DPD: Renal disease Flashcards

(35 cards)

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
List 2 complications of CKD
Calcification of abdominal aorta | Predisposes to cardiovascular disease
26
What is nephrotic syndrome?
Proteinuria >3g/24h or PCR >300mg/mmol Hypoalbuminuria Oedema
27
What primary renal aetiologies can cause nephrotic syndrome?
Minimal change disease (glomerular) | Membranous nephropathy
28
What secondary renal aetiologies can cause nephrotic syndrome?
DM SLE Myeloma Amyloid
29
What investigations are necessary in nephrotic syndrome?
``` 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
How is nephrotic syndrome managed?
Control oedema: low salt diet, diuretics ACEi/ARB (reduce proteinuria) Treat the cause Sometimes steroids or immunosuppression
31
What is uncontrolled proteinuria is a major risk for?
Progressive CKD | Ultimate ESKD
32
Where is the pathology in haematuria? What may cause this?
Glomerulus Thin glomerular basement membrane disease or variant e.g. Alport’s syndrome IgA nephropathy
33
What investigations are used for haematuria if cancer/ kidney stones are most likely the cause?
Imaging (US, CT) | Cystoscopy
34
What investigations are used for haematuria if glomerular injury is most likely the cause?
Check urine for protein eGFR Blood tests for underlying systemic or immune disease Renal biopsy.
35
What is the prognosis for ESKD?
No recovery possible | Need dialysis or a transplant or not do either + treat symptoms (conservative care)