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302/308 > Introduction to kidney tests - Acid-Base metabolism > Flashcards

Introduction to kidney tests - Acid-Base metabolism Flashcards

1
Q

What is GFR based on

A
  • Based on serum-creatinine
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2
Q

Sensitivity of GFR to kidney damage

A
  • Poor sensitivity for minor kidney damage
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3
Q

When does serum-creatinine start to rise

A
  • 50% flomeruli lost

- Marker of progressive kidney damage

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4
Q

plasma creatinine sensitivity - GFR

A
  • Creatinine has poor sensitivity in reference range (clinically silent stage)
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5
Q

Hierarchy of kidney function tests (inaccurate to accurate)

A
  • S-urea
  • 24h creatinine clearance
  • S-creatinine
  • eGFR estimated from s-Creatinine
  • Direct GFR measurement used for research
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6
Q

What is CKD-EPI

A

CKD-EPI creatinine equation is based on the same four variables as the MDRD Study equation, but uses a 2-slope spline to model the relationship between estimated GFR and serum creatinine, and a different relationship for age, sex and race

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7
Q

How does diabetic ketoacidosis cause lower eGFR and increased s-creatinine and urea

A
  • Glycosuria causes an osmotic diuresis
  • Decrease in plasma volume
  • Dehydrated from loss of fluid in urine
  • Due to osmotic diuresis caused by urine glucose
  • Decreased blood flow to kidneys
  • Decreased glomerular filtration
  • eGFR decreased
  • s-creatinine and urea increased
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8
Q

Hyperkalaemia

A
  • Decreased renal excretion
  • Shift of intracellular potassium (due to insulin lack, acidosis, tissue catabolism)
  • Total body potassium lower
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9
Q

Potassium influences

A
  • Decreased renal excretion
  • Re-distribution (shift of intracellular potassium), metabolic acidosis, extracellular h+ exchanged for intracellular k+, tissue catabolism
  • Serum K+ is high but total body K+ is low
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10
Q

Anion gap

A

Consider un-measured anions

  • Ketones
  • Lactate
  • Ethylene glycol
  • Salicylate
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11
Q

Sodium - influences in DKA

A

Water retention - acute kidney injury
Excessive water intake - polydipsia
Artefactual - high glucose

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12
Q

AKI

A
  • Urgent patient review

- GFR maybe compromised - low BP, shock (decreased blood flow to kidneys)

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13
Q

What should be considered in AKI

A
  • Obstruction, hydration, infection

- Drugs - most important that maybe harmful to kidneys: ACEI/ARB, NSAID, Diuretics

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14
Q

Waste products that accumulate in AKI

A
  • Creatinine, urea, acid
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15
Q

Management of DKA

A
  • Probs dehydrated - fluid saline
  • Review drugs: ACEI/ARB. NSAID, Diuretics
  • BP
  • Monitor urine output
  • Saline + insulin
  • Monitor Na, K, HCO3, eGFR, glucose
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16
Q

Complications of AKI

A 
- Volume overload, raised K+, H+, PO4  
Initial assessment: 
- Volume status - possible dehydration, CHF 
- s-K, HCO3, PO4, calcium, albumin 
- s-uric acid, magnesium 
- FBC
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17
Q

Glomerular disease

A

Manifest in a variety of ways ranging from:

  • Aymptomatic urinary abnormalities
  • Acute kidney injury (AKI)
  • End-stage kidney disease
18
Q

Glomerular disease clinical manifestations

A
  • Glomerular basement membrane (GBM)
  • Barrier to the passage of macromolecules (both size- and charge-selective)
    Clinical manifestations:
  • Hematuria and/or albuminuria/proteinuria
  • Kidney insufficiency
  • Hypertension
  • Oedema etc
19
Q

Albuminuria - proteinuria

A

Change in clinical use

  • From proteinuria
  • To albuminuria

Urine albumin measurements improved
Urine protein measurements more variable
Diabetes kidney disease research used albuminuria

20
Q

Identification of albuminuria

A
  • Urine dipstick
  • Quantitative measurement of urine albumin excretion
  • Usually as ACR - albumin creatinine ratio
  • ACR allows for differences in urine concentration
21
Q

Persistent albuminuria categories urine ACR (mg/mmol) description and range

A

A1 - normal male<2.5 female<3.5
A2 - microalbuminuria male 2.5-25. female 3.5 - 35
A3 - macroalbuminuria male > 25 female > 35

22
Q

eGFR categories (mL/min/1.73 min^2) Description and range

A

G1 Normal or high >90
G2 Mildly decreased 60-89
G3a Mildly to moderately decreased 45-59
G3b Moderately to severely decreased 30-44
G4 Severely decreased 15-29
G5 Kidney failure <15

23
Q

Diabetic nephropathy - albuminuria

A

Major clinical manifestation is albuminuria

Moderately increased albuminuria - predicts high risk for future nephropathy

24
Q

Features of diabetic microvascular disease

A
  • Nephropathy, retinopathy, neuropathy
25
Q

Risk factor for diabetic microvascular disease

A
  • Hypertension
26
Q

Nephrotic syndrome

A 
Urine albumin loss 
- Low serum albumin 
Low oncotic pressure stimulates 
- Liver albumin synthesis 
- also lipoprotein synthesis 
- Hypercholesterolemia and hypertriglyceridemia 
Also synthesis clotting factors 
- thrombotic disease
27
Q

What is nephrotic syndrome defined by

A
  • Heavy albuminuria ACR > 250 mg/mmol
  • ACR > 70 mg/mmol = 1g protein/24h
  • Protein excretion > 3.5g/24h
  • Low serum albumin <30 g/L
28
Q

What is ACR

A

Urine albumin to creatinine ratio, also known as urine microalbumin, helps identify kidney disease that can occur as a complication of diabetes

29
Q

Main way in which nitrogenous end products are excreted

A
  • The kidneys are the main route by which nitrogenous end products are excreted
  • The loss of renal function is characterised by the increase of nitrogenous waste products in the blood
  • High protein intake will lead to increase of production of urea which must be filtered through the kidneys
30
Q

Urea origin

A

Protein - amino acids - urea

Alanine -ALT-> urea + pyruvate
Aspartate -AST-> urea + oxalo-acetate -> glucose

ALT - Alanine transaminase
AST - Aspartate transaminase
Enhanced by stress - cortisol (glucocorticoid)

31
Q

Creatinine origin

A 
Muscle mass - creatine - creatinine 
Creatine + ATP -ck-> Creatine-P + ADP 
Creatinine -constant decay-> creatinine 
CK - creatine kinase 
creatine-p - high energy phosphate
32
Q

Creatine kinase - CK

A
  • Levels related to muscle mass
  • Women < men
  • Children < adults
  • Black africans - greater muscle mass
  • After physical exertion, increase - slight-moderate
  • If raised, repeat with 3 days with no exertion
33
Q

Kidney stones - types of stones

A
  • 80pc are composed of calcium salts
  • Calcium oxalate - mc
  • Calcium phosphate
  • Uric acid
  • Ammonium - infection
  • Cysteine - inborn error
  • Xanthine - very rare - inborn error
34
Q

Causes of kidney stones - calcium related

A

Calcium

  • Primary hyperparathyroidism
  • Renal tubular acidosis - distal
  • High sodium intake

Oxalate(hyperoxaluria)

  • Low calcium/high ovalate diet
  • Primary hyperoxaluria

Low urine citrate - Rx potassium citrate

35
Q

Kidney stone causes - uric acid

A 
Uric acid 
- high purine diet
-Alcohol. Obesity, drugs
Ammonium – infection
Cystine – inborn error
Xanthine – very rare – inborn error
36
Q

Kidney stones - investigations - serum

A

Fluid intake especially Hot environment
Radiology – residual stones, nephrocalcinosis
Urine culture
Urine pH
Serum sodium, potassium, chloride, bicarbonate, creatinine, calcium, albumin, phosphate, alkaline phosphatase, uric acid, vitamin D, PTH,

37
Q

Kidney stones - investigations - urine

A
  • Volume, creatinine: fluid intake
  • Sodium - increases u-calcium
  • Calcium
  • Phosphate
  • Oxalate - diet, inborn error -
  • Citrate - helps solubilise calcium
  • Uric acid - xanthine, cystine (transport defect dibasic aa)
  • Albumin - rare
38
Q

RTA - renal tubular acidosis - distal

A
  • Nephrocalcinosis/kidney stones

- Bone disease in older age

39
Q

Diagnosis RTA

A
  • s-potassium usually low
  • Metabolic acidosis - normal anion gap
  • Increased s-chloride
  • Inappropriately alkaline urine
  • Clinical context
  • Urine pH, citrate, bicarbonate
  • Urine acidification test
40
Q

Treatment of RTA - distal

A
  • Rx - potassium citrate

- correct acidosis, potassium

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