Complications
Your Organisational Guidance
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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: 2017Anaemia of chronic kidney disease is due to a deficiency of erythropoietin as the glomerular filtration rate (GFR) declines.
Anaemia is typically identified in GFR category G3a/G3b CKD. Patients should be screened with a full blood count at least every 6 to 12 months, and an erythropoietin-stimulating agent may be considered once the haemoglobin (Hb) falls to <100 g/L (<10 g/dL) and there are symptoms of anaemia.
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The target Hb is 100 to 110 g/L (10 to 11 g/dL).[101][104][137]
If the patient is iron-deficient, oral or intravenous supplementation may also be prescribed.[108]
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Patients with CKD on erythropoietin-stimulating agents for the treatment of anaemia have a higher risk of death and cardiovascular complications if the Hb is normalised >130 g/L (>13 g/dL).[102][103][138][139][140]
May be caused by an elevation in parathyroid hormone (PTH) as a result of phosphorus retention and hypocalcaemia from 1,25 vitamin D deficiency as the glomerular filtration rate (GFR) declines. Severe hyperparathyroidism and hyperphosphataemia are risk factors for death, cardiovascular disease, and vascular calcification in patients with CKD.[111][Evidence 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 PTH levels, considered together.[111]
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).[109][110]
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, and the overwhelming majority of patients with CKD will die prior to reaching the need for renal replacement therapy.
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.[142][143]
As the glomerular filtration rate falls, patients develop anorexia, nausea, vomiting, and lack of protein intake. Previously, patients with advanced CKD were placed on very-low- to low-protein diets to reduce the risk for end-stage kidney disease, but this recommendation has limitations due to its worsening of malnutrition. It is recommended for patients with CKD stages 3 to 5 who are metabolically stable to have 0.6 g/kg body weight protein intake daily and those with diabetes (not on dialysis) to have 0.6 to 0.8 g/kg body weight protein intake daily.[141] 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.[141]
Metabolic acidosis is common in patients with CKD, due to the inability of the kidney to excrete acid once the estimated glomerular filtration rate is <50 mL/minute. The anion gap is typically normal, but may be increased in uraemia with retention of phosphate anions. Rarely does the serum bicarbonate level fall below 12 mmol/L (12 mEq/L). Metabolic acidosis may worsen renal osteodystrophy and cause malnutrition, hypercatabolism, and growth retardation.
Treatment involves the administration of sodium bicarbonate 0.5 to 1.0 mmol/kg/day (0.5 to 1.0 mEq/kg/day) for a target serum bicarbonate level >20 mmol/L (>20 mEq/L). Sodium citrate as a bicarbonate source is generally avoided in patients with CKD, as it increases the absorption of aluminium and may contribute to bone disease and dementia.[144][145]
Hyperkalaemia is common in patients with CKD, due to the kidney's inability to excrete potassium from the diet as the estimated glomerular filtration rate declines. Hyperkalaemia is more common in patients with oliguria, resistant or deficient aldosterone state, or co-existing metabolic acidosis. Most patients with hyperkalaemia 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 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 renal replacement therapy.
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