The Adrenal Glands: Two Organs in One Coat

A cap on the kidney — but not part of it

The name says "above the kidney", and for once the name is honest about the geography and misleading about everything else. Each adrenal gland is retroperitoneal, plastered against the muscles of the posterior abdominal wall at about the level of the twelfth thoracic vertebra, capping the superomedial pole of its kidney. It is a small organ — roughly five centimetres tall, three wide, one thick, and weighing four to five grams in the adult — and it is deeply buried: behind the peritoneum, inside the renal (Gerota's) fascia, embedded in perinephric fat. But the crucial detail is that the fascia sends a thin SEPTUM OF FAT between the gland and the kidney beneath it. The two organs are neighbours in a shared envelope, not partners. That septum is why the adrenal is left behind in a simple nephrectomy: the surgeon removing a kidney for a lower-pole tumour peels the kidney out of its fat and the gland stays, still perched on the diaphragm, still doing its work. It is also why the adrenal does not follow the kidney downwards in the rare cases where a kidney is congenitally low or ectopic — the gland develops separately and stays where it was built. Everything you need to know about the kidney itself, its fascial layers and its own vessels is set out in the kidneys and ureters.

The two glands are not mirror images, and telling them apart on a scan is a genuine skill. The RIGHT adrenal is PYRAMIDAL — a three-sided cocked hat — and sits higher, wedged into a tight space between the bare area of the liver in front and above, the right crus of the diaphragm behind, and, most importantly, the INFERIOR VENA CAVA in front and medially: part of the gland actually lies BEHIND the cava, which is what makes the right side hard surgical country. The LEFT adrenal is SEMILUNAR or crescentic, longer and flatter, and sits a little lower and more medially along the upper part of the kidney. Its anterior surface is related above to the stomach across the lesser sac, below to the body of the pancreas and the splenic artery running along its upper border, and behind it lies the left crus of the diaphragm. Both glands rest posteriorly on the diaphragm described in the diaphragm — which is why a large adrenal mass can be felt to move, faintly, with respiration.

The cortex: three zones, three hormones

Cut the gland across and the cortex is a yellow rind about a millimetre thick, banded into three layers you can name from the outside in. The mnemonic that has survived every curriculum reform is "GFR — salt, sugar, sex", and it works because the order of the zones matches the order of their products. The ZONA GLOMERULOSA is the outermost, a thin band of cells in rounded clusters immediately beneath the capsule; it makes MINERALOCORTICOIDS, chiefly aldosterone, which acts on the distal nephron to retain sodium and water and excrete potassium. Crucially, this zone does NOT take its orders from the pituitary: it is driven by the renin–angiotensin–aldosterone system, and secondarily by plasma potassium. The ZONA FASCICULATA is the broad middle layer — about three quarters of the cortex — with cells arranged in long straight cords like fence palings, foamy and pale because they are stuffed with lipid droplets of stored cholesterol; it makes GLUCOCORTICOIDS, chiefly cortisol, under the control of ACTH from the anterior pituitary. The ZONA RETICULARIS is the innermost, a network of branching cords abutting the medulla; it makes the ADRENAL ANDROGENS — dehydroepiandrosterone (DHEA), its sulphate, and androstenedione — weak in themselves but converted peripherally to testosterone, and the reason a woman has any androgen at all.

Two consequences follow immediately from that architecture. First, because only two of the three zones answer to ACTH, disease of the pituitary spares aldosterone: a patient with secondary adrenal insufficiency loses cortisol and androgens but keeps their salt, which is why they are far less likely to collapse in circulatory shock than a patient whose entire adrenal cortex has been destroyed. Second, because every cortical hormone is a STEROID built from cholesterol along a shared assembly line, a block at any single enzyme diverts the raw material down the remaining paths. That single sentence is the whole of congenital adrenal hyperplasia: a missing enzyme (most often 21-hydroxylase) means no cortisol, no negative feedback, relentless ACTH drive, a gland that hypertrophies until it is huge — and all that unusable precursor shunted into the androgen pathway, virilising a female newborn while she quietly loses salt.

The medulla: a ganglion that never grew axons

This is the single most beautiful piece of design in the abdomen, and it is easy to miss. The medulla forms about a tenth of the gland's mass and consists of CHROMAFFIN CELLS — so called because they stain brown with chromium salts. Developmentally they are neural crest cells that migrated to exactly the same place as the sympathetic ganglia and then took a different final step: instead of growing an axon to reach a distant target, they simply secreted their transmitter into the bloodstream. They ARE postganglionic sympathetic neurons, minus the axon. And because they are postganglionic, the fibres that reach them must be PREGANGLIONIC — myelinated fibres running from the lateral horn of spinal segments T5 to T9, out through the sympathetic chain WITHOUT SYNAPSING, into the greater splanchnic nerve, and straight onto the chromaffin cells. This is the one place in the entire body where a preganglionic fibre reaches its target organ without an intervening ganglion, an exception explained in its wider context in the autonomic nerves of the abdomen. That short circuit is why the adrenaline surge is essentially instantaneous: the brainstem's alarm signal has to cross exactly one synapse before it becomes a hormone in your blood.

The chromaffin cells secrete CATECHOLAMINES: roughly eighty per cent adrenaline (epinephrine) and twenty per cent noradrenaline (norepinephrine), with a trace of dopamine. That ratio matters, because the rest of the sympathetic nervous system releases almost pure noradrenaline at its nerve endings. The adrenal medulla is therefore the body's only significant source of circulating ADRENALINE — the molecule that widens the pupils, opens the bronchi, speeds and strengthens the heart, dilates the vessels of skeletal muscle while clamping those of the skin and gut, mobilises glucose from the liver and free fatty acids from fat. A nerve ending delivers a message to one organ; the adrenal medulla broadcasts to all of them at once and keeps broadcasting for a minute or two after the danger has passed. That is the difference between the sympathetic nervous system and the fight-or-flight surge, and it is the reason your hands are still shaking after the car has swerved safely by.

Three arteries in, one vein out

Gram for gram, the adrenal is one of the most richly perfused organs in the body — and it is supplied from three separate sources. The SUPERIOR suprarenal arteries — usually six to a dozen small twigs — come from the INFERIOR PHRENIC ARTERY as it runs across the diaphragm above the gland. The MIDDLE suprarenal artery arises DIRECTLY FROM THE ABDOMINAL AORTA, at about the level of the superior mesenteric artery; it is one of the very few small branches the aorta gives to a paired organ in its own right, and its origin is worth remembering when reading the branches of the abdominal aorta. The INFERIOR suprarenal arteries come from the RENAL ARTERY of the same side. So the gland is fed from above, from the middle and from below, and the three sets anastomose freely in a subcapsular plexus before breaking up into the sinusoids that run inwards through the cortex. This triple supply is generous by design: an organ that must sustain a maximal secretory burst within seconds cannot afford to depend on a single vessel. It is also why adrenal infarction is rare, and why surgical dissection of the gland is bloody out of all proportion to its size.

Then the elegance stops. The venous drainage is a single vein on each side — and the two sides are not the same. All that arterial blood, having passed through cortex and then medulla, is collected into ONE suprarenal vein emerging from the hilum. On the LEFT, that vein is comfortably long: it descends and drains into the LEFT RENAL VEIN, usually joining it near the point where the left inferior phrenic vein also enters. On the RIGHT, the vein is VERY SHORT — often less than a centimetre — and it passes almost immediately, and at a steep angle, into the posterior wall of the INFERIOR VENA CAVA. There is no margin. A right adrenalectomy therefore means dissecting a stubby, fragile, high-pressure-adjacent vein directly off the cava, and if it tears or avulses the surgeon is left with a hole in the largest vein in the body, in a deep space behind the liver, with the bleeding described in the inferior vena cava as catastrophic for good reason. The same asymmetry defeats the radiologist: in adrenal vein sampling — the test that decides which gland is over-producing aldosterone in Conn's syndrome — cannulating the long left vein is routine and cannulating the short right one, which enters the cava at an awkward angle, is the technical step that most often fails.

Lymph from the gland drains, as you would expect from a retroperitoneal organ at this level, into the LUMBAR (para-aortic) NODES that lie along the aorta and the cava, and from there into the lumbar trunks and the cisterna chyli — the route traced in the lymphatics of the abdomen. This is why adrenal metastases, which are common (the adrenal is a favourite landing site for carcinoma of the lung, breast, kidney, stomach and melanoma, precisely because of its lavish blood supply), are staged and searched for alongside para-aortic nodal disease. The gland's fame in oncology is not for the tumours that arise in it, but for the tumours that arrive.

Four diseases, one gland

Because the gland has four secretory compartments, it fails in four recognisable ways, and each maps onto a zone. Too much CORTISOL from the fasciculata is CUSHING'S SYNDROME: central obesity with thin limbs, a rounded plethoric face, a dorsocervical fat pad, purple striae on a thin bruisable skin, proximal muscle weakness, hypertension, diabetes, osteoporosis and mood change — the body catabolising its own periphery to feed a permanent stress state. Too much ALDOSTERONE from the glomerulosa is CONN'S SYNDROME (primary hyperaldosteronism): hypertension that resists three drugs, a low or low-normal serum potassium with a metabolic alkalosis, often with muscle cramps and polyuria — an important and genuinely curable cause of secondary hypertension. Too much CATECHOLAMINE from the medulla is PHAEOCHROMOCYTOMA, and its classic triad is episodic HEADACHE, SWEATING and PALPITATIONS on a background of paroxysmal or sustained hypertension; the teaching "rule of tens" holds that about ten per cent are bilateral, ten per cent extra-adrenal (arising in the paraganglia, most famously the organ of Zuckerkandl near the aortic bifurcation), ten per cent malignant and ten per cent occur in children — though modern genetics shows a far higher proportion than ten per cent are familial. And too LITTLE of everything is ADDISON'S DISEASE.

ADDISON'S DISEASE is primary adrenocortical failure — worldwide most often tuberculous, in the developed world usually autoimmune — and it is the one to recognise, because it kills. The patient is tired beyond explanation, has lost weight and appetite, feels dizzy on standing, craves salt, and is PIGMENTED: a tan in the palmar creases, on the buccal mucosa, on scars and pressure areas, because the pituitary, freed from cortisol feedback, is pouring out POMC-derived peptides that stimulate melanocytes. Biochemistry shows low sodium, high potassium and, if you look, a low cortisol that fails to rise on stimulation. Then an infection, an injury or an operation arrives, and the gland that cannot mount a stress response fails outright: ADRENAL CRISIS — vomiting, abdominal pain that can mimic a surgical abdomen, profound hypotension unresponsive to fluids alone, hypoglycaemia, collapse. The treatment is intravenous hydrocortisone and saline, immediately, before the diagnosis is confirmed. And this is exactly why long-term steroid therapy must NEVER be stopped abruptly: exogenous steroid suppresses ACTH, the zona fasciculata atrophies from disuse over weeks, and a patient who stops their prednisolone on Monday may have no functioning cortisol reserve by Thursday — an iatrogenic Addisonian crisis in a person who never had adrenal disease at all.