Introduction to kidney tests - Acid-Base metabolism Flashcards
What is GFR based on
- Based on serum-creatinine
Sensitivity of GFR to kidney damage
- Poor sensitivity for minor kidney damage
When does serum-creatinine start to rise
- 50% flomeruli lost
- Marker of progressive kidney damage
plasma creatinine sensitivity - GFR
- Creatinine has poor sensitivity in reference range (clinically silent stage)
Hierarchy of kidney function tests (inaccurate to accurate)
- S-urea
- 24h creatinine clearance
- S-creatinine
- eGFR estimated from s-Creatinine
- Direct GFR measurement used for research
What is CKD-EPI
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
How does diabetic ketoacidosis cause lower eGFR and increased s-creatinine and urea
- 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
Hyperkalaemia
- Decreased renal excretion
- Shift of intracellular potassium (due to insulin lack, acidosis, tissue catabolism)
- Total body potassium lower
Potassium influences
- 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
Anion gap
Consider un-measured anions
- Ketones
- Lactate
- Ethylene glycol
- Salicylate
Sodium - influences in DKA
Water retention - acute kidney injury
Excessive water intake - polydipsia
Artefactual - high glucose
AKI
- Urgent patient review
- GFR maybe compromised - low BP, shock (decreased blood flow to kidneys)
What should be considered in AKI
- Obstruction, hydration, infection
- Drugs - most important that maybe harmful to kidneys: ACEI/ARB, NSAID, Diuretics
Waste products that accumulate in AKI
- Creatinine, urea, acid
Management of DKA
- Probs dehydrated - fluid saline
- Review drugs: ACEI/ARB. NSAID, Diuretics
- BP
- Monitor urine output
- Saline + insulin
- Monitor Na, K, HCO3, eGFR, glucose
Complications of AKI
- Volume overload, raised K+, H+, PO4 Initial assessment: - Volume status - possible dehydration, CHF - s-K, HCO3, PO4, calcium, albumin - s-uric acid, magnesium - FBC
Glomerular disease
Manifest in a variety of ways ranging from:
- Aymptomatic urinary abnormalities
- Acute kidney injury (AKI)
- End-stage kidney disease
Glomerular disease clinical manifestations
- 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
Albuminuria - proteinuria
Change in clinical use
- From proteinuria
- To albuminuria
Urine albumin measurements improved
Urine protein measurements more variable
Diabetes kidney disease research used albuminuria
Identification of albuminuria
- Urine dipstick
- Quantitative measurement of urine albumin excretion
- Usually as ACR - albumin creatinine ratio
- ACR allows for differences in urine concentration
Persistent albuminuria categories urine ACR (mg/mmol) description and range
A1 - normal male<2.5 female<3.5
A2 - microalbuminuria male 2.5-25. female 3.5 - 35
A3 - macroalbuminuria male > 25 female > 35
eGFR categories (mL/min/1.73 min^2) Description and range
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
Diabetic nephropathy - albuminuria
Major clinical manifestation is albuminuria
Moderately increased albuminuria - predicts high risk for future nephropathy
Features of diabetic microvascular disease
- Nephropathy, retinopathy, neuropathy