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.
• Located behind the peritoneum in the posterior abdomen.
• Positioned on either side of the vertebral column.
• Partially protected by the lower ribs.

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 produced by the kidneys flows through the ureters to the bladder.

🔬 Meet the Nephron: The Kidney’s Working Unit

Each kidney contains around one million nephrons, although the number varies between individuals.

A nephron includes:

• The glomerulus.
• Bowman’s capsule.
• Proximal convoluted tubule.
• Loop of Henle.
• Distal convoluted tubule.
• Connections to the collecting-duct system.

The easiest way to understand kidney function is:

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

1. Filtration

Blood enters the glomerulus, a specialised network of capillaries. Water and small solutes move into Bowman’s capsule to form glomerular filtrate.

Blood cells and most large proteins are normally retained within the circulation.

2. Reabsorption

As filtrate travels through the tubules, the kidneys return useful substances to the blood, including:

• Most filtered water.
• Sodium and other electrolytes.
• Bicarbonate.
• Glucose and amino acids under normal conditions.

3. Secretion

Selected substances move from the blood into the tubular fluid. This contributes to the removal of hydrogen ions, potassium, some medicines and other compounds.

4. Excretion

What remains eventually becomes urine and passes through the collecting system, renal pelvis and ureter to the bladder.

🧪 Around 180 Litres Filtered, But Not 180 Litres of Urine

A commonly quoted estimate is that healthy adult kidneys form approximately 180 litres of glomerular filtrate each day.

That figure is based on a typical glomerular filtration rate of about 125 mL per minute:

125 mL × 60 minutes × 24 hours ≈ 180 litres

It does not mean 180 litres of completely separate blood passes through once. Water and small solutes from the plasma are filtered repeatedly as blood continually circulates through the kidneys.

Actual filtration varies with factors such as body size, age, sex, pregnancy, blood pressure and kidney function.

Most of that filtered water and its useful contents are reabsorbed. Only a small proportion leaves the body as urine, often around one to two litres daily in a typical adult, although urine volume varies considerably with fluid intake, losses, medication, illness and kidney function (Cleveland Clinic, 2025).

Your kidneys are not simply removing waste. They are continually deciding what should be:

• Retained.
• Returned.
• Adjusted.
• Secreted.
• Excreted.

That is what makes them impressive.

💧 What Happens During Dehydration?

When the body loses water, reduced circulating volume and increased plasma osmolality trigger several regulatory responses.

These include:

• Increased release of antidiuretic hormone, also called vasopressin.
• Activation of the renin–angiotensin–aldosterone system.
• Increased thirst.
• Greater renal conservation of water and sodium.
• Production of a smaller volume of more concentrated urine.

The kidneys do not simply “go on strike”. They respond to hormonal and haemodynamic signals in an attempt to preserve circulating volume and maintain blood pressure.

However, significant hypovolaemia can reduce renal perfusion and glomerular filtration. If severe or prolonged, this can contribute to acute kidney injury.

Possible signs of dehydration or hypovolaemia may include:

• Thirst.
• Dry mucous membranes.
• Reduced urine output.
• Darker, concentrated urine.
• Tachycardia.
• Postural symptoms.
• Hypotension.
• Altered cognition.
• Delayed capillary refill.

None of these signs should be interpreted alone. Dark urine does not automatically equal dehydration, and reduced urine output is not always caused by poor fluid intake.

🫀 The Kidneys Help Regulate Blood Pressure

Specialised cells within the kidney can release renin when they detect signals such as reduced renal perfusion, reduced sodium chloride delivery or sympathetic stimulation.

Renin initiates the renin–angiotensin–aldosterone system:

1. Renin contributes to the conversion of angiotensinogen to angiotensin I.
2. Angiotensin-converting enzyme helps convert angiotensin I to angiotensin II.
3. Angiotensin II promotes vasoconstriction.
4. Aldosterone supports sodium retention, with water following.
5. Antidiuretic hormone and thirst may also contribute to restoring circulating volume.

This system can help maintain blood pressure and organ perfusion. Persistent or inappropriate activation, however, may contribute to hypertension and cardiovascular disease.

The kidneys and blood pressure have a two-way relationship:

• Kidney function influences blood pressure.
• Persistent high blood pressure can damage the kidneys.

⚖️ They Are Electrolyte and Acid–Base Managers

Healthy kidneys help regulate concentrations of:

• Sodium.
• Potassium.
• Calcium.
• Phosphate.
• Magnesium.
• Bicarbonate.
• Hydrogen ions.

They also contribute to acid–base balance by reabsorbing bicarbonate and excreting acid.

This is why impaired kidney function can become dangerous even before anyone is worried about urine itself. Complications may include:

• Hyperkalaemia.
• Metabolic acidosis.
• Fluid overload.
• Pulmonary oedema.
• Uraemic complications.

NICE recommends immediate referral for renal replacement therapy when complications such as hyperkalaemia, metabolic acidosis, uraemic symptoms, fluid overload or pulmonary oedema are not responding to medical management (NICE, 2024).

🩸 Your Kidneys Talk to the Bone Marrow

The kidneys produce erythropoietin, commonly shortened to EPO.

EPO signals the bone marrow to increase red blood-cell production. When kidney function is severely or chronically impaired, reduced EPO production can contribute to anaemia (Oxford University Hospitals NHS Foundation Trust, 2026).

So when a patient with chronic kidney disease has a low haemoglobin, the explanation may involve more than iron intake or bleeding.

🦴 They Also Activate Vitamin D

The kidneys convert vitamin D into its active hormonal form, calcitriol.

involve moreCalcitriol supports calcium and phosphate regulation and contributes to bone health. Reduced kidney function can disrupt this process, contributing to abnormalities involving calcium, phosphate, parathyroid hormone and bone metabolism.

Once again: the kidneys are doing far more than making urine.

🚨 Is Urine Output an Early Warning Sign?

It can be, but it is not a perfect kidney alarm.

Reduced urine output may occur with:

• Hypovolaemia.
• Sepsis.
• Shock.
• Heart failure.
• Reduced renal perfusion.
• Intrinsic kidney injury.
• Urinary obstruction.
• A blocked, kinked or displaced catheter.
• Some medicines.
• Normal physiological variation.

NICE defines oliguria as urine output below 0.5 mL/kg/hour and includes persistent oliguria within the diagnostic criteria for acute kidney injury (NICE, 2024).

However:

• AKI can occur without oliguria.
• Oliguria can occur before creatinine rises.
• Reduced output does not reveal the cause by itself.
• A catheter bag containing little urine does not automatically prove kidney failure.

Urine output is one part of the clinical picture, not the whole diagnosis.

🧠 Why Creatinine Is Not a Perfect Warning Light

Creatinine is produced through normal muscle metabolism and is cleared mainly by the kidneys.

When glomerular filtration falls, serum creatinine often rises. Comparing the current result with the patient’s baseline can therefore help detect acute changes in kidney function.

NICE criteria for detecting AKI include:

• A serum creatinine rise of 26 micromol/L or more within 48 hours.
• A rise of 50% or more within the previous seven days.
• Urine output below 0.5 mL/kg/hour for more than six hours in adults (NICE, 2024).

But creatinine has limitations:

• It may take time to rise after kidney injury.
• It is influenced by muscle mass.
• A frail person may have significant renal impairment without a markedly raised creatinine.
• A muscular person may naturally have a higher baseline.
• Fluid balance can affect the measured concentration.
• It does not explain whether the cause is pre-renal, intrinsic renal or post-renal.
• A single result is less informative than the trend and clinical context.

A raised creatinine is not always caused by reduced perfusion, and a normal-looking creatinine does not always guarantee normal kidney function.

The useful question is not:

“Is the creatinine high?”

It is:

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

🔍 Three Broad Places the Problem Can Begin

A useful framework for AKI is:

Pre-renal: before the kidney

The kidneys may be structurally intact but receiving inadequate perfusion.

Possible causes include:

• Hypovolaemia.
• Haemorrhage.
• Sepsis.
• Hypotension.
• Reduced cardiac output.

Intrinsic renal: within the kidney

The kidney tissue itself is affected.

Possible causes include:

• Acute tubular injury.
• Glomerulonephritis.
• Interstitial nephritis.
• Vascular disorders.
• Nephrotoxic exposure.

Post-renal: after the kidney

Urinary outflow is obstructed.

Possible causes include:

• Prostatic enlargement.
• Stones.
• Tumours.
• Ureteric obstruction.
• Blocked urinary catheters.

This framework helps organise thinking, but patients may have more than one contributing factor.

Student Nurse POV: What Should You Notice?

When caring for a patient at risk of kidney injury, look beyond the number in the urine bag.

Consider:

• Current urine output and the trend.
• Whether output has been measured accurately.
• Fluid intake and other losses.
• Vomiting, diarrhoea, drains, bleeding or fever.
• Blood pressure, pulse and NEWS2 trend.
• Signs of hypovolaemia or fluid overload.
• Peripheral or pulmonary oedema.
• Daily weight where prescribed.
• Serum creatinine compared with baseline.
• Urea, potassium, bicarbonate and eGFR.
• Urinalysis results.
• Recent illness, surgery or sepsis.
• Medicines that may affect kidney function.
• Possible urinary obstruction.
• Whether a catheter is kinked, blocked, displaced or positioned incorrectly.

Do not flush, manipulate or replace a catheter unless authorised, competent and following local policy.

📞 When Should You Escalate?

Escalate promptly if you identify:

• New or persistent oliguria.
• Anuria.
• A rising creatinine or confirmed AKI alert.
• Hyperkalaemia.
• Worsening acidosis.
• Hypotension or deteriorating NEWS2.
• Signs of sepsis or shock.
• New breathlessness, oedema or suspected pulmonary oedema.
• Haematuria or significant proteinuria.
• Suspected urinary obstruction.
• A sudden unexplained change in fluid balance.
• Concern that a medicine may be accumulating or causing harm.

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

🧠 Bleepbook Memory Line

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

Urine output and creatinine can reveal that something has changed. They cannot, by themselves, tell you exactly why.

Think:

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

The Takeaway

The kidneys:

• Filter plasma.
• Reabsorb useful substances.
• Excrete waste and many medicines.
• Regulate fluid and electrolytes.
• Maintain acid–base balance.
• Influence blood pressure.
• Produce erythropoietin.
• Activate vitamin D.
• Support bone and cardiovascular health.

So yes, they make urine.

But reducing the kidneys to urine production is like saying a smartphone “just tells the time”.

References

Cleveland Clinic (2025) Kidneys: Location, anatomy, function and health. Available at: https://my.clevelandclinic.org/health/body/21824-kidney.

National Institute for Health and Care Excellence (NICE) (2024) Acute kidney injury: Prevention, detection and management. NG148. Available at: https://www.nice.org.uk/guidance/ng148.

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) (2025) Your kidneys and how they work. Available at: https://www.niddk.nih.gov/health-information/kidney-disease/kidneys-how-they-work.

Oxford University Hospitals NHS Foundation Trust (2026) Kidney disease: About your kidneys. Available at: https://www.ouh.nhs.uk/oku/about-kidneys/.

Think Kidneys (2017) Almost everything you need to know about your kidneys. Available at: https://www.thinkkidneys.nhs.uk/aki/wp-content/uploads/sites/2/2016/07/Infographic-poster-March-2017.pdf.