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Support of Renal Function 483

+
excretion as blood pressure rises. It also responds effec- ammonia (NH 3 ) in the renal tubule to form ammonium
+
tively to a rise in sodium intake by reducing angiotensin (NH 4 ), which is unable to be reabsorbed. Coinciden-
+
II formation and allowing a larger natriuresis, resulting tally, raised H excretion increases the reabsorption of
in maintenance of sodium balance, a key to tissue fluid sodium, which increases the alkalytic ion, bicarbonate
−
distribution and balance. 10 (HCO 3 ). Conversely, during alkalosis the reabsorption
of hydrogen ions is increased. These changes in secretion
Aldosterone is a mineralocorticoid excreted from the
adrenal cortex in response to angiotensin II. Aldosterone of hydrogen ion concentration in the renal filtrate alter
increases the reabsorption of sodium, and hence water, the pH of the urine down to a maximum level of 4. The
+
in the cortical collecting tubules and increases the rate of buffering of H with ammonia reduces the acidifying
potassium excretion. This has a dual effect of regulating effect of the hydrogen ions, particularly as some ammo-
sodium balance and extracellular fluid volume. As fluid nium combines with chloride to form ammonium
10
volume accumulates, the rise in glomerular filtration rate chloride.
self-limits the volume effect by increasing both diuresis
and natriuresis. Role as an Endocrine Organ
The kidney has two homeostatic roles as an endocrine
Atrial Natriuretic Peptide organ. Although neither have effects relevant to acute
Atrial natriuretic peptide (ANP) is a hormone released illness, patients with chronic renal dysfunction often
need supplementation to overcome the loss of renal
from the atria of the heart in response to atrial stretching endocrine support. Erythropoietin is important in stimu-
during periods of increased circulating fluid volume. ANP lating the generation of new red blood cells and is released
is therefore often described as having an antagonising from the kidney in response to a sustained drop in arte-
effect to the RAAS (which acts primarily to preserve rial blood oxygen levels. Calcitriol helps regulate the
sodium and water). These natriuretic, and hence diuretic, absorption of calcium from the gut, which in turn pro-
effects are mild and self-limiting, and occur in response motes bone resorption of calcium and the reabsorption
to mild rises in GFR and reductions in sodium reabsorp- of calcium in the kidney. The kidney also acts to convert
tion. As blood pressure falls, the drop in GFR compen- vitamin D to its active form, which is necessary for the
sates for the effect of ANP, ensuring that excessive loss of maintenance of body calcium levels. 10
sodium and water does not occur. 10

Regulation of Acid–base and PATHOPHYSIOLOGY AND
Electrolyte Balance CLASSIFICATION OF RENAL FAILURE

The kidney assists in the management of body pH by Diseases of the kidneys affect structure and therefore the
−
+
regulation of the excretion of H and HCO 3 ions. While function of the nephrons in some way. Pathology such as
the renal response to alkalosis or acidosis is slow in com- this, if untreated, may not cause complete loss of renal
parison with plasma buffers and respiratory regulation function (i.e. ARF), but is dependent on the amount of
+
(see Chapter 13), it does result in a net loss of H ions or nephron damage or ‘injury’ occurring at the time of the
−
recovery of HCO 3 ions, which are the basis of human pH illness, and whether the patient has had any previous
11
balance (see Figure 18.5). During acidosis the kidney illness that resulted in undetected kidney damage. By
+
raises H secretion by active transport to combine with focusing on factors that resulted in kidney injury, both
individually and collectively, then more serious damage
that may result in failure can be averted. This concept is
more clearly described in the later section on ATN and
Capillary lumen Renal tubule AKI which includes the RIFLE Criteria. 1,2
The conventional classification of ARF is based on
the perceived causative mechanisms, as outlined by
numerous authors, 12,13 however, irrespective of causative
H2CO3 mechanism, the same renal replacement therapies are
Active
HCO 3 – transport suitable to treat this: 14
H + ● prerenal
H + H + ● intrarenal (intrinsic)
+ ● postrenal.
+
+ NH 3
NH 3 PRERENAL CAUSES
=
NH 4 + Prerenal factors affecting blood supply to the kidneys,
such as hypovolaemia, cardiac failure or hypotension/
shock, can cause ARF. The mechanism and outcome are
easily related. As blood flow to the kidneys is reduced,
Tubular epithelium
less glomerulofiltration occurs, urine production dimin-
ishes and wastes accumulate. This state can be reversed
FIGURE 18.5 Hydrogen ion regulation in the kidney. by restoration of blood volume or blood pressure. In the