DPD: Renal disease Flashcards

1
Q

What are 5 main functions of the kidney?

A

Filtration + excretion of waste products
Electrolyte homeostasis
Hormone production (EPO+ 1.25 Calcitriol)
BP control via RAAS, prostaglandins + bradykinin
Acid base homeostasis

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2
Q

What must be considered when interpreting eGFR?

A

Only relevant in stable patients
Not valid in AKI
Dependent on muscle mass

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3
Q

What variation in urine colour may be seen? What causes each of these?

A

Red: myoglobinuria or haemoglobinuria, food dyes, beetroot, porphyria, rifampicin
White: pyuria, phosphate crystals, chyluria
Black: haemoglobinuria , alkaptonuria

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4
Q

What is urine PCR?

A

Total urine protein excretion (albumin, light chains + other globulins) divided by urine creatinine

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5
Q

What is urine ACR?

A

Urine albumin concentration divided by urine creatinine.

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6
Q

What is AKI?

A

A rapid deterioration in renal function over days
with
Accumulation of nitrogenous waste products
Potentially life threatening metabolic consequences
+/- reduction in urine output

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7
Q

What figures define AKI?

A

Serum Cr rise >26 umol/L within 48 hrs
Or
Serum Cr rise 1.5x the reference value known or presumed to have occurred within 1 week
Or
Urine output < 0.5ml.kg/hr for 6 consecutive hours

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8
Q

List 10 risk factors for AKI?

A
Age >75
Pre existing CKD (eGFR <60)
Previous ep of AKI
Debility + dementia
HF
Liver disease
DM
Hypotension
Sepsis
Hypovolaemia 
Nephrotoxins e.g. gentamicin, NSAIDs
Continued antihypertensives in setting of hypotension
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9
Q

How can the causes of AKI be classified? What is the prevalence of each cause?

A

Pre-renal ~20%
Intrinsic renal ~50%: problem in kidney
Post renal ~15%

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10
Q

What is the problem in pre-renal AKI? List 3 causes of this What do you need to examine

A
Hypovolaemia 
Low CO
Hypotension
Renal artery thrombosis
is BP low? volume status, JVP, BP + postural drop?
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11
Q

List 8 causes of renal AKI

A
Acute tubular necrosis
Glomerulonephritis
Myeloma
Vasculitis 
Nephrotoxins, contrast, rhabdomyolysis
Interstitial nephritis
HUS/ TTP
Malignant HTN
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12
Q

What is the problem in post-renal AKI? List 3 causes of this. What investigation should you perform?

A
Ureteric obstruction
Urethral obstruction
Blocked urinary catheter
Bladder tumour 
US scan
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13
Q

What is CKD?

A

impaired kidney function, usually progressive, potentially resulting in ESKD over months to years, often multifactorial.
Not reversible.

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14
Q

What signs and symptoms are caused by AKI?

A

Symptoms of uraemia (nausea, vomiting, anorexia)
Decreased urine output
Features of the underlying disease
Systemic features (rash, myalgia, arthralgia, headaches)

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15
Q

What biochemistry may be found in AKI?

A

High serum urea + creatinine
Acidosis
Hyperkalaemia
Salt + water retention

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16
Q

What is found in the urine in the 3 classes of AKI?

A

Glomerular disease: red cells, red cell casts, proteinuria (often heavy)
Tubular disease: Minimal blood, small protein, granular or white cell casts
Post-renal: no blood or protein, no casts

17
Q

What 9 investigations are necessary in AKI?

A
Volume status (for ATN)
Urine microscopy + dipstick
US scan to detect obstruction 
ANCA, Anti-GBM, SLE immunology (ANA, dsDNA, complements) 
Creatinine kinase 
FBC, clotting
Inflammatory markers
Myeloma screen (protein electrophoresis, urine BJP)
May need biopsy
18
Q

What immediate complications of AKI need urgent treatment?

A
Potassium (kills)
Pulmonary oedema (kills)
Acidosis 
HTN
Uraemia (brain, nerves, heart)
19
Q

How is hyperkalaemia treated?

A
IV Ca
Insulin + dextrose
Nebulised salbutamol
Calcium resonium or newer binding agent
Dialysis
20
Q

What is the aetiology of CKD? Often CKD patients present at what stage? What size are their kidneys?

A

A “syndrome” for which there is a cause, although often not identified
End stage
Often small kidneys

21
Q

What is the epidemiology of CKD?

A

Common

>40% of >75s

22
Q

List 7 risk factors for CKD

A
Elderly 
HTN 
Diabetes 
IHD 
FH CKD 
African American 
Obesity
23
Q

List 6 causes of CKD

A

Diabetes (~30%)
Chronic glomerulonephritis (~30%)
Vascular diseases inc. HTN, IHD (~15%)
Autosomal dominant polycystic kidney disease (~10%)
Congenital/reflux/childhood infections
Genetic risks .. with another insult (eg ApoL1 risk variants in black patients)

24
Q

What is the key to preventing progression of CKD? How is this achieved?

A

BP control (v low) + reducing proteinuria
ACEi/ARBs
Increasingly SGLTi drugs
Minimising other CV risks eg smoking

25
Q

List 2 complications of CKD

A

Calcification of abdominal aorta

Predisposes to cardiovascular disease

26
Q

What is nephrotic syndrome?

A

Proteinuria >3g/24h or PCR >300mg/mmol
Hypoalbuminuria
Oedema

27
Q

What primary renal aetiologies can cause nephrotic syndrome?

A

Minimal change disease (glomerular)

Membranous nephropathy

28
Q

What secondary renal aetiologies can cause nephrotic syndrome?

A

DM
SLE
Myeloma
Amyloid

29
Q

What investigations are necessary in nephrotic syndrome?

A
Quantitate proteinuria (urine PCR) 
Serum albumin + cholesterol 
Serum creatinine, U+Es 
Glucose
SLE tests
Virology (Hep B,C + HIV)
Myeloma screen 
Renal US
Renal biopsy
30
Q

How is nephrotic syndrome managed?

A

Control oedema: low salt diet, diuretics
ACEi/ARB (reduce proteinuria)
Treat the cause
Sometimes steroids or immunosuppression

31
Q

What is uncontrolled proteinuria is a major risk for?

A

Progressive CKD

Ultimate ESKD

32
Q

Where is the pathology in haematuria? What may cause this?

A

Glomerulus
Thin glomerular basement membrane disease or variant e.g. Alport’s syndrome
IgA nephropathy

33
Q

What investigations are used for haematuria if cancer/ kidney stones are most likely the cause?

A

Imaging (US, CT)

Cystoscopy

34
Q

What investigations are used for haematuria if glomerular injury is most likely the cause?

A

Check urine for protein
eGFR
Blood tests for underlying systemic or immune disease
Renal biopsy.

35
Q

What is the prognosis for ESKD?

A

No recovery possible

Need dialysis or a transplant or not do either + treat symptoms (conservative care)