Renal medicine

The ageing kidney

Kidney function tends to decline with age, but unless there is additional disease, function is usually sufficient to remove waste and to regulate volume and electrolyte balance; it is only when stressed that lack of renal reserve becomes apparent. The relative contribution of cumulative exposure to risk factors (extrinsic ageing), disease acquisition (often occult) and intrinsic ageing is unknown, but not all the changes described are universal in an older population.

Falling renal reserve

Glomerular filtration rate (GFR) falls steadily after the age of 40 in most healthy older people, possibly due to the following age-related changes:

Rise in blood pressure within the normal range
Numbers of glomeruli fall (˜50% fewer age 70 than age 30)
Increase in sclerotic glomeruli

Renal blood flow decreases by around 10% per decade (cortex more than medulla, leading to patchy cortical defects on renal scans).

Lower GFR and renal blood flow are the major causes of reduced renal reserve, with the following clinical implications:

Renally excreted substances are likely to be retained longer (especially drugs) making prescription amendments necessary (see ‘Pharmacology in older patients’, p.126)
Reduced threshold for damage with ischaemia or nephrotoxins

The normal range for plasma urea and creatinine does not change with age. However, as production of urea and creatinine decreases with falling body muscle mass, renal function is often substantially diminished in an older person, even with apparently normal blood chemistry.

▶GFR is a better estimate of renal function than plasma urea and creatinine (see

‘HOW TO … Estimate the glomerular filtration rate’, p.393)

Blunted fluid and electrolyte homeostasis

The following changes occur with age:

A blunted response to sodium loading and depletion, so equilibrium is achieved more slowly
Reduced ability to dilute and concentrate urine (falls 5% every decade)
Lower renin and aldosterone levels (30-50% less than young people)
Loss of the sensation of thirst, even when plasma tonicity is high (reasons unclear—may relate to altered baroreceptor function, dry mouths or altered mental capacity)
Reduced response to vasopressin
In addition, many commonly prescribed drugs interfere with renal function (diuretics, NSAIDs, ACE inhibitors, lithium, sedatives, etc.)

Hyponatraemia is therefore common (low sodium intake combined with renal sodium wasting), but in times of acute illness (increased fluid demand and decreased intake) the slower adaptive mechanisms make hypernatraemic dehydration more common.

Hypokalaemia is common because of poor intake and frequent diuretic use, but lower GFR and hypoaldosteronism lead to a vulnerability to hyperkalaemia especially when exacerbating drugs (NSAIDs, spironolactone, ACE inhibitors) are used.

Structural changes

Renal mass falls by 20-30% between 30 and 90 years, making kidneys appear smaller on ultrasound scanning, without necessarily implying disease
Distal nephrons develop diverticulae (3 per tubule by age 90) that may become retention cysts (benign finding in older people)

Other changes

Renal 1-hydroxylase activity decreases with age leading to decreased vitamin D production. Combined with low phosphate intake, this can mildly elevate parathyroid hormone levels
There is a loss of the circadian rhythm, owing to altered sodium handling and patterns of aldosterone secretion, so that over the age of 60 the proportion of water, sodium, and potassium excretion occurring at night increases, causing nocturia

Acute kidney injury

Previous called acute renal failure. This is more common in older people, but with a similar prognosis if occurring de novo and treated correctly.

▶Do not deny treatment based on age alone—even anuric patients can make a full recovery

Causes

80% of cases of acute kidney injury (AKI) are caused by pre-renal failure and ATN (acute tubular necrosis).

Pre-renal causes

Due to poor renal perfusion. May be caused by:

Dehydration (commonly associated with sepsis)
Volume loss (eg bleeding, over-diuresis)
Volume redistribution (eg with low serum albumin)
Poor cardiac output (eg post-MI)
Aggravated by many drugs (eg diuretics, ACE inhibitors, NSAIDs)

Older patients are prone to sepsis, have less capacity to maintain circulating volume in the face of stress and are more likely to be on aggravating medications, making this a very common problem (eg urinary sepsis in a patient taking diuretics and NSAIDs can often cause pre-renal renal impairment, and responds well to antibiotics, fluids, and drug cessation).

▶All unwell elderly patients should have renal function checked routinely and repeatedly. Consider stopping diuretics and ACE inhibitors during an acute illness.

Renal causes

Due to direct damage to the kidney. Commonly ATN, which may be:

Ischaemic (occurs when pre-renal failure is not corrected quickly, eg with sepsis, surgical procedures, prolonged hypotension, etc.)
Nephrotoxic (usually medication such as aminoglycoside antibiotics, eg gentamicin)
Due to pigment deposition (eg myoglobin in rhabdomyolysis, See ‘Rhabdomyolysis’, p.505)

Not all renal failure is ATN. Other (rarer) causes include:

Glomerulonephritis—diffuse inflammatory change to glomeruli with resulting haematuria and red cell casts
Acute interstitial nephritis—consider drug induced nephritis. May have flank pain, rash, fever, eosinophilia, and urine white blood cells/casts but consider if new drug recently even in absence of these features

These less common causes are important because they are often responsive to specific treatment (usually steroids). The patient should be assessed by a renal physician promptly and often need a biopsy.

Post-renal causes

Obstruction of the renal tract at some point, eg prostatic enlargement, renal stones, urethral strictures, pelvic tumours
Ultrasound scan shows a dilated collecting system
These conditions are all more common in older people, and are very responsive to treatment if found early, often with full recovery of renal function

Acute kidney injury: management

Is this acute kidney injury?

Older people are more likely to have underlying chronic kidney disease (CKD), and this confers a worse prognosis. Check old notes, ask the patient, family, and GP about history, and look back at blood test results.

Generally, management does not differ significantly from younger patients.

Investigations

See Table 13.1
Treat cause

Older people respond as well to most treatments

Monitor meticulously

Pulse and blood pressure, cardiac monitor, input (iv and oral) and output (urine, faecal matter, vomit, drains, sweat)
May be best done on HDU
Aim for euvolaemia (assessed clinically may need to correct deficit) then maintain by matching input to output on an hourly basis initially
Fluid balance is likely to be harder in older people because of comorbidity (especially heart failure)

▶The presence of peripheral oedema does not necessarily indicate fluid overload. Circulating volume is best assessed by blood pressure, pulse, JVP, and skin turgor (see

‘Challenges to volume status assessment in elderly patients’, p.405)

May need central venous catheter and urinary catheter initially, but remove as soon as possible because of infection risk
Document daily weight and total fluid balance summary
Be prepared for polyuria in the recovery phase, and ensure that the patient does not become fluid depleted

Treat complications

Importantly hyperkalaemia, acidosis, and pulmonary oedema.

Refer early for further renal support (filtration or dialysis) a patient can remain oliguric for some time while renal recovery is occurring, but it is sensible to make the relevant teams aware of a potential patient. The indications for renal replacement therapy are as follows:

Refractory pulmonary oedema (older people are particularly prone to this after over enthusiastic initial fluid replacement)
Persistent hyperkalaemia (K >7 mmol/L) that cannot be controlled by insulin/glucose infusions and iv calcium
Worsening acidosis (pH <7.2)
Uraemic pericarditis
Uraemic encephalopathy

HOW TO … Perform a fluid challenge in AKI/anuria

Many older patients are clearly dehydrated with mildly impaired renal function tests and these patients can be simply rehydrated orally or parenterally.

If the patient presents with established AKI or is found to be anuric despite simple rehydration then a fluid challenge should be contemplated.

This is an important clinical skill to develop and requires advanced clinical acumen and an investment of time. The key is an accurate assessment of fluid status with the aim of rendering the patient euvolaemic.

A urinary catheter is needed and a central venous pressure monitoring device is helpful if facilities exist.

Start by assessing and clearly documenting baseline fluid status as this will inform your management and will be helpful when the patient is reassessed
If the patient is already fluid overloaded then a single bolus of iv loop diuretic and early contact with the renal specialist team is need
If the patient appears to be hypovolaemic, give 500mL of normal saline (sodium bicarbonate may be considered if they are profoundly acidotic) over 30-60min and review
If the patient appears to be euvolaemic then the fluid challenge should be more cautious. Give 100mL bolus intravenously and review after about 15min
For the review repeat and document the fluid status and urine output. Repeat this cycle of fluid prescription and do a careful review as the clinical progression becomes clear