Dr.
Dalya Shakir
PhD.Clinical Biochemistry
21\4\2020
Renal function PART 3
Renal handling of sodium and potassium
The amount of Na+ excreted in the urine controls the ECF volume since, when
osmoregulation is normal, the amount of extracellular water is controlled to
maintain a constant concentration of extracellular Na+. A number of mechanisms
are important regulators of Na+ excretion:
1. The renin-angiotensin-aldosterone system: Renin is secreted in response to a
fall in renal afferent arteriolar pressure or to a reduction in supply of Na+ to the
distal tubule. It converts angiotensinogen in plasma to angiotensin I (AI), which
in turn is converted to angiotensin II (AII) by angiotensin-converting enzyme
(ACE). Both AII and its metabolic product angiotensin III (AIII) are
physiologically active, and stimulate the release of aldosterone from the adrenal
cortex. Aldosterone acts on the distal tubule to promote Na+ reabsorption in
exchange for urinary loss of H+ or K+.
2. The glomerular filtration rate (GFR): The rate of Na+ excretion is often
related to the GFR. When the GFR falls acutely, less Na+ is filtered and
excreted, and vice versa. However, this only becomes a limiting factor in Na+
excretion at very low levels of GFR.
3. Atrial natriuretic peptide (ANP): This peptide secreted by cardiocytes of the
right atrium of the heart promotes Na+ excretion by the kidney, apparently by
causing a marked increase in GFR. The importance of the ANP regulatory
mechanism is not yet clear, but it probably only plays a minor role. Other
structurally similar peptides have been identified, including brain or B-type
natriuretic peptide (BNP), secreted by the cardiac ventricles and with similar
properties to ANP. BNP is increasingly being used in the assessment of patients
suspected of having cardiac failure.
Aldosterone secretion
The principal physiological function of aldosterone is to conserve Na+, mainly by
facilitating Na+ reabsorption and reciprocal K+ or H+ secretion in the distal renal
tubule and in other epithelial cells. Aldosterone is a major regulator of water and
electrolyte balance, as well as blood pressure. The renin–angiotensin system is the
most important system controlling aldosterone secretion.
Renin-Angiotensin System
Renin is proteolytic enzyme released from the renal juxtaglomerular cells (JC) in
response to hypotension, low blood volume or sodium depletion. Renin catalyses
the conversion of angiotensinogen in plasma to angiotensin I. During passage
through the lung, angiotensin-converting enzyme (ACE) catalyses the production
of angiotensin II from angiotensin I. The angiotensin II stimulates release of
aldosterone from the adrenal glomerulosa and the mineralocorticoid then promotes
reabsorption of sodium in the distal tubules of the kidney.
Sodium excretion
The kidneys are essential for maintaining sodium balance, normally filtering about
21 000 mmol Na+/day through the glomeruli. On a diet of 100 mmol Na+, and in
the absence of any pathological loss of Na+, the kidney matches this intake with
an excretion of 100 mmol Na+, which represents about 0.5% of the filtered Na+
load. As the GFR declines in chronic renal failure, the proportion of the filtered
Na+ that is excreted needs to increase progressively to maintain Na+ balance. Most
patients with chronic renal failure tolerate normal levels of dietary Na+ if the GFR
is more than 10 mL/min. However, if the GFR falls below this level, Na+ retention
occurs, leading to expansion of the ECF, weight gain and worsening hypertension.
In chronic renal failure, excessive Na+ loss may also occur. The capacity of the
kidneys to adapt to changes in Na+ intake is limited, and a requirement to conserve
Na+ (e.g. in response to excessive use of diuretics or if the patient has severe
diarrhoea) may not be met by the damaged kidneys.
Potassium excretion.
About 90% of K+ in the glomerular filtrate is normally reabsorbed in the proximal
tubules, the distal tubules regulating the amount of K+ excreted in the urine. The
rate of secretion of K+ by the distal tubules is influenced by the transtubular
potential and by the tubular cell [K+], and is usually maintained adequately,
provided the daily urine flow rate is greater than 1 L.
In the presence of a normal GFR, about 550 mmol K+ is filtered daily at the
glomerulus. An average dietary intake of K+ is about 80 mmol/day, and external
K+ balance is normally achieved by excreting about 15% of the filtered K+. A
reduction in GFR to about 10 mL/min requires an increase in the proportion of the
filtered K+ . Distal tubular secretion of K+ is needed to achieve this.
Generally, the normal daily intake of K+ can be tolerated if the GFR is 10
mL/min. At a GFR of about 5 mL/min, however, the limit of adaptation is reached,
leading K+ retention and hyperkalaemia. The ability of the GI tract to increase
excretion of K+ helps to delay the onset of hyperkalaemia. In chronic renal disease,
excessive renal losses of K+ are rare, but the Na+ depletion that sometimes
develops in renal disease .
