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MSC: Disease of major orgns > Biochemical Assessment of Kidney Function and Damage > Flashcards

Biochemical Assessment of Kidney Function and Damage Flashcards

1
Q

What is the function of a nephron?

A
  • NEPHRON = basic functional unit responsible for filtration of plasma and production of urine.
  • There are around 1 000 000 nephrons per kidney
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2
Q

What are major functions of the kidney?

A
  • Nitrogen Excretion​
  • Fluid (blood volume) Regulation
  • Electrolyte regulation
  • Acid-Base regulation
  • Calcium Metabolism
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3
Q

How does the kidney carry Red Blood Cell Production?

A
  • Erythropoetin is secreted mainly by the peri-tubular cells of the renal cortex. It is required to stimulate rbc production.
  • Levels of EPO are increased when O2 delivery to the kidney is low.
  • EPO stimulate bone marrow to make more rbc.
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4
Q

How is nitrogen excretion carried?

A
  • Urea is major waste product. Filtered by the glomerulus.
  • Some urea diffuses back into kidney from filtrate.
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5
Q

How does the kidney regulate fluid?

A
  • Dehydration may be significant enough to reduce blood pressure – reduces GFR and fluid loss.
  • RENIN secretion results in ANGIOTENSIN II production
  • ALDOSTERONE increases Na+ reabsorption (water follows).
  • ADH increases aquaporins in collecting duct
  • BNP counteracts this – prevents fluid overload by reducing renin secretion and causing vasodilation to reduce blood pressure.
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6
Q

How does Electrolyte regulation take place?

A
  • PTH regulates Ca2+ reabsorption and PO4- excretion
  • Excretion of Mg2+ and other ions is largely passive – more being filtered = more being excreted
  • In steady state, K+ is inversely related to Na+ (Aldosterone activity)
  • Renal Failure – limited capacity to excrete potassium
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7
Q

How does ACID-BASE regulation take place?

A
  • Metabolic process result in acid production (phosphoric, sulfuric and carbonic – CO2 is excreted via lungs).
  • Carbonic Anhydrase is key to HCO3-
  • Reabsorption in the PCT.
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8
Q

How is Calcium metabolism regulated?

A
  • Cells in the kidney respond to PTH by increasing 1 α-hydroxylase activity
  • Required to form 1, 25 (OH) Vit D (active form).
  • This is required for normal bone metabolism and absorption of Ca2+ and PO4-
  • PTH acts on the DCT to increase phosphate excretion and increase caclium reabsorption.
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9
Q

What is the effect of Renal disease on the glomerulus?

A

Reduced filtration

  • Reduced urine volume
  • Increased plasma creatinine /urea
  • Hyperkalaemia
  • Hyperphosphataemia
  • Metabolic acidosis

Damage to glomerular membrane

  • Proteinuria – large proteins
  • Haematuria
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10
Q

What is the effect of renal disease on tubular?

A

Reduced reabsorption (general or specific inherited conditions).

  • Polyuria, low urine osmolality
  • Metabolic acidosis
  • Proteinuria - small proteins (ß2 microglobulin, amino acids)
  • Glycosuria
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11
Q

What is the effect of renal disease on hormonal disease?

A
  • Anaemia
  • Hypocalcaemia
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12
Q

What is the clinical presentation of Renal Disease?

A

Uraemic Syndrome

  • Dermatological: Pruritus, Pigmentation, Slow wound healing
  • Gastrointestinal: Vomiting, Nausea, Anorexia
  • Genitourinary: Impotence, Polyuria/Nocturia
  • Neurological: Lethargy, Headache, Peripheral neuropathy, Muscle weakness
  • Immunological: Increased susceptibility to infection
  • Cardiovascular: Hypertension, Percarditis, CCF, Anaemia
  • Skeletal: Renal osteodystrophy, Stunted growth
  • Azotaemia – increased urea
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13
Q

What is Biochemical Assessment useful for?

A
  • Detection and staging of renal disease
  • Identification and management of biochemical complications.
  • Prognosis
  • Monitoring disease progression
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14
Q

What is the use of kidney test?

A

Tests for Glomerular function

  • Ability to remove waste products
  • Integrity of glomerular membrane and ability to prevent large particles entering the filtrate

Tests for Tubular function

  • Ability to adjust Na+, K+, H+ ions, water composition of filtrate & reabsorb small proteins, amino acids & glucose

Tests for hormonal production

  • Vitamin D, erythropoietin

Urinalysis

  • Detect disease
  • Proteinuria
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15
Q

What is Albuminuria and Microalbuminuria?

A

MICROALBUMINURIA: Predictor of CVD, increased risk of diabetic nephropathy

  • 24 hour urine sample 30 – 300 mg/L albumin (not detectable using a dipstick, measured using turbidometric immuoassay)

ALBUMINURIA

  • > 300 mg
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16
Q

What is Albumin:Creatinie Ratio?

A

Used to screen diabetic patients, can use random urine sample.

  • > 2.5 mg/mmol (male), > 3.5 mg/mmol (female)
  • ACR 3 – 70 mg/mmol – confirm with early morning repeat
  • ACR > 70 mg/mmol – no repeat required

MACR has high intraindividual variation (60 – 80 % CV)

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17
Q

What is Clinical Proteinuria?

A

Clinical Proteinuria:

  • > 500 mg/24 hour
  • +ve dipstick
  • Increased ACR or PCR
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18
Q

What is overflow, tubular and Glomerular Proteinuria?

A

OVERFLOW (Mw ≤ Albumin)

  • Abnormal small proteins over flow into urine (eg. multiple myeloma)
  • Kappa/lambda light chains (Bence Jones Proteins)

TUBULAR

  • Decreased reabsorption of filtered proteins
  • N-Acetyl Glucosaminidase (NAG) – released from lysed tubular cells

GLOMERULAR (Mw ≥ Albumin)

  • Increased glomerular permeability – larger proteins present
  • IgG, Transferrin, retinol binding protein, α1-macroglobulin
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19
Q

How is proteinuria, severe proteinuria, heavy proteinuria and nephrotic syndrome catgorised?

A
20
Q

What is clearance?

A
  • Clearance (ability to remove waste products)
  • The volume of plasma that is filtered by the kidneys and from which a substance is completely cleared per unit of time
21
Q

What is the equation?

A

Clearance (mL.min<span>-1​</span> )= Urine Marker concentration (µmol/L) x Urine Volume (mL) / Plasma Marker concentration (µmol/L) x time (min)

22
Q

What makes an ideal marker of GFR?

A

Ideal Marker (clearance = GFR)

  • Stable plasma concentration
  • Freely filtered at the glomerulus
  • Not secreted or reabsorbed by renal tubular cells
  • Renal excretion ONLY (i.e. not metabolised by liver)
  • Easy and cheap to measure
23
Q

How are exogenous markers delivered?

A
  • Bolus injection: disappearance from plasma
  • IV infusion: clearance
24
Q

What are some exogenous markers of GFR?

A

Inulin Clearance - gold standard.

  • Difficult and expensive to measure

51Cr-EDTA - clinical standard

  • Difficult and expensive to measure, not available for clinical use in the UK beyond March 2019
  • IOHEXOL – non-ionic contrast media containing iodine.

99mTc-DTPA (diethylenetriaminepentacetic acid)

  • Difficult and expensive to measure
  • Allows imaging of kidney

P-aminohippuric acid

  • Determines renal plasma flow
  • Completely cleared in single passage through kidney
25
Q

What are some endogenous markers of GFR?

A
  • Urea
  • Creatinine
  • Cystatin C
26
Q

What are characterisitics of Urea?

A
  • End product of nitrogenous compound metabolism (esp amino acids)
  • Freely filtered at glomerulus
  • Quick, cheap & convenient
  • NOT steady plasma levels: effected by diet and protein catabolism e.g. raised in GI bleed
  • Low in liver disease
  • Some passive reabsorption in renal tubules
  • Under estimation of GFR
27
Q

What are characterisitics of Creatinine?

A
  • From breakdown of skeletal muscle cells.
  • Normally filtered and excreted in the urine.
  • Small amount secreted by PCT – creatinine slightly overestimates GFR
  • Quick, cheap & convenient
  • Dependent on body mass /ethnicity/diet
  • Assay Interferences with Jaffe method (ketones, bilirubin & glucose). Can use Jaffe kinetic method to reduce interference.
  • Enzymatic method (creatinase and creatininase coupled method)

N.B. GFR falls to <50ml/min before creatinine rises

28
Q

What are characteristics of Cystatin C?

A
  • Protein produced stadily by all nucleated cells
  • Protease inhibitor: Lysosomal proteinases and extracellular cysteine proteinases
  • Small MW 13kDa that is freely filtered by glomerulues
  • Serum levels independant of age, muscle mass, weight, height and sex
  • Expensive assay
29
Q

How is Cystatin C affected by thyroid disease?

A
  • Hypothyroid - Lower serum levels overestimates GFR
  • Hyperthyroid - Higher serum levels underestimates GFR
30
Q

How do you collect 24hr urine?

A

Day 1

  • 8am empty bladder (discard output)
  • Commence 24h urine collection
  • All urine now passed until 8am next day must be collected into container.

Day 2

  • 8am collect final urine output into container

Collect blood sample with 24 hr period

31
Q

What is the equation of Creatinine Clearance?

A

Creatinine clearance (mL/min) = [Creat]u x V (mL/min) / [Creat]p

32
Q

What is the eGFR (Estimated Glomerular Filtration rate)?

A

Calculated result based on [Creatinine] in plasma/serum

  • Creatinine-based eGFR
  • Should use CKD-EPI equation
  • When Cystatin C requested, should use CKD-EPI cystatin C equation
  • Calculated eGFR is added to all U&E profiles
33
Q

When is eGFR not validated?

A

NOT validated for use in

  • Children
  • Acute kidney injury
  • Amputees
  • Pregnancy
  • Malnourished
  • Odematous
  • Muscle wasting
34
Q

What are variables for eGFR?

A
  • creatinine
  • age
  • sex
  • ethnicity
35
Q

What are features of MDRD equation?

A
  • Study only included patients with known renal failure.
  • Under-estimates GFR (>60 mL/min).
  • The normal kidney patients have measured GFR that is slightly higher than the estimated GFR - MDRD equation underestimates GFR in persons with normal kidney function
36
Q

What are features of CKD-EPI?

A
  • Study used CKD and normal renal function patients
  • More accurate than MDRD esp when GFR >60 mL/min
37
Q

How is Tubular function assessed?

A

-Ability to excrete / retain water

  • Determined by ability to concentrate / dilute urine
  • Tests: Urine sodium, osmolality and volume/Serum sodium & osmolality/Fluid deprivation test

-Ability to maintain acid-base balance

  • Usually see metabolic acidosis
  • Renal tubular acidosis
  • Urine / blood pH & Anion gap& Serum bicarbonate

-Ability to maintain electrolyte balance

  • Serum sodium & potassium
  • Random Urine sodium & potassium
  • FRACTIONAL EXCRETION: Relative to creatinine, Excretion over same time and volume

-Ability to reabsorb small proteins, amino acids & glucose

  • Tubular proteinuria – low molecular weight proteins (α1-microglobin, Retinol binding protein, RBP & β2-microglobin)
  • Serum and urine aminoacids. (specific defects – aminoaciduria).
  • Urine glucose – renal threshold = 11mmol/L
38
Q

What is Fanconi syndrome and causes?

A
  • Decreased reabsorption of solutes by PCT.
  • Hypophosphataemia, Glycosuria, Hypouricaemia, aminoaciduria, low Mw proteinuria, Type 2 RTA

Caused by: cystinosis, Wilsons, Gentamicin, Cisplatin, heavy metal intoxication

39
Q

What is the equation for Fractional Excretion?

A

FENa = 100 x(Urine [x] x Plasma [creat]) / (Plasma [x] x Urine [creat])

40
Q

How are hormone production assessed?

A

-Ability to produce active Vitamin D (1,25 (OH) Vit D)

  • PTH
  • Serum adjusted calcium

-Ability to secrete erythropoetin

  • EPO and FBC
41
Q

What is Renal Osteodystrophy?

A
  • Seen in dialysis patients/ CKD
  • Hypocalcaemia and hyperphosphataemia
  • Secondary hyperparathyroidism
42
Q

What are some microscopy in urinalysis?

A
  • Red cell
  • Granular (cell debris)
  • Hyaline (Tamm-Horsfall protein)
  • White cell
43
Q

What are types of Renal Stones?

A

Calcium oxalate ± phosphate (hypercalcaemia) - 67%

Triple phosphate/struvite (Mg, Ca, NH4) (UTI) - 12%

Calcium phosphate (alkaline urine) - 8%)

Uric acid (purine metabolism) - 8%

Cystine (cystinuria) - 1-2%

44
Q

How are Renal Stones induced?

A
  • Increased concentration of urinary constituents above natural solubility
  • Lack of physiological inhibitors of stone growth (e.g mucopolysaccarides,citrate & pyrophosphate)
  • Changes in urine pH (alkaline pH favours NH4 ion formation → precipitate)
  • Seeding (i.e stone formed can be different to the nucleus that the stone started from & colonisation of bacteria can accelerate stone growth)
45
Q

How is Urinalysis used for Renal Stones?

A
  • Calcium
  • Phosphate
  • Urate
  • Oxalate
  • Cystine
  • pH
  • Sodium
  • Magnesium
  • Citrate
  • Microbiology
  • Stone Analysis
46
Q

What are novel biomarkers of Renal Function?

A
  • Neutrophil Gelatinase-Associated Lipocalin (NGAL) – 25 kDa epithelial protein, covalently bound to gelatinase from human neutrophils. Forms a complex with MMP-9
  • Kidney Injury Molecule 1 (KIM-1) – type 1 transmembrane protein, with immunoglobulin and mucin domains. Expression is upregulated in PCT post injury.
  • Liver Fatty Acid Binding Protein (L-FABP) – localises in PCT and is excreted in urine in response to oxidative stress
  • Tissue Inhibitor Metalloproteinase 2 (TIMP2) and Insulin-Like Growth Factor Binding Protein 7 (IGFBP7) - Nephrocheck (Astute Medical [TIMP2] x [IGFBP7] = < 0.3

MSC: Disease of major orgns (23 decks)

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