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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: 2017

A significant proportion of people with chronic kidney disease (CKD) are asymptomatic, and the diagnosis relies on pathological evidence of kidney damage such as haematuria and/or proteinuria, or laboratory evidence of a reduction in the glomerular filtration rate (GFR) with an elevated serum creatinine.

History

Signs and symptoms vary with stage of disease. They are often vague, and commonly include fatigue (which may be related to uraemia or the anaemia associated with CKD), nausea, and possibly the development of oedema.[49][50]

Uraemic illness is due largely to the accumulation of organic waste products that are normally cleared by the kidneys, and symptoms may be present to some degree in the early stages of kidney failure.[49] As kidney failure progresses to the more advanced stages of uraemia, patients will often describe anorexia, nausea, vomiting, restless legs, pruritus, fatigue, and feeling generally ill.[51]

Changes in the frequency of urination (e.g., polyuria, oliguria, or nocturia) and appearance of urine are sometimes reported. Patients may describe their urine as foamy if significant proteinuria is present, or cola- or tea-coloured in the setting of haematuria.[2]​ If patients begin to have a lack of urine production, resulting fluid overload may be present with dyspnoea and orthopnoea due to pulmonary oedema. Cognition may be affected in all stages of CKD.[2] In the most advanced stages of uraemia, patients may present with seizures or coma.[52]

Examination

Signs of CKD include hypertension, peripheral oedema (due to sodium retention and exacerbated by hypoalbuminaemia), and pallor due to anaemia.[2] In patients with fluid overload/congestion, leg oedema is usually bilateral and pitting; additional signs of fluid overload include pulmonary crepitations, dullness to percussion and decreased air entry in lung bases, wheezing, elevated jugular venous pressure, and ascites.

Assess for end-organ damage

Physical examination includes assessment of end-organ damage associated with causative disease states such as diabetes or hypertension. A fundoscopic eye examination is critical for the diagnosis of diabetic or hypertensive retinopathy as evidence of microvascular damage that has probably occurred in the kidney, resulting in CKD.

In men, a rectal examination for prostatic enlargement or for the diagnosis of prostate nodules can be helpful in determining a diagnosis of obstructive uropathy. In glomerular nephrotic and nephritic syndromes, the signs and symptoms of CKD may present more acutely with accelerated hypertension, peri-orbital and peripheral oedema, rashes, or arthritis on musculoskeletal examination for patients with autoimmune disorders.[53]

Initial investigations

Most people are unaware that they have CKD and are informed only after abnormalities are discovered by blood and/or urine tests.[2]

The first diagnostic tests to order are serum creatinine (as part of renal chemistry), estimated GFR (eGFR), and urinalysis to assess for haematuria and proteinuria.[1][2]

Interpretation of eGFR creatinine results should be individualised, including consideration of muscle mass. 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 Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) Equation with Creatinine, without Race (2021) Opens in new window ]

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 CKD.[2][57]

Nephrotic level proteinuria is conventionally defined as >3.5 g proteinuria per 24 hours.[58]

Renal ultrasound may be 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 review of history, past or repeat measurements, imaging findings (e.g., reduced kidney size and cortical thickness), or pathological findings (e.g., fibrosis and atrophy).[1]

Additional investigations

Comorbidities of CKD may not be identified unless intentionally assessed; therefore, comprehensive examination is important.

If not already known, consider screening for diabetes. See Type 2 diabetes in adults.

Anaemia and secondary hyperparathyroidism are commonly seen in patients with later stages of CKD (GFR category G3-G5 [eGFR <15-59 mL/minute/1.73 m²]). Full blood count (including haemoglobin concentration, red cell indices, white blood cell count and differential, and platelet count) and other tests for anaemia (iron studies, vitamin B12) are recommended.[61]

Assessment for hyperparathyroidism includes measurement of calcium, phosphorus, and intact parathyroid hormone (PTH) levels.[62]​ Frequency of monitoring for anaemia and secondary hyperparathyroidism depends on stage, with more frequent testing as CKD stage increases.

Biopsy and further imaging studies

Kidney biopsies are performed in a minority of patients with CKD to help evaluate cause and guide treatment.[1]

A kidney biopsy to determine a pathological diagnosis is indicated if a glomerular nephrotic or nephritic syndrome is suspected, or in people with diabetes with atypical presentations such as rapidly progressive kidney failure. Nephrotic syndrome may be suggested by proteinuria, and both nephritic and nephrotic syndromes may be suggested by severe presenting symptoms (accelerated hypertension, periorbital and peripheral oedema) or with symptoms of underlying autoimmune diseases (rashes or arthritis). Certain infections, such as hepatitis B and C, syphilis, and streptococcal pharyngitis, are associated with glomerular disorders.[63]​ A kidney biopsy is critical in these cases to determine the correct diagnosis.[58]

Imaging of the genitourinary tract may be helpful in the evaluation of a patient with CKD. A plain abdominal x-ray is a non-specific test that may aid in the detection of calcium-containing kidney stones. Other radiological tests are not used routinely.​[59][60]

Genetic testing is not carried out routinely, but may be useful in some cases to establish cause and inform management.[1][64][65]​​​​​ Actionable genes in kidney diseases have been suggested by expert consensus.[1][20]

Venepuncture and phlebotomy animated demonstration
Venepuncture and phlebotomy animated demonstration

How to take a venous blood sample from the antecubital fossa using a vacuum needle.

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