Chempath: Renal Flashcards

1
Q

What are the functions of the kidney?

A

The kidney has various functions - broadly broken down into;
1. Removal of waste

  1. Homeostatic -> acid/base, fluid, electrolytes
  2. Hormonal -> renin, EPO, 1a-hydroxylase
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2
Q

What is GFR? what is the normal level?

A

Glomerular filtration rate is a measure of kidney function and normal rate is 120ml/min

GS = INSULIN CLEARANCE

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3
Q

How is GFT calculated?

A

Clearance is used to calculate GFR -> volume of plasma that can be completely cleared of a marker substance per unit time

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4
Q

What makes the ideal marker to be used in assessing GFR?

A

1) not bound to serum proteins
(2) freely filtered at the glomerulus
(3) not secreted or reabsorbed by tubular cells

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5
Q

What is the gold standard for measuring GFR?

A

INULIN, however, steady state infusion required, therefore only really used in research

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6
Q

What is used in clical practice to measure GFR?

A

Endogenous marker aka creatinine

However, creatine isn’t a perfect marker –> factors affecting it + secreted into tubules

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7
Q

What factors can affect creatinine levels?

A

Muscle mass (↑ with more muscle mass)

Age (↓ with age)

Sex (M > F)

Ethnicity (Black > Caucasian > Chinese)

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8
Q

How can you use creatinine as a better marker for GFR?

A

By using th CKD-EPI equations equation estimates the creatinine clearance, taking into account age, weight and sex

The old equation (cockgroft gault) may overestimate GFR

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9
Q

What is the better way to measure proteinuria?

A

Spot urine > 24 hour urine collection when measuring proteinuria

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10
Q

How is protein uria measured?

A

Spot urine + Protein:creatinine ratio (PCR) = quantitative assessment of amount of proteinuria

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11
Q

What can urine dipstick testing show?

A
pH
Specific gravity (SG) - concentration of urine

Blood:

  • If –ve - reliably EXCLUDES haematuria
  • If +ve - may be due to blood OR myoglobin

Protein

Nitrites - detects bacteria (coliform)

Leucocyte esterase (-ve result = important)

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12
Q

What microscopy is used in renal tests?

A

Crystals (calcium oxalate, calcium phosphate, uric acid, cystine, struvite)
RBCs (infections, stones, cancers)
WBCs (bacterial or non bacterial inflammation)
Casts (cellular vs acellular)
Bacteria

+ imaging can be used depending on diagnosis suspected

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13
Q

What is the gold standard for renal issues?

A

Renal biopsy

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14
Q

What is the definition of AKI?

A

Rapid reduction in kidney function leading to inability to maintain electrolyte, acid base and fluid homeostasis.

NB - THIS IS A MEDICAL EMERGENCY NEEDS REFERRAL TO NEPHROLOGIST FOR DX + TX

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15
Q

What is the criteria for AKI?

A

Increase in serum creatinine by >26mmol/L within 48 hours OR

Increase in serum creatinine to 1.5x baseline within 7 days OR

Urine output <0.5mL/kg/hr for 6hrs

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16
Q

What are the different stages of AKI?

A

Stage 1: ↑ in serum Cr by ≥ 26micromol/L OR by 1.5-1.9 x reference serum Cr

Stage 2: ↑ in serum Cr by 2-2.9 x the reference serum Cr

Stage 3: ↑ in serum Cr by ≥ 3 x the reference serum Cr OR ↑ by ≥ 354micromol/L

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17
Q

What is the most common cause of AKI?

A

pre-renal + ATN (occurs when a pre-renal AKI isnt treated)

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18
Q

What are the different causes of pre-renal AKI?

A

Hypotension
Oedematous states
Selective renal ischaemia
Drugs affecting glomerular blood flow

19
Q

What drugs can cause prerenal AKI and how?

A

NSAIDs- ↓ afferent dilation

ACEi/ ARBs- ↓ efferent constriction

Diuretics- ↓ preload, affects tubular function

Calcineurin inhibitors- ↓ afferent dilation

20
Q

How can you distinguish between renal and pre-renal AKI?

A

RESPONDS TO RESTORATION OF CIRCULATING VOLUME (fluid resus) - this is because there is no structural damage unlike in renal (prlonged insult -> ATN)

21
Q

What causes pre-renal?

A

Generally = INTRINSIC DAMAGE

Vasculitis
Glomerular disease (GN-itides)
Interstitial disease (analgesics)
Tubular disease

22
Q

What are some tubular disease causes of renal AKI?

A

Ischaemia- MOST COMMON (ACN)

Endogenous toxins

MYOGLOBIN!

Immunoglobulins (paraprotein)

Exogenous toxins

Aminoglycosides

Amphotericin

Aciclovir

23
Q

What is the triad of rhabdomyolysis?

A

New onset AKI + bruising + dark urine

24
Q

What causes post-renal AKI?

A

Obstruction to urine flow

  • Intra-renal
  • Ureteric (bilateral)
  • Prostatic
  • Blocked urinary catheter

Severe obstruction -> hydronephrosis

25
Q

What happens in post-renal AKI depending on length of obstruction?

A

Immediate relief of obstruction:

  • Restores GFR
  • NO structural damage

Immediate relief of obstruction:

  • Restores GFR
  • NO structural damage
26
Q

What are the indications for emergency dialysis?

A
Acidosis -> metabolic acidosis
Electrolytes -> refractory hyperkalaemia
Intoxication -> lithium, aspirin
Oedema -> pulmonary oedema
Uraemia -> encephalopathy, pericarditis

AEIOU

27
Q

Which drugs / toxins are dialysable?

A

I STUMBLED

Isopropyl alcohol (antifreeze)

Salicylates
TheophyllineUraemia
Methanol
Barbiturates
Lithium
Ethylene glycol
Dabigatran
28
Q

What suggests a pathological response to AKI?

A

Hallmark of pathological response to AKI = imbalance between scarring and remodelling

Replacement of renal tissue with scar tissue causes chronic kidney disease.

29
Q

What is CKD?

A

Abnormalities of kidney function >3 months with implications for health.

GFR < 60 OR 1+ of:

  • Albuminuria/proteinuria
  • Urine sediment abnormalities (haematuria)
  • Electrolyte abnormalities
  • Histological abnormality
  • Structural abnormalities (on imaging)
  • History of kidney transplantation
30
Q

What are the different causes of CKD?

A
Diabetes mellitus (commonest)
Hypertension (2nd commonest)

Atherosclerotic renal disease

Obstructive or infective uropathy

Glomerular nephrotic and nephritic syndromes

Polycystic kidney disease

31
Q

What are the different stages of CKD?

A
G1 : GFR >90 +evidence of kidney damage
G2: GFR 60-89
G3: GFR 45-59
G4: GFR 15-29
G5: GFR <15
32
Q

What consequences of CKD affect the kidneys function to Excrete of waste

A

Uraemia + death

Uraemic cardiomyo/encephalopathy

33
Q

What consequences of CKD affect the kidneys function to Acid-base balance

A

Metabolic acidosis

34
Q

What consequences of CKD affect the kidneys function to electrolyte balance? ECG changes?

A

HyperK -> ECG: Tented T waves, broad QRS, flat/ loss of P waves, U waves

35
Q

What consequences of CKD affect the kidneys function to endocrine function?

A

Vit D hydroxylation:
Renal bone disease - E.g. Osteomalacia, osteitis fibrosa cystica, mixed osteodystrophy etc.

EPO production:
Anaemia- Normocytic, normochromic

RAAS:
CVD - Calcified vascular plaques

36
Q

How can problems in CKD due to issues with waste excretion be treated?

A

Dialysis

37
Q

How can problems in CKD due to issues with acid-base balance be treated?

A

PO Sodium bicarbonate

Dialysis

38
Q

How can problems in CKD due to issues with electrolyte balance be treated?

A
Calcium gluconate
Insulin (+ dextrose)
Nebulised salbutamol
Calcium resonium
Dialysis
39
Q

How can problems in CKD due to issues with endocrine function be treated?

A

Vit D:
PO4 limiting control: diet, PO4 binders
Vit D receptor activators: 1a-calcidol
PTH suppression: Cinacalcet

EPO:
Erythropoiesis stimulating agents: EPO alpha, EPO beta, Darbopoietin

RAAS:
Control risk factors, e.g. cholesterol, BP

40
Q

What does renal replacement therapy involve?

A

Dialysis - haemodialysis (3x w dialysis centre -av fistula / tesio line) + peritoneal (at home but infection risk - tenckoff catheter)

Transplant = only definitive mx - lasts 25y (needs lifelong immunosupressants)

41
Q

Indications for renal replacement therapy:

A

G5 CKD

Uraemia

42
Q

What are absolute CI for renal transplant?

A

Active HIV infection
Uncontrolled malignancy
Life expectancy <2yrs due to other cause

43
Q

DIfferences between AKI and CKD?

A

AKI:
Abrupt decline in GFR
Potentially reversible
Treatment: precise diagnosis and reversal

CKD:
Longstanding decline in GFR
Irreversible
Treatment: prevention of (1) progression and (2) complications