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
Risk factor for diabetic microvascular disease
- Hypertension
26
Nephrotic syndrome
``` 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
What is nephrotic syndrome defined by
- 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
What is ACR
Urine albumin to creatinine ratio, also known as urine microalbumin, helps identify kidney disease that can occur as a complication of diabetes
29
Main way in which nitrogenous end products are excreted
- 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
Urea origin
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
Creatinine origin
``` Muscle mass - creatine - creatinine Creatine + ATP -ck-> Creatine-P + ADP Creatinine -constant decay-> creatinine CK - creatine kinase creatine-p - high energy phosphate ```
32
Creatine kinase - CK
- 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
Kidney stones - types of stones
- 80pc are composed of calcium salts - Calcium oxalate - mc - Calcium phosphate - Uric acid - Ammonium - infection - Cysteine - inborn error - Xanthine - very rare - inborn error
34
Causes of kidney stones - calcium related
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
Kidney stone causes - uric acid
``` Uric acid - high purine diet -Alcohol. Obesity, drugs Ammonium – infection Cystine – inborn error Xanthine – very rare – inborn error ```
36
Kidney stones - investigations - serum
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
Kidney stones - investigations - urine
- 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
RTA - renal tubular acidosis - distal
- Nephrocalcinosis/kidney stones | - Bone disease in older age
39
Diagnosis RTA
- 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
Treatment of RTA - distal
- Rx - potassium citrate | - correct acidosis, potassium