Kidney Anatomy and Function: Why These Two Beans Are Brilliant

Ask most student nurses what the kidneys do and you will probably hear:

“They make urine and balance fluid.”

Correct, but wildly incomplete.

Your kidneys filter blood, fine-tune electrolytes, control acid–base balance, influence blood pressure, activate vitamin D and produce a hormone needed for red blood-cell production.

They are less like two simple filters and more like a highly selective laboratory, recycling centre and control system rolled into one.

First, Where Are the Kidneys?

Most people have two kidneys. They are bean-shaped, roughly fist-sized and lie retroperitoneally in the posterior abdomen on either side of the vertebral column. The lower ribs provide some protection, and the right kidney usually sits slightly lower than the left because of the liver.

Blood reaches each kidney through a renal artery and leaves through a renal vein. Urine drains from the renal pelvis through the ureters to the bladder.

Meet the Nephron: The Kidney’s Working Unit

Each kidney contains roughly one million nephrons, although nephron number varies considerably between individuals.

The nephron includes the renal corpuscle (the glomerulus and Bowman’s capsule), proximal convoluted tubule, loop of Henle and distal convoluted tubule. Tubular fluid then enters the collecting-duct system.

Filter first. Reclaim what is needed. Add selected substances. Excrete the remainder.

1. Filtration

Blood enters the glomerulus, a specialised capillary network. Hydrostatic pressure drives water and small solutes across the glomerular filtration barrier into Bowman’s space. Blood cells and most large plasma proteins are normally retained in the circulation.

2. Reabsorption

As filtrate travels through the tubules, substances the body needs are selectively returned to the circulation. These include most filtered water and sodium, bicarbonate, and normally virtually all filtered glucose and amino acids.

3. Secretion

Selected substances are transported from the peritubular blood into tubular fluid. Tubular secretion contributes to acid–base and potassium regulation and to the renal handling of many medicines and metabolites.

4. Excretion

The final urine passes through the collecting ducts into the renal calyces and renal pelvis, then through the ureter to the bladder.

Around 180 Litres Filtered, But Not 180 Litres of Urine

A commonly taught estimate is that healthy young adults form around 180 litres of glomerular filtrate per day. This is based on a GFR of approximately 125 mL/min:

125 mL × 60 minutes × 24 hours ≈ 180 litres

This is an illustrative physiological estimate, not a fixed normal value for every adult. GFR varies with factors including age, sex, body size, pregnancy and kidney function.

Almost all filtered water is reabsorbed. Typical daily urine volume is therefore far smaller and varies substantially with fluid intake, physiological losses, medicines and illness.

What Happens During Dehydration?

Water deficit and reduced effective circulating volume stimulate coordinated responses including thirst, vasopressin (antidiuretic hormone) release and, where appropriate, activation of the renin–angiotensin–aldosterone system (RAAS). The kidneys conserve water and sodium, so urine commonly becomes lower in volume and more concentrated.

Significant hypovolaemia can reduce renal perfusion and GFR. If sufficiently severe or prolonged, this may contribute to acute kidney injury (AKI).

Possible findings include thirst, dry mucous membranes, reduced urine output, tachycardia, postural symptoms, hypotension, altered cognition and delayed capillary refill. These findings must be interpreted together: dark urine alone does not diagnose dehydration, and oliguria has many possible causes.

The Kidneys Help Regulate Blood Pressure

Renin is released by juxtaglomerular cells in response to signals including reduced renal perfusion pressure, reduced sodium chloride delivery to the macula densa and sympathetic stimulation.

Renin cleaves angiotensinogen to angiotensin I. Angiotensin-converting enzyme then contributes to formation of angiotensin II. Angiotensin II causes vasoconstriction and stimulates aldosterone release; aldosterone increases distal sodium reabsorption, which supports retention of extracellular fluid. Angiotensin II also promotes thirst and vasopressin release.

RAAS therefore helps defend blood pressure and perfusion. Persistent inappropriate activation can contribute to hypertension and cardiovascular disease. The relationship is two-way: the kidneys influence blood pressure, while sustained hypertension can damage the kidneys.

Electrolyte and Acid–Base Control

Healthy kidneys are central to regulation of sodium, potassium, calcium, phosphate, magnesium and water. They also maintain acid–base homeostasis through bicarbonate reclamation and generation and renal acid excretion.

Significant kidney dysfunction can therefore cause clinically important complications including hyperkalaemia, metabolic acidosis and fluid overload.

NICE advises immediate referral for renal replacement therapy when hyperkalaemia, metabolic acidosis, uraemic symptoms or complications, fluid overload or pulmonary oedema are not responding to medical management. The decision should be based on the patient’s overall clinical condition rather than an isolated urea, creatinine or potassium result.

Your Kidneys Talk to the Bone Marrow

The kidneys produce erythropoietin (EPO), a hormone that stimulates red-blood-cell production in the bone marrow. In chronic kidney disease, reduced renal EPO production is an important contributor to renal anaemia, although iron deficiency, inflammation and other factors may also contribute.

They Also Activate Vitamin D

The kidneys perform the final activation step that converts 25-hydroxyvitamin D to the active hormone calcitriol (1,25-dihydroxyvitamin D).

Calcitriol contributes to calcium and phosphate homeostasis and bone health. Chronic kidney disease can reduce calcitriol production and phosphate excretion, contributing to disturbances of calcium, phosphate and parathyroid hormone collectively recognised within chronic kidney disease–mineral and bone disorder (CKD-MBD).

Is Urine Output an Early Warning Sign?

It can be. Oliguria may accompany hypovolaemia, sepsis, shock, heart failure, intrinsic renal disease or urinary obstruction. In a catheterised patient, always consider simple mechanical causes such as a kinked, blocked or displaced catheter as well.

NICE uses urine output below 0.5 mL/kg/hour for more than 6 hours in adults as one criterion for detecting AKI. Importantly, AKI may be non-oliguric, and oliguria does not establish the cause.

Why Creatinine Is Not a Perfect Warning Light

Creatinine is generated from muscle metabolism and eliminated mainly by the kidneys. When GFR falls, serum creatinine usually rises, but the change can lag behind an acute reduction in kidney function and is influenced by factors including muscle mass and fluid status.

NICE criteria for detecting AKI in adults include:

• A rise in serum creatinine of 26 micromol/L or more within 48 hours.
• A rise in serum creatinine of 50% or more within the previous 7 days.
• Urine output below 0.5 mL/kg/hour for more than 6 hours.

A single creatinine result is therefore less informative than the patient’s baseline, trend and clinical context. Estimated GFR is also less reliable during rapidly changing kidney function because serum creatinine is not in steady state.

Ask: How does this compare with baseline, what is the trend, and what is happening to the patient?

Three Broad Places the Problem Can Begin

Pre-renal: before the kidney

Renal perfusion is reduced without primary structural kidney damage initially. Causes include hypovolaemia, haemorrhage, hypotension, sepsis and reduced cardiac output. If hypoperfusion persists, intrinsic tubular injury can develop.

Intrinsic renal: within the kidney

Kidney tissue itself is affected. Examples include acute tubular injury, glomerulonephritis, acute interstitial nephritis and vascular causes.

Post-renal: after the kidney

Urinary outflow is obstructed. Causes include prostatic enlargement, calculi, tumours and ureteric or bladder-outflow obstruction. A blocked catheter can mimic or contribute to apparent post-renal oliguria in a catheterised patient.

This framework is useful for organising clinical reasoning, but AKI is often multifactorial.

Student Nurse POV: What Should You Notice?

Look beyond the number in the urine bag. Consider the urine-output trend and whether it has been measured accurately; fluid intake and losses; vomiting, diarrhoea, drains, bleeding and fever; blood pressure, pulse and NEWS2 trend; signs of hypovolaemia or fluid overload; weight where clinically indicated; creatinine compared with baseline; urea, potassium and bicarbonate; urinalysis; recent illness, surgery or sepsis; medicines that may affect renal function; and possible urinary obstruction.

In a catheterised patient, check the drainage system for visible kinks, dependent loops and bag position according to local policy. Do not irrigate, manipulate or replace a catheter unless this is within your competence, authorised role and local policy.

When Should You Escalate?

Escalate promptly according to local policy if you identify new or persistent oliguria or anuria, a rising creatinine or AKI warning, hyperkalaemia, worsening acidosis, hypotension or deteriorating NEWS2, suspected sepsis or shock, new breathlessness or pulmonary oedema, significant haematuria/proteinuria, suspected obstruction, an unexplained fluid-balance change, or concern about medicine-related kidney harm or accumulation.

Use observation trends, fluid balance, blood results and the patient’s clinical appearance together. Do not wait for severe oliguria before sharing a genuine concern.

Bleepbook Memory Line

The kidneys do not lie, but they do need interpreting.

Urine output and creatinine can show that something has changed. Neither tells you the cause on its own.

Perfusion. Kidney tissue. Obstruction. Then look at the whole patient.

The Takeaway

The kidneys filter plasma, selectively reabsorb useful substances, excrete metabolic waste and many medicines, regulate water and electrolytes, maintain acid–base balance, influence blood pressure, produce erythropoietin and activate vitamin D.

So yes, they make urine. But reducing the kidneys to urine production is like saying a smartphone “just tells the time”.

References

National Institute for Health and Care Excellence (NICE) (2024) Acute kidney injury: prevention, detection and management. NG148. Available at: NICE NG148.

UK Kidney Association (2019) Clinical Practice Guideline: Acute Kidney Injury. Available at: UK Kidney Association.

UK Kidney Association (2024) Anaemia in Chronic Kidney Disease. Available at: UK Kidney Association.

Think Kidneys (n.d.) Information for the public: Chronic Kidney Disease. Available at: Think Kidneys.