Serum potassium

Serum levels of potassium are usually low or low-normal in patients with primary hyperaldosteronism (Conn’s syndrome). This is often associated with high or high-normal serum levels of sodium.

Low levels of potassium sometimes occur in patients who take diuretics, but usually, thiazide diuretics only lower potassium by 0.5 mmol/l. If hypokalaemia is marked, it is possible that it is related to underlying aldosterone excess. Patients with malignant hypertension may have mild hypokalaemia because of aldosterone excess, secondary to high levels of renin caused by juxtaglomerular cell ischaemia. As blood pressure is brought under control, this hypokalaemia often normalises. If serum levels of potassium remain low without diuretic treatment despite good control of blood pressure over a few months, primary hyperaldosteronism should be excluded.

Hyperkalaemia may develop in patients with renal failure and those who take drugs such as angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and potassium sparing diuretics (e.g. spironolactone and amiloride). Spironolactone is increasingly used as third-line treatment in patients with resistant hypertension, and potassium and renal function need to be monitored regularly. Low table salt alternatives, which contain potassium salts, should be used cautiously with angiotensin-blocking drugs as dangerous hyperkalaemia can occur, particularly if spironolactone is also being used. This is a problem which is becoming more common as angiotensin-blocking drugs and spironolactone are frequently used together in both hypertension and heart failure.

Serum sodium

Serum levels of sodium may be high or high-normal in patients with primary hyperaldosteronism (Conn’s syndrome). This is usually associated with low or low-normal serum levels of potassium. In patients with secondary hyperaldosteronism as a result of malignant hypertension or renal disease, serum levels of sodium can be low or low-normal. Low levels of sodium may also be present with overuse of diuretics.

Profound hyponatraemia, which may cause confusion and hypotension, is occasionally seen in patients even on low doses of diuretics.

Serum urea and creatinine

Non-malignant essential hypertension only rarely causes renal impairment, but associated co-morbid disease (such as diabetes mellitus) and concomitant treatment with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers can lead to renal impairment.

Almost all intrinsic renal diseases can cause hypertension, and levels of urea and creatinine in serum should be part of the initial work up in a patient with newly diagnosed hypertension. Even a modest increase in levels of creatinine in serum needs more detailed investigation.

Estimated glomerular filtration rate

In recent years, it has become fashionable to assess renal function using a formula devised from the US Modification of Diet in Renal Disease (MDRD) study. This has proved a little controversial. It has long been recognised that serum creatinine levels do not rise above the so-called normal range until renal function is about halved. The MDRD study attempted to correct for this. The estimated glomerular filtration rate (eGFR) formula takes into account age, gender, body weight (as a surrogate for muscle bulk) and ethnicity (African American vs. non-African American). The grade of renal impairment can then be calculated but this should also take into account the presence of other abnormalities including proteinuria and haematuria. Taking these criteria, patients with a eGFR above 90 ml/min (excellent) will be labeled as having grade 1 chronic kidney disease (CKD) (Table 7.2). It would appear that all patients, regardless of their eGFR, have some form of CKD.

Serum uric acid

High levels of uric acid in serum are found in about 40% of patients with hypertension, especially in association with renal impairment. Increased ingestion of alcohol and the use of thiazide diuretics can also lead to higher levels of uric acid. Whether high levels of uric acid are harmful in their own right, or only by association with hypertension, hyperlipidaemia and diabetes remains uncertain. There is no information as to whether the treatment of hyperuricaemia with allopurinol in symptomless hypertensive patients with normal renal function is of any value.

Liver function tests

There is an increased prevalence of abnormal liver function tests (LFTs) in patients with hypertension. (Figure 7.2). This is partly explained by the association between excess alcohol intake in the causation of hypertension. However, abnormal LFT are also seen in people who consume no alcohol at all. Such patients are often overweight and/or have type 2 diabetes, as part of Non-Alcoholic Fatty Liver Disease (NAFLD). This syndrome is usually reversible with weight reduction but may progress to Non-Alcoholic Steato-Hepatitis (NASH) or even cirrhosis.