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Renal Flashcards

1
Q

What is renal function?

A

How much blood flow goes through the glomerulus = Glomerular filtration rate. Should be >90ml/mom

Endogenous marker is blood urea and serum creatinine (this is dependent on age/sex/weight/muscle mass).

Can give EDTA to clinically assess

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2
Q

What conditions raises blood urea levels?

A

GI bleeds, hepatic function and nutrition states

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3
Q

What is normal urea:creatinine ratio?

A

40:1 to 100:1

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4
Q

What does metformin predispose for in poor kidney function patients?

A

lactic Acidosis

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5
Q

Features of AKI?

A

Fluid -> oliguria, volume overload
Electrolyte - > hyperkalae,ia
Acid-base -> metabolic acidosis

Measured by urea or creatinine

Potentially reversible

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6
Q

CKD features?

A

Impaired renal function for >3 months.

Abnormal structure/function or GFR <60ml/min for >3months
+/- evidence of idney damage

usuualy progressive and irreversible

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7
Q

Symptoms of AKI?

A

Underlying cause
Oliguria/anuria

N+V
SOB
Dehydration
Confusion (encephalopathy from uraemia)

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8
Q

Signs of AKI?

A

HTN, distended bladder, dehydration (postural hypotension)

Fluid overload e.g. HF, cirrhosis, nephrotic syndrome) = raised JVP, pulmonary and peripheral oedema

Pallor, rash and bruising from vascular disease

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9
Q

How to classify AKI?

A

Stage 1: 1.4x rise in Creatinine to baseline of urine <0.5ml/kg/hr for >6hours

Stage 2: 2x Cr rise r urine output the same for >12hours

Stage 3: 3x Cr rise of <0.3ml/kg/hour for >24hrs or anuria>12hours

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10
Q

RFs for AKI?

A

Hypovolaemia

CKD, diabetes, HF, renal transplant, ?75YO, contrast administration

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11
Q

Pre-renal causes of AKI?

A

40-70% AKI= reduced urine output and raised urea:creatinine ratio

Hypovolaemia: either renal loss from diruetic overuse or extrarenal loss e.g. V+D, burns, sweating and blood loss

Systemic vasodilation e.g. Sepsis and neurogenic shock

Decreased CO e.g. MI or HF

Intrarenal vasoconstriction

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12
Q

Renal AKI causes?

A

Tubular = acute tubular necrosis

Glomerular = glomerulonephritis

Interstitial = iterstitial nephritis

Vascular = vessel obstruction e.g. thrombosis, vasculitis and haemolytic microangiopathy

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13
Q

What can cause acute tubular necrosis?

A

Paracetamol, NSAIDs, ACEi, contrast and myoglobinuria in rhabdomyolysis

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14
Q

What causes intrarenal vasoconstriction in pre-renal AKI?

A

Renal artery stenosis, fibromuscular dysplasia, cardiorenal syndrome, hepatorenal syndrome,

NSAIDS, ACEi and ARB

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15
Q

How to manage pre-renal AKI?

A

NEWS and identify causitive problem e.g. hypovolaemia and monitor fluid balance, K+, lactate and daily creatinine

Bolus and maintenance fluid

Stop nephrotoxic meds and change medications that are renal excreted
e.g. metformin and LMWH
Avoid contrast

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16
Q

What drugs can commonly cause AKI?

A

Abx such as aminoglycosides e.g. gentamicin and amikacin

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17
Q

What causes Acute Tubular Necrosis (ATN)?

A

> 50% of renal causes of AKI

Renal tubular epithelial cell injury due to ischaemia from shock/sepsis or nephrotoxic agents

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18
Q

What Exogenous substances causes ATN?

A

NSIADS, aminoglycosiides, amphotericin B, contrast media, calcineurin inhibitors, cisplatin

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19
Q

What endogenous substances cause ATN?

A

Myoglobiunuria (rhabdomyolysis), haemoglobinuria, crystals (uric acid) e.g. gout, and myeloma (IgG light chains)

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20
Q

Features of ATN?

A

Urine = muddy brown granular casts, myoglobiunuria and haemoglobiunrura

Features of raised AKI: e.g. urea, creatinine, potassium and metabolic acidosis
Urea:creatinine ratio <40:1

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21
Q

Indicators of rhabdomyolysis?

A

Raised CK, hypocalcaemia and elevated phosphate

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22
Q

Hyperkalaemia management?

A

Escalate + ABCDE
Continuous cardiac monitoring + IV acess and redo bloods
Review drugs e.g. stop neprotoxic
10ml 10% calcium gluconate IV over 10 mins
100ml 20% dextrose with 8U insulin over 15mins
Nebulised salbutamol 5-10mg
Sodium bicarbonate to correct acidosis

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23
Q

ECG changes in hyperkalaemia?

A

Tall tented T wave, small absent p wave, broad QRS, increased PR interval, sine wave, bradycardia

24
Q

What is glomerulonephritis and what can it causes?

A

Inflammation of the glomeruli and nephrons.

Can cause increase in BP to malignant HTN
Urine dipstick can show blood and protein
Decreased renal function due to loss of filtering capacity

25
Features of nephrotic syndrome?
Proteinuria?3.5mg/24hours Hypoalbunaemia <25g/L oedema Hyperlidaemia +-hypercoagulative state
26
features of nephritic syndrome?
Hypertension haematuria + red cell casts Oedema Oliguria and progressive renal impairment
27
Primary Causes of nephrotic syndromer?
Minimal changes disease Membranous nephropathy Focal segmental glomerulosclerosis
28
Secondary causes of nephrotic syndrome?
DM - glomerulosclerosis SLE Amyloid
29
Primary causes of nephritic syndrome?
``` Membranoprolifertive (MPGN) Raid progressive (RPGN) with types: 1=Anti-GBM (goodpastures) 2=Immune complex deposition 3= pauci immune ``` Thin BM disease Alports syndrome
30
Secondary causes of nephritic syndrome?
``` Post-streptococcal IgA nephropathy (bergers) HSP Small vessel vasculitiis SLE Anti-GBM disease ``` Cryoglobineamia (IgM secondary to MM, CLL and waldenstroms)
31
What is minimal change disease?
Affects youn population with normal biopsy ecept electron = podocyte effacement Associated with Hodgkins lymphoma Steroid responsive
32
Features of membranouse nephropathy | ?
100% nephrotic Granular IC depositon with spike and dome pattern on microscopy Primary= autoimmune (ab for PLA2R) Secondary = Malignancy, drugs and infection e.g. HEPB/C and SLE
33
What drugs can cause secondary membranous nephropathy | ?
Gold, penicillamine and captopril
34
What is FSGS?
Nephrotic Focal scarring with IgM deposition In Afro-caribbeans Heroin, HIV and HIV-associated hephropathy Bisphosphonate use e.g. Pamidronate
35
Differences in diabetic and amyloid nephropathy?
Nephrotic Congo red staining = aple green birefringence for amyloid Diabetic = Nodular glomerulosclerosis and Kimmelstiel-Wilson nodules
36
What us MPGN?
nephrotic + nephritic Immune complex associated with deposition causing mixed nephritic Type 1 = Hep C>B Type 2 = C3 nephritic factor (low C3) Presents tram tacking appearence and mesangial proliferation on microscopy
37
What is IgA nephropathy?
Days after URTI causes deposition of complexes and episodic macroscopic haematuria Nephritic syndrome
38
What is Henoch Schonlein Purpura?
Nephritic variant of IgA nephropathy Systemic vasculitis and depostion = purpuric rahs and arthralgia
39
What is post-strep GN?
1-2 weeks after throat or skin infection causes IgA depostion and high ASOT with Low C3 'smoky urine'
40
What are the Rapidly progressive GN?
Nephritic syndromes Anti-GBM goodpastures Immune complex deposition Pauci immune
41
GFeatures of Anti-GBM type 1 RPGN?
Haematuria, haemopysis, proteinuria young M>F | Auto-abs to Type 4 collahen so linear stain
42
Features of Type 2 immune complex mediated RPGN?
Any immune complex deposition = granular pattern | SLE< IgA nephrotpathy and HSP
43
Features of Pauci-immune Type 3 RPGN?
Negtaive stain and ANCA associated cANCA = ENT+lungs+kidneys = granulomatous polyangiitis pANCA=asthma+eosinophilia+mononeuritis multiplex and purpura = eosinophilic granulomatosis with polyangiitis [purpura = microscopic polyangiitis]
44
What drugs cause glomerular damage?
Rifampicine, dapsone, penicillins, isonazid
45
What drugs cause post-renal tubular blockage?
Aciclovir and sulphonamides
46
What drugs cause acute interstitial nephritis?
Penicillins, anti-Tb therapy, sulphadiazine and cephalosporins
47
Symptoms of CKD?
Often asymptomatic. Severe = anorexia, N+V, fatigue, pruritis, peripheral oedema, msucle cramps, pulmonary oedema, sexual dysfunction
48
Signs of CKD?
Underlying disease e.g. SLE Skin pigmentation and excoriations from uraemia, pallor, HTN, peripheral oedem,a peripheral vascular disease and renal bone disease
49
Consequences of CKD?
Progressive failure of homeostatic = acidosis and hyperkalaemia Progressive hormonal failure = anaemia and renal bone disease e.g. osteomalacia CVD = vascular calcification, uraemic cardiomyopathy Uraemia, encephalopathy and death
50
CKD Ix?
bedside: BP, dipstick urine, fundoscopy, ECG for cardiac changes Bloods: bicarb for metabolic acidosis, U&Es, Hb for renal normocytic anaemia, PTHCa/phosphate studies BM and HbA1c Imaging: USS and CXR, biopsy if no diagnosis
51
CKD management?
1) limit progression 2) symptom control 3) Prep for renal replacement therapy
52
How to limit CKD progression?
BP target so lifestyle and drugs Tight sugar control decreased CVS risk Diet to reduces phosphate and salts
53
How to symptom control for CKD?
Human EPO or iron for anaemia Sodium bicarb for acidosis Loop diuretics and fluid restriction for oedema HTN treatment Phosphate binders for hyperphosphataemai e.g. sevelamer HypoCaHyperPth e.g. cholecaliferol, alfa, cincacimet
54
How to renal replacement therapy for CKD?
Haemodialysis, peritoneal dialysis and renal transplant
55
Indications for urgent haemodialysis?
``` AEIOU Refractory Acidosis Refractory hyperkalaemia (electrolytes) Drug OD (ingestion) Refractory pulmonary oedema Uraemia with complications ```

MedEd (32 decks)

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