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
Risk factor for diabetic microvascular disease
- Hypertension
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
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
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
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
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)
Creatinine origin
Muscle mass - creatine - creatinine Creatine + ATP -ck-> Creatine-P + ADP Creatinine -constant decay-> creatinine CK - creatine kinase creatine-p - high energy phosphate
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
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
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
Kidney stone causes - uric acid
Uric acid - high purine diet -Alcohol. Obesity, drugs Ammonium – infection Cystine – inborn error Xanthine – very rare – inborn error
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,
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
RTA - renal tubular acidosis - distal
- Nephrocalcinosis/kidney stones
- Bone disease in older age
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
Treatment of RTA - distal
- Rx - potassium citrate
- correct acidosis, potassium
