Investigations
Your Organisational Guidance
ebpracticenet urges you to prioritise the following organisational guidance:
Chronisch nierlijden (multidisciplinaire aanpak)Published by: WORELLast published: 2017GPC pluridisciplinaire sur la néphropathie chronique (IRC)Published by: Groupe de travail Développement de recommandations de première ligneLast published: 20171st investigations to order
renal chemistry
Test
Includes sodium, potassium, chloride, bicarbonate, urea, creatinine, and glucose.
Serum creatinine alone is insufficient to determine chronic kidney disease (CKD) and may be falsely low in conditions of low muscle mass, as in older or malnourished people, or patients with liver failure.[72]
Normal creatinine in men is 70-120 micromol/L (0.8 to 1.4 mg/dL), and in women 50-97 micromol/L (0.6 to 1.1 mg/dL). However, there is significant variation due to calibration methods between laboratories.[2]
Electrolyte abnormalities may indicate an underlying cause of CKD, such as tubular disorders.[1] Adaptations in acid excretion by the kidneys initially prevent a fall in serum bicarbonate concentration, but as GFR declines, metabolic acidosis develops.[1]
Result
elevated serum creatinine; electrolyte abnormalities
estimation of GFR using serum creatinine
Test
A GFR estimating equation using serum creatinine is recommended for initial assessment.
Determines more accurately, by mathematical equations such as the chronic kidney disease (CKD) EPI equation, the GFR and the severity and stage of CKD.[73]
Interpretation of estimated GFR creatinine results should be individualised, including consideration of muscle mass. Reduced muscle mass may result in over-estimation of GFR; increased muscle mass may lead to under-estimation.[1]
In circumstances where creatinine-based eGFR is less accurate or uncertain (e.g., extremes of muscle mass, above-knee amputation, BMI >40 kg/m²), cystatin C should be measured, if available, and GFR estimated using a combination of creatinine and cystatin C, or cystatin alone.[1]
Laboratories should estimate GFR using an equation without a race variable.[54][55][56] National Kidney Foundation: eGFR calculator Opens in new window
Result
<60 mL/minute/1.73 m²
estimation of GFR using cystatin C with or without serum creatinine
Test
In circumstances where creatinine-based eGFR is less accurate or uncertain (e.g., extremes of muscle mass, above-knee amputation, BMI >40 kg/m²), cystatin C should be measured, if available, and GFR estimated using a combination of creatinine and cystatin C, or cystatin alone.[1]
Laboratories should estimate GFR using an equation without a race variable.[54][55][56] National Kidney Foundation: eGFR calculator Opens in new window
[ Glomerular Filtration Rate Estimation (eGFR) by CKD-EPI Equation with Cystatin C, without Race (2012) Opens in new window ] [ Glomerular Filtration Rate Estimation (eGFR) by CKD-EPI Equation with Creatinine and Cystatin C, without Race (2021) Opens in new window ]
Result
<60 mL/minute/1.73 m²
urinalysis
Test
Screening test to determine for pathological markers of kidney damage excreted in the urine.
Result
haematuria and/or proteinuria
urinary albumin
Test
Urinary albumin assessment is preferred to total urine protein, with calculation of the albumin to creatinine ratio (ACR) or the albumin excretion rate (AER).[1][54]
Albuminuria is both a diagnostic and a prognostic variable in the evaluation of patients with chronic kidney disease (CKD).[2][57]
Moderately increased albuminuria is a risk factor for the development of progressive CKD and coronary artery disease associated with diabetes and hypertension. Indicated in patients with diabetes and CKD if there was no evidence of proteinuria on urine dipstick.[74]
Result
moderately increased (AER 30-300 mg/24 hours; ACR 3-30 mg/mmol [30-300 mg/g])
renal ultrasound
Test
Used to evaluate kidney size, mass lesions, urinary tract obstruction, and, with a duplex examination, renal arterial flow.[59][60]
Ultrasound is indicated in patients with a history of kidney stones or obstruction, renal artery stenosis, frequent urinary tract infections, or a family history of autosomal dominant polycystic kidney disease.[59]
Chronicity (duration of at least 3 months) may be established by imaging findings (e.g., reduced kidney size and cortical thickness).[1]
Result
small kidney size; presence of obstruction/hydronephrosis; kidney stones
Investigations to consider
kidney biopsy
Test
Helps to determine pathological diagnosis of chronic kidney disease in glomerular nephrotic and nephritic syndromes, or in people with diabetes with atypical presentations such as rapidly progressive kidney failure.
Also essential in determining whether pathological lesions are due to infection (e.g., hepatitis B and C, syphilis, and streptococcal pharyngitis).
Chronicity (duration of at least 3 months) may be established by pathological findings (e.g., fibrosis and atrophy).[1]
Provides insight into treatment options based on severity or chronicity of scarring of glomeruli and interstitium.
Result
variable depending on aetiology
plain abdominal radiograph
diabetes screen
Result
hyperglycaemia
mineral bone disorder assessment
Test
Assessment for hyperparathyroidism includes measurement of calcium, phosphorus, and intact parathyroid hormone (PTH) levels.[62]
Frequency of monitoring depends on stage, with more frequent testing as chronic kidney disease stage increases.
Result
low serum calcium; elevated serum phosphorus; elevated serum intact PTH
anaemia assessment
Test
Full blood count (FBC) and iron studies are recommended to assess for anaemia.
FBC should include haemoglobin concentration, red cell indices, white blood cell count and differential, and platelet count.[61]
Iron studies include serum ferritin and serum transferrin saturation (TSAT).
Measurement of vitamin B12 and folate may also be considered to assess for deficiencies.
Result
low haemoglobin; serum ferritin and TSAT levels will depend on presence of iron deficiency; serum vitamin B12 may be low; serum folate may be low
Emerging tests
genetic testing
Test
May be useful in establishing cause and, in some cases, informing management.[1][64][65] Actionable genes in kidney diseases have been suggested based on expert consensus.[1][20]
Result
positive for genetic variant in chronic kidney disease-related gene, e.g., APOL1, COL4A3, COL4A4, COL4A5, NPHS1, UMOD, HNF1B, PKD1, PKD2
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