Renal Flashcards
1
Q
What is eGFR
A
Creatinine clearance used to estimate GFR
2
Q
What is creatinine
A
Chemical waste product from muscle metabolism
3
Q
Why are diuretics nephrotoxic?
A
Due to the hypovolaemia caused
4
Q
RAAS physiology
A
RAAS activated when low BP at afferent arteriole
Secretion of renin from kidneys (juxtaglomerular cells), Renin (enzyme) converts angiotensinogen -> angiotensin, ACE in lungs converts to angiotensin II
Angiotensin II = vasoconstrictor & Stimulates aldosterone release (adrenal cortex)
Aldosterone = inc sodium and water retention, inc K+ loss
5
Q
What is secreted during high volume? Where from?
A
ANP/BNP
From heart
6
Q
What is Activated during low volume?
A
RAAS
7
Q
Angiotensin II effect on kidneys
A
Constrict efferent arteriole
- This is to maintain GFR during hypotension
8
Q
ACEi SE
A
May impair renal function (Angiotensin II efferent constriction lost) and dec GFR
Hyperkalaemia due (less aldosterone)
Bradykinin mediated cough
9
Q
ARB (e.g. Losartan)
- Use
- indication
- SE
- CI
A
Modulation of RAAS but no dry cough (direct renin inhibitor)
HTN, HF, diabetic nephropathy
Renal impari, hyperkalemia
Preg, use with other RAAS drugs
10
Q
Where is Na+ reabsorbed
A
70% proximal tubule
25% loop of Henle
11
Q
Potassium control kidney
A
Free filtration in proximal tubule/loop of henle
Distal secretion determines secretion (collecting duct - Aldosterone mediated)
12
Q
Meds causing hypokalaemia
A
Loop diuretics
Thiazide diuretics
Na+ retaining diuretics
13
Q
Meds causing Hyprekalaemia
A
(drugs causing aldosterone block or reduction)
Spironolactone
Amiloride
ACEi, ARB
14
Q
Important roles of Kidneys:
A
- Fluid and electrolyte balance
- BP control
- Activates Vti D: Ca absorption, PO4 secretion
- EPO production: at low GFR anaemia can occur
15
Q
What makes up glomerulus
A
Capillary bed + Bowman’s capsule
16
Q
Osmolarity PCT DescendingLH DCT CD
A
300mOsm
600->1200mOsm (At bottom)
100-300 mOsm
1200mOsm
17
Q
Where is the majority of water reabsorbed
A
Descending loop of Henle
18
Q
Site where they work:
- Carbonic anhydrase inhibitors
- Furosemide (loop diuretic)
- Thiazides (indapemide)
- K+ sparing (Spironolactone)
- Desmopressin
A
Carbonic anhydrase inhibitors
- Proximal convoluted tubule
Furosemide
- Thick ascending loop of Henle
Thiazides
- Distal convoluted tubule
K+ sparing
- Cortical Collecting duct
Desmopressin
- ADH agonists (Vasopressin receptors in Kidney)
19
Q
Proximal convolute tubule:
- What is reabsorbed here
A
70% filtrate
Most essential things
- 100% glucose and Aminos (passive and active transport)
- Ions: Na (Na2HCA3 or NaCl), K+, Cl
20
Q
Loop of Henle
- Main job
- Key luminary’s transporter (on urine side)
- Diuretic with action here
- effect of diuretic and why
A
Descending limb reabsorbs water
Ascending limb concentrates or dilutes fluid in urine
20% of Na reabsorption
NKCC2 (Na, K and 2X Cl)
Inhibit NKCC2 - hypotension, hyponatraemia, hypokalaemia, hypochloraemia, indirect hypomagnesia/ hypocalcaemia/alkalosis
21
Q
Distal convoluted tubule and Collecting duct:
- Na reabsorption
- Transporters
- Hormone action here
A
5% at early DCT
Sodium/Potassium ATPase
Sodium reabsorption regulated by aldosterone (stim) and ADH (inhibit)
22
Q
DCT
- function
- channel
- Horomones (and effect)
- diuretic:
A
Reabsorbs Na and swaps for either H+ or K+ (they compete) via aldosterone
Acidifies urine
Na/Cl passive cotransporter (reabsorbes Na and H2O)
Na/K
PTH + Vit D: Ca absorbed, PO4 secreted
Aldosterone: Na absorption
ANP: Na excretion
Thiazide (e.g. indapemide): Hypotension, hyponatraemia
23
Q
Collecting duct:
- function
- Channels
- Hormones
A
Concentrates urine
Apical (urine side)
ENaC (reabsorption of sodium) and ROMK (potassium secretion)
Basolateral (blood side of cell)
Na/K - at BV
Aldosterone, ADH (Vasopressin)
24
Q
Renal tubular acidosis:
- What is happening
- What is the result
A
Dec H+ excretion or Dec reabsorption of Bicarbonate
Metabolic acidosis with normal anion gap (Even if low bicarb, renal tubule acidosis is hyperchloraemic)
Affects children
25
Causes of Renal tubular acidosis
Type 1) Mutation of proton pump (H-ATPase) giving inability to excrete H+ in distal tubule
Type 2) Sodium bicarb co-transporter mutation = inability to reabsorb bicarbonate
Fanconi's syndrome: Myeloma proteins and various drugs cause proximal tubule injury giving inability to secrete H+
26
Renal tubular acidosis:
- Investigations
- Tx
Low serum bicarb
high chloride
Variable K+
low pH w normal anion gap
Sodium alkali or potassium alkali
27
Renal tubular acidosis Complications
Volume depletion: loss of Na+
Osteoporosis due to acidosis causing bone buffering (demineralisation)
Growth retardation: Acidosis = muscle catabolism
28
Causes of End-stage renal failure
```
Glomerulonephritis
Pyelonephritis
Diabetes
PKD
End stage CKD
```
29
Pyelonephritis
- Def
- Causes
- Route of infection
- Epidemiology
Infection/inflammation of renal parenchyma, calyces and pelvis
Enteric bacteria (Escherichia coli, UPEC (Uropathic E.coli)
Ascending from Lower urianry tract or haematogenous
Women under 35 most common
30
Whe is pyelonephritis complicated
All men, pregnant, those with structural abnormalities (PKD, Horseshoe kidney, vesicle-ureteric reflux), immunosuppressed, (steroids, HIV, Radio/Chemo/Malig, transplant, sickle cell) Obstruction (posterior ureteral valve, stone, BPH)
More severe infection assoc with these
31
Pyelonephritis:
| Pres triad
1) Loin pain
2) Fever, Rigors
3) Costovertebral tenderness
May also have N&V,
32
Pyelonephritis Invesitgation
Urine dip (Blood, protein nitrites)
Urinalysis (microscopy) - WBC/RBC
Gram stain (G-ve rods (e.coli, klebsiella)
FBC: Leukocytosis
ESR/CRP: raised
Bacteraemia (Risk Sepsis)
Imaging: Renal USS, CT, DMSA(reals structural scan)
33
Pyelonephritis Treatment & complications
Mild/Moderate: Ciprofloxacin
Severe/complicated:
- Admit
- IV ceftriaxone or ciprofloxacin
- IV fluids
- IV para
Complications: Renal failure, abscess formation, parenchymal scarring, recurrence
34
Renal cell carcinoma
- Def
- Types
- Pres
- What is difficulty with Tx
Malignancy of renal parenchyma
80% clear cell
15% papillary tumour
```
Often asymp
Triad:
1) Abdo mass +
2) Haematuria +
3) Loin/Flank pain
Also: weight loss, anorexia, malaise
```
High levels P-glycoprotein (multiple chemo resistant)
35
RCC
- RF
- What LNs 1st to be affected
- Problem with surgery and mets
Smoking, obesity, HTN, age, Renal transplant, Polycystic kidney, Von Hipple Lindau
Para-aortic and Hilar LN
Very vascular - lots of bleeding
36
What is assoc with left sided RCC
Left sided varicocele due to invasion of Left renal vein
37
RCC Spread
| Mets description
Direct - renal vein
LN - Paraaortic then mediastinal
Haem - Bone, Liver, Lung
Cannonball mets
38
Principles in investigating RCC
Check kidney function
Check structure
Check for Mets
39
RCC Ix
BP: inc renin = inc BP
FBC: polycythemia (EPO)
Urinalysis haematuria ± proteinuria
Cr raised with reduced clearance
Percutaneous biopsy (histology)
LFT - AST/ALT raised in mets
Abdo pelvis USS & CT - mass staging and mets (LN, Bone, Liver)
MRI for local invasion
CXR: cannonball mets to lung
Bone scan
40
RCC paraneoplastic syndrome
```
Anaemia
Hypercalcaemia
Erythrocytosis
SIADH
Hepatosplenomegaly
```
41
RCC Tx & Prognosis
Surgical resection or Radiofrequency ablation
T3 = radical nephrectomy
T4 = Tyrosine kinase inhibitor (Sunitinib) ± locale radiation
Bisphosphnates for bone mets
Prognosis = 70% 5 year survival, 10% for mets
42
Childhood renal Ca name and Pres:
Wilms tumour - Nephroblastoma (primitive renal tubules)
Abdo mass + hameaturia
43
AKI
- Def
- Effect
Acute decline in GFR: inc in Creatinine with/without oliguria(under 0.5 ml/kg/hr)/anuria (under 50ml/day)
Impaired clearance (urea/creatinine --> Azotaemia), imparted acid-base/electrolye/volume regulation
44
AKI Causes
Pre (50%)
- reduced perfusion (hypovolaemia, sepsis, haemorrhage, HF
- Hepatorenal syndrome - GFR not responsive to fluids (liver failure = splanchnic dilation)
- Renovascular disease (Bilateral stenosis) and drugs (NSAIDs, ACEi)
Intrinsic (30%)
- Tubular necrosis (mainly sepsis - exogenous toxins, Abx and contrast also )
- Glomerulonephritis
- Interstitial nephritis
Post (20%)
- Mechanical obstruction
- calculi, BPH, Retention, pyelonephritis, retroperitoneal fibrosis, lymphoma
45
Commonest pathology of AKIA
Acute tubular necrosis as a result of ischaemia (poor perfusion)
Hypoxaemia results in ROS, decreased ATP, cellular death
46
Nephrotoxic drugs
Pre-renal
Intrarenal
Post renal
CANT DAMAG
Pre-renal
- NSAIDS -> hypoperfusion
- ACEI if compromised renal perfusion (e.g. renal artery stenosis) (DO NOT PRESCRIBE WITH NSAID)
Intrarenal
- Glomerulonephritis: captopril, penicillamine, gold, penicillins, rifampicin
- Interstitial nephritis: penicillins, cephalosporins, thiazide, furosemide, NSAID, rifampicin
- ATN: aminoglycosides, ciclosporin
Post renal
- Anticholinergics (TCA) + alcohol -> retention
CANT DAMAG
Contrast, antibiotics (penicillin/ceph), NSAIDs, Therapeutic index (narrow), diuretics, ACEI, metformin, ARB, gentamicin/GOLD
47
Staging AKI
| - What is used
Creatinine: more than 3x baseline = stage 3
Urine output: les than 0.3mL/kg for 24 hours or anuria for 12hrs = Stage 3
48
AKI
- RFs
- Pres
Older, underlying kidney disease, nephrotixics, DM, contrast, Liver failure + Ascites (Hepatorenal)
```
Decreased urine
Altered mental state (uraemia)
Peripheral oedema
Hypotension (suggests pre-renal)
Hypertension
```
49
AKI investigaitons
U&E + Cr: elevated Cr, High serum K+, metabolic acidosis
Urine dip: infection (leukocytosis, nitrites), glomerular disease (blood/protein)
FBC: anaemia (blood loss), Leukocytosis (inf)
ECG: hyperkalaemia (inc PR, Wide QRS, Peaked T)
50
AKI Tx approach
1) STOP nephrotoxics
2) ABCDE
3) Catheterise (monitor output)
4) VBG/ABG for K+ and ECG
5) USS KUB for obstruction
6) Urine dip (Inf, Blood/protein)
7) Dialysis for uraemia, acidosis, hyperkalaemia
51
CKD
- defa
- epi
- cause
- pres
Evidence kidney damage (Prot/Haematuria)
+ reduced GFR
For over 3 months
10% of adult pop. Inc due to age.
DM and HTN commonly
Smoking
Obesity
AI disorders (focal segmental glomerulonephritis)
Majority of people are asymptomatic
52
CKD
- Tx
- Complications
Glycaemic control
Increased risk of Cardiovascular disease -> main cause of death HF
53
```
CKD stages (%GFR)
1
2
3
4
5
```
```
>90%
60-89%
59-30%
15-29%
< 15%
```
Remember: minus 30 then half twice
90, 60, 30, 15, under 15
54
What is stage 5 CKD and what must be done?
This is end stage renal disease
Requires renal replacement therapy
- Haemodialysis
- Peritoneal dialysis
- Tranplant
55
CKD Aetiology (5 sections)
DM (50% ESRF)
- diabetic nephropathy due to glucose = albuminuria ± reduced GFR
HTN (30% ESFR)
- Atherosclerotic disease = stenosis
- HTN = renal scarring (glomerulosclerosis)
Nephrotic/nephritic syndromes
- focal glomerulosclerosis
- lupus nephritis
- membranous nephropathy
PKD
Obstruction
- Myelome
- RCC
- BPH
- Stones
56
Primary prevention CKD
Secondary prevention CKD
Good control DM (HbA1c under 7%) and BP ( under 140-90)
Smoking cessation
BMI under 27
As above, protein and salt restriction (control uraemia, prevent dialysis)
57
CKD presentation
Hypertensive diabetic over 50
```
Fatigue (anaemia)
oedema (salt/water retention)
Nausea (uraemia)
Arthralgia (If SLE)
Pruritus (uraemia)
```
58
Uremic syndrome
- Symp
- Signs
Metallic taste
anorexia
N&V (gastritis)
seizures
```
Skin- grey, pruritus
Uraemic encephalopathy
Pericardial rub
Bone pain
Anaemia
```
59
CKD complications
Anaemia (diminished EPO)
OSteodystrophy ( hypocalcaemia/phosphate retention due to Vit D def causes PTH release)
Cardiorenal syndrome (Na/H2O retention, volume expansion inc BP. inc pre-load due to renal hypoperfusion. HF & HTN as a result. These have knock on negative effect on kidneys)
Metabolic acidosis (unable to excrete acid)
Hyperkalaemia (unable to excrete as GFR declines)
Pulmonary oedema (fluid overload)
60
CKD investigations
Serum Creatinine (elevated), if osteodystropthy - hyperphosphataemia, hypocalcaemia
eGFR (under 60% for significant
Urinalysis: haemorrhage/prot
Renal USS: obstruct/hydronephrosis, large kidney (RCC, Myeloma, amyloid)
FBC: anaemia
Antibodies: Autoantibodies (ANA), antibodies to strep antigens (glomerulonephritis)
61
Management of CKD
Reversible causes: Obstruction, Nephrotixics
Glycaemic control
BP + CVD risk
- ACEi/ARB2: target 140/90
- statin, smoking, weight loss
Anaemia:
- Epoeitin alfa (stimulates SPO)
Bone disease:
- Dietary inc in Ca, Calcitriol if low (active Vit D)
- Phosphate binding drug (Calcium acetate)
Acidosis: oral sodium bicarb
Low protein and salt diet
62
Renal replacement therapy
- When used
- Indicating factors
- Inc risk to death
Severe AKI and ESRD (stage 5, eGFR < 15%)
Uraemia (pericarditis, gastritis, encephalopathy)
Pulmonary oedema (fluid retention)
Hyperkalaemia over 6.5% / Metabolic acidosis unresponsive to tx
Urea over 30
Each year dialysis inc risk of death by 6% (cardiovascular death)
63
Haemodialysis
- Mech
- Access
- Typical regimen
Blood passed over semipermeable membrane against dialysis fluid (opposite direction)
Blood meets less conc solution, small solutes can diffuse across conc grad.
```
AV fistula (bypassing capillary bed) Can also use a graft
Need Heparin infusion
```
Hospital 3X week for 4 hours OR home 5X 2-3 hours
64
Haemodialysis complications;
Access: infection, thrombosis, aneurysm,
Hypotension
Air emboli
N&V
Anaphylaxis (sterilising agent)
Disequilibriation: restless, tremor, coma
65
Who is harm-dialysis good for
Lives alone
Elderly
Cant have peritoneal dialysis
66
Peritoneal dialysis
- Mech
- Access
Dialysate infused into peritoneal cavity.
Uses blood from peritoneal capillaries. altering osmolality of dialysate determines how much fluid removed
Catheter to peritoneum
67
Peritoneal dialysis regimen
Continuous ambulatory with exchanges (last 20 min)
OR
Overnight
68
Peritoneal dialysis
- CI
- Complications
- Who does it suit
Intra-abdominal surgery/adhesions
Stoma
Obesity
Intestinal disease
```
Infection (peritonitis, catheter)
Catheter block/leak
Constipation
Hyperglycaemia + weight gain
Hernia
```
Young, indépendant, lack of healthcare access
69
Renal transplant
- Advantages
- Types
- Location
Inc survival, QoL, Economic advantage in long term, enable pregnancy (Kidney disease/Dialysis affects eggs and menstruation)
Cadaveric (90%), living donor (10%)
Right iliac fossa
70
Matching a renal transplant (3 things)
ABO group and crossmatch
HLA
- On 6 loci
- A and B (X2) present Ag to CD8 (cytotoxic) cell
- DR (X2) present to CD4 (Th) cell
Antibody screening
71
Immunosuppression in kidney transplant
Induction (at time): Basiliximab + IV methylprednisolone
Maintain: Prednisolone, Calcineurin inhibition's (Block t-cell activation e.g. tacrolimus/ciclosporin), antimetabolites (azathioprine)
72
CI for renal transplant
Cancer
Active infection
Uncontrolled Ischaemic heart disease
AIDs with opportunistic infection
73
Renal transplant Risks
Surgery: Infection, DVT, pain
Immunosuppression:
BM suppression, Ca (Skin, Lymphoma), infection
CV disease (HTN, dyslipidemia)
Rejection:
- hyper acute:mins, cross match error
- Accelerated: days, T-cell. fever swollen kidney, inc Cr. Give IV steroids
- Acute cellular: weeks (25%), fluid retention, inc BP and Cr. Give high dose IV steroids
- Chronic: years, gradual Cr rise and proteinuria, HTN. fibrosis and atrophy on graft biopsy. Not responsive to immunosuppression will need RRT again
74
Renal tranplant prognosis
Cadaver
1yr 90%,
10yr 65%
Live
1yr 96%,
10yr 80%
75
Glomerular disease classifications
Nephrotic:
- Proteinuria
- Peripheral oedema
- In children minimal change disease commonest - Steroids
- Hypoalbuminaemia and hyperlipidaemia (liver synthetic compensation)
Nephritic:
- Inflamation of glomeruli = Oliguria + Hematuria (cola coloured)
- Berger's disease (IgA nephropathy) commonest cause
76
Glomerulonephritis
- def
- complication
- common type
Glomerular injury due to immune mediated damage of glomerular capillaries and basement membrane (e.g. Berger's IgA nephropathy, SLE)
3rd most common cause ESRD
Focal segmental glomerulonephritis
77
Causes of Glomerulonephritis
Systemic disease
Infection
Drugs
Other
SLE, RA, Goodpastures, Wegners, HSP, HUS, Scleroderma
Group A strep (pyogenes) - immune complex, Hep B/C
Penicillamine (DMARD and used in Wilsons to bind copper), Ciclosporin, NSAIDs, Gold
DM, HTN, Lunc/colorectal cancer
78
Glomerulonephritis pathophysiology
Immune mediated injury due to 2 possible mech
1) cellular immune response: Leukocyte and macrophage infiltration (focal glomerulosclerosis)
2) immune complex formation and deposition + complement activation in glomerulus
- antibodies may bind with autoantigens e.g. in anti basement membrane disease
- extrinsic antigens bound to antibodies may deposit e.g. post infection
- complement, cytokine and growth factor activation = structural and functional changes
Non-immune: Hyperglycaemia, high intraglomerular pressure (HTN)
79
Nephrotic Vs Nephritic
Nephrotic = non-proliferative disease
- Proteinuria,
- hypoalbuminaemia,
- peripheral oedema,
- hyperlipidaemia
Nephritic = proliferative disease
- Oliguria/AKI
- HTN
- Haematuria (Red cells and casts)
80
Causes of Nephrotic syndrome
Deposition disease (Amyloid, light chain deposition - myeloma = Bence jones)
Minimal change disease
Other:
Focal, segmental, membranous, mebranoproliferative
81
Causes of Nephritic syndrome:
```
IgA Nephropathy (Berger's)
Postinfective
```
Vasculitis
Anti-GBM
82
Nephrotic syndrome
- Children: cause, Tx
- Young adults: Cause
Minimal change
Light microscopy normal, immunoflourscence = no deposition
Steroids (Prednisalone)
Focal segmental glomerulonephritis: idiopathic or secondary to HIV.
Light micro shows focal areas of sclerosis
83
Ddx nephrotic syndrome
Other diseases causing Peripheral oedema
- Congestive heart failure
- Liver disease (Dec albumin)
84
Nephrotic syndrome complications
Infection: IgG loss or secondary to steroids
Hypercholesterolaemia: inc hepatic synthesis of lipoproteins
Hypervoleamia: Dec in GFR, oedema
HTN: GFR impaired (not as much as nephritic)
85
Nephritic syndrome
- def
- most common
- Other
Acute kidney injury with deterioration of function
Most common = Buergers
- Macroscopic haematuria 2due to IgA deposition
Membranoproliferative: secondary to SLE causes thickening of GBM
Post infective: immune complex post Group A strep
Rapidly progressive (crescenteric)
- Vasculitis: Wegner's (cANCA), microscopic polyangitis (pANCA)
- AntiGBM
86
Glomerulonephritis
- Pres
- other symp
Haematuria + Oedema + HTN + Oliguria
weight loss (systemic), nausea (vasculitic), fever (Infection), arthralgia (Vasculitic), haemoptysis (antiGBM)
87
Glomerulonephritis investigatons
U&E, Cr - GFR normal or reduced
Urinalysis: haematuria, proteinuria, RBC casts
```
ESR - vasculitis
Complement - low in immune complex
antiGBM antibody
ANA - SLE
Renal biopsy
```
88
Glomerulonephritis management
Abx if post strep (phenoxymethylpenicillin)
moderate: haematuria + proteinuria + low GFR
- Reduce proteinuria: ACEi + furosemide + prednisolone
- immunosuppressive: cyclophosphamide
Rapidly progressive:
- antiGBM: plasma exchange + IV methylprednisolone + IV cyclophosphamide
- Lupus nephritis: IV methylpred + Cyclophosphamide
89
PKD
- Def
- Forms
- Characterised by
inherited cystic disease of kidneys
ADPKD (most common)
ARPKD
Renal cysts, intracranial aneurysms, aortic root dilatation and aneurysms, mitral prolapse, extra-renal cysts
90
PKD complications
HTN, CV morbidity (aneurysms rupture), CKD, End stage renal disease
91
Genes in PKD
Autosomal Dominant or recessive
Two PKD loci
- PKD1 - 85% ESRF at 50
PKD2 - 15% ESRF at 50
92
PKD pathophysiology
POlycystin 1 and 2 make protein complex involved in Ca regulation
Disruption affects cell signalling and inc proliferation
cAMP activation (Ca) and cAMP mediated cysts expansion/fluid secretion
Cysts form in tubular portion of nephron compress renal architecture and infrarenal vasculature (interstitial fibrosis and tubular atrophy
93
ARPKD
More severe form
High mortality
Neonated often present with large kidneys, renal cysts, hepatic cysts and fibrosis
15 year survival is low (50-80%)
94
PKD presentation
FH or PKD/ESRD or Haemorrhagic stroke
Lumbar pain (females), haematuria (males), HTN at 25-30yr (renal USS to screen)
Palpable kidneys
headache (aneurysms)
Hepatomegaly (Liver)
95
PKD extra renal cyst locations
Liver (80%)
Pancreas (10%)
Seminal vesicles (40%)
Brain (10%)
96
PKD investigations
Renal USS for cysts
Genetic testing (PKD1 or PKD2 mutation)
CT abdo pelvis (kidney and extra renal cysts)
Urinalysis (protein), ECG (LVH - HTN), ECH) (aortic root dilatation)
MR angio (aneurysm screen)
SCREEN FAMILY Kidneys and SAH (MR angio)
97
PKD management
UTI/infected cyst: Ciprofloxacin
PAin: analgesia (para, naproxen) ± laparoscopic cystectomy ± nephrectomy
ESRD: RRT (transplant or dialysis)
Target cell proliferation ( somatostatin (GH)
Intracranial: neurosurgical + nimodipine (CCB helps improve blood flow after aneurysm)
Genetic counselling
98
Types of Post Strep Glomerulonephritis (giving heamaturia)
IgA (1-2 days post URTI)
Immune complex (1-2 weeks post-URTI)
99
4 things in renal failure (Aki)
Uraemia
Acidosis
Hyperkalaemia
Fluid overload
100
Fluid overload in AKI
Pulmonary oedema (CXR)
101
Aki and glomerulonephritis
Two types of glomerulonephritis (phrotic/phritic)
Both are cause of AKI
