The kidneys are among the most sophisticated organs in the body. Each day, they filter about 180 litres of blood plasma, reclaim almost all of it, and produce only 1–2 litres of urine. That selective filtration and recovery is the kidney’s masterwork. Understanding how the kidney achieves this — the structure of the nephron, the processes of filtration, reabsorption, secretion, and concentration — is central to both NEET preparation and understanding human physiology.
Key Terms & Definitions
Nephron: The structural and functional unit of the kidney. Each kidney contains approximately 1 million nephrons.
Glomerulus: A tuft of capillaries inside the Bowman’s capsule. The site of ultrafiltration. High blood pressure forces fluid from blood into the Bowman’s capsule.
Bowman’s capsule: Cup-shaped structure surrounding the glomerulus. Collects the filtered fluid (glomerular filtrate).
Renal tubule: The tubular portion of the nephron where reabsorption, secretion, and concentration of filtrate occur. Consists of proximal convoluted tubule (PCT), loop of Henle, distal convoluted tubule (DCT), and collecting duct.
Glomerular Filtration Rate (GFR): Volume of filtrate produced per unit time. Normal human GFR: ~125 mL/min (~180 L/day).
Ultrafiltration: High-pressure filtration in the glomerulus that forces water, ions, glucose, amino acids, urea, and other small molecules from blood into the Bowman’s capsule. Large molecules (plasma proteins, blood cells) are retained.
Tubular reabsorption: The recovery of useful substances (glucose, amino acids, most water, Na⁺, K⁺) from the filtrate back into the blood.
Tubular secretion: Active transfer of waste substances (creatinine, H⁺, K⁺, some drugs) from blood into the tubular fluid.
Osmoregulation: Regulation of blood osmolarity and water content. The kidney is the primary osmoregulatory organ in vertebrates.
ADH (Antidiuretic hormone): Released by the posterior pituitary when blood osmolarity rises. Makes the collecting duct more permeable to water → more water reabsorption → concentrated urine.
Aldosterone: Mineralocorticoid hormone from the adrenal cortex. Stimulates Na⁺ reabsorption and K⁺ secretion in the DCT and collecting duct → water follows Na⁺ → blood volume increases.
Kidney Structure
Gross Anatomy
Each kidney is bean-shaped, about 10–12 cm long. The outer region is the cortex (contains glomeruli and convoluted tubules). The inner region is the medulla (contains loops of Henle and collecting ducts, organised into renal pyramids). The apex of each pyramid opens into a calyx → renal pelvis → ureter → urinary bladder.
Blood supply: The renal artery brings all blood to be filtered. About 20–25% of cardiac output goes to the kidneys at rest — an enormous blood flow relative to kidney mass.
Nephron Structure
Two types of nephrons:
- Cortical nephrons (~85%): Short loops of Henle that barely penetrate the medulla. Less important for urine concentration.
- Juxtamedullary nephrons (~15%): Long loops of Henle that penetrate deep into the medulla. These are critical for producing concentrated urine.
Parts of a nephron in order:
- Bowman’s capsule (surrounding the glomerulus)
- Proximal Convoluted Tubule (PCT) — in the cortex
- Loop of Henle (descending and ascending limbs) — dips into medulla
- Distal Convoluted Tubule (DCT) — in the cortex
- Collecting duct — passes through medulla to renal pelvis
Process 1: Glomerular Filtration (Ultrafiltration)
Blood enters the glomerulus via the afferent arteriole (wider) and leaves via the efferent arteriole (narrower). The difference in diameters creates high blood pressure within the glomerular capillaries (~60–75 mmHg versus normal capillary pressure of ~35 mmHg).
This pressure forces water and small solutes through three filtration barriers:
- Capillary endothelium (fenestrated — has pores)
- Basement membrane (negatively charged — repels proteins)
- Podocyte foot processes of Bowman’s capsule (filtration slits)
What passes: Water, glucose, amino acids, Na⁺, K⁺, Cl⁻, HCO₃⁻, urea, creatinine, uric acid. What is retained: Plasma proteins (albumin, globulins), blood cells (too large for filtration slits), protein-bound substances.
The filtrate entering the Bowman’s capsule is called glomerular filtrate or primary urine — it has the same composition as blood plasma minus proteins.
GFR = 125 mL/min × 1440 min/day = 180 L/day of filtrate produced. But only 1–2 L becomes urine — so 99% of the filtrate is reabsorbed!
Why such a high filtration rate? Because the kidney needs a high throughput to accurately regulate blood composition. If you only filtered 1 L/day, small changes in blood composition would be very difficult to fine-tune. The high GFR allows the kidney to make continuous, precise adjustments to blood pH, ion concentrations, and osmolarity.
Process 2: Tubular Reabsorption
As the filtrate moves through the renal tubule, almost everything useful is recovered:
Proximal Convoluted Tubule (PCT)
The PCT does the bulk of reabsorption — about 65–70% of filtered Na⁺, water, and Cl⁻ is reabsorbed here, along with 100% of glucose and amino acids (in a healthy person).
Glucose reabsorption: Active transport (Na⁺-glucose cotransporter). Glucose is completely reabsorbed because blood glucose levels are below the renal threshold (~180 mg/dL). Above this threshold (as in uncontrolled diabetes), the transporters are saturated and glucose appears in urine (glucosuria).
Na⁺ reabsorption: Na⁺ is actively pumped from tubular cells into the interstitial fluid by Na⁺/K⁺-ATPase on the basolateral side. Na⁺ enters tubular cells from filtrate via various cotransporters (with glucose, amino acids) and exchangers.
Water reabsorption: Follows Na⁺ by osmosis. PCT cells are highly permeable to water (many aquaporins). This is called obligatory water reabsorption.
HCO₃⁻ reabsorption: Critical for acid-base balance. PCT reabsorbs ~80% of filtered bicarbonate.
Loop of Henle — Counter-current Multiplier
This is where the kidney builds the concentration gradient in the medulla that enables it to produce concentrated urine:
Descending limb (permeable to water, not ions): As filtrate descends into the hypertonic medulla, water leaves by osmosis → filtrate becomes concentrated (osmolarity rises from ~300 mOsm at the top to ~1200 mOsm at the hairpin turn).
Ascending limb (permeable to ions, not water): Na⁺, K⁺, Cl⁻ are actively pumped out into the medullary interstitium. But water cannot follow (this segment lacks aquaporins). Filtrate becomes dilute as it rises (osmolarity falls from ~1200 to ~100 mOsm entering the DCT).
The net result: a concentration gradient is established in the medulla, high at the inner medulla (near the papilla), low at the cortex. This gradient drives water reabsorption in the collecting duct.
A memory aid for the loop of Henle: “D-ow-n is D-iffusion of water (osmosis); U-p is active ion transport U-p and out.” Descending = water leaves by osmosis. Ascending = ions pumped out.
Distal Convoluted Tubule (DCT)
The DCT is the fine-tuning site — it adjusts Na⁺, K⁺, H⁺, and HCO₃⁻ based on hormonal signals:
- Aldosterone (from adrenal cortex): Stimulates Na⁺ reabsorption and K⁺ secretion in the DCT. Triggered by low blood pressure (via angiotensin II) or high K⁺.
- PTH (Parathyroid hormone): Stimulates Ca²⁺ reabsorption in the DCT.
- H⁺ secretion: Important for pH regulation. DCT cells secrete H⁺ (using carbonic anhydrase) to acidify urine.
Collecting Duct — ADH Control
The collecting duct passes through the hypertonic medullary gradient built by the loop of Henle. Whether the kidney produces concentrated or dilute urine depends entirely on water permeability of the collecting duct, which is controlled by ADH:
High ADH (when blood is concentrated/dehydrated): ADH inserts aquaporin-2 (AQP2) water channels into collecting duct cells → water flows out by osmosis into the hypertonic medulla → concentrated urine produced.
Low ADH (when blood is dilute/overhydrated): No AQP2 insertion → collecting duct is water-impermeable → dilute urine produced.
Normal urine osmolarity ranges from 50–1200 mOsm depending on hydration status. Maximum concentration of human urine is ~1200–1400 mOsm — about 4× more concentrated than blood plasma (~300 mOsm).
Process 3: Tubular Secretion
While reabsorption moves substances from the tubule into blood, secretion does the reverse — substances move from blood (peritubular capillaries) into the tubular fluid:
- H⁺: Secreted in PCT and DCT. Critical for maintaining blood pH at 7.35–7.45.
- K⁺: Secreted in DCT and collecting duct (regulated by aldosterone).
- Creatinine: Secreted in the PCT. Used clinically to measure kidney function (GFR estimation).
- Organic acids and drugs (penicillin, aspirin, some diuretics): Secreted by the PCT.
- NH₄⁺: Produced in tubular cells from glutamine. Secreted into filtrate to carry acid out of the body.
Secretion allows the kidney to eliminate substances that were not filtered initially (because they were protein-bound) or that need to be cleared rapidly.
Urine Formation — Final Composition
After filtration, reabsorption, and secretion, the final urine contains:
- Urea: ~200× more concentrated than blood (kidney is excellent at concentrating urea)
- Creatinine: Not reabsorbed at all — entirely excreted
- Uric acid: Partially reabsorbed, partially secreted
- Na⁺, K⁺, Cl⁻: Variable depending on dietary intake and hormonal status
- NO glucose (in healthy people)
- NO protein (absence indicates normal glomerular function)
Normal urine is slightly acidic (pH 4.5–8, usually ~6) and yellow due to urochrome (a pigment from haemoglobin breakdown).
Hormonal Regulation of Kidney Function
The kidney doesn’t work in isolation — it responds to multiple hormones:
| Hormone | Source | Effect on Kidney |
|---|---|---|
| ADH (vasopressin) | Posterior pituitary | Increases water reabsorption in collecting duct |
| Aldosterone | Adrenal cortex | Increases Na⁺ reabsorption, K⁺ secretion in DCT/CD |
| ANP (Atrial natriuretic peptide) | Heart atria (when stretched) | Decreases Na⁺ reabsorption, increases urine output |
| PTH | Parathyroid glands | Increases Ca²⁺ reabsorption in DCT |
| Renin | Juxtaglomerular cells | Initiates RAAS cascade → angiotensin II → aldosterone |
Solved Examples
Example 1 — CBSE Level
Q: Why is glucose normally absent in urine but present in urine of diabetic patients?
A: Glucose is freely filtered at the glomerulus. In healthy individuals, all filtered glucose is reabsorbed in the PCT by Na⁺-glucose cotransporters. These transporters have a maximum capacity — the renal threshold for glucose is ~180 mg/dL (blood glucose concentration).
In uncontrolled diabetes mellitus, blood glucose exceeds 180 mg/dL. The transporters become saturated — they are working at maximum capacity but cannot reabsorb all the filtered glucose. Excess glucose remains in the tubule and is excreted in urine (glucosuria). The presence of glucose in urine is a diagnostic indicator of diabetes.
Example 2 — NEET Level
Q: How does ADH regulate urine concentration? What would happen if ADH secretion stopped completely?
A: ADH (antidiuretic hormone) is released by the posterior pituitary when blood osmolarity rises (dehydration) or blood volume falls. ADH binds to V2 receptors on collecting duct cells → activates cAMP signalling → aquaporin-2 (AQP2) channels are inserted into the apical membrane → collecting duct becomes permeable to water → water moves from the tubular fluid into the hypertonic medullary interstitium by osmosis → water returns to blood → concentrated urine is produced.
If ADH stopped completely: The collecting duct remains impermeable to water. Despite the hypertonic medulla, water cannot leave the tubule. Dilute urine (as dilute as ~50 mOsm) would be produced in enormous volumes (10–15 L/day). This condition is called diabetes insipidus — characterised by polyuria (excessive dilute urine) and polydipsia (excessive thirst).
Example 3 — Challenging
Q: A patient has protein in urine (proteinuria). What part of the nephron is likely damaged?
A: Protein in urine indicates that plasma proteins (normally retained during filtration) are passing into the tubule and are not reabsorbed. The filtration barrier consists of: fenestrated capillary endothelium, glomerular basement membrane (GBM), and podocyte foot processes.
Damage to any of these components allows protein leakage into the filtrate. The most common cause is damage to the glomerular basement membrane or podocyte injury — seen in nephrotic syndrome, diabetic nephropathy, and glomerulonephritis. Since the proximal tubule can only reabsorb small amounts of protein, most of the leaked protein appears in the urine.
Exam-Specific Tips
NEET (Chapter 19 — Excretory Products): Focus on: (1) full structure and function of each nephron segment, (2) counter-current mechanism in the loop of Henle — this is a high-frequency conceptual question, (3) ADH and aldosterone mechanisms, (4) GFR calculation type questions (125 mL/min × time), (5) the conditions diagnosed from urine analysis (glucosuria → diabetes; proteinuria → glomerular damage; haematuria → kidney stones or infection).
CBSE Class 11/12: Diagrams are important. Practise drawing and labelling the nephron with all parts and the associated blood vessels (afferent arteriole, glomerulus, efferent arteriole, peritubular capillaries, vasa recta). Know the difference between cortical and juxtamedullary nephrons and why it matters.
Common Mistakes to Avoid
Mistake 1 — Glomerular filtration is based on size only: The glomerular filtration barrier has both size and charge selectivity. The GBM is negatively charged, which repels negatively charged proteins (like albumin). This is why even small proteins (which might fit through pore size) are retained.
Mistake 2 — All reabsorption is active transport: While Na⁺ reabsorption is active (Na⁺/K⁺-ATPase), water reabsorption is entirely passive (osmosis) — it follows the osmotic gradient created by Na⁺ reabsorption. Glucose and amino acids use secondary active transport (co-transport with Na⁺). Students sometimes say “water is actively reabsorbed” — incorrect.
Mistake 3 — The loop of Henle is entirely in the medulla: The PCT and DCT are entirely in the cortex. Only the loop of Henle dips into the medulla. Students sometimes place the whole nephron in the medulla.
Mistake 4 — ADH is produced in the anterior pituitary: ADH is produced in the hypothalamus (by neurosecretory cells) and stored/released from the posterior pituitary. The distinction matters — some questions ask about the site of production vs release.
Practice Questions
Q1: What is the significance of the counter-current mechanism in the loop of Henle?
The counter-current mechanism creates a high osmolarity gradient in the medulla (300 mOsm at the cortex → ~1200 mOsm deep in the medulla). This gradient is essential for concentrating urine.
The descending limb loses water (permeable to water, impermeable to ions). The ascending limb pumps ions out (impermeable to water, active ion transport). Because these two flows run in opposite directions (“counter-current”), they amplify the medullary gradient — each segment of the descending limb is in contact with the ascending limb that has already concentrated the medulla further down.
Without this gradient, the collecting duct would have no driving force to reabsorb water even if ADH were present. The counter-current multiplier of the loop of Henle is what makes concentrated urine possible.
Q2: What is the renin-angiotensin-aldosterone system (RAAS) and how does it regulate blood pressure?
When blood pressure falls or blood Na⁺ is low, juxtaglomerular (JG) cells in the afferent arteriole wall secrete renin. Renin cleaves angiotensinogen (from the liver) to angiotensin I. ACE (angiotensin-converting enzyme) in the lung converts angiotensin I to angiotensin II.
Angiotensin II acts to: (1) constrict blood vessels (raises blood pressure directly); (2) stimulate the adrenal cortex to release aldosterone; (3) stimulate ADH release from the posterior pituitary; (4) stimulate thirst.
Aldosterone increases Na⁺ reabsorption in the DCT and collecting duct → water follows Na⁺ → blood volume and blood pressure increase.
This RAAS cascade restores blood pressure. ACE inhibitors (common antihypertensive drugs like enalapril) block this cascade, reducing blood pressure in hypertensive patients.
Q3: Why do marathon runners sometimes experience hyponatraemia (low blood Na⁺) after races?
During a marathon, runners lose salt in sweat and drink large amounts of plain water (or water-based drinks). If they drink excessive water without replacing lost Na⁺, blood Na⁺ concentration falls.
The kidneys cannot solve this problem quickly because:
- Low blood osmolarity (low Na⁺) suppresses ADH → more dilute urine is produced
- But if the runner keeps drinking excessive water, the kidneys cannot excrete water fast enough (maximum urine flow is ~20 mL/min)
Result: Blood becomes hypo-osmolar → cells swell from osmosis → brain cells swell → neurological symptoms (confusion, seizures). Severe hyponatraemia can be fatal.
Prevention: Drink sports drinks with electrolytes (Na⁺, K⁺) rather than plain water, especially in long events.
FAQs
Q: How is kidney function measured clinically? The most common test is serum creatinine — creatinine is produced at a relatively constant rate (from muscle creatine metabolism), is freely filtered, and barely secreted/reabsorbed. Blood creatinine levels inversely reflect GFR: when GFR falls (kidney damage), creatinine accumulates. GFR can be estimated from serum creatinine using the CKD-EPI or MDRD formula. A more accurate measurement uses creatinine clearance: collect 24-hour urine, measure creatinine in urine and plasma, calculate GFR = (urine creatinine × urine volume) / plasma creatinine.
Q: Can you survive with just one kidney? Yes — the remaining kidney undergoes compensatory hypertrophy (increases in size and functional capacity) to maintain adequate filtration. GFR with one kidney is typically 60–75% of normal two-kidney GFR — sufficient for a healthy life. Kidney donors live normal life expectancy.
Q: Why does drinking alcohol cause dehydration? Ethanol inhibits ADH secretion from the posterior pituitary. Without ADH, the collecting duct becomes impermeable to water → dilute urine is produced in large volumes → dehydration. This is why alcoholic beverages cause frequent urination and a hangover thirst the next morning.
Q: What is the difference between the kidney and the juxtaglomerular apparatus? The juxtaglomerular apparatus (JGA) is a specialised structure at the junction of the afferent arteriole and the DCT. It consists of juxtaglomerular (JG) cells (granular cells in the afferent arteriole wall that secrete renin) and the macula densa (specialised DCT cells that sense Na⁺ and Cl⁻ concentration in the tubular fluid). The JGA is the kidney’s blood pressure sensor and regulator — it monitors both blood pressure (via JG cells) and tubular Na⁺ delivery (via macula densa), and adjusts renin secretion accordingly.