The kidney is normally responsible for excreting waste and excess water from the body, and for regulating various hormones. If the kidney is damaged, it can pose significant health risks, including mineral and bone disorder. Hormones and minerals play an essential role for bones and cardiovascular health.5
Hyperphosphatemia and Secondary Hyperparathyroidism (SHPT) are currently the conditions we are focusing on within the mineral and bone disease management:
Phosphorus is a mineral which plays an essential role in bone metabolism and cellular functions. An abnormal elevation of phosphorus levels – Hyperphosphatemia – in the blood, is a common and serious condition in CKD patients on dialysis, because the kidneys cannot remove extra phosphorus. Most patients are treated with a phosphate binder, however up to 50% of patients – depending on the region – are unable to achieve and maintain their target serum phosphorus levels6. In some patients, non-compliance due to the high pill burden and poor tolerability appear to be key factors behind this7,8. On average, dialysis patients take approximately 19 pills per day, with phosphate binders9 comprising around 50% of this daily pill burden.
Secondary Hyperparathyroidism (SHPT)
SHPT is characterised by increased secretion of parathyroid hormone (PTH) due to disrupted mineral and vitamin D homeostasis in chronic kidney disease (CKD) patients. It affects 40–82% of patients with stage 3 or 4 CKD.10-13 The loss of mineral homeostasis leads to an enlargement of the parathyroid glands, as well as bone and vascular complications, which are linked with increased morbidity (the rate of disease in a person or population) and mortality.12,13
Hyperkalaemia is defined as abnormally elevated levels of potassium in the blood, a serious condition in cardio-renal patients that can be responsible for cardiac arrhythmias leading to cardiac arrest and death, with a resulting mortality rate of up to 30%. Severe hyperkalaemia is an independent predictor of mortality and hospitalisations. Recurrent hyperkalaemia frequently occurs in patients with chronic kidney disease suffering from hypertension or diabetes, with or without heart failure19. It is often triggered by treatment with renin-angiotensin-aldosterone system inhibitors (RAASi), the cornerstone therapy for a number of conditions in cardio-renal patients20 such as hypertension or heart failure. As a consequence, RAASi therapy is often down-titrated or discontinued, compromising its cardio-renal protective benefit.