Absorption of orally administered medicines may be reduced in patients with renal impairment as a result of factors including:

• Nausea, vomiting or diarrhoea associated with uraemia (raised levels of waste compounds in the blood)
• Reduced gastrointestinal (GI) motility and delayed gastric emptying time
• An increase in pH in the gut from increased gastric ammonia production in uraemia
• Co-administration of medicines which increase gastric pH (e.g. H2-antagonists) 
• Co-administration of chelating agents such as those used for binding phosphate.

Changes to the distribution of medicines in the body in patients with renal impairment may occur as a result of factors including:

• Changes in their hydration
• Alterations in how medicines attach to proteins
• Alterations in how medicines attach to tissue.

Metabolism is slower in chronic kidney disease. The effect of this is to increase serum medicine concentrations of the parent medicine. This may lead to higher prevalence of adverse effects and toxicity.

Two examples are hydroxycholecalciferol to active vitamin D and the metabolism of insulin. For patients requiring vitamin D, either the active medicine (calcitriol) or a preparation requiring metabolism to active medicine by the liver (alfacalcidol) should be used. For diabetic patients required insulin will be reduced.

The kidney is involved in the elimination of medicines by glomerular filtration (the first step in making urine), renal tubular secretion (the process where solutes and water are removed from tubular fluid, leaving only urine) and reabsorption. All of these functions are reduced by renal impairment, resulting in medicines being removed by the kidneys at a slower rate.