating anaemia (due to epo deficiency) with excess epo (or if smoke as well) can increase BP (partially due to haematocrit increase) and be prothrombotic.
75
Uraemia (CKD) and HTN?
Uraemia impairs NO synthesis and endothelium-mediated vasodilation (i.e. CKD causing HTN)
76
6 factors that may cause HTN in CKD?
1. Impaired Na+ excretion (increased volume)
2. RAAS (vasoconstriction, SNS potentiation)
3. SNS (renin release, vasoconstriction)
4. Prostaglandin/kinin imbalance (vasoconstriction)
5. Endothelin (direct vasoconstiction, renal injury)
6. Reduced NO (uraemia) causes loss of dilation.
77
What does renal ischaemia trigger?
RAAS! and therefore HTN
78
Essential crux of HTN/CKD?
HTN damages arteries; kidneys are full of arteries; kidneys cannot regulate BP; get more HTN.
79
Consequences of 5/6 nephrectomy model?
Mimics CKD. See RAAS upregulation, proteinuria, glomerular hypertrophy, mesangial expansion, focal and segmental sclerosis, fibrosis; soon get widespread sclerosis and tubulointerstitial fibrosis.
80
Why does nephron damage/fibrosis cause CKD?
One nephron fails; others work harder; get 5/6 model effects; they fail, domino-style.
81
BP targets of nephropathies?
Diabetic = 130/80, proteinuric (non-diabetic) = 130/80, non-diabetic/non-proteinuric = 140/90. Technically diabetes with end-organ damage is 130/80; without is 140/80
82
When does renal artery stenosis need revascularising?
Recurrent pulmonary oedema, solitary kidney, transplant kidney, worsening renal failure, very high blood pressure; if not do medical management
83
Indication for bilateral nephrectomy?
Refractory HTN in dialyisis patients; underperfused kidneys can still produce renin and therefore cause HTN (reduced renin, aldosterone and SNS activity). Alternative is catheter based denervation.
84
USS findings in CKD?
Reduced cortical thickness, loss of corticomedullary differentiation
85
Haematuria and diabetic nephropathy?
Not common, but doesn't exclude it. However, would not be likely to have casts with just + blood, even if it glomerular in origin. More likely with GN/vasculitis.
86
How to tell if epo will benefit in anaemic CKD patients/?
Check iron stores; if ferritin low, and transferrin sat low, then supplementing iron should be done. If these are normal, then epo will probably help. NB: Transferrin is measure of actual bioavailable iron (reduced in CKD) so may need IV iron if <20%.
87
Why is transferrin sat low in CKD?
Hepcidin accumulates; decreases bioavailibity of iron i.e. circulating iron; this can be measured with transferrin sat, even if ferritin is normal.
88
Why not ACEI in 5a CKD?
Better at stopping progression of proteinuric disease, particularly diabetic nephropathy. At this point, they are not going to do much for kidney function, though are still advised for hypertension. However, they can reduce GFR (particularly if there is marked renal artery stenosis ie dual pathology) and can cause hyperkalaemia; this must be corrected before they can be started. Stopping ACEI in advanced CKD (EGFR <20) means rise in GFR but poorer CV outcomes. Less evidence for them in this zone.
89
What to do if phosphate high?
Accumulates because is renally excreted. Low phosphate diet and giving phosphate binders can help. Important because high phosphate actually stimulates PTH release and therefore exacerbates renal osteodystrophy.
90
Causes of recurrent UTI?
Urological pathology e.g. stones, stasis, incomplete voiding; pregnancy; sex; menopause (oestrogen protects tissues). Most common pathology is reinfection with original isolate. Increased frequency of sex, new sexual partners, use of spermicide also increase risk.
91
Antibiotics in recurrent UTI?
Can go on low-dose prophylaxis for a couple of years if frequent and disabling, or take a single dose after sex if this seems to be the precipitant
92
Abx and pyelonephritis?
Abx given in UTI to make symptoms go away faster, but have side effect of stopping ascending infection; this is not the indication for giving them
93
Investigating recurrent UTI?
If have clear precipitant e.g. sex then may not be needed. US is investigation of choice. Doing cultures and sensitivities is more important because reinfeciton is likely.
94
Non-drug methods of reducing UTI risk?
Peeing after sex, staying hydrated, using non-barrier contraception, cranberry juice, probiotics.
95
Pathogenesis of diabetic nephropathy?
Fundamentally about imbalance in renal vascular regulation (excess RAAS). ATII is key mediator; get efferent vasoconstriction and glomerular hypertension. Along with systemic HTN, obesity,and glucose-dependent pathways stimulating fibroblast proliferation and mesangial expansion of glomerulus, means get podocytopathy (hence proteinuria) and fibrosis. Constriction of ea leaves glomerulus working overtime; get increase in GFR initially, but stress contributes to the above changes, then glomerulus fails and others have increased work so also fall!
96
Clinical features of progressive CKD?
Usually none! (identified by fall in GFR). Comorbidity (DM, CVA, CVD, PVD, AI disesase) common, and may lead you to suspect it, as could certain medicine e.g. NSAIDs, lithium
97
Management of progressive CKD?
1. Treat cause! May just be vascular risk factors
2. BP control; <140/90 or <130/80 if ACR >30 ie A3 (aim is to relieve glomerular HTN)
3. ACEI reduce proteinuria, cardioprotective
4. Glycaemic control (HbA1c <53)
5. Low salt intake
6. Lifestyle measures e.g. smoking
7. Reduce CV risk
98
Why are ACEI/ARB important in CKD?
Proteinuria associated with greater mortality (and nasty symptoms); ACEI relieve glomerular HTN by dilating efferent arteriole.
99
How do ACEI affect 'direction' of GFR/CKD?
Get initial decrease (greater dip may actually be good) as efferent dilates; if more than 30% panic. Then hopefully plateaus; most effective in proteinuric disease. However, may get progressive fall e.g. if have renal artery stenosis, and barely any flow "in" then dilating the efferent could cause GFR to collapse.
100
Complications of severe CKD i.e. GFR<20?
Uraemia, acidaemia, mineral bone disorder, anaemia.
101
Phosphate and PTH?
High phosphate stimulates PTH therefore can contribute to osteodystrophy
102
CKD: Uraemia px and rx?
Fatigue, nausea, loss of appetite, itch; supportive and dialysis
103
CKD: high phosphate px and rx?
Itch (can also be uraemia); diet restriction and phosphate binders.
104
Rare features of advanced CKD?
Pruritis, uraemic frost, encephalopathy, asterixis, pericarditis (an absolute indication for dialysis because of risk of tamponade and arrest), neuropathy.
105
Haemodialysis?
Either use central venous dialysis catheter (temporary, risk of infection high) or AV graft/fistula for access. Home or hospital; done for 4 hours, three times a week. Use counter-current multiplier
106
Peritoneal dialysis?
Peritoneum acts as membrane. Put fluid in (at home), leave it in for ~4 hours, then drain and repeat; can do overnight. Risk of infection, causing peritonitis, but have more freedom.
107
Benefits of transplant?
Good outcomes, actually corrects metabolic problems unlike dialysis, increased quality of life, cost effective (after first year).
108
HLA matching and ABO matching in transplant?
'0,0,0' mismatch is perfect match in key HLA domains; called haplotype matched. '0,1,0' still pretty good; 2,1,0 etc. not good. Can do incompatible on ABO/HLA, with immunoabsorption and special immunosuppression, but outcomes are worse.
109
Features of tubulointerstitial nephritis?
Caused by infection, drugs (NSAIDs, penicillins, phenytoin); can be acute or chronic.
1. Urine shows white cells, red cells, white cell casts
2. Proteinuria; normal or mildly increased (unlike in glomerular disease)
3. Fever, rash and eosinophilia (visible on biopsy); may not be apparent if caused by NSAIDs.
110
How might one diagnose haemolysis?
Blood film, LDH
111
KCO in pulmonary haemorrhage?
INCREASED!
112
Investigating small vessel vasculitis?
CXR may show diffuse alveolar shadowing, KCO increased, BAL bloody, anti-PR3/MPO +ve, biopsy confirms.
113
Crescentic GN?
Signifies severe and aggressive immune damage; inflammatory cells move into Bowman's space; fibroblasts proliferate, hypercellular area compresses glomerulus and its capillaries so renal function deteriorates. Glomerulus ill-defined; % of affected glomeruli on biopsy predicts response. Often seen in rapidly progressive GN (includes IgA, vasculitis, SLE etc.)
114
Recurrent UTI with clear precipitant (e.g. sex)?
Doesn't really need investigating, but cultures with sensitivities key because likely to be reinfection with original culture
115
Prophylactic Abx for UTI?
Low dose proph Abx are effective, but should be reserved for those with frequent, disabling UTIs to avoid resistance. Treat for 1-2 years then reassess. Can also give single dose after sex if this seems to be the cause.
116
Indications for urgent dialysis?
High K+, refractory pulmonary oedema, severe acidosis, uraemia signs and symptoms e.g. encephalitis, pericarditis!
117
Why US apparent diabetic kidney disease?
May have concurrent reversible pathology e.g. obstruction, renal artery stenosis (suspect if one kidney smaller than the other)
