Chronic kidney disease
Complications
Anaemia of chronic kidney disease (CKD) is due to a deficiency of erythropoietin as the glomerular filtration rate (GFR) declines.
Anaemia is typically identified in patients with GFR category G3a/G3b CKD. Patients should be screened with haemoglobin (Hb) measurement at least annually for patients with GFR category G3 disease and twice a year for patients with G4 to G5 disease not on dialysis.[61][150]
Treatment of anaemia with the use of an erythropoietin-stimulating agent is recommended for patients with CKD after other causes of anaemia have been excluded.[61]
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Erythropoietin-stimulating agents may be initiated if the Hb level falls to <100 g/L (<10 g/dL) and the patient has signs and symptoms of anaemia. A target Hb of 100-115 g/L (10.0 to 11.5 g/dL) is appropriate, as normalisation of Hb (>130 g/L [>13 g/dL]) has resulted in increased risk for death and cardiovascular disease in this population.[140][141][142] For most patients, Hb concentration should be maintained at <115 g/L (<11.5 g/dL) with erythropoietin-stimulating agents to manage anaemia.[61][143][144]
If the patient is iron-deficient, oral or intravenous supplementation should also be prescribed.[149]
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Hyperparathyroidism may be caused by low calcium levels and phosphorus retention, attributable to 1,25 vitamin D deficiency and declining kidney function.
Severe hyperparathyroidism and hyperphosphataemia increase risk for death, cardiovascular disease, and vascular calcification in patients with chronic kidney disease (CKD).[62][Evidência C]
Patients with GFR category G3 to G5 CKD should be routinely monitored for hyperparathyroidism and treatments based on serial assessments of phosphorus, calcium, and parathyroid hormone levels, considered together.[62]
25-OH vitamin D should be monitored and treatment initiated if the serum level of 25-OH vitamin D is <75 nanomol/L (<30 nanograms/mL).[151][152]
The initial approach to managing secondary hyperparathyroidism is to maintain serum calcium and phosphorus levels in the normal range with dietary restriction and/or phosphate-binding drugs.[62]
Chronic kidney disease (CKD) is a risk factor for cardiovascular disease independent of comorbidities such as diabetes, hypertension, and dyslipidaemia. Cardiovascular disease is the leading cause of death for these patients.[196][197][198] The majority of patients with CKD will die prior to requiring kidney replacement therapy.[191]
The goal in treatment of cardiovascular disease in patients with CKD is early recognition and risk factor modification, including lipid therapy, optimisation of blood pressure and glycaemic control, tobacco cessation, and aspirin use.[199][200]
There is a high prevalence of atrial fibrillation in people with chronic kidney disease (CKD); it may be asymptomatic. The same principles of diagnosis and management apply to those with and without CKD.
Kidney Disease: Improving Global Outcomes (KDIGO) guidelines recommend considering opportunistic pulse-based screening (e.g., when taking blood pressure) in people with CKD, followed by a 12-lead ECG if an irregularly irregular pulse is identified.[1]
Direct oral anticoagulants (DOACs) are preferred over warfarin for thromboprophylaxis in patients with G1 to G4 CKD.[1]
As the glomerular filtration rate falls, patients develop anorexia, nausea, and vomiting, and are at risk for protein malnutrition.
Guidelines suggest that patients at risk of chronic kidney disease progression should avoid high protein intake, and that those with G3 or higher category disease with diabetes (not on dialysis) should aim for a target protein intake of 0.8 g/kg body weight per day.[80][92] Severe protein restriction should not be recommended until late GFR category G4 or G5 disease as a management strategy to delay the initiation of dialysis.[171]
In patients on dialysis, a dietary protein intake of 1.0 to 1.2 g/kg body weight daily is recommended to maintain a stable nutritional status.[195]
Hyperkalaemia is more common in patients who have chronic kidney disease with oliguria, resistant or deficient aldosterone state, or co-existing metabolic acidosis. Most patients are asymptomatic, but some may present with muscle weakness.
The hallmark for the severity of hyperkalaemia is identification of cardiac disturbances on an ECG with peaked T waves, prolongation of the conduction system, sine wave, or asystole. Hyperkalaemia associated with cardiac conduction disturbances is a medical emergency and is treated with intravenous calcium; drugs to shift potassium into the cells, such as insulin and dextrose; beta-agonists and the focused removal of potassium from the body with loop diuretics, if kidney function is intact; oral potassium binders (e.g., sodium polystyrene sulfonate, patiromer, sodium zirconium cyclosilicate); and, in severe cases, haemodialysis.
Fluid overload occurs in patients with chronic kidney disease (CKD), especially those with concomitant congestive heart failure. Treatment of fluid overload with loop diuretics is often used to prevent episodes of pulmonary oedema and manage peripheral oedema. In some instances, a combination diuretic regimen (e.g., a loop and a thiazide diuretic) provides a more effective diuresis in patients.
Failure to maintain fluid balance in those with advanced glomerular filtration rate category G4 and G5 CKD is an indication to start kidney replacement therapy.
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